Episodes

6d ago

In this episode, the CardioNerds (Dr. Natalie Tapaskar, Dr. Jenna Skowronski, and Dr. Shazli Khan) discuss the process of heart transplantation from the initial donor selection to the time a patient is discharged with Dr. Dave Kaczorowski and Dr. Jason Katz. We dissect a case where we understand criteria for donor selection, the differences between DBD and DCD organ donors, the choice of vasoactive agents in the post-operative period, complications such as cardiac tamponade, and the choice of immunosuppression in the immediate post-operative period. Most importantly, we highlight the importance of multi-disciplinary teams in the care of transplant patients. Audio editing for this episode was performed by CardioNerds Intern, Dr. Julia Marques Fernandes. Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. CardioNerds Heart Success Series PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls When thinking about donor selection, you need to consider how much physiologic stress your recipient can tolerate, and this may guide your selection of “higher risk” or “lower risk” donors. The use of DCD donors has increased the potential donor pool and shortened waitlist times with very similar perioperative outcomes to DBD transplantation. Post-operative critical care management rests on a fundamental principle to apply as much inotropic/vasoactive therapy as needed to achieve some reasonable physiologic hemostasis, and then getting “the heck out of the way!” There are no standard regimens as practices vary across centers, but rest on providing adequate RV support, maintaining AV synchrony, and early resuscitation. The RV is fickle and doesn’t take a joke too well. RV dysfunction post-transplant is important to watch for, and it can be transient or require aggressive support. Don’t miss assessing for cardiac tamponade which can require surgical evacuation- “where there’s space, that space can be filled with fluid.” Induction immunosuppression post-transplant varies across centers, but some considerations for use may include (1) high sensitization of the patient, (2) high risk immunologic donor-recipient matching, and (3) recipient renal dysfunction to provide a calcineurin inhibitor (CNI) sparing regimen long term. Management of heart transplant patients is a multi-disciplinary effort that requires coordination amongst heart failure/transplant cardiologists, cardiac surgeons, anesthesiologists, pathology/immunologists and a slew of ancillary services. Without a dynamic and collaborative team, successful cardiac transplantation could not be possible. Notes Notes: Notes drafted by Dr. Natalie Tapaskar What are the basic components of donor heart selection? In practicality, it can be a very inexact science, but we use some basic selection criteria such as: (1) size matching (2) ischemic time (3) donor graft function (4) immunologic compatibility (5) age of the potential donor and recipient (6) severity of illness of the recipient (7) regional variation in donor availability When thinking about accepting older donors (>50 years old), we ideally would screen for donor coronary disease and try to keep ischemic times as short as possible. We may accept an older donor for a recipient who is highly sensitized, which leaves a smaller potential donor pool. There is no clear consensus on size matching, but the predicted heart mass is most used. We are generally more comfortable oversizing than under-sizing donor hearts. Serial echocardiography is important in potential donors as initially reduced ejection fractions can improve on repeat testing, and these organs should not be disregarded automatically. For recipients who are more surgically complex, (i.e. multiple prior sternotomies or complex anatomy), it’s probably preferable to avoid older donors with some graft dysfunction and favor donors with shorter ischemic times. What is the difference between DBD and DCD? DBD is donation after brain death- these donors meet criteria for brain death. Uniform Determination of Death Act 1980: the death of an individual is The irreversible cessation of circulatory and respiratory functions or The irreversible cessation of all functions of the entire brain, including those of the brain stem DCD is donation after circulatory death- donation of the heart after confirming that circulatory function has irreversibly ceased. Only donors in category 3 of the Maastricht Classification of DCD donors are considered for DCD donations: anticipated circulatory arrest (planned withdrawal of life-support treatment). DCD hearts can be procured via direct procurement or normothermic regional perfusion (NRP). The basic difference is the way the hearts are assessed, either on an external circuit or in the donor body. For the most complex recipient, DCD may not be utilized at some centers due to concern for higher rates of delayed graft function, but this is center specific and data is still evolving. What are some features surgeons consider when procuring the donor heart? Visual assessment of the donor heart is key in DBD or NRP cases. LV function may be hard to assess, but visually the RV can be inspected. Palpation of the coronary arteries is important to assess any calcifications or abnormalities. Ventricular arrhythmias at the time of procurement may be concerning. Key considerations in the procurement process: (1) Ensuring the heart remains decompressed at all times and doesn’t become distended (2) adequate cardioplegia delivery (3) aorta is cross-clamped properly all the way across the vessel (4) avoiding injury to adjacent structures during procurement What hemodynamic parameters should we monitor and what vasoactive agents are used peri-heart transplant? There is no consensus regarding vasoactive agent use post-transplant and practice varies across institutions. Some commonly seen regimens may include: (1) AAI pacing around 110 bpm to support RV function and preserve AV synchrony (2) inotropic agents such as epinephrine and dobutamine to support RV function (3) pulmonary vasodilators such as inhaled nitric oxide to optimize RV afterload Early post-transplant patients tend to have low cardiac filling pressures and require preload monitoring and resuscitation initially. Slow weaning of inotropes as the patient shows signs of stable graft function and hemodynamics. RV dysfunction may manifest as elevated central venous pressure with low cardiac index or hypotension with reducing urine output. Optimize inotropic support, volume status, metabolic status (acidosis and hypoxia), afterload (pulmonary hypertension), and assess for cardiac tamponade. Tamponade requires urgent take-back to the operating room to evacuate material. Refractory RV failure requires mechanical circulatory support, with early consideration of VA-ECMO. Isolated RV MCS may be used in the right clinical context. Why do pericardial effusions/cardiac tamponade happen after transplant? They are not uncommon after transplant and can be due to: Inherent size differences between the donor and recipient (i.e. if the donor heart is much smaller than the recipient’s original heart) Bleeding from suture lines and anastomoses, pacing wires, and cannulation sites Depending on the hemodynamic stability of the patient and the location of the effusion, these effusions may require urgent return to the OR for drainage/clot evacuation via reopening the sternotomy, mini thoracotomy, and possible pericardial windows. What are the basics of immunosuppression post-transplant? Induction immunosuppression is variably used and is center-specific. Considerations for using induction therapy may include: (1) high sensitization of the patient (2) younger patients or multiparous women with theoretically more robust immune systems (3) crossing of recipient antibodies with donor antigens (3) renal function to provide a CNI sparing regimen long term Some considerations for avoiding induction may include: (1) older age of the recipient (2) underlying comorbid conditions such as infections or frailty of the recipient What are expected activity restrictions post-transplant? Sternal precautions are important to maintain sternal wire integrity. Generally avoiding lifting >10 pounds in the first 4-12 weeks, no driving usually in the first 4 weeks, monitoring for signs and symptoms of wound infections, and optimizing nutrition and physical activity. Cardiac rehabilitation is incredibly important as soon as feasible. References Kharawala A , Nagraj S , Seo J , et al. Donation after circulatory death heart transplant: current state and future directions. Circ: Heart Failure. 2024;17(7). doi: 10.1161/circheartfailure.124.011678 Copeland H, Knezevic I, Baran DA, et al. Donor heart selection: Evidence-based guidelines for providers. The Journal of Heart and Lung Transplantation. 2023;42(1):7-29. doi:10.1016/j.healun.2022.08.030 Moayedifar R, Shudo Y, Kawabori M, et al. Recipient Outcomes With Extended Criteria Donors Using Advanced Heart Preservation: An Analysis of the GUARDIAN-Heart Registry. J Heart Lung Transplant. 2024;43(4):673-680. doi:10.1016/j.healun.2023.12.013 Kharawala A, Nagraj S, Seo J, et al. Donation After Circulatory Death Heart Transplant: Current State and Future Directions. Circ Heart Fail. 2024;17(7):e011678. doi:10.1161/CIRCHEARTFAILURE.124.011678 Copeland H, Hayanga JWA, Neyrinck A, et al. Donor heart and lung procurement: A consensus statement. J Heart Lung Transplant. 2020;39(6):501-517.

Dec 5

In this episode, the CardioNerds (Dr. Naima Maqsood, Dr. Akiva Rosenzveig, and Dr. Colin Blumenthal) are joined by renowned educator in electrophysiology, Dr. Joshua Cooper, to discuss everything atrial flutter; from anatomy and pathophysiology to diagnosis and management. Dr. Cooper’s expert teaching comes through as Dr. Cooper vividly describes atrial anatomy to provide the foundational understanding to be able to understand why management of atrial flutter is unique from atrial fibrillation despite their every intertwined relationship. A foundational episode for learners to understand atrial flutter as well as numerous concepts in electrophysiology. Audio editing for this episode was performed by CardioNerds intern Dr. Bhavya Shah. CardioNerds Atrial Fibrillation PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls "The biggest mistake is failure to diagnose”. Atrial flutter, especially with 2:1 conduction, is commonly missed in both inpatient and outpatient settings so look carefully at that 12-lead EKG so you can mitigate the stroke and tachycardia induced cardiomyopathy risk Decremental conduction of the AV node makes it more challenging to rate control atrial flutter than atrial fibrillation Catheter Ablation is the first line treatment for atrial flutter and is highly successful, but cardioversion can be utilized as well prior to pursuing ablation in some cases. Class I AADs like propafenone and flecainide may stability the atrial flutter circuit by slowing conduction and thus may worsen the arrhythmia. Therefore, the preferred anti-arrhythmic medication in atrial flutter are class III agents. Atrial flutter can be triggered by firing from the left side of the heart, so in patients with both atrial fibrillation and flutter, ablating atrial fibrillation makes atrial flutter less likely to recur. BONUS PEARL: Dr. Cooper’s youtube video on atrial flutter is a MUST SEE! Notes Notes: Notes drafted by Dr. Akiva Rosenzveig What are the distinguishing features of atrial fibrillation and flutter? Atrial flutter is an organized rhythm characterized by a wavefront that continuously travels around the same circuit leading to reproducible P-waves on surface EKG as well as a very mathematical and predictable relationship between atrial and ventricular activity Atrial fibrillation is an ever changing, chaotic rhythm that consists of small local circuits that interplay off each other. Consequently, no two beats are the same and the relationship between the atrial activity and ventricular activity is unpredictable leading to an irregularly irregular rhythm What are common atrial flutter circuits? Cavo-tricuspid isthmus (CTI)-dependent atrial flutter is the most common type of flutter. It is characterized by a circuit that circumnavigates the tricuspid valve. Typical atrial flutter is characterized by the circuit running in a counterclockwise pattern up the septum, from medial to lateral across the right atrial roof, down the lateral wall, and back towards the septum across the floor of the right atrium between the IVC and the inferior margin of the tricuspid valve i.e. the cavo-tricuspid isthmus. Surface EKG will show a gradual downslope in leads II, III, and AvF and a rapid rise at end of each flutter wave. Atypical CTI-dependent flutter follows the same route but in the opposite direction (clockwise). Therefore, we will see positive flutter waves in the inferior leads Mitral annular flutter is more commonly seen in atrial fibrillation patients who’ve been treated with ablation leading to scarring in the left atrium. Roof-dependent flutter is characterized by a circuit that travels around left atrium circumnavigating a lesion (often from prior ablation), traveling through the left atrial roof, down the posterior wall, and around the pulmonary veins Surgical/scar/incisional flutter is seen in people with a history of prior cardiac surgery and have iatrogenic scars in right atrium due to cannulation sites or incisions How does atrial flutter pharmacologic management differ from other atrial arrhythmias? The atrioventricular (AV) node is unique in that the faster it is stimulated, the longer the refractory period and the slower it conducts. This characteristic is called decremental conduction. In atrial fibrillation, the atrial rate is so fast that the AV node becomes overwhelmed and only lets some of those signals through to the ventricles creating an irregular tachycardia but at lower rates. In atrial flutter, the atrial rate is slower, therefore the AV node has more capability to conduct allowing for higher ventricular rates. Therefore, to achieve rate control one will need a higher dose of AV blocking medications. Atrial tachycardia may require even higher doses due to the increased ability of the AV node to conduct, as the atrial rates are slower than in atrial flutter. Sodium channel blockers (Class I) such as flecainide and propafenone slow wavefront propagation, making it easier for the AV node to handle the atrial rates. This will end up leading to increased ventricular rates which can be dangerously fast. That is why AV nodal blockers should be used in conjunction with flecainide and propafenone. What is the role of cardioversion in atrial flutter management? Due to high success rate with atrial flutter ablation, ablation is the first line treatment. However, sometimes cardioversion may be utilized in patients depending on how symptomatic they are and how long it will take to get an ablation. Cardioversion may also be utilized preferentially when the atrial flutter was triggered by infection or cardiac surgery to see if it will come back. If cardioversion is pursued, the patient will need to be anticoagulated due to the stroke risk after the procedure due to post-conversion stunning. How effective is atrial flutter ablation? The landmark Natale et al study in 2000 demonstrated 80% success rate after radiofrequency ablation as compared to 36% in patients on anti-arrhythmic therapy. The LADIP study in 2006 further corroborated these findings. Contemporary data shows above 90% success rate of atrial flutter ablation. In patients who have had both atrial fibrillation and atrial flutter, most electrophysiologists would ablate both. However, in patients with atrial fibrillation, the atrial flutter usually is initiated by trigger spots firing in the left atrium. Once the atrial fibrillation is ablated, the flutter will become less likely. Therefore, there are those who say there’s no need to ablate the flutter circuit as well. Alternatively, if a patient has severe comorbidities and/or is high risk for ablation, one may consider performing the atrial flutter ablation only since atrial flutter is harder to manage medically compared with atrial fibrillation. How do you manage atrial flutter in the acute inpatient setting? In the inpatient setting, electrical cardioversion is often limited by blood pressure and the hypotensive effects of the sedatives required. If one is awake and too hypotensive, chemical cardioversion can be pursued. The most effective anti-arrhythmic for this is ibutilide. Amiodarone is not effective for acute cardioversion. Since ibutilide prolongs refractoriness in atrial and ventricular tissue, there’s a risk of long QT induced torsades de pointes. Pretreating with magneisum reduces the risk to 1-2%. References Jolly WA, Ritchie WT. Auricular flutter and fibrillation. 1911. Ann Noninvasive Electrocardiol. 2003;8(1):92-96. doi:10.1046/j.1542-474x.2003.08114.x McMichael J. History of atrial fibrillation 1628-1819 Harvey - de Senac - Laënnec. Br Heart J. 1982;48(3):193-197. doi:10.1136/hrt.48.3.193 Lee KW, Yang Y, Scheinman MM; University of Califoirnia-San Francisco, San Francisco, CA, USA. Atrial flutter: a review of its history, mechanisms, clinical features, and current therapy. Curr Probl Cardiol. 2005;30(3):121-167. doi:10.1016/j.cpcardiol.200 2023 ACC/AHA/ACCP/HRS Guideline for the Diagnosis and Management of Atrial Fibrillation: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. Circulation. 2024;149(1):e167. doi:10.1161/ Cosío F. G. (2017). Atrial Flutter, Typical and Atypical: A Review. Arrhythmia & electrophysiology review, 6(2), 55–62. https://doi.org/10.15420/aer.2017.5.2 https://www.escardio.org/Journals/E-Journal-of-Cardiology-Practice/Volume-11/Atrial-flutter-common-and-main-atypical-forms Natale A, Newby KH, Pisanó E, et al. Prospective randomized comparison of antiarrhythmic therapy versus first-line radiofrequency ablation in patients with atrial flutter. J Am Coll Cardiol. 2000;35(7):1898-1904. doi:10.1016/s0735-1097(00)00635-5 Da Costa A, Thévenin J, Roche F, et al. Results from the Loire-Ardèche-Drôme-Isère-Puy-de-Dôme (LADIP) trial on atrial flutter, a multicentric prospective randomized study comparing amiodarone and radiofrequency ablation after the first episode of symptomatic atrial flutter. Circulation. 2006;114(16):1676-1681. doi:10.1161/CIRCULATIONAHA.106.638395 https://www.acc.org/Membership/Sections-and-Councils/Fellows-in-Training-Section/Section-Updates/2015/12/15/16/58/Atrial-Fibrillation#:~:text=The%20first%20'modern%20day'%20account,in%20open%20chest%20animal%20models.&text=In%201775%2C%20William%20Withering%20first,(purple%20foxglove)%20in%20AFib.

Nov 24

In this episode, the CardioNerds (Dr. Rachel Goodman, Dr. Shazli Khan, and Dr. Jenna Skowronski) discuss a case of AMI-shock with a focus on listing for heart transplant with faculty expert Dr. Kelly Schlendorf. We dive into the world of pre-transplant management, discuss the current allocation system, and additional factors that impact transplant timing, such as sensitization. We conclude by discussing efforts to increase the donor pool. Audio editing for this episode was performed by CardioNerds Intern, Julia Marques Fernandes. Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. CardioNerds Heart Success Series PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls The current iteration of heart allocation listing is based on priority, with status 1 being the highest priority. The are multiple donor and recipient characteristics to consider when listing a patient for heart transplantation and accepting a heart offer. Desensitization is an option for patients who need heart transplantation but are highly sensitized. Protocols vary by center. Acceptance of DCD hearts is one of many efforts to expand the donor pool Notes Notes: Notes drafted by Dr. Rachel Goodman Once a patient is determined to be a candidate for heart transplantation, how is priority determined? The current iteration of heart listing statuses was implemented in 2018. Priority is determined by acuity, with higher statuses indicating higher acuity and given higher priority. Status 1 is the highest priority status, and Status 7 is inactive patients. (1,2) What criteria should be considered in organ selection when listing a patient for heart transplant? Once it is determined that a patient will be listed for heart transplantation, there are certain criteria that should be assessed. These factors may impact pre-transplant care and/or donor matching (3). (1) PVR (2) Height/weight (3) Milage listing criteria (4) Blood typing/cPRA/HLA typing What is desensitization and why would it be considered? Desensitization is an attempt to reduce or remove anti-HLA antibodies in the recipient. It is done to increase the donor pool. In general, desensitization is reserved for patients who are highly sensitized. Desensitization protocols vary by transplant center, and some may opt against it. When considering desensitization, it is important to note two key things: first, there is no promise that it will work, and second desensitization involves the use of immunosuppressive agents, thereby putting patients at increased risk of infection and cytopenia. (4) Can you explain DCD and DBD transplant? DBD: donor that have met the requirements for legal definition of brain death. DCD: donors that have not met the legal definition of brain death but have been determined to have circulatory death. Because the brain death criteria have not been met, organ recovery can only take place once death is confirmed based on cessation of circulatory and respiratory function. Life support is only withdrawn following declaration of circulatory death—once the heart has stopped beating and spontaneous respirations have stopped. (5,6) References 1: Maitra NS, Dugger SJ, Balachandran IC, Civitello AB, Khazanie P, Rogers JG. Impact of the 2018 UNOS Heart Transplant Policy Changes on Patient Outcomes. JACC Heart Fail. 2023;11(5):491-503. doi:10.1016/j.jchf.2023.01.009 2: Shore S, Golbus JR, Aaronson KD, Nallamothu BK. Changes in the United States Adult Heart Allocation Policy: Challenges and Opportunities. Circ Cardiovasc Qual Outcomes. 2020;13(10):e005795. doi:10.1161/CIRCOUTCOMES.119.005795 3: Copeland H, Knezevic I, Baran DA, et al. Donor heart selection: Evidence-based guidelines for providers. J Heart Lung Transplant. 2023;42(1):7-29. doi:10.1016/j.healun.2022.08.030 4: Kittleson MM. Management of the sensitized heart transplant candidate. Curr Opin Organ Transplant. 2023;28(5):362-369. doi:10.1097/MOT.0000000000001096 5: Kharawala A, Nagraj S, Seo J, et al. Donation After Circulatory Death Heart Transplant: Current State and Future Directions. Circ Heart Fail. 2024;17(7):e011678. doi:10.1161/CIRCHEARTFAILURE.124.011678 6: Siddiqi HK, Trahanas J, Xu M, et al. Outcomes of Heart Transplant Donation After Circulatory Death. J Am Coll Cardiol. 2023;82(15):1512-1520. doi:10.1016/j.jacc.2023.08.006

Nov 20

CardioNerds (Dr. Kelly Arps, Dr. Naima Maqsood, and Dr. Elizabeth Davis) discuss chronic AF management with Dr. Edmond Cronin. This episode seeks to explore the chronic management of atrial fibrillation (AF) as described by the 2023 ACC/AHA/ACCP/HRS Guideline for the Diagnosis and Management of Atrial Fibrillation: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. The discussion covers the different AF classifications, symptomatology, and management including medications and invasive therapies. Importantly, the episode explores current gaps in knowledge and where there is indecision regarding proper treatment course, as in those with heart failure and AF. Our expert, Dr. Cronin, helps elucidate these gaps and apply guideline knowledge to patient scenarios. Audio editing for this episode was performed by CardioNerds intern Dr. Bhavya Shah. CardioNerds Atrial Fibrillation PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls Review the guidelines- Catheter ablation is a Class I recommendation for select patient groups Appropriately recognize AF stages- preAF conditions, symptomatology, classification system (paroxysmal, persistent, long-standing persistent, permanent) Be familiar with the EAST-AFNET4 trial, as it changed the approach of rate vs rhythm control Understand treatment approaches- lifestyle modifications, management of comorbidities, rate vs rhythm control medications, cardioversion, ablation, pulmonary vein isolation, surgical MAZE Sympathize with patients- understand their treatment goals Notes Notes: Notes drafted by Dr. Davis. What are the stages of atrial fibrillation? The stages of AF were redefined in the 2023 guidelines to better recognize AF as a progressive disease that requires different strategies at the different therapies Stage 1 At Risk for AF: presence of modifiable (obesity, lack of fitness, HTN, sleep apnea, alcohol, diabetes) and nonmodifiable (genetics, male sex, age) risk factors associated with AF Stage 2 Pre-AF: presence of structural (atrial enlargement) or electrical (frequent atrial ectopy, short bursts of atrial tachycardia, atrial flutter) findings further pre-disposing a patient to AF Stage 3 AF: patient may transition between these stages Paroxysmal AF (3A): intermittent and terminates within ≤ 7 days of onset Persistent AF (3B): continuous and sustained for > 7 days and requires intervention Long-standing persistent AF (3C): continuous for > 12 months Successful AF ablation (3D): freedom from AF after percutaneous or surgical intervention Stage 4 Permanent AF: no further attempts at rhythm control after discussion between patient and clinician The term chronic AF is considered obsolete and such terminology should be abandoned What are common symptoms of AF? Symptoms vary with ventricular rate, functional status, duration, and patient perception May present as an embolic complication or heart failure exacerbation Most commonly patients report palpitations, chest pain, dyspnea, fatigue, or lightheadedness. Vague exertional intolerance is common Some patients also have polyuria due to increased production of atrial natriuretic peptide Less commonly can present as tachycardia-associated cardiomyopathy or syncope Cardioversion into sinus rhythm may be diagnostic to help determine if a given set of symptoms are from atrial fibrillation to help guide the expected utility of more aggressive rhythm control strategies. What are the current guidelines regarding rhythm control and available options? COR-LOE 1B: In patients with reduced LV function and persistent (or high burden) AF, a trial of rhythm control should be recommended to evaluate whether AF is contributing to the reduced LV function COR-LOE 2a-B: In patients with reduced LV function and persistent (or high burden) AF, a trial of rhythm control should be recommended to evaluate whether AF is contributing to the reduced LV function. In patients with a recent diagnosis of AF (<1 year), rhythm control can be useful to reduce hospitalizations, stroke, and mortality. In patients with AF and HF, rhythm control can be useful for improving symptoms and improving outcomes, such as mortality and hospitalizations for HF and ischemia. In patients with AF, rhythm-control strategies can be useful to reduce the likelihood of AF progression. COR-LOE 2b-C: In patients with AF where symptoms associated with AF are uncertain, a trial of rhythm control (eg, cardioversion or pharmacological therapy) may be useful to determine what if any symptoms are attributable to AF. COR-LOE 2b-B: In patients with AF, rhythm-control strategies may be useful to reduce the likelihood of development of dementia or worsening cardiac structural abnormalities. While both rate and rhythm control can improve AF symptoms, several studies (such as AF-CHF) show improved quality of life with rhythm control EAST-AFNET 4 was significant in that it showed rhythm control was associated with a 25% reduction in the combined endpoint of mortality rate, stroke, and hospitalizations due to HF or ACS Acute rhythm control can be achieved with electrical or pharmacological cardioversion. Electrical is more effective and faster than pharmacological and is preferred for patients with hemodynamic instability attributable to AF. However, both approaches involved considerations for anticoagulation and thromboembolic risk. Pharmacologic options for cardioversion include ibutilide, amiodarone, flecainide, propafenone, procainamide, dofetilide, and sotalol. COR-LOE 1-A: In patients with symptomatic AF in whom antiarrhythmic drugs have been ineffective, contraindicated, not tolerated or not preferred, and continued rhythm control is desired, catheter ablation is useful to improve symptoms. AF ablation is also a suitable first-line option in some patients with paroxysmal AF to reduce recurrence and burden. Patient selection is important. Younger patients, those with minimal atrial enlargement, less myocardial fibrosis, and less persistent forms are more likely to have successful ablations, meaning less likely to have recurrence of AF after ablation. HFrEF patients derive greater benefit than others from AF ablation in terms of improved functional status, LV function, and cardiovascular outcomes Surgical ablation can be considered in those undergoing cardiac surgery for some other etiology such as valve surgery or CABG and is associated with increased survival, but some risk of pacemaker placement and renal dysfunction How would you monitor for AF recurrence in post-ablation or cardioversion? Is there a role for monitoring in every patient? Cardiac monitoring may be advised to AF patients for various reasons, such as for detecting recurrences, screening, or response to therapy Long-term surveillance to detect recurrent AF can be beneficial and can be accomplished by various modalities, including wearable devices, smart watches, random monitoring (Holter, event, mobile telemetry), and implantable loop recorders. This is especially helpful in those who had AF-induced cardiomyopathy, especially if their LVEF recovered after rate/rhythm control. This is a population in whom recurrence of AF would want to be promptly noted and addressed. Loop recorders can also be helpful in detecting subclinical AF or in patients with stroke or TIA of undetermined cause (COR-LOE 2a-B) What AF burden warrants intervention? It is important to recognize that AF is a chronic condition and tends to recur, so treatment often is focused on reducing risk of recurrence Patient-clinician shared decision making is important when deciding when/how to intervene, as there is no cut-off for “significant” burden (COR-LOE 1-B) What are some options for antiarrhythmic drugs and their characteristics? Antiarrhythmic drugs are reasonable for long-term maintenance of sinus rhythm for patients with AF who are not candidates for, or decline, catheter ablation, or who prefer antiarrhythmic therapy Amiodarone can be used in patients with or without HFrEF, as opposed to many other anti-arrhythmics that are (relatively) contraindicated in HFrEF or should be used with caution in such patients, such as flecainide, propafenone, dronedarone, and sotalol. However, due to its adverse effects and multiple drug interactions, is should be used only in patients in which other antiarrhythmic drugs are contraindications, ineffective, or not preferred. Dofetilide can also be used in patients with HFrEF. In patients on amiodarone, labs should be checked regularly for thyroid, liver and kidney functions. There is also a role for pulmonary function testing and chest x-rays to monitor for pulmonary fibrosis, but frequency is not clearly established. It should be noted that amiodarone-induced lung toxicity occurs between 6 months and 2 years of use. Flecainide is well tolerated, but is contraindicated in patients with significant coronary artery disease and possibly structural heart disease in general. It can also lead to the development of atrial flutter. Dofetilide and sotalol require regular renal function monitoring and QTC monitoring When should AV node ablation (AVNA) be considered? In patients with AF and uncontrolled rapid ventricular response refractory to rate-control medications (who are not candidates for or in whom rhythm control has been unsuccessful), AVNA can be useful to improve symptoms and QOL (COR-LOE 2a-B) AVNA is effective for rate control and does not require continuation of medications; however,

Nov 7

CardioNerds kicks off its advanced therapies series with Chair of the CardioNerds Heart Failure Council, Dr. Jenna Skowronski, co-chair of the series, Dr. Shazli Khan, and Episode FIT lead, Dr. Jason Feinman. In this first episode, they discuss the process of advanced therapies evaluation with Dr. Michelle Kittleson, Professor of Medicine and Director of Education in Heart Failure and Transplantation at Cedars-Sinai. In this case-based discussion, they cover the signs and symptoms of end-stage heart failure, the initial management strategies, and the diagnostic workup required when considering advanced therapies. Importantly, they discuss the special considerations for pursuing left-ventricular assist device (LVAD) versus heart transplantation as well as the multidisciplinary, team-based approach needed when advanced therapies are indicated. Notes were drafted by Dr. Shazli Khan. Audio editing for this episode was performed by CardioNerds Intern, Julia Marques Fernandes. Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. CardioNerds Heart Success Series PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls Guideline-directed medical therapy (GDMT) is indicated in all heart failure patients and improves survival, but progressive symptoms and intolerance to GDMT can be warning signs of disease progression. The I-NEED-HELP mnemonic is an excellent reference when considering referral for advanced therapies (Figure). Management of acute decompensation includes diuretics and possible inotropic support. The inotropic agent used should be whichever best suits your specific patient. Milrinone may result in more hypotension, whereas dobutamine may result in more tachycardia. Tachycardic and normotensive patients may do better with milrinone, while hypotensive patients with normal heart rates may do better with dobutamine. Notably, DoReMi found no difference between milrinone and dobutamine for patients with cardiogenic shock. The initial diagnostic evaluation includes an echocardiogram, right heart catheterization (RHC), and often cardiopulmonary exercise testing (CPET) to objectively assess the status of the heart. Comprehensive labs, imaging and cancer screening are also needed to assess all other organs. When making the decision to pursue advanced therapies, always ask: Is the heart sick enough? Is the rest of the body well enough? These two questions provide a framework to guide if patients are optimal candidates for transplant versus LVAD. The advanced therapies evaluation is a team sport! Patients will meet not only with advanced heart failure cardiologists, but also cardiac surgeons, psychiatrists, social workers, nutritionists and pharmacists. All team members are of critical value in the process. Notes 1.) What are the key features of advanced cardiomyopathy, and when should providers consider referral for advanced therapies? Advanced cardiomyopathy may present as recurrent hospitalizations for decompensated heart failure, intolerance to GDMT with symptomatic orthostasis and hypotension, and progressive symptoms of heart failure despite medical therapy. The I-NEED-HELP mnemonic is a helpful tool to identify patients at risk of heart failure and is defined as follows: Need for Inotropic support, New York Heart Association (NYHA) Class IV symptoms, End-Organ Dysfunction, Ejection fraction <20%, Defibrillator shocks for ventricular arrhythmias, Recurrent HF hospitalizations, Escalating diuretic dose, Low blood pressure and Progressive intolerance of GDMT. See the Figure designed by Dr. Gurleen Kaur. When patients demonstrate any of the above warning signs, they should be referred to advanced heart failure specialists for consideration of advanced therapies. 2.) What diagnostic testing is pursued when working up patients for advanced therapies? How does this workup differ whether you are in the inpatient or outpatient setting? Work-up generally answers two key questions: is the heart sick enough and is the rest of the body well enough? Workup includes an echocardiogram that may show specific features concerning for end-stage heart failure (EF <20%, dilated and remodeled left ventricle, reduced right ventricular function, etc.). A RHC provides information on the filling pressures of the heart for management in the acute setting, but also helps give an objective measure of the cardiac output to assess how sick the heart is. Importantly the RHC also provides key information on the presence of pulmonary hypertension. Obtaining a comprehensive metabolic panel provides valuable information on end-organ dysfunction, as kidney or liver abnormalities are suggestive of worsening disease. Outpatients presenting for referral may also undergo CPET as an objective confirmation of decreased functional capacity. Typically, a peak VO2 max of <14 mL/kg/min is indicative of advanced disease. CT imaging, as well as other cancer screening tools, may be employed to ensure there is no systemic disease that would prohibit advanced therapies. 3.) Who makes up the multidisciplinary advanced therapies team? The ACC/AHA/HFSA 2022 guidelines for heart failure support using a multidisciplinary team approach in managing HF. This collaborative care model has been shown to reduce hospital admissions and healthcare expenses while enhancing patient adherence to self-care practices and recommended medical treatments. The multidisciplinary team consists of cardiologists, cardiac surgeons, advanced practice providers, psychiatrists, pharmacists, social workers, nutritionists, and other specialists. 4.) What are the medical factors to consider when deciding between transplant versus LVAD, and what social determinants of health play a role? The medical evaluation and workup done during the advanced therapies evaluation help answer two crucial questions: Is the heart sick enough? Is the rest of the body well enough? All patients should be assessed for extracardiac disease that may impact survival after advanced therapies. While selection between transplant versus LVAD varies by program and institution, general principles considered include the allocation system and regional wait times, patient’s age, and extracardiac comorbidities. Generally, patients being considered for heart transplantation should be devoid of conditions that have a five-year survival of <70% or a ten-year survival of <50%. This is also because patients undergoing organ transplantation require immunosuppressive medications, which may further exacerbate their other systemic conditions. Social support and internal motivation also play a role, as it is important for patients to attend multiple follow-up appointments and maintain strict adherence to their immunosuppressive medications. Graphic - Stage D (Advanced) Heart Failure Designed by Dr. Gurleen Kaur References Morris AA, Khazanie P, Drazner MH, et al; American Heart Association Heart Failure and Transplantation Committee of the Council on Clinical Cardiology; Council on Arteriosclerosis, Thrombosis and Vascular Biology; Council on Cardiovascular Radiology and Intervention; Council on Hypertension. Guidance for timely and appropriate referral of patients with advanced heart failure: a scientific statement from the American Heart Association. Circulation. 2021;144(15):e238-e250. doi:10.1161/CIR.0000000000001016 https://www.ahajournals.org/doi/10.1161/CIR.0000000000001016 Truby LK, Rogers JG. Advanced heart failure: epidemiology, diagnosis, and therapeutic approaches. JACC Heart Fail. 2020;8(7):523-536. doi:10.1016/j.jchf.2020.01.014 https://www.sciencedirect.com/science/article/pii/S2213177920302080?via%3Dihub Heidenreich PA, Bozkurt B, Aguilar D, Allen LA, Byun JJ, Colvin MM, Deswal A, et al; ACC/AHA Joint Committee Members. 2022 AHA/ACC/HFSA guideline for the management of heart failure: a report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. Circulation. 2022;145(18):e895-e1032. doi:10.1161/CIR.0000000000001063 https://www.ahajournals.org/doi/10.1161/CIR.0000000000001063 Guglin M, Zucker MJ, Borlaug BA, Breen E, Cleveland J, Johnson MR, Panjrath GS, et al; ACC Heart Failure and Transplant Member Section and Leadership Council. Evaluation for heart transplantation and LVAD implantation: JACC Council perspectives. J Am Coll Cardiol. 2020;75(12):1471-1487. doi:10.1016/j.jacc.2020.01.034 https://www.sciencedirect.com/science/article/pii/S0735109720304150?via%3Dihub

Nov 5

In this second episode of a collaborative series with the AHA Women in Cardiology (WIC) Committee, CardioNerds (Dr. Gurleen Kaur and Dr. Anna Radhakrishnan) are joined by four leading experts in Cardio-Obstetrics to explore this rapidly evolving field. Dr. Rina Mauricio (Director of Women's Cardiovascular Health and Cardio-Obstetrics at UT Southwestern Medical Center), Dr. Afshan Hameed (Director of Maternal Fetal Medicine and Cardio-Obstetrics at UC Irvine), Dr. Doreen DeFaria Yeh (Co-director of the MGH Cardiovascular Disease and Pregnancy Program), and Dr. Garima Sharma (Director of Women's Cardiovascular Health and Cardio-Obstetrics at Inova) define Cardio-Ob as encompassing not only care of women during pregnancy, but also the complex decision-making that extends through the preconception and postpartum periods. From counseling patients with pre-existing or congenital heart disease before pregnancy to managing cardiovascular health during pregnancy and after delivery, they trace how the field has developed in response to the urgent need to address maternal mortality. Listeners will gain valuable insight into the multidisciplinary teamwork, patient-centered decision-making, and advocacy that drive this field - along with the importance of expanding Cardio-Ob education for clinicians and trainees, and innovations and system-level changes shaping its future. Audio editing by CardioNerds academy intern, Grace Qiu. This episode was planned in collaboration with the AHA CLCD Women in Cardiology Committee with mentorship from Dr. Monika Sanghavi. The PA-ACC & CardioNerds Narratives in Cardiology PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron!

Oct 29

Dr. Jeanne De Lavallaz and Dr. Ramy Doss discuss the results of the TRANSFORM-AF Trial with expert faculty Dr. Sanjeev Saksena and Dr. Varun Sundaram. The TRANSFORM-AF trial enrolled 2,510 patients with atrial fibrillation (AF), type 2 diabetes, and obesity across 170 Veterans Affairs hospitals to evaluate the impact of diabetes-dose GLP-1 receptor agonists on AF-related outcomes. Participants were assigned to receive either a GLP-1 receptor agonist, a DPP-IV inhibitor, or a sulfonylurea. The primary composite outcome included AF-related hospitalizations, cardioversions, ablation procedures, and all-cause mortality. Over a median follow-up of 3.2 years, GLP-1 use was associated with a 13% reduction in major AF-related events compared to other therapies. The study population was predominantly male, with a high prevalence of severe obesity (BMI >40 kg/m²) in whom the benefit appeared most pronounced. Notably, the observed benefit occurred despite only modest additional weight loss, suggesting potential non-weight-mediated effects of GLP-1 therapy This episode was planned in collaboration with Heart Rhythm TV with mentorship from Dr. Daniel Alyesh and Dr. Mehak Dhande. CardioNerds Journal Club PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron!

Oct 24

Dr. Naima Maqsood, Dr. Kelly Arps, and Dr. Jake Roberts discuss the acute management of atrial fibrillation with guest expert Dr. Jonathan Chrispin. Episode audio was edited by CardioNerds Intern Dr. Bhavya Shah. This episode reviews acute management strategies for atrial fibrillation. Atrial fibrillation is the most common chronic arrhythmia worldwide and is associated with increasingly prevalent comorbidities, including advanced age, obesity, and hypertension. Atrial fibrillation is a frequent indication for hospitalization and a complicating factor during hospital stays for other conditions. Here, we discuss considerations for the acute management of atrial fibrillation, including indications for rate versus rhythm control strategies, treatment targets for these approaches, considerations including pharmacologic versus electrical cardioversion, and management in the post-operative setting. CardioNerds Atrial Fibrillation PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls A key component to the management of acute atrial fibrillation involves addressing the underlying cause of the acute presentation. For example, if a patient presents with rapid atrial fibrillation and signs of infection, treatment of the underlying infection will help improve the elevated heart rate. Selecting a rate control versus rhythm control strategy in the acute setting involves considerations of comorbid conditions such as heart failure and competing risk factors such as critical illness that may favor one strategy over another. Recent data strongly supports the use of rhythm control in heart failure patients. Patients should be initiated on anticoagulation prior to pursuing a rhythm control strategy. There are several strategies for rate control medications with therapies including beta-blockers, non-dihydropyridine calcium channel blockers, and digoxin. The selection of which agent to use depends on additional comorbidities and the overall clinical assessment. For example, a patient with severely decompensated low-output heart failure may not tolerate a beta-blocker or calcium channel blocker in the acute phase due to hypotension risks but may benefit from the use of digoxin to provide rate control and some inotropic support. Thromboembolic prevention remains a cornerstone of atrial fibrillation management, and considerations must always be made in terms of the duration of atrial fibrillation, thromboembolic risk, and risks of anticoagulation. While postoperative atrial fibrillation is more common after cardiac surgeries, there is no major difference in management between patients who undergo cardiac versus non-cardiac procedures. Considerations involve whether the patient has a prior history of atrial fibrillation, surgery-specific bleeding risks related to anticoagulation, and monitoring in the post-operative period to assess for recurrence. Notes 1. Our first patient is a 65-year-old man with obesity, hypertension, obstructive sleep apnea, and pre-diabetes presenting for evaluation of worsening shortness of breath and palpitations. The patient has no known history of heart disease. Telemetry shows atrial fibrillation with ventricular rates elevated to 130-140 bpm. What would be the initial approach to addressing the acute management of atrial fibrillation in this patient? What are some of the primary considerations in the initial history and chart review? An important first step involves taking a careful history to understand the timing of symptom onset and potential underlying causes contributing to a patient’s acute presentation with rapid atrial fibrillation. Understanding the episode trigger determines management by targeting reversible causes of the acute presentation and elucidating whether the episode is triggered by a cardiac or non-cardiac condition. For example, if a patient presents with a few days of infectious symptoms, treating the infection is likely to lead to improvements in heart rate. Determining the tempo of symptoms has further importance for assessing the risk of thromboembolism and anticoagulation consideration. 2. How would the initial evaluation be different for patients who have a new diagnosis of atrial fibrillation compared to those who have a known prior history of this arrhythmia? The acuity of symptom onset plays an essential role in these considerations. For example, a patient may describe symptoms that have been ongoing for several months, which indicate a diagnosis beyond the acute phase of their presentation and would involve different considerations than for a patient who first noticed symptoms within the past few hours. One way to view RVR rates in a patient with longstanding or permanent atrial fibrillation is to consider this vital sign as that patient’s version of sinus tachycardia in response to another physiologic process. In that setting, you would not try an approach to directly lower their heart rate but would instead attempt to determine and address the underlying cause of their presentation. An additional consideration for patients without known prior atrial fibrillation is that they have likely never been on any rate-controlling agents and may have variable initial responses to these interventions. 3. In cases for which acute rate control of atrial fibrillation is indicated, what is the recommended heart rate target and how quickly should we aim to reach that target? The initial first step in management should focus on addressing the underlying cause of the patient’s elevated heart rate while in atrial fibrillation. Once those factors are addressed and elevated heart rates persist, a rate-controlling agent can be considered. Often, a primary reason for rate control is for symptom relief since patients can be very symptomatic from an elevated heart rate alone. A reasonable goal for the intermediate setting is to achieve a heart rate of less than 100-110 bpm. One study compared lenient (resting heart rate <110 bpm) versus strict (resting heart rate <80 bpm and heart rate during moderate exercise <110 bpm) rate control in patients with atrial fibrillation and found no difference in outcomes related to mortality, hospitalization for heart failure, stroke, embolism, bleeding, or life-threatening arrhythmic events but that lenient control was easier to achieve.1 For this reason, aggressive rate control in the acute setting may not have a significant impact apart from symptom relief. There are not often clear indications to rapidly lower a patient’s heart rate, for example, from 140 to 90 bpm. Conversely, lowering a patient’s heart rate too rapidly can be detrimental by causing bradycardia or hypotension with excessive use of nodal blocking agents. 4. What are some of the considerations for the selection of rate-controlling agents? Beta-blockers and non-dihydropyridine calcium channel blockers remain the mainstay of therapies used for rate control. The choice between these agents often depends on the comorbidities present. For example, if a patient has a known reduced LVEF, you may often avoid calcium channel blockers and opt for careful titration of beta-blockers. Often, the use of beta-blockers also allows for the management of additional comorbidities, including heart failure and coronary disease. Digoxin is another agent to consider when a patient presents with acutely decompensated heart failure with a low LVEF and may not tolerate a beta-blocker or calcium channel blocker due to the risk of hypotension or worsening cardiogenic shock. Digoxin provides rate control while adding some positive inotropy. In terms of chronic management, digoxin use can be more challenging with close follow-up required to monitor levels. In some cases, amiodarone can be used as an acute rate-control agent, but there is a risk of conversion to sinus rhythm and thromboembolism if not on anticoagulation. 5. In what clinical scenarios might it be more optimal to consider an upfront rhythm control strategy? Recent data support the benefit of an upfront rhythm control approach in heart failure patients, with complications including cardiovascular death, stroke, or hospitalization for worsening of heart failure or for acute coronary syndrome, reduced in heart failure patients managed with any early rhythm control strategy.2,3 In certain patients with known atrial fibrillation and heart failure, cardioversion can be considered as a strategy to help improve their heart failure symptoms. In these patients, initiating an anti-arrhythmic drug (AAD) prior to cardioversion can improve the likelihood of remaining in sinus rhythm after cardioversion. 6. Our second patient is a 58-year-old woman with a history of heart failure with reduced EF presenting to the ED with progressive lower extremity swelling and shortness of breath. She has a prior diagnosis of paroxysmal atrial fibrillation, and her most recent echo demonstrated an LVEF of 35%. She is found to have bilateral lower extremity pitting edema to her knees and elevated jugular venous pressure while requiring 2L of oxygen by nasal cannula. She is in rapid atrial fibrillation on presentation. Interrogation of her primary prevention ICD shows that she has been in atrial fibrillation for the past 3 weeks. In this scenario involving a patient with an acute heart failure exacerbation, are there considerations for a more upfront rhythm control strategy and perhaps electrical cardioversion? In this scenario, there is an indication for utilizing an early rhythm control strategy. Even if an initial trial of diuresis and beta-blockers is used initially,

Oct 9

In this powerful kickoff to a collaborative series with the AHA Women in Cardiology (WIC) Committee, CardioNerds (Dr. Apoorva Gangavelli, Dr. Gurleen Kaur, and Dr. Jenna Skowronski) explore the evolving landscape of women in advanced heart failure and transplant cardiology, featuring insights from two inspiring leaders in the field. Dr. Mariell Jessup, Chief Science and Medical Officer of the American Heart Association, reflects on her decades-long journey in heart failure cardiology, from navigating early career barriers to becoming a trailblazer in clinical leadership and research. Dr. Nosheen Reza, an advanced heart failure and transplant cardiologist at the University of Pennsylvania, shares how Dr. Jessup’s pioneering work has inspired her own career and shaped her approach to mentorship, advocacy, and academic development. Together, they discuss the systemic challenges women continue to face, the importance of sponsorship, and the evolving culture within cardiology. Listeners will gain a multigenerational perspective on how far the field has come and what is still needed to ensure equity, excellence, and innovation in advanced heart failure care. Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. CardioNerds Narratives in Cardiology Series PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! References DeFilippis EM, Moayedi Y, Reza N. Representation of Women Physicians in Heart Failure Clinical Practice. Card Fail Rev. 2021;7:e05. Published 2021 Mar 31. doi:10.15420/cfr.2020.31

Sep 28

CardioNerds (Dr. Abby Frederickson, Dr. Claire Cambron, and Dr. Rawan Amir) are joined by Dr. Leigh Reardon for a powerful conversation on navigating adult congenital heart disease as both a patient and provider. Dr. Reardon shares his personal journey with congenital heart disease and how it shaped his path to becoming an expert in the field himself. The discussion highlights patient-centered perspectives, barriers to care within the healthcare system, and the importance of advocacy and empathy. This episode was planned by the CardioNerds ACHD Council. CardioNerds Adult Congenital Heart Disease PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron!

Sep 15

Dr. Kelly Arps, Dr. Naima Maqsood, and Dr. Sahi Allam discuss modifiable risk factors and lifestyle management of atrial fibrillation with Dr. Prash Sanders. Atrial fibrillation is becoming more prevalent across the world as people are living longer with cardiovascular disease. While much of our current focus lies on the pharmacological and procedural management of atrial fibrillation, several studies have shown that targeted reduction of risk factors, such as obesity, sleep apnea, hypertension, and alcohol use, can also significantly reduce atrial fibrillation burden and symptoms. Today, we discuss the data behind lifestyle management and why it is considered the “4th pillar” of atrial fibrillation treatment. We also explore ways to incorporate prevention strategies into our general cardiology and electrophysiology clinics to better serve the growing atrial fibrillation population. Audio editing for this episode was performed by CardioNerds Intern, Julia Marques Fernandes. CardioNerds Atrial Fibrillation PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls More people have atrial fibrillation because it is being detected earlier using wearable technology, and patients are living longer with subclinical or clinical cardiovascular disease There are 3 components of atrial fibrillation: an electrical “trigger” + a susceptible substrate (due to age, sex, genetics) + “perpetuators” that cause the trigger to continue stimulating the substrate (lifestyle risk factors such as obesity, smoking, diabetes, etc.) Obesity is the highest attributable risk factor for atrial fibrillation. Treating obesity often helps to treat other risk factors, such as hypertension and sleep apnea. Counseling is patient-dependent. Most patients are unable to make major behavioral changes cold-turkey and will need to make small, incremental changes. Dr. Sanders’ tip: He tells his own patients that “atrial fibrillation is the body’s response to stress.” The key to treating atrial fibrillation is to control your underlying stressors - procedures and medications are simply band-aids that do not fix the root of the problem. Notes Notes drafted by Dr. Allam. 1. How common is atrial fibrillation? Atrial fibrillation is the most common sustained arrhythmia. Currently, an estimated 50-60 million individuals worldwide are estimated to have atrial fibrillation, or roughly 1 in 4 individuals over the age of 45.1 The rising global prevalence of atrial fibrillation can be attributed to the aging of the population, increased rates of obesity, and greater accumulation of cardiovascular risk factors and survival with clinical cardiovascular disease.2 Atrial fibrillation is also being detected earlier through digital and wearable devices.2 Annually, we spend approximately $5,312 per adult on the management of atrial fibrillation in the United States.3 2. What is the underlying pathophysiology of atrial fibrillation? How do risk factors like sleep apnea or obesity “trigger” atrial fibrillation? For atrial fibrillation to occur, there is an electrical “trigger”, a susceptible substrate (due to age, sex, genetics), and “perpetuators” that allow the trigger to continue stimulating the substrate.2 90% of electrical “triggers” come from the pulmonary veins “Perpetuators” influence how the autonomic nervous system interacts with the triggers and substrate to perpetuate atrial fibrillation. Sleep apnea, obesity, and other risk factors are the “perpetuators” Over time, as atrial fibrillation recurs, the substrate remodels to result in persistent atrial fibrillation. 3. What are some of the risk factors for atrial fibrillation and what are the possible benefits of controlling them? Reference 4 provides an excellent review of the individual risk factors Tobacco use Nicotine patches/gums and counseling are associated with successful nicotine cessation in RCTs. In the long term, nicotine itself can cause atrial fibrosis. However, it is safe to use patches and gums in the short term to abet cessation. Obesity The highest attributable risk factor for atrial fibrillation. Treating obesity often helps to treat other risk factors, such as hypertension and sleep apnea In addition to regular exercise, reducing caloric intake can help combat obesity. Eating more fiber-laden food such as vegetables instead of carbohydrates, limiting portions, sugary drinks, and alcohol, and increasing fasting periods can all help decrease weight. GLP-1 agonists can significantly reduce obesity and improve both symptoms and mortality for patients with comorbid conditions, such as HFpEF. Obstructive sleep apnea This is an evolving area of research with upcoming randomized trial data Sleep apnea is probably not a static condition. Our likelihood of having sleep apnea changes with how rested we are, how much we’ve exercised, or whether we’ve consumed alcohol, etc. The testing and treatment of the future will reflect the changeable nature of sleep apnea. Current data: In the atrial fibrillation ablation population, treatment of sleep apnea was associated with an improvement in time to arrhythmia recurrence. Another observational study from Norway, which included various patients who used dental sleep appliances, found no significant difference in atrial fibrillation between those who were treated for sleep apnea and those who were not. It was severely underpowered to detect a difference. Caffeine There is no evidence to support cessation of caffeine in patients with atrial fibrillation For patients with bothersome palpitations, caffeine cessation can be tried if it improves their symptoms Alcohol use Per data from the UK Biobank, a single drink of alcohol daily does not increase your risk for developing atrial fibrillation. However, multiple drinks per day will increase your risk. A proof-of-concept study showed that patients who abstained from alcohol for at least 6 months had complete resolution of atrial fibrillation. However, the dropout rate was very high as most patients could not completely abstain from alcohol Dr. Sanders recommends alcohol consumption of ≤ 3 drinks/week, which is the cutoff used in lifestyle management studies. Heart Failure For patients with heart failure, the 4 pillars of heart failure management are also crucial to treating atrial fibrillation. SGLT2 inhibitors in particular are likely to confer benefits. 40-50% of patients in the SGLT2 inhibitor clinical trials had co-morbid atrial fibrillation. About half of patients undergoing atrial fibrillation ablation appear to have HFpEF based on their hemodynamics. 4. Can atrial fibrillation be treated with only lifestyle modifications? Potentially. This is an evolving area of research without much published data. Empirically, Dr. Sanders has noticed that in patients referred for atrial fibrillation ablation, aggressive lifestyle modifications result in 40% of them no longer requiring ablation. After a 10-year follow-up, 20% still do not require ablation. However, ablation is still an effective modality to achieve rhythm control. It is also becoming a safer procedure owing to novel techniques, such as pulse field ablation. In the future, we foresee most patients utilizing a combination of lifestyle modification and rhythm control strategies (ablation and/or medications) to control their atrial fibrillation. 5. What are the benefits of exercise in patients with atrial fibrillation? How much exercise do you recommend to your patients? Also, on the other end of the spectrum, does participation in endurance sports paradoxically promote atrial fibrillation? The ACTIVE-AF study tested whether an intensive aerobic exercise regimen, up to 210 minutes per day, is safe and effective in controlling atrial fibrillation. Intensive exercise was associated with a significant reduction in atrial fibrillation burden and symptoms as well as an increase in quality of life and maintenance of sinus rhythm.5 Endurance athletes do have an approximately 5-fold higher risk of atrial fibrillation compared to sedentary people.6 However, this occurs at very high levels of exercise, exceeding 4 hours per day. Low to moderate levels of exercise have been shown to reduce rates of atrial fibrillation.4,5 6. How should we counsel patients about lifestyle management? Are there any good resources to use? Dr. Sanders’ tip: Counseling is patient-dependent. For the majority of patients, the key to behavioral change is to make incremental adjustments over time, accompanied by encouragement. Some patients respond well to continuous feedback from digital devices. We can also supplement pharmacological therapies, such as medications to assist with weight loss or tobacco/alcohol cessation, to behavioral counseling. Risk factor modification should be the central pillar of atrial fibrillation management and reviewed early on with patients in their atrial fibrillation course. It may be beneficial to have clinic sessions specifically dedicated to lifestyle counseling, which can be run by a multidisciplinary team of electrophysiologists, general cardiologists, and nurse educators. 7. How should we explain what atrial fibrillation is to our patients? Dr. Sanders’ tip: He tells his own patients that “atrial fibrillation is the body’s response to stress. It occurs because the heart is not coping well with increased stress. Procedures and medications for atrial fibrillation are simply band-aids that do not fix the root of the problem, but controlling the risk factors contributing to increased stress will.

Sep 11

CardioNerds (Drs. Amit Goyal, Elizabeth Davis, and Keerthi Gondi) discuss the approach to asymptomatic severe aortic stenosis with expert faculty Drs. Parth Desai and Tony Bavry. They review the natural history of aortic stenosis, current guidelines for treating severe aortic stenosis, multiparametric risk stratification, trial data on aortic valve replacement for patients with asymptomatic severe aortic stenosis, and a practical approach for our patients today. This episode was supported by an educational grant from Edwards Lifesciences. All CardioNerds education is planned, produced, and reviewed solely by CardioNerds. Managing asymptomatic severe aortic stenosis | AKH CME Enjoy this Circulation Paths to Discovery article to learn more about the CardioNerds mission and journey. US Cardiology Review is now the official journal of CardioNerds! Submit your manuscripts here. CardioNerds Aortic Stenosis SeriesCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron!

Sep 8

CardioNerds join Dr. Neel Patel, Dr. Victoria Odeleye, and Dr. Jay Ramsay from the University of Tennessee, Nashville, for a deep dive into cardiovascular medicine in the vibrant city of Nashville. They discuss the following case: A 57-year-old male with a history of prior cardiac surgery, hypertension, and polysubstance use presented with syncope and chest pain. Initial workup revealed a large saccular ascending aortic aneurysm. While under conservative management, he experienced acute hemodynamic collapse, leading to the discovery of an unprecedented aorto-right ventricular fistula. This episode examines the clinical presentation, diagnostic journey, and management challenges of this rare and complex aortic pathology, highlighting the role of multimodal imaging and the interplay of multifactorial risk factors. Expert commentary is provided by Dr. Andrew Zurick III. Episode audio was edited by CardioNerds Intern student Dr. Pacey Wetstein. US Cardiology Review is now the official journal of CardioNerds! Submit your manuscript here. CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls Saccular Aneurysm Risk: Saccular aortic aneurysms, though less common than fusiform, carry a higher inherent rupture risk due to concentrated wall shear stress, often exacerbated by prior cardiac surgery, chronic hypertension, and polysubstance use. Unprecedented Rupture: The direct rupture of an aortic aneurysm into a cardiac chamber, specifically the right ventricle, is an exceedingly rare event, with no prior reported cases in the literature, highlighting the unpredictable nature of complex aortic pathology. Hemodynamic Catastrophe: A large aorto-right ventricular fistula creates a massive left-to-right shunt, leading to acute right ventricular pressure and volume overload, culminating in rapid cardiogenic shock and refractory right ventricular failure. Multimodal Imaging Imperative: Multimodal imaging (CT angiography for anatomy, TTE/TEE for real-time hemodynamics and fistula detection, CMR for tissue characterization) is indispensable for rapid diagnosis and comprehensive characterization of life-threatening cardiovascular emergencies. High-Risk Intervention: Emergent surgical repair of a ruptured aortic aneurysm with an aorto-right ventricular fistula is a high-risk procedure associated with significant mortality, underscoring the need for prompt multidisciplinary care and realistic outcome expectations. Notes - Notes (drafted by Dr Neel Patel): What are the unique characteristics and rupture risk of saccular aortic aneurysms? Saccular aortic aneurysms are less common than fusiform aneurysms. They are generally considered more prone to rupture due to higher wall shear stress concentrated at the neck of the aneurysm, acting as a focal point of weakness. Contributing Factors to Aneurysm Formation and Rupture in this Case: Prior Cardiac Surgery: Aortic cannulation during the VSD/ASD repair decades ago likely created a localized structural weakness or predisposition. Chronic, Poorly Controlled Hypertension: Imposed relentless systemic stress on the arterial walls, accelerating dilation and weakening. Polysubstance Use: Particularly stimulants like cocaine and methamphetamines, which directly contribute to vascular damage by inducing severe, uncontrolled hypertension and direct arterial wall injury. This significantly increases the risk of aneurysm formation and rupture, especially with pre-existing conditions. The direct rupture of an aortic aneurysm into a cardiac chamber, specifically the right ventricle, is an exceedingly rare event, with no prior reported cases in the literature, making this a "first of its kind" report. What are the hemodynamic consequences and management challenges associated with aorto-right ventricular fistulas? Hemodynamic Impact: A large aorto-right ventricular fistula results in a significant anatomic left-to-right shunt, where blood from the high-pressure aorta is shunted directly into the lower-pressure right ventricle. This leads to acute right ventricular pressure and volume overload, causing rapid right ventricular dilation, increased right ventricular wall stress, and ultimately, acute right ventricular failure. This directly explained the sudden onset of cardiogenic shock, as the right ventricle was unable to maintain forward flow, leading to systemic hypoperfusion and shock. Management Challenges: The patient required emergent, extremely high-risk salvage aortic aneurysm repair surgery. Marked hemodynamic instability occurred immediately after anesthesia induction (systolic blood pressure dropped to 50 mmHg), necessitating immediate initiation of external cardiopulmonary bypass. Intra-operatively, a large (2 cm diameter) hole in the ascending aorta communicating with the saccular aneurysm was found, along with a massive (4-5 cm) fistula into the right ventricular outflow tract (RVOT) area, just proximal to the pulmonic valve, with several smaller holes. Surgical repair involved a 5x10 cm bovine pericardial patch for the right ventricular wall and replacement of a 5 cm segment of the ascending aorta with a 34 mm gelweave straight graft. Post-operative Course: Severely complicated by severe coagulopathy and extensive bleeding (requiring multiple blood products and a Cabral fistula). Continued severe right ventricular dysfunction necessitated the placement of a Right Ventricular Assist Device (RVAD). Despite support, hemodynamic function continued to decline, with severely depressed Left Ventricular (LV) function observed. The patient ultimately passed away due to refractory right heart failure and hemodynamic collapse, highlighting the extremely high mortality risk associated with such complex, emergent cardiac surgical interventions. What is the role of multimodal imaging in diagnosing this complex and rare cardiovascular emergency? CT Angiography: Crucial for initial identification and comprehensive characterization of the large saccular ascending aortic aneurysm, providing precise dimensions, revealing layered thrombus, and understanding anatomical relationships. Its high spatial resolution and wide field of view are excellent for aortic assessment. Transthoracic and Transesophageal Echocardiography (TTE/TEE): Absolutely critical for real-time diagnosis of the fistula during acute deterioration. Bedside echocardiography, particularly TEE, allowed for visualization of the new continuous, turbulent flow from the aorta directly into the right ventricle, quantification of acute right ventricular dilation, and estimation of significantly increased RVSP. Its accessibility and real-time capabilities are unmatched for acute hemodynamic assessment and shunt detection. Cardiac MRI (CMR): Provided additional tissue characterization of the aneurysm, confirming partial thrombosis and, importantly, showing no significant late gadolinium enhancement (LGE) in the myocardium, which was reassuring regarding the absence of significant myocardial scar related to the aneurysm itself. CMR offers superior soft tissue characterization compared to CT. Complementary Nature: This case demonstrated the complementary nature of these modalities: CT provided the initial anatomical roadmap, echocardiography offered real-time hemodynamic assessment and immediate diagnosis of the acute rupture and shunt, and CMR contributed valuable tissue characterization. Imaging choices are guided by clinical questions, urgency, and specific information needed for critical management decisions. What are the multi-factorial risk factors contributing to complex aortic disease, including the often-overlooked impact of polysubstance use? Prior Cardiac Surgery: The patient's history of open-heart surgery decades prior, involving aortic cannulation for cardiopulmonary bypass, is a recognized risk factor for the subsequent development of iatrogenic aneurysms, creating a localized structural weakness or predisposition. Chronic, Poorly Controlled Hypertension: Imposes relentless systemic stress on the arterial walls, accelerating dilation and weakening, significantly contributing to aneurysm progression. Polysubstance Use: The patient's long-standing history of polysubstance use, particularly stimulants like cocaine and methamphetamines, represents a significant contributing factor to his vascular pathology. These substances are not merely comorbidities; they directly contribute to vascular damage. Chronic stimulant use can induce severe, uncontrolled hypertension and direct arterial wall injury. This significantly increases the risk of aneurysm formation and rupture, especially when combined with pre-existing conditions like essential hypertension and prior cardiac surgery. Multi-hit Phenomenon: This case illustrates a multi-factorial pathology where various insults on vascular integrity over time converge to create a highly complex and catastrophic cardiovascular event. The presence of these factors emphasizes the critical importance of a thorough social history in cardiovascular risk assessment, moving beyond a superficial listing to understanding the profound pathophysiological impact on vascular health. References - Lavall D, Schäfers HJ, Böhm M, Laufs U. Aneurysms of the ascending aorta. Dtsch Arztebl Int. 2012 Mar;109(13):227-33. doi: 10.3238/arztebl.2012.0227. Epub 2012 Mar 30. PMID: 22532815; PMCID: PMC3334714. Shang EK, Nathan DP, Boonn WW, Lys-Dobradin IA,

Aug 29

CardioNerds guest host Dr. Colin Blumenthal joins Dr. Juma Bin Firos and Dr. Aishwarya Verma from the Trinity Health Livonia Hospital to discuss a fascinating case involving malignant ventricular arrhythmias. Expert commentary is provided by Dr. Mohammad-Ali Jazayeri. Audio editing for this episode was performed by CardioNerds Intern,Julia Marques Fernandes. This case explores the puzzling presentation of exercise-induced ventricular tachycardia in a young, otherwise healthy male who suffered recurrent out-of-hospital cardiac arrests. With no traditional risk factors and an unremarkable ischemic workup, the challenge lay in uncovering the underlying cause of his malignant arrhythmias. Electrophysiology studies and advanced imaging played a pivotal role in systematically narrowing the differentials, revealing an unexpected arrhythmogenic substrate. This episode delves into the diagnostic dilemma, the role of EP testing, and the critical decision-making surrounding ICD placement in a patient with a concealed but life-threatening condition. US Cardiology Review is now the official journal of CardioNerds! Submit your manuscript here. CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls- Malignant Ventricular Arrhythmias This case highlights the challenges and importance of diagnosing and managing ventricular arrhythmias in young, seemingly healthy individuals. Here are five key takeaways from the episode: Electrophysiology (EP) studies play a crucial role in identifying arrhythmogenic substrates in patients with exercise-induced ventricular tachycardia (VT) without obvious structural heart disease. In this case, substrate mapping revealed late abnormal ventricular afterdepolarizations in the basal inferior left ventricle, providing valuable insights into the underlying mechanism. Cardiac MRI can be a powerful tool for detecting subtle myocardial abnormalities. The subepicardial late gadolinium enhancement (LGE) in the lateral and inferior LV walls suggested an underlying myocardial process, even when other imaging modalities appeared normal. The VT morphology can provide clues about the underlying mechanism. In this case, the right bundle branch block pattern with a northwest axis and shifting exit sites pointed towards a scar-mediated mechanism rather than a channelopathy or idiopathic VT. Implantable cardioverter-defibrillator (ICD) placement is crucial for secondary prevention of sudden cardiac death (SCD) in patients with malignant ventricular arrhythmias, even in young individuals. The patient's initial deferral of ICD implantation highlights the importance of shared decision-making and patient education in these complex cases. "Scar-mediated VT introduces the risk of new arrhythmogenic substrates over time, reinforcing the need for ICD therapy even when catheter ablation is considered." This pearl emphasizes the dynamic nature of the arrhythmogenic substrate and the importance of long-term risk mitigation strategies. Notes - Malignant Ventricular Arrhythmias Notes were drafted by Juma Bin Firos. 1. What underlying pathologies cause ventricular arrhythmias in young patients without overt structural heart disease? Myocardial fibrosis: Detected via late gadolinium enhancement (LGE) on cardiac MRI Present in 38% of nonischemic cardiomyopathy cases Increases sudden cardiac death (SCD) risk 5-fold Often localized to subepicardial regions, particularly in the inferolateral left ventricle (LV) May precede overt systolic dysfunction by years Subclinical cardiomyopathy: 67% of young VT patients show subtle cardiac dysfunction Suggests VT may be the first manifestation of cardiomyopathy Can include early-stage genetic cardiomyopathies (e.g., ARVC, LMNA mutations) Often associated with preserved ejection fraction (EF >50%) Arrhythmogenic substrate: EP studies localize re-entry circuits to specific regions: Basal inferior LV near the mitral annulus (as in this case) Right ventricular outflow tract (RVOT) in idiopathic VT Papillary muscles or fascicular regions Substrate can exist even with normal EF and no visible structural abnormalities on echocardiography Channelopathies: Long QT syndrome (LQTS): QTc >460ms in males, >470ms in females Brugada syndrome: Coved ST elevation in V1-V3 Catecholaminergic polymorphic VT (CPVT): Normal resting ECG, bidirectional VT with exercise Short QT syndrome: QTc <330ms Inflammatory conditions: Myocarditis: Can cause transient or persistent arrhythmogenic substrate Cardiac sarcoidosis: Patchy inflammation and fibrosis, often affecting the septum 2. How do electrophysiology studies differentiate scar-mediated VT from channelopathies? Substrate mapping: Identifies late abnormal potentials (LAPs) with 92% specificity for re-entry circuits Utilizes multi-electrode catheters (e.g., Penta Ray) for high-density mapping LAPs indicate slow conduction through fibrotic tissue, key for re-entry Absent in purely electrical disorders like channelopathies Inducibility: Programmed electrical stimulation (PES) protocols: Up to triple extra stimuli at multiple sites (RV apex, RVOT, LV) Burst pacing at cycle lengths down to 200-250ms Scar-mediated VT is often inducible with aggressive stimulation Polymorphic VT/VF induction suggests a structural substrate Channelopathies like Catecholaminergic polymorphic ventricular tachycardia CPVT) typically requires isoproterenol or exercise for induction VT morphology analysis: Right bundle branch block (RBBB) + northwest axis localizes to LV basal inferior wall Left bundle branch block (LBBB) + inferior axis suggests RVOT origin Fascicular VT: RBBB + left anterior or posterior fascicular block pattern Papillary muscle VT: RBBB or LBBB with variable axis Entrainment mapping: Performed during sustained monomorphic VT Post-pacing interval minus tachycardia cycle length (PPI-TCL) <30ms indicates critical isthmus Not applicable to polymorphic VT or channelopathies Electroanatomic voltage mapping: Low voltage areas (<1.5mV bipolar) indicate scar tissue Normal voltage throughout suggests functional (non-scar) VT mechanism 3. What are key management considerations for recurrent VT/VF in young patients? ICD for secondary prevention: Class I indication after cardiac arrest or sustained VT without a reversible cause Reduces mortality from 13% (8-year untreated) to <5%, especially with LGE present Device selection: Single-chamber ICD if no pacing indication Subcutaneous ICD (S-ICD) in young patients to avoid transvenous lead complications Consider cardiac resynchronization therapy defibrillator (CRT-D) if LBBB or wide QRS LifeVest limitations: Bridges ≤3 months; not a long-term solution Recurrent arrests double mortality vs. prompt ICD implantation Compliance issues: must be worn consistently to be effective Oral antiarrhythmic medications: Amiodarone: Effective for acute VT suppression Long-term use limited by side effects (thyroid, liver, pulmonary toxicity) Beta-blockers: First line for most VT/VF, especially exercise-induced Sotalol: Alternative for those with preserved LV function Mexiletine: Adjunct for frequent ICD shocks, especially with LQT3 Catheter ablation: Consider early in the course for recurrent ICD shocks Success rates 60-80% for scar-related VT May reduce ICD shocks and improve quality of life Limitations: deep intramural or epicardial substrates may require specialized approaches Lifestyle modifications: Exercise restrictions: Avoid high-intensity activities that trigger arrhythmias Stress management: Consider cognitive behavioral therapy or mindfulness training Avoidance of QT-prolonging medications in LQTS patients Genetic testing and family screening: Recommended for suspected inherited arrhythmia syndromes Can guide management and risk stratification for family members 4. Why does exercise exacerbate arrhythmia risk in these patients? Sympathetic surge: Increases myocardial oxygen demand Enhances automaticity and triggered activity Can unmask concealed conduction abnormalities Hemodynamic changes: Increased preload and afterload stress fibrotic regions Volume shifts may alter electrolyte concentrations locally Metabolic factors: Lactic acid accumulation can promote ectopic beats Catecholamine release exacerbates ion channel dysfunction in channelopathies Exercise-induced VT/VF correlates with 8× higher SCD risk vs. rest-onset arrhythmias: Warrants activity restrictions tailored to individual risk profile May indicate more malignant substrate or advanced disease process Treadmill testing: Should guide therapy in asymptomatic patients with exercise-related VT Protocols: Bruce protocol for general assessment Modified protocols (e.g., longer stages) for specific arrhythmia provocation Endpoints: Induction of sustained VT/VF Achieving target heart rate (85% of age-predicted maximum) Development of concerning symptoms (pre-syncope, chest pain) Cardiac rehabilitation: Supervised exercise programs can improve outcomes Gradual increase in intensity with continuous monitoring Helps define safe exercise thresholds for patients 5. How does LGE on cardiac MRI refine risk stratification? Late gadolinium enhancement (LGE) on cardiac MRI acts like a "scar map" of the heart, revealing areas of damaged or fibrotic tissue. These scars create electrical instability,

Aug 19

CardioNerds (Drs. Rick Ferraro and Georgia Vasilakis Tsatiris) discuss ATTR cardiac amyloidosis with expert Dr. Justin Grodin. This episode is a must-listen for all who want to know how to diagnose and treat ATTR with current available therapies, as well as management of concomitant diseases through a multidisciplinary approach. We take a deep dive into the importance of genetic testing, not only for patients and families, but also for gene-specific therapies on the horizon. Dr. Grodin draws us a roadmap, guiding us through new experimental therapies that may reverse the amyloidosis disease process once and for all. Audio editing by CardioNerds academy intern, Christiana Dangas. This episode was developed in collaboration with the American Society of Preventive Cardiology and supported by an educational grant from BridgeBio. Enjoy this Circulation Paths to Discovery article to learn more about the CardioNerds mission and journey. US Cardiology Review is now the official journal of CardioNerds! Submit your manuscripts here. CardioNerds Cardiac Amyloid PageCardioNerds Episode Page Pearls: You must THINK about your patient having amyloid to recognize the pattern and make the diagnosis. Start with a routine ECG and TTE, and look for a disproportionately large heart muscle with relatively low voltages on the ECG. Before you diagnose ATTR amyloidosis, AL amyloidosis must be ruled out (or ruled in) with serum light chains, serum/urine immunofixation, and/or tissue biopsy. Genetic testing is standard of care for all patients and families with ATTR amyloidosis, and the future is promising for gene-specific treatments. Current FDA-approved treatments for TTR amyloidosis are TTR stabilizers and TTR silencers, but TTR fibril-depleting agents are on their way. Early diagnosis of ATTR affords patients maximal benefit from current amyloidosis therapies. TTR amyloidosis patients require a multidisciplinary approach for success, given the high number of concomitant diseases with cardiomyopathy. Notes: Notes: Notes drafted by Dr. Georgia Vasilakis Tsatiris. What makes you most suspicious of a diagnosis of cardiac amyloidosis from the typical heart failure patient? You must have a strong index of suspicion, meaning you THINK that the patient could have cardiac amyloidosis, to consider it diagnostically. Some characteristics or “red flags” to not miss: Disproportionately thick heart muscle with a relatively low voltages on EKG Bilateral carpal tunnel syndrome – estimated that 1 in 10 people >65 years old will have amyloidosis Previously tolerated antihypertensive medications Atraumatic biceps tendon rupture Bilateral carpal tunnel syndrome Spinal stenosis Concomitant with other diseases: HFpEF, low-flow low-gradient aortic stenosis How would you work up a patient for cardiac amyloidosis? Start with a routine ECG (looking for disproportionally low voltage) and routine TTE (looking for thick heart muscle) CBC, serum chemistries, hepatic function panel, NT proBNP, and troponin levels NOTE: It is critical to differentiate between amyloid light chain (AL amyloidosis) and transthyretin ATTR amyloidosis, as both make up 95-99% of amyloidosis cases. Obtain serum free light chains, serum & urine electrophoresis, and serum & urine immunofixation to rule out AL amyloidosis. (See table below) AL Amyloidosis ATTR Amyloidosis → Positive serum free light chains and immunofixation (Abnormal M protein) → Tissue biopsy (endomyocardial, fat pad) to confirm diagnosis → Negative serum free light chains and immunofixation (ruled out AL amyloidosis) → Cardiac scintigraphy (Technetium pyrophosphate with SPECT imaging) What treatment options do we have to offer now for ATTR CM, and how has this compared to prior years? Before 2019, treatment options were limited outside of cardiac transplantation and prophylactic liver transplants for hereditary ATTR amyloidosis. Treatments since 2019 have utilized the amyloidogenic cascade: TTR protein is formed in the liver and circulates in the bloodstream. Current treatments aim to either slow ATTR progression by stopping deposition or clearing amyloid deposits Only FDA-approved treatments are for stopping deposition, while agents that clear amyloid deposits remain investigational. Two classes of agents that stop amyloid deposition are TTR stabilizers and TTR Silencers. (See table below) TTR Stabilizers TTR Silencers Tafamidis (ATTR-ACT, 2018) Acoramidis (ATTRibute-CM, 2024) Inotersen (Clinical Trial, 2018) Eplontersen (Clinical Trial, 2023) Patisiran (Clinical Trial, 2018) Vutrisiran* (Clinical Trial, 2022) Mechanism: prevents dissociation of, or stabilizes, the TTR tetramer to halt disease progression Mechanism: inhibit the liver’s production of TTR in the bloodstream via small interfering RNAs (siRNAs)/antisense oligonucleotides Route of administration: PO (pills) Route of Administration: IV infusions *Vutrisiran is a subQ injection q3months Outcomes: improve morbidity and mortality in both wildtype (wtATTR) and hereditary ATTR (hATTR) amyloidosis Outcomes: only approved for treatment of hATTR with polyneuropathy Agents that clear amyloid deposits are still in clinical trials (ALXN2200, Coramitug PRX004). Liver transplantation is the only method of clearing amyloid fibril deposits until the FDA approves a fibril-depleting agent, as perhaps one of the aforementioned agents. How do you use genetic testing in your practice? How does the role of genetic testing impact treatment options for patients and their families? Genetic testing = standard of care; everyone with ATTR-CM should get genetic sequencing! Family screening is also important, as hATTR is an autosomal dominant disease. Patients and families can be referred to genetic counseling, become educated on the GINA Act, and choose to start cascade screening for family members. Family members can be affected in different ways, as penetrance can occur at different ages Due to current FDA labeling patients must have hereditary ATTR with polyneuropathy and a pathologic variant to qualify for TTR silencer treatment. Patients can have concomitant cardiomyopathy but must also have polyneuropathy and pathologic variant. TTR stabilizers are approved for ATTR cardiomyopathy regardless of the presence of the pathogenic TTR variant. Are there differences in treatment response between wtATTR or hATTR? What about differences in men and women? Epidemiological studies suggest variant (hereditary) ATTR patients have more aggressive disease than wildtype ATTR patients. Since current treatments do not cure the disease and work to slow progression, patients with advanced stages of disease do not show much benefit from current therapies. Whether it is wild type or hereditary, diagnosing ATTR as early as possible will afford patients the greatest therapeutic impact of current treatments. The current data does not suggest a therapeutic difference in response between men and women with ATTR cardiac amyloidosis What is the role of CRISPR/Cas9 in the treatment of cardiac amyloidosis? ATTR amyloidosis is an elegant disease model because it is one gene responsible for one protein and ultimately one disease process. NTLA 2001 (currently in a phase-three clinical trial, link to phase one) is an agent administered in a single infusion to silence hepatic production of TTR indefinitely. We are awaiting promising results from this trial at the time of this recording. How can we best call on our friends in other subspecialities to take care of the concomitant diseases – peripheral neuropathy, symptomatic atrial fibrillation, aortic stenosis? Do any ATTR specific treatments show improvement in these manifestations? TTR amyloidosis patients need a multidisciplinary care model for success. Carpal tunnel syndrome is common in ATTR amyloidosis, so referrals to neurology and hand surgery are common Patients with autonomic dysfunction secondary to autonomic neuropathy could benefit from neurology referral for blood pressure strategies and gastroenterology due to gut dysmotility and constipation. Electrophysiology (EP) referral is common for atrial fibrillation and atrial flutter ATTR is a disease of aging, so collaborating with geriatricians is important to help coordinate care and establish the patient’s individualized goals. What is your management of subclinical ATTR and strategies for early detection? Again, having a strong index of suspicion for cardiac amyloidosis is prudent. The most common TTR variant that causes hATTR on earth is the V122I mutation (PV142I), which is very common in Western African ancestry. We suspect 1.5 million carriers of this variant in the USA alone, which puts individuals at 2-3x higher risk for heart failure than their age, sex, and race-matched non-carrier controls. Expert consensus suggests monitoring individuals with this variant about 10 years before when the proband (i.e. if patient was diagnosed at 70, family members start screening at 60). Initial work-up should include standard tests: ECG, echocardiogram, blood work. Upcoming clinical trial will enroll patients in this critical 10-year window and randomize them into acoramadis vs placebo to see if treatment before symptom/disease onset can prevent amyloid disease. References Arbelo E, Protonotarios A, Gimeno JR, et al. 2023 ESC Guidelines for the management of cardiomyopathies: Developed by the task force on the management of cardiomyopathies of the European Society of Cardiology (ESC). Eur Heart J. 2023;44(37):3503-3626. doi:10.1093/eurheartj/ehad194 Maron MS, Masri A, Nassif ME, et al.

Aug 3

CardioNerds (Dr. Rick Ferraro and Dr. Dan Ambinder) join Dr. Sahar Samimi and Dr. Lorraine Mascarenhas from Baylor College of Medicine, Houston, Texas, at the Houston Rodeo for some tasty Texas BBQ and a tour of the lively rodeo grounds to discuss an interesting case full of clinical pearls involving a patient with nonbacterial thrombotic endocarditis (NBTE). Expert commentary is provided by Dr. Basant Arya. Episode audio was edited by CardioNerds Intern Dr. Bhavya Shah. (Photo by Xu Jianmei/Xinhua via Getty Images)Xinhua News Agency via Getty Images We discuss a case of a 38-year-old woman with advanced endometrial cancer who presents with acute abdominal pain, found to have splenic and renal infarcts, severe aortic regurgitation, and persistently negative blood cultures, ultimately diagnosed with nonbacterial thrombotic endocarditis (NBTE). We review the definition and pathophysiology of NBTE in the context of malignancy and hypercoagulability, discuss initial evaluation and echocardiographic findings, and highlight important management considerations. Emphasis is placed on the complexities of anticoagulation choice, the role of valvular surveillance, and the need for coordinated, multidisciplinary care. US Cardiology Review is now the official journal of CardioNerds! Submit your manuscript here. CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls- Nonbacterial Thrombotic Endocarditis Eliminate the Usual Suspects. NBTE is a diagnosis of exclusion! Always rule out infective endocarditis (IE) first with serial blood cultures and serologic tests. More than Meets the Echo. Distinguishing NBTE from culture-negative endocarditis can be tricky. Look beyond the echo—focus on clinical context (underlying malignancy, autoimmune issues) and lab findings to clinch the diagnosis. TEE for the Win... Mostly. While TEE is more sensitive than TTE, NBTE vegetations can be sneaky and may embolize quickly. Don’t hesitate to use advanced imaging (i.e., cardiac MRI, CTA) or repeat imaging if you still suspect NBTE. Choose your champion. In cancer-associated NBTE, guideline recommendations for anticoagulation choice are lacking. Consider DOACs and LMWH as agents of choice, but ultimately use shared decision-making to guide management. No obvious trigger? Go hunting for hidden malignancies or autoimmune disorders. A thorough workup is essential to uncover the driving force behind NBTE. Check out this state-of-the-art review for a comprehensive, one-stop summary of NBTE: European Heart Journal, 46(3), 236–245. Please note that the figures and tables referenced in the following notes are adapted from this review. notes- Nonbacterial Thrombotic Endocarditis Notes were drafted by Dr. Sahar Samimi. What is nonbacterial thrombotic endocarditis (NBTE)? NBTE, previously known as marantic endocarditis, is a rare condition in which sterile vegetations form on heart valves.1 It occurs most commonly in association with malignancies and autoimmune conditions (i.e, antiphospholipid antibody syndrome or systemic lupus erythematosus).1 In addition, NBTE has been reported in association with COVID-19 infection, burns, sepsis, and indwelling catheters.2 Precise mechanisms remain unclear, but an interplay of endothelial injury, hypercoagulability, hypoxia, and immune complex deposition contributes to the formation of these sterile vegetations. 1 How do we diagnose NBTE? Physicians should have a high level of suspicion for NBTE in at-risk patients (e.g., with active malignancy) who present with recent or recurrent embolic events (i.e., stroke, splenic, renal, or mesenteric infarct, and acute coronary syndrome).1 Once vegetations are observed, the diagnosis of NBTE is focused on ruling out IE, followed by looking for the underlying etiology, if not already evident.1 A focused clinical assessment, including a thorough history, physical exam, and relevant microbiological and serological tests, should aim to rule out IE using the modified Duke criteria.3 Persistently negative blood cultures after adequate sampling increase the likelihood of NBTE but do not exclude culture-negative endocarditis. Vegetations found in patients with risk factors raise the suspicion for NBTE, whereas signs of systemic infection—such as ongoing fever, recent antibiotic exposure, or potential zoonotic sources—may point instead toward CNE.1 New diagnostic techniques, including specialized serology and metagenomic sequencing, have significantly enhanced our ability to detect elusive pathogens in CNE.1 How should imaging be approached in suspected NBTE? In cases of suspected endocarditis, guidelines from the American College of Cardiology, the American Heart Association, and the European Society of Cardiology recommend starting the assessment with a TTE to visualize potential valvular vegetations. 4,5 TTE is less sensitive than TEE, particularly for detecting smaller vegetations < 5 mm that are often associated with NBTE. Therefore, a subsequent TEE is recommended due to its superior ability to detect subtle valvular abnormalities. 4,5 Echocardiographic features of vegetations alone do not reliably distinguish NBTE from IE; hence, clinical context, along with laboratory and microbiological findings, is crucial for accurate diagnosis. 1 Uncertainty may remain following a TEE or in cases where TEE is not feasible. In such situations, advanced imaging techniques like cardiac MRI and CT scanning are emerging tools for more detailed cardiac tissue characterization. 1 What are the management strategies for NBTE? NBTE’s complexity necessitates a multidisciplinary treatment strategy, with each patient’s prognosis shaped by individual clinical factors. 1 Primary therapy involves anticoagulation, alongside targeted management of malignancy or autoimmune disorder driving the hypercoagulable state. 1 While the criteria for surgical intervention are similar to those used in IE, surgery generally has a more limited role in NBTE. 1 What factors into choosing the anticoagulation agent? Anticoagulation outcomes in NBTE can vary greatly: some patients have vegetations resolve, while others experience disease progression to new valves despite therapy.1 Because NBTE-specific evidence remains sparse, the underlying clinical context primarily guides the choice of anticoagulant: Multiple case reports describe DOAC failure with recurrent embolization in patients with cancer and NBTE. 6-8 LMWH remains a mainstay for patients with cancer or when patients experience thrombotic complications on DOACs. 1 Warfarin is the preferred anticoagulant among patients with thrombotic antiphospholipid syndrome. 9 The duration of anticoagulation should take into consideration the status of the underlying disease, the presence of valvular lesions on follow-up imaging, and an individualized assessment of risks and benefits. 1 References - Nonbacterial Thrombotic Endocarditis Ahmed O, King NE, Qureshi MA, et al. Non-bacterial thrombotic endocarditis: a clinical and pathophysiological reappraisal. European Heart Journal. 2025;46(3):236-49. Balata D, Mellergård J, Ekqvist D, et al. Non-bacterial thrombotic endocarditis: a presentation of COVID-19. European journal of case reports in internal medicine. 2020;7(8). Li JS, Sexton DJ, Mick N, et al. Proposed modifications to the Duke criteria for the diagnosis of infective endocarditis. Clin Infect Dis 2000;30: 633–8. Otto CM, Nishimura RA, Bonow RO, et al. 2020 ACC/AHA guideline for the management of patients with valvular heart disease: a report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. J Am Coll Cardiol 2021;77:e25–197. Vahanian A, Beyersdorf F, Praz F, et al.; ESC/EACTS Scientific Document Group. 2021 ESC/EACTS Guidelines for the management of valvular heart disease. Eur Heart J. 2022 Feb 12;43(7):561-632. Mantovani F, Navazio A, Barbieri A, Boriani G. A first described case of cancer- associated non-bacterial thrombotic endocarditis in the era of direct oral anticoagulants. Thromb Res 2017;149:45–7. Panicucci E, Bruno C, Ferrari V, Suissa L. Recurrence of ischemic stroke on direct oral anticoagulant therapy in a patient with marantic endocarditis related to lung cancer. J Cardiol Cases 2021;23:242–5. Shoji MK, Kim JH, Bakshi S, et al. Nonbacterial thrombotic endocarditis due to primary gallbladder malignancy with recurrent stroke despite anticoagulation: case report and literature review. J Gen Intern Med 2019;34:1934–40. Khairani CD, Bejjani A, Piazza G, et al. Direct oral anticoagulants vs vitamin K antagonists in patients with antiphospholipid syndromes: meta-analysis of randomized trials. J Am Coll Cardiol 2023;81:16–30. Case Media TTE and TEE

Jul 25

Drs. Rick Ferraro and Sneha Nandy discuss ‘Diagnosis of ATTR Cardiac Amyloidosis’ with Dr. Venkatesh Murthy. In this episode, we explore the diagnosis of ATTR cardiac amyloidosis, a condition once considered rare but now increasingly recognized due to advances in imaging and the availability of effective therapies. Dr. Venkatesh Murthy, a leader in multimodality imaging, discusses key clinical and laboratory features that should raise suspicion for the disease. We also examine the role of nuclear imaging and genetic testing in confirming the diagnosis, as well as the importance of early detection. Tune in for expert insights on navigating this challenging diagnosis and look out for our next episode on treatment approaches for cardiac amyloidosis! Audio editing for this episode was performed by CardioNerds Intern, Julia Marques Fernandes. Enjoy this Circulation Paths to Discovery article to learn more about the CardioNerds mission and journey. US Cardiology Review is now the official journal of CardioNerds! Submit your manuscripts here. CardioNerds Cardiac Amyloid PageCardioNerds Episode Page Pearls: - Diagnosis of Transthyretin amyloid cardiomyopathy 1. Recognizing the Red Flags – ATTR cardiac amyloidosis often presents with subtle but telling signs, such as bilateral carpal tunnel syndrome, low-voltage ECG, and a history of lumbar spinal stenosis or biceps tendon rupture. If you see these features in a patient with heart failure symptoms, think amyloidosis! 2. “Vanilla Ice Cream with a Cherry on Top” – On strain echocardiography, apical sparing is a classic pattern for cardiac amyloidosis. While helpful, it’s not foolproof—multimodal imaging and clinical suspicion are key! 3. Nuclear Imaging is a Game-Changer – When suspicion for cardiac amyloidosis is high à a positive PYP scan with SPECT imaging (grade 2 or 3 myocardial uptake) in the absence of monoclonal protein (ruled out by SPEP, UPEP, and free light chains) is diagnostic for ATTR amyloidosis—no biopsy needed! 4. Wild-Type vs. Hereditary? Know the Clues – Older patients (70+) are more likely to have wild-type ATTR, while younger patients (40s-60s), especially those with neuropathy and a family history of heart failure, should raise suspicion for hereditary ATTR. Genetic testing is crucial for distinguishing between the two. Note that some ATTR variants may predispose to a false negative PYP scan! 5. Missing Amyloidosis = Missed Opportunity – With multiple disease-modifying therapies now available, early diagnosis is critical. If you suspect cardiac amyloidosis, don’t delay the workup—early treatment improves outcomes! Notes - Diagnosis of Transthyretin amyloid cardiomyopathy What clinical features should raise suspicion for ATTR cardiac amyloidosis? ATTR cardiac amyloidosis is underdiagnosed because symptoms overlap with other forms of heart failure. Red flags include bilateral carpal tunnel syndrome (often years before cardiac symptoms), low-voltage ECG despite increased LV wall thickness, heart failure with preserved ejection fraction (HFpEF) with a restrictive pattern, and history of lumbar spinal stenosis, biceps tendon rupture, and/or peripheral neuropathy, including possible autonomic dysfunction (e.g., orthostatic hypotension). Remember: If an older patient presents with heart failure and unexplained symptoms like neuropathy or musculoskeletal issues, think amyloidosis! What is the differential diagnosis for a thick left ventricle (LVH) and how does ATTR amyloidosis fit into it? Hypertension: Most common cause of LVH, typically with a history of uncontrolled high blood pressure. Aortic stenosis: May present with concentric LVH. Hypertrophic cardiomyopathy (HCM): Genetic disorder typically presenting with asymmetric LVH, especially in younger patients. Infiltrative cardiomyopathy: Often due to amyloidosis, sarcoidosis, or hemochromatosis. Storage disorder: Fabry’s, Danon, Pompe, etc. What are the key imaging modalities used to diagnose ATTR cardiac amyloidosis? Echocardiography: Thickened LV walls (>12 mm) with a restrictive filling pattern, Speckled appearance on 2D echo (not specific), apical sparing on strain imaging (“Vanilla ice cream with a cherry on top”). Cardiac MRI (CMR): Late gadolinium enhancement (LGE) in a global subendocardial pattern, T1 mapping & extracellular volume (ECV) expansion are supportive findings. Nuclear Scintigraphy (99mTc-PYP scan): Gold standard noninvasive test for ATTR. Grade 2 or 3 uptake (equal to or greater than bone uptake) is diagnostic if monoclonal protein is absent in the right clinical scenario. What lab tests are used to diagnose ATTR cardiac amyloidosis? Check troponin and NTproBNP (useful for staging) Rule out AL amyloidosis with monoclonal protein studies like serum protein electrophoresis (SPEP) and urine protein electrophoresis (UPEP) with immunofixation and serum free light chain (FLC) assay (to detect clonal plasma cell disorders) Why is ruling out AL amyloidosis critical before diagnosing ATTR? They are treated very differently- AL amyloidosis is an oncologic emergency requiring chemotherapy, while ATTR is treated with medications. If workup for AL amyloidosis, such as SPEP/UPEP or serum free light chains ratio, comes back positive, you do not need to pursue further testing for ATTR amyloidosis. When should genetic testing be performed in suspected ATTR amyloidosis? All patients diagnosed with ATTR amyloidosis should undergo genetic testing to distinguish wild-type from hereditary forms. Wild-type ATTR: More common in older men (≥70 years), no known mutation, sporadic occurrence, often presents with predominantly cardiac involvement Familial ATTR: Autosomal dominant inheritance, more common in Black patients (V122I mutation), more likely to have neuropathy and earlier onset of heart failure (4th or 5th decade). Specific variants have typical geographic distribution and predilection to causing neuropathy and/or cardiomyopathy. When is a biopsy necessary to confirm ATTR amyloidosis? Biopsy is not needed if PYP scan is positive (Grade 2-3) and AL amyloidosis is ruled out. If the diagnosis remains uncertain, a biopsy can be performed of either a fat pad or salivary gland biopsy (easier, lower sensitivity) or an endomyocardial biopsy (gold standard but invasive). References - Diagnosis of Transthyretin amyloid cardiomyopathy Dorbala S, Ando Y, Bokhari S, et al. ASNC/AHA/ASE/EANM/HFSA/ISA/SCMR/SNMMI expert consensus recommendations for multimodality imaging in cardiac amyloidosis: Part 1 of 2-evidence base and standardized methods of imaging [published correction appears in J Nucl Cardiol. 2021 Aug;28(4):1761-1762. doi: 10.1007/s12350-021-02711-w.]. J Nucl Cardiol. 2019;26(6):2065-2123. doi:10.1007/s12350-019-01760-6 https://pubmed.ncbi.nlm.nih.gov/31468376 Writing Committee, Kittleson MM, Ruberg FL, et al. 2023 ACC Expert Consensus Decision Pathway on Comprehensive Multidisciplinary Care for the Patient With Cardiac Amyloidosis: A Report of the American College of Cardiology Solution Set Oversight Committee [published correction appears in J Am Coll Cardiol. 2023 Mar 21;81(11):1135. doi: 10.1016/j.jacc.2023.02.013.]. J Am Coll Cardiol. 2023;81(11):1076-1126. doi:10.1016/j.jacc.2022.11.022 https://pubmed.ncbi.nlm.nih.gov/36697326

Jul 10

CardioNerds (Dr. Claire Cambron and Dr. Rawan Amir) join Dr. Ayan Purkayastha, Dr. David Song, and Dr. Justin Wang from NewYork-Presbyterian Queens for an afternoon of hot pot in downtown Flushing. They discuss a case of congenital heart disease presenting in adulthood. Expert commentary is provided by Dr. Su Yuan, and audio editing for this episode was performed by CardioNerds Intern, Julia Marques Fernandes. A 53-year-old woman with a past medical history of hypertension visiting from Guyana presented with 2 days of chest pain. EKG showed dominant R wave in V1 with precordial T wave inversions. Troponin levels were normal, however she was started on therapeutic heparin with plan for left heart catheterization. Her chest X-ray revealed dextrocardia and echocardiogram was suspicious for the systemic ventricle being the morphologic right ventricle with reduced systolic function and the pulmonic ventricle being the morphologic left ventricle. Patient underwent coronary CT angiography which confirmed diagnosis of congenitally corrected transposition of the great arteries (CCTGA) as well as minimal non-obstructive coronary artery disease. Her chest pain spontaneously improved and catheterization was deferred. Patient opted to follow with a congenital specialist back in her home country upon discharge. US Cardiology Review is now the official journal of CardioNerds! Submit your manuscript here. CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls- A Case of Congenital Heart Disease Presenting in Adulthood Congenitally Corrected Transposition of the Great Arteries (CCTGA) is a rare and unique structural heart disease which presents as an isolated combination of atrioventricular and ventriculoarterial discordance resulting in physiologically corrected blood flow. CCTGA occurs due to L looping of the embryologic heart tube. As a result, the morphologic right ventricle outflows into the systemic circulation, and the morphologic left ventricle outflows into the pulmonary circulation. CCTGA is frequently associated with ventricular septal defects, pulmonic stenosis, tricuspid valve abnormalities and dextrocardia. CCTGA is often asymptomatic in childhood and can present later in adulthood with symptoms of morphologic right ventricular failure, tricuspid regurgitation, or cardiac arrhythmias. Systemic atrioventricular valve (SAVV) intervention can be a valuable option for treating right ventricular failure and degeneration of the morphologic tricuspid valve. notes- A Case of Congenital Heart Disease Presenting in Adulthood Notes were drafted by Ayan Purkayastha. What is the pathogenesis of Congenitally Corrected Transposition of the Great Arteries? Occurs due to disorders in the development of the primary cardiac tube Bulboventricular part of the primary heart forms a left-sided loop instead of right-sided loop, leading to the normally located atria being connected to morphologically incompatible ventricles This is accompanied by abnormal torsion of the aortopulmonary septum (transposition of the great vessels) As a result, there is ‘physiologic correction’ of blood flow. Non-oxygenated blood flows into the right atrium and through the mitral valve into the morphologic left ventricle, which pumps blood into the pulmonary artery. Oxygenated blood from the pulmonary veins flows into the left atrium and through the tricuspid valve to the morphologic right ventricle, which pumps blood to the aorta. Compared with standard anatomy, the flow of blood is appropriate, but it is going through the incorrect ventricle on both sides. Frequent conditions associated with CCTGA include VSD, pulmonic stenosis and dextrocardia What is the presentation of Congenitally Corrected Transposition of the Great Arteries? In cases without concomitant deficits CCTA is asymptomatic early in life and often for several decades. Cyanosis and dyspnea are common presenting symptoms. Systemic right ventricular dysfunction due to high systemic pressures over time Arrythmias, commonly AV block, due to abnormal structure of the conduction system Tricuspid valve regurgitation resulting from dilation of the right ventricle and tricuspid valve annulus What is Dextrocardia and how is it associated with CCTGA? Dextrocardia is a cardiac positional anomaly where the heart is located in the right hemithorax with base to apex axis directed to the right and caudad Dextrocardia can occur in up to 20% cases of CCTGA Can be associated with both situs solitus (normal anatomic arrangement of chest and abdominal organs) or situs inversus (chest and abdominal organs are mirrored from their normal positions) How is CCTGA Diagnosed? Transthoracic echocardiography is the primary diagnostic tool in CCTGA Assessment of the systemic RV function is crucial but can be challenging. Techniques such as speckle tracking echocardiography and global longitudinal strain can help with assessment of systemic RV function Cardiac MRI can also provide accurate measurements of ventricular volumes as well as quantification of valvular regurgitation What is the long-term management of CCTGA in adults? Many patients with CCTGA and no associated lesions have long life expectancies with minimal or non-specific symptoms Symptoms of circulatory failure occur mainly in 5th and 6th decades of life The 2018 AHA/ACC Guidelines for the Management of Adults with Congenital Heart Disease recommends the following routine follow-up and testing intervals for CCTGA Physiologic stage A: Outpatient ACHD follow up every 12 months with ECG(12 months), TTE(12-24 months), Holter monitor(12-60 months), CMR/CCT and exercise test(36-60 months) Physiologic stage B: outpatient ACHD follow up every 12 months with ECG and TTE(12 months), Holter monitor(12-60 months), CMR/CCT and exercise test(36-60 months) Physiologic stage C: outpatient ACHD follow up every 6-12 months with ECG and TTE(12 months), pulse oximetry at each visit, Holter monitor(12-36 months), CMR/CCT and exercise test(12-24 months) Physiologic stage D: outpatient ACHD follow up every 3-6 months, ECG and TTE every 12 months, pulse oximetry at each visit, Holter monitor, CMR/CCT and exercise test every 12 months What is the role of Systemic Atrioventricular Valve Surgery (SAVV) for treatment of CCTGA as an adult? In CCTGA the morphologic tricuspid valve acts as the SAVV and is subject to functional deterioration from high systemic pressures Tricuspid valve regurgitation is a key prognostic overall survival determinant in CCTGA patients Studies have shown that 94% of patients with CCTGA suffered from intrinsic tricuspid valve abnormalities SAV surgery remains a valuable option with low early mortality and good long-term outcomes, especially with ejection fraction > 40%. The 2018 AHA/ACC Guidelines for the Management of Adults with Congenital Heart Disease recommends tricuspid valve replacement for symptomatic adults with CCTGA and severe TR and preserved or mildly depressed systemic ventricular function (class IB recommendation). References - A Case of Congenital Heart Disease Presenting in Adulthood 1. Baruteau AE, Abrams DJ, Ho SY, Thambo JB, McLeod CJ, Shah MJ. Cardiac Conduction System in Congenitally Corrected Transposition of the Great Arteries and Its Clinical Relevance. J Am Heart Assoc. 2017;6(12). doi:10.1161/JAHA.117.007759 2. Susheel Kumar TK. Congenitally corrected transposition of the great arteries. J Thorac Dis. 2020;12(3):1213-1218. doi:10.21037/jtd.2019.10.15 3. Osakada K, Ohya M, Waki K, Nasu H, Kadota K. Congenitally Corrected Transposition of the Great Arteries at Age 88 Years. CJC Open. 2020;2(6):726-728. doi:10.1016/j.cjco.2020.08.003 4. Munaf M, Farooqui S, Kazmi SK, Ul-Haque I. Congenitally Corrected Transposition of Great Arteries with Dextrocardia, Patent Ductus Arteriosus, Atrial Septal Defects and Ventricular Septal Defects in a 15-Year-Old Marfanoid Habitus Patient: A Case Study. Cureus. Published online July 1, 2020. doi:10.7759/cureus.8937 5. Abdelrehim AA, Stephens EH, Miranda WR, et al. Systemic Atrioventricular Valve Surgery in Patients With Congenitally Corrected Transposition of the Great Vessels. J Am Coll Cardiol. 2023;82(23):2197-2208. doi:10.1016/j.jacc.2023.09.822 6. Lippmann MR, Maron BA. The Right Ventricle: From Embryologic Development to RV Failure. Curr Heart Fail Rep. 2022;19(5):325-333. doi:10.1007/s11897-022-00572-z 7. Brida M, Diller GP, Gatzoulis MA. Systemic Right Ventricle in Adults with Congenital Heart Disease. Circulation. 2018;137(5):508-518. doi:10.1161/CIRCULATIONAHA.117.031544 8. Bevilacqua F, Pasqualin G, Ferrero P, et al. Overview of Long-Term Outcome in Adults with Systemic Right Ventricle and Transposition of the Great Arteries: A Review. Diagnostics. 2023;13(13). doi:10.3390/diagnostics13132205 9. Maldjian PD, Saric M. Approach to dextrocardia in adults: Review. American Journal of Roentgenology. 2007;188(6 SUPPL.). doi:10.2214/AJR.06.1179 10. Kandakure PR, Katta Y, Batra MJ, Timmanwar A, Lakka VK, Reddy B. Dextrocardia and corrected transposition of the great arteries with rheumatic tricuspid stenosis: a unique association. Indian J Thorac Cardiovasc Surg. 2019;35(2):230-232. doi:10.1007/s12055-018-0778-0 11. Stout KK, Daniels CJ, Aboulhosn JA, et al.

Jun 20

In this episode, CardioNerds Dr. Gurleen Kaur, Dr. Richard Ferraro, and Dr. Jake Roberts are joined by Cardio-Rheumatology expert, Dr. Monica Mukherjee, to discuss the role of utilizing multimodal imaging for cardiovascular disease risk stratification, monitoring, and management in patients with chronic systemic inflammation. The team delves into the contexts for utilizing advanced imaging to assess systemic inflammation with cardiac involvement, as well as the role of imaging in monitoring various specific cardiovascular complications that may develop due to inflammatory diseases. Audio editing by CardioNerds academy intern, Christiana Dangas. CardioNerds Prevention PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls - Cardiovascular Multimodality Imaging & Systemic Inflammation Systemic inflammatory diseases are associated with an elevated CVD risk that has significant implications for early detection, risk stratification, and implementation of therapeutic strategies to address these risks and disease-specific complications. As an example, patients with SLE have a 48-fold increased risk for developing ASCVD compared to the general population. They may also develop disease-specific complications, such as pericarditis, that require focused imaging approaches to detect. In addition to increasing the risk for CAD, systemic inflammatory diseases can also result in cardiac complications, including myocardial, pericardial, and valvular involvement. Assessment of these complications requires the use of different imaging techniques, with the modality and serial studies selected based on the suspected disease process involved. In most contexts, echocardiography remains the starting point for evaluating cardiac involvement in systemic inflammatory diseases and can inform the next steps in terms of diagnostic study selection for the assessment of specific cardiac processes. For example, if echocardiography is completed in an SLE patient and demonstrates potential myocardial or pericardial inflammation, the next steps in evaluation may include completing a cardiac MRI for better characterization. While no current guidelines or standards of care directly guide our selection of advanced imaging studies for screening and management of CVD in patients with systemic inflammatory diseases, our understanding of cardiac involvement in these patients continues to improve and will likely lead to future guideline development. Due to the vast heterogeneity of cardiac involvement both across and within different systemic inflammatory diseases, a personalized approach to caring for each individual patient remains central to CVD evaluation and management in these patients. For example, patients with systemic sclerosis and symptoms of shortness of breath may experience these symptoms due to a range of causes. Echocardiography can be a central guiding tool in assessing these patients for potential concerns related to pulmonary hypertension or diastolic dysfunction. Based on the initial echocardiogram, the next steps in evaluation may involve further ischemic evaluation or right heart catheterization, depending on the pathology of concern. Show notes - Cardiovascular Multimodality Imaging & Systemic Inflammation Episode notes drafted by Dr. Jake Roberts. What are the contexts in which we should consider pursuing multimodal cardiac imaging, and are there certain inflammatory disorders associated with systemic inflammation and higher associated CVD risk for which advanced imaging can help guide early intervention? Systemic inflammatory diseases are associated with elevated CVD risk, which has significant implications for early detection, risk stratification, prognostication, and implementation of therapeutic strategies to address CVD risk and complications in these patient populations.The most well-characterized autoimmune diseases with an association between systemic inflammation and CVD risk are inflammatory arthritic conditions such as rheumatoid arthritis. Additional inflammatory diseases with elevated CVD risk include spondyloarthropathies and psoriatic arthritis.Patients with rheumatoid arthritis have a 1.5- 2x risk of developing coronary artery disease compared to the general population.The mechanism of elevated CVD risk in inflammatory disease patients is likely related to a combination of abnormalities in lipid metabolism, endothelial dysfunction, and vascular inflammation. Conditions including systemic lupus erythematosus (SLE), myositis, vasculitis disorders, and systemic sclerosis may have additional cardiovascular complications beyond CAD, including pericarditis, myocarditis, electrical, and valvular complications. Are there any established or emerging technologies to help with improving early detection or characterization of cardiac involvement in systemic inflammatory diseases? Echocardiography remains the most common and useful starting point for screening and early detection of cardiac involvement in systemic inflammatory diseases due to its widespread availability, real-time interpretation, low cost, and noninvasive nature. Furthermore, echocardiography remains a crucial tool in serial monitoring for disease progression and the detection of therapeutic effects. This modality additionally provides significant utility for early detection and screening of pericardial and valvular involvement. Given that patients with inflammatory disorders have an elevated risk for developing CAD, utilizing CAC scores and CCTA are often additionally helpful for CAD detection in these patient populations. Are there different imaging techniques that should be used to assess complications specific to different systemic inflammatory diseases? Based on the specific disease involved, the choice of imaging technique may vary depending on the clinical context and the cardiovascular complication requiring further investigation. As an example, in systemic sclerosis, there can be a wide range of variable cardiac manifestations that emerge depending on the subtype of the disease, with the cardiac complications developing either because of the fibrotic disease process or from other secondary effects of the disease. Specifically, if the patient's phenotype involves interstitial lung disease, the right ventricle of the heart will encounter chronic increased afterload, which can lead to adverse adaptive responses and remodeling over time. As a result, screening tools such as echocardiography can be very useful in this patient population, with these patients often requiring regular annual screening echocardiograms coupled with pulmonary function testing to screen for coupled changes in individual patients’ physiology. When these patients develop complications of their disease, including pulmonary hypertension, echocardiography can help evaluate the underlying cause of this complication and inform subsequent diagnostic steps. In terms of assessing myocardial disease and inflammation in myocardial tissue, cardiac MRI remains a valuable tool in detecting subclinical myocardial disease and can identify areas of low-grade myocardial inflammation. One of the advantages of cardiac MRI over other imaging techniques involves its ability to allow for noninvasive tissue characterization. For disease complications such as pericarditis, which can commonly develop in SLE, 2D echocardiography remains the first-line imaging modality of choice to detect pericardial disease involvement. In SLE patients who have long-standing pericardial disease with progression, they can also develop constrictive symptoms resulting from this process. In those cases, either CT or cardiac MRI can assist in defining the pericardial or myocardial anatomy. As an example, what would be the approach to utilizing advanced imaging to assess for CVD detection and monitoring in a patient with SLE with relatively well-controlled symptoms on chronic immunosuppressive agents and no prior history of heart failure or CVD? As a starting point, all patients with systemic inflammatory diseases should undergo comprehensive ASCVD risk assessment. Initial stratification involves completing a laboratory assessment with a standard lipid panel and diabetes screening studies. Further evaluation of any symptoms that a patient may describe, which could indicate potential early cardiovascular disease processes, should also be thoroughly assessed and may influence the next steps in screening. In the context of SLE, pericardial disease is common, and therefore, obtaining a baseline echocardiogram to assess for any early pericardial involvement should be the initial step in evaluation. If the patient also has an elevated ASCVD risk, they should also undergo assessment for coronary artery disease. What should be the approach to the sequence of imaging technique selection, serial imaging, monitoring, and follow-up in patients with systemic inflammatory disorders undergoing evaluation of CVD screening and monitoring? The initial selection of imaging modality should be based on what is suspected to be the primary driver of the patient’s symptoms or as the primary underlying process of concern that requires further evaluation. As an important consideration in the context of systemic inflammatory diseases such as SLE, ischemic disease may involve atypical presentations due to underlying myocardial dysfunction and microvascular disease. Therefore, imaging and other diagnostic studies may be warranted to assess for reversible ischemia. There is emerging evidence that cardiac PET perfusion and cardiac MRI may be particularly useful in this patient population to assess coronary flow reserve to evaluate for coronary microvascular disease.

Jun 4

In this episode, CardioNerds Dr. Anna Radakrishnan and Dr. Apoorva Gangavelli are joined by prevention expert Dr. Martha Gulati and heart failure expert Dr. Anu Lala to discuss heart failure with preserved ejection fraction (HFpEF), a multifactorial, evolving challenge, particularly in women. In this episode, we delve into the distinctive clinical presentation and pathophysiology of HFpEF among women, exploring both traditional and gender-specific risk factors, from metabolic and inflammatory processes to the impact of obesity, sleep apnea, and gender-specific conditions. We also discussed the latest evidence on prevention strategies and emerging therapies that not only target HFpEF symptoms but also address underlying risk factors. This conversation highlights the importance of multidisciplinary, holistic care to advance diagnosis, management, and ultimately, patient outcomes for women with HFpEF. Audio editing by CardioNerds academy intern, Christiana Dangas. Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. CardioNerds Heart Success Series PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls - HFpEF in Women HFpEF Is a Multisystem Syndrome:HFpEF in women involves more than just diastolic dysfunction—it represents a convergence of metabolic, inflammatory, and hormonal factors that make its diagnosis and management uniquely challenging. Visceral Adiposity Drives Risk:Obesity isn’t just excess weight; central or visceral adiposity actively promotes inflammation, insulin resistance, and microvascular dysfunction, which are crucial in triggering HFpEF in women. Early Identification Is Key:Recognizing—and treating—subtle risk factors such as sleep-disordered breathing, hypertension, and subtle metabolic dysfunction early, especially in women who may underreport symptoms, can prevent progression to HFpEF. Holistic, Lifespan Approach Matters:Effective HFpEF care involves managing the whole cardiometabolic profile with tailored lifestyle interventions, advanced medications (e.g., SGLT2 inhibitors, GLP-1 agonists), and even cardiac rehabilitation, which remain critical at every stage, even after diagnosis. Tailoring Prevention to Unique Risks in Women:Gender-specific factors such as postmenopausal hormonal changes, pregnancy-related complications, and autoimmune conditions demand a customized prevention strategy, reminding us that prevention isn’t one-size-fits-all. Show notes - HFpEF in Women Notes drafted by Dr. Apoorva Gangavelli 1. What are the gender-based differences in HFpEF presentation? HFpEF in women often presents with more subtle symptoms such as exertional dyspnea and fatigue, which may be mistakenly attributed to aging or obesity. Women tend to have a higher prevalence of preserved ejection fraction despite a similar heart failure symptom burden to men. The diagnostic challenge is compounded by lower natriuretic peptide levels influenced by hormonal factors, particularly postmenopausal estrogen deficiency, leading to false negatives and underdiagnosis. 2. How do traditional and gender-specific risk factors contribute to the development of HFpEF in women? Traditional risk factors include obesity, hypertension, diabetes, and metabolic syndrome. Gender-specific risk factors encompass pregnancy-related complications, menopause, and autoimmune diseases, which may uniquely affect cardiovascular structure and function in women. The interaction between visceral adiposity and systemic inflammation is central in predisposing women to HFpEF. 3. What underlying pathophysiological mechanisms make women more susceptible to HFpEF? Chronic inflammation and endothelial dysfunction contribute to myocardial stiffness and diastolic dysfunction. Insulin resistance results in impaired myocardial metabolism and lipotoxicity. Microvascular dysfunction, with reduced nitric oxide bioavailability, is more pronounced in women, exacerbating cardiac remodeling and fibrosis. 4. What prevention strategies can be tailored across different life stages to reduce HFpEF risk in women? Early detection and aggressive management of traditional risk factors (e.g., blood pressure control, weight management) during perimenopause and early adulthood. Incorporating lifestyle modifications such as structured exercise programs, improved dietary habits, and sleep optimization. Preventive interventions might also include screening for gender-specific risk factors like pregnancy complications and autoimmune conditions early in life. 5. What current and emerging therapeutic approaches are used in the management of HFpEF in women? Use of mineralocorticoid receptor antagonists and nonsteroidal alternatives shows promise, particularly in reducing hospitalizations. Novel pharmacologic agents such as SGLT2 inhibitors and GLP-1 receptor agonists address both heart failure symptoms and metabolic dysfunction. Cardiac rehabilitation is advocated to improve functional capacity and quality of life despite challenges with insurance coverage. References - HFpEF in Women Borlaug BA, Sharma K, Shah SJ, Ho J. Heart Failure With Preserved Ejection Fraction. Journal of the American College of Cardiology. 2023;81(18). doi:https://doi.org/10.1016/j.jacc.2023.01.049 ‌Kittleson MM, Gurusher Panjrath, Kaushik Amancherla, et al. 2023 ACC Expert Consensus Decision Pathway on Management of Heart Failure With Preserved Ejection Fraction. Journal of the American College of Cardiology. 2023;81(18). doi:https://doi.org/10.1016/j.jacc.2023.03.393 Radakrishnan A, Agrawal S, Singh N, et al. Underpinnings of Heart Failure With Preserved Ejection Fraction in Women - From Prevention to Improving Function. A Co-publication With the American Journal of Preventive Cardiology and the Journal of Cardiac Failure. Journal of Cardiac Failure. Published online February 2025. doi:https://doi.org/10.1016/j.cardfail.2025.01.008

May 14

In this webinar, the CardioNerds collaborated with the Cardiogenic Shock Working Group (CSWG) to discuss LV unloading and the updated AMI guidelines, which upgraded transvalvular flow pumps to a Class 2A recommendation in AMI shock. Dr. Rachel Goodman and Dr. Gurleen Kaur from CardioNerds were joined by Dr. Navin Kapur (Tufts Medical Center), Dr. Shashank Sinha (INOVA Fairfax Hospital), and Dr. Rachna Kataria (Brown University) from the CSWG. Together, they explore a case of an older woman who presented with inferior STEMI and was found to have complete occlusion of an anomalous single coronary artery originating from the right coronary cusp and supplying the entire left ventricle. She was treated with DES to the anomalous RCA. Her course was complicated by AMI shock with re-occlusion of the DES, which was treated with thrombectomy and balloon angioplasty. An IABP was placed. After transfer to a tertiary care center, a pulmonary artery catheter revealed a CI of 0.96. With worsening shock, rising lactate, and end organ dysfunction, the team proceeded with VA-ECMO and Impella CP for LV unloading. Her lactate subsequently normalized. Produced by CardioNerds in collaboration with the Cardiogenic Shock Working Group. CardioNerds Cardiac Critical Care PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron!

May 9

CardioNerds Critical Care Cardiology Council members Dr. Gurleen Kaur and Dr. Katie Vanchiere meet with Dr. Yash Patel, Dr. Akanksha, and Dr. Mohammed El Nayir from Trinity Health Ann Arbor. They discuss a case of pulmonary air embolism, RV failure, and cardiac arrest secondary to an ocular venous air embolism. Expert insights provided by Dr. Tanmay Swadia. Audio editing by CardioNerds Academy intern, Grace Qiu. A 36-year-old man with a history of multiple ocular surgeries, including a complex retinal detachment repair, suffered a post-vitrectomy collapse at home. He was found hypoxic, tachycardic, and hypotensive, later diagnosed with a pulmonary embolism from ocular venous air embolism leading to severe right heart failure. Despite a mild embolic burden, the cardiovascular response was profound, requiring advanced hemodynamic support, including an Impella RP device (Abiomed, Inc.). Multidisciplinary management, including fluid optimization, vasopressors and mechanical support to facilitate recovery. This case underscores the need for early recognition and individualized intervention in cases of ocular venous air embolism. US Cardiology Review is now the official journal of CardioNerds! Submit your manuscript here. CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls- Clear Vision, Clouded Heart: Ocular Venous Air Embolism with Pulmonary Air Embolism, RV Failure, and Cardiac Arrest Hypoxia, hypotension and tachycardia in a patient following ocular instrumentation are classic findings suggestive of pulmonary embolism from possible air embolism. The diagnosis of RV failure is based on clinical presentation, echocardiographic findings (such as McConnell’s sign), and invasive hemodynamic assessment via right heart catheterization. Mechanical circulatory support can be considered as a temporary measure for patients with refractory RV failure. Central Figure: Approach to Pulmonary Embolism with Acute RV Failure Notes - Clear Vision, Clouded Heart: Ocular Venous Air Embolism with Pulmonary Air Embolism, RV Failure, and Cardiac Arrest 1. What is an Ocular Venous Air Embolism (VAE), and how can it be managed in critically ill patients? An Ocular Venous Air Embolism is defined as the entry of air into the systemic venous circulation through the ocular venous circulation, often during vitrectomy procedures. Early diagnosis is key to preventing cardiovascular collapse in cases of Ocular Venous Air Embolism (VAE). The goal is to stop further air entry. This can be done by covering the surgical site with saline-soaked dressings and checking for air entry points. Adjusting the operating table can help, especially with a reverse Trendelenburg position for lower-body procedures. The moment VAE is suspected, discontinue nitrous oxide and switch to 100% oxygen. This helps with oxygenation, speeds up nitrogen elimination, and shrinks air bubbles. Hyperbaric Oxygen Therapy can reduce bubble size and improve oxygenation, especially in cases of cerebral air embolism, when administered within 6 hours of the incident. Though delayed hyperbaric oxygen therapy can still offer benefits, the evidence is mixed. VAE increases right heart strain, so inotropic agents like dobutamine can help boost cardiac output, while norepinephrine supports ventricular function and systemic vascular resistance, but this may also worsen pulmonary resistance. Aspiration of air via multi-orifice or Swan-Ganz catheters has limited success, with success rates ranging from 6% to 16%. In contrast, the Bunegin-Albin catheter has shown more promise, with a 30-60% success rate. Catheterization for acute VAE-induced hemodynamic compromise is controversial, and there's insufficient evidence to support its widespread emergency use. 2. What are the key hemodynamic parameters used to assess RV function? On echocardiogram, there are a number of parameters that can assess RV function: Tricuspid Annular Plane Systolic Excursion (TAPSE): Measures the lateral tricuspid annulus’ movement during systole. A TAPSE value below 1.6 cm is associated with poor prognosis.RV Outflow Tract (RVOT) Acceleration Time: Measured via pulsed wave Doppler, an acceleration time of <100 ms is abnormal, with values ≤60 ms indicating a worse prognosis.Global RV Longitudinal Strain: Assessed via speckle tracking, with a strain value of −20% being highly predictive of RV dysfunction (normal values typically range -24.5 to -28.5%).Tricuspid Regurgitation (TR) Jet Velocity: Helps estimate pulmonary systolic pressure and provides prognostic information.Inferior Vena Cava (IVC) Collapsibility: Useful in estimating right atrial pressure and guiding volume resuscitation, though it lacks prognostic significance. The RV:LV diameter ratio offers prognostic value, with a ratio greater than 0.9 linked to worse outcomes. Invasive Hemodynamic Monitoring (Right heart catheterization, PA Catheter) The Pulmonary Artery Pulsatility Index (PAPI) is an invasive hemodynamic parameter used to assess right ventricular (RV) function, particularly in cases of RV failure and cardiogenic shock. PAPi is the pulmonary arterial pulse pressure divided by the RA pressure. A PAPi of <0.9 is a poor indicator, especially in the acute myocardial infarction population. 3. What are the core principles in managing a patient with RV failure? The management to optimize RV function is centered around optimizing preload, afterload, and contractility.Optimizing preload - Optimizing preload is one of the most important aspects in the management of acute decompensated RV failure. The majority of us are taught that the RV is “preload dependent” and patients should be fluid resuscitated. However, many patients are actually volume overloaded and may benefit from diuresis. Overall, this is a patient-to-patient decision, depending on the clinical picture, to optimize preload; though the use of pulmonary artery (PA) catheters in this setting is not well supported.Reducing afterload - Avoid intubation if clinically feasible, as they may increase PVR; however, if essential, ideally, oxygen saturation (SaO₂) should be maintained above 92%, and ventilator settings should be adjusted to optimize lung volume and maintain a normal pH and PCO₂. Nitric oxide has also been beneficial in improving oxygenation and reducing PVR with its vasodilatory effects. Support cardiac output May support with the use of inotropes as well as mechanical circulatory support.Pressors: The ideal vasopressor increases systemic arterial pressure and RV contractility without raising pulmonary vascular resistance.Norepinephrine: Primarily an α1 agonist, it improves systemic blood pressure with some β1 stimulation. It has shown benefits in maintaining RV-PA coupling.Dobutamine: A β1 agonist that improves myocardial contractility and RV-PA coupling, though it can cause vasodilation at higher doses.In general, dobutamine is considered the best for acute RVF with PH, unless hypotension is a significant concern, in which case norepinephrine might be preferred. Milrinone is another option. MCS: short-term MCS should be considered in patients with cardiogenic shock as a bridge to recovery, a bridge to decision, or a bridge to bridge whilst the underlying causes for cardiogenic shock are addressed further described below Options include:Venous-arterial extracorporeal membranous oxygenation (V-A ECMO)RA to PA extracorporeal pump. (surgical RVAD) Flow device with an intake in the RA and an output in the PA. (Impella RP, Protek Duo) 4. When should we consider mechanical circulatory support for right ventricular (RV) failure? Short-term MCS should be considered in patients with cardiogenic shock as a bridge to recovery, a bridge to decision, or a bridge to bridge whilst the underlying causes for cardiogenic shock are addressed. Clinical parameters that suggest acute MCS use include signs of relative hypoperfusion plus hemodynamic features suggestive of RV failure, which were present in our patient. A specific additional consideration relates to where acute left-sided MCS reveals acute RV failure. Discerning whether this is intrinsic RV failure or due to persistently elevated RV afterload from inadequate LV support is also essential, as it will define management. The goal of percutaneous mechanical support is to bypass the right ventricle and improve hemodynamics, while allowing time for optimization of the patient and recovery of the RV. References Arrigo, Mattia, et al. “Diagnosis and Treatment of Right Ventricular Failure Secondary to Acutely Increased Right Ventricular Afterload (Acute Cor Pulmonale). A Clinical Consensus Statement of the Association for Acute CardioVascular Care (ACVC) of the ESC.” European Heart Journal. Acute Cardiovascular Care, vol. 13, no. 3, 22 Dec. 2023, pp. 304–312, https://doi.org/10.1093/ehjacc/zuad157. Accessed 17 May 2024. Chen, Guohai, et al. “INCIDENCE of ENDOPHTHALMITIS after VITRECTOMY: A Systematic Review and Meta-Analysis.” Retina (Philadelphia, Pa.), vol. 39, no. 5, May 2019, pp. 844–852, pubmed.ncbi.nlm.nih.gov/29370034/, https://doi.org/10.1097/IAE.0000000000002055. Fakkert, Raoul A, et al. “Early Hyperbaric Oxygen Therapy Is Associated with Favorable Outcome in Patients with Iatrogenic Cerebral Arterial Gas Embolism: Systematic Review and Individual Patient Data Meta-Analysis of Observational Studies.” Critical Care, vol. 27, no. 1, 12 July 2023, https://doi.org/10.1186/s13054-023-04563-x. Accessed 7 June 2024. Flaxel, Christina J., et al. “Idiopathic Epiretinal Membrane and Vitreomacular Traction Preferred Practice Pattern®.” Ophthalmology, vol. 127, no. 2, Feb. 2020, pp. P145–P183,

Apr 23

CardioNerds ACHD Council members Dr. Rawan Amir and Dr. Claire Cambron lead a profound conversation with ACHD faculty Dr. Allison Tsao, Dr. Jill Steiner, and Dr. Katherine Salciccioli. Together, they explore the emotional and professional challenges that ACHD providers face across the lifespan of congenital heart disease. Topics discussed include navigating challenging case scenarios, empowering patients through tough decisions, leveraging multi-subspecialty expertise, celebrating the successes, preparing for and grieving loss, and more. This episode was planned by the CardioNerds ACHD Council. CardioNerds Adult Congenital Heart Disease PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron!

Apr 10

CardioNerds (Drs. Daniel Ambinder and Eunice Dugan) are joined by Namrita Ashokprabhu, incoming medical student, along with Drs. Yulith Roca Alvarez and Mehmet Yildiz from The Christ Hospital. Expert insights provided by Dr. Odayme Quesada. Audio editing by CardioNerds intern Christiana Dangas. This episode explores how cardiac MRI and coronary function testing revealed coronary vasospasm in a case of MINOCA. Cardiac MRI is crucial in evaluating myocardial infarction with nonobstructive coronary arteries (MINOCA) and diagnosing myocarditis, but findings must be interpreted within clinical context. A 58-year-old man with hypertension, hyperlipidemia, diabetes, a family history of cardiovascular disease, and smoking history presented with sudden chest pain, non-ST-elevation on EKG, and elevated troponin I (0.64 µg/L). Cardiac angiography revealed nonobstructive coronary disease, including a 40% stenosis in the LAD, consistent with MINOCA. Eight weeks later, another event (troponin I 1.18 µg/L) led to cardiac MRI findings suggesting myocarditis. Further history revealed episodic chest pain and coronary vasospasm, confirmed by coronary functional angiography showing severe vasoconstriction, resolved with nitroglycerin. Management included calcium channel blockers and long-acting nitrates, reducing symptoms. Coronary vasospasm is a frequent MINOCA cause and can mimic myocarditis on CMRI. Invasive coronary functional testing, including acetylcholine provocation testing, is indicated in suspicious cases. US Cardiology Review is now the official journal of CardioNerds! Submit your manuscript here. CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Notes - Coronary Vasospasm What are the potential underlying causes of MINOCA (Myocardial Infarction with Non-Obstructive Coronary Arteries)? Plaque Rupture: Plaque disruption, which includes plaque rupture, erosion, and calcified nodules, occurs as lipids accumulate in coronary arteries, leading to inflammation, necrosis, fibrosis, and calcification. Plaque rupture exposes the plaque to the lumen, causing thrombosis and thromboembolism, while plaque erosion results from thrombus formation without rupture and is more common in women and smokers. Intravascular imaging, such as IVUS and OCT, can detect plaque rupture and erosion, with studies showing plaque disruption as a frequent cause of MINOCA, particularly in women, though the true prevalence may be underestimated due to limited imaging coverage. Coronary Vasospasm: Coronary vasospasm is characterized by nitrate-responsive chest pain, transient ischemic EKG changes, and >90% vasoconstriction during provocative testing with acetylcholine or ergonovine, due to hyper-reactivity in vascular smooth muscle. It is a common cause of MINOCA, with approximately half of MINOCA patients testing positive in provocative tests, and Asians are at a significantly higher risk than Whites. Smoking is a known risk factor for vasospasm. In contrast, traditional risk factors like sex, hypertension, and diabetes do not increase the risk, and vasospasm is associated with a 2.5–13% long-term risk of major adverse cardiovascular events (MACE). Spontaneous Coronary Artery Dissection: Spontaneous coronary artery dissection (SCAD) involves the formation of a false lumen in epicardial coronary arteries without atherosclerosis, caused by either an inside-out tear or outside-in intramural hemorrhage. SCAD is classified into four types based on angiographic features, with coronary angiography being the primary diagnostic tool. However, in uncertain cases, advanced imaging like IVUS or OCT may be used cautiously. While the true prevalence is unclear due to missed diagnoses, SCAD is more common in women and is considered a cause of MINOCA when it results in non-obstructive lesions, with various predisposing factors including genetics, fibromuscular dysplasia, and emotional stress. Coronary Embolism/Thrombosis: Coronary embolism, often underdiagnosed, can be classified based on thrombus origin as direct, paradoxical, or iatrogenic, with atrial fibrillation being the most common cause. A Japanese study found that only 2.9% of AMI patients were related to coronary embolism, and 73% of these cases were due to atrial fibrillation, with recurrent thromboembolic events occurring in 10% of patients during follow-up. Risk factors for coronary thromboembolism include hereditary thrombophilia, with 14% of MINOCA patients having hereditary thrombophilia, and an extensive evaluation, including a hypercoagulable workup and screening for atrial fibrillation or patent foramen ovale, is crucial to determine the underlying cause. Coronary Microvascular Dysfunction: The role of microvascular dysfunction in MINOCA remains uncertain due to limited data, though it is characterized by impaired vasodilation, increased vasoconstriction, and abnormal microcirculation remodeling, which affects coronary flow reserve without epicardial disease. Microvascular dysfunction is often underdiagnosed because it requires invasive functional testing, and studies in patients with ischemia but no obstructive coronary disease (INOCA) show a prevalence of up to 41%. A small study of MINOCA patients found that 25% had low myocardial perfusion reserve, suggesting potential involvement, but further research is needed to establish its role as a cause of MINOCA. MINOCA mimickers: Myocarditis: Myocarditis, often caused by viral infections, can also result from bacterial infections, toxic substances, or autoimmune disorders, and is more common in younger patients, though it can affect all ages. Fulminant myocarditis, though rare, can lead to life-threatening cardiogenic shock, and is diagnosed through CMR showing diffuse myocardial edema on T2 and myocardial biopsy. A meta-analysis found that one-third of MINOCA patients had myocarditis, particularly younger patients and those with elevated C-reactive protein levels. Non-ischemic Cardiomyopathy: Non-ischemic cardiomyopathy encompasses conditions like dilated, hypertrophic, restrictive, and arrhythmogenic cardiomyopathy, with dilated cardiomyopathy being the most common. A longitudinal study found that 25% of MINOCA patients had non-ischemic cardiomyopathy, which was associated with the highest mortality compared to other MINOCA mechanisms. Stress CMR has also identified underlying microvascular dysfunction in patients with dilated cardiomyopathy. Takotsubo Cardiomyopathy: Takotsubo cardiomyopathy, or stress-induced cardiomyopathy, is characterized by reversible wall motion abnormalities without obstructive CAD. It is often triggered by emotional or physical stress and is associated with a catecholamine surge. The condition is more common in postmenopausal women and has four main anatomical variants, with apical ballooning being the most common. Diagnosis typically involves coronary angiography, ventriculography, and CMRI to rule out other causes of AMI, with risks of cardiogenic shock and death comparable to those of AMI patients with CAD. What are the key diagnostic tests to evaluate MINOCA, and how are they applied in this case? Coronary Intravascular Imaging: Coronary intravascular imaging with IVUS and OCT is essential for diagnosing plaque disruption in MINOCA and should be performed during coronary angiography of all three major epicardial arteries. IVUS identifies plaque disruption in up to 40% of MINOCA cases, while OCT detects the culprit lesion in about 50%. These imaging techniques are also valuable for evaluating SCAD in cases of diagnostic uncertainty. Cardiac Imaging: Transthoracic echocardiography is valuable for assessing cardiac function after MINOCA, diagnosing Takotsubo and non-ischemic cardiomyopathy, and monitoring recovery of left ventricular function. Transesophageal echocardiography may be considered when coronary embolism is suspected. CMR is recommended for uncertain MINOCA diagnoses, providing accurate results in 74–87% of cases. It can differentiate between ischemic and non-ischemic MI, diagnose myocarditis, and detect coronary microvascular dysfunction through perfusion imaging. CMR's diagnostic accuracy improves when performed closer to the event and also serves as a prognostic tool for long-term cardiovascular outcomes. Invasive Coronary Functional Testing: Provocative spasm testing with intracoronary acetylcholine helps diagnose coronary vasospasm (epicardial or microvascular) and endothelial-dependent microvascular dysfunction, with a low complication rate (0.5%). In MINOCA patients, spasm testing is positive in about half, with epicardial spasm in 65% and microvascular spasm in 35%. CFR assessed by doppler flow velocity or thermodilution (with values 25) are used to assess microvascular dysfunction, though CFR is more sensitive. While coronary microvascular dysfunction is linked to worse outcomes in INOCA, its prognostic impact in MINOCA is less clear. However, low CFR has been associated with increased mortality across various patient populations. How is MINOCA treated based on its underlying etiology? Plaque Rupture: Patients with plaque disruption should be treated with aspirin and high-intensity statin therapy. Additionally, for those with plaque disruption who do not require stenting, dual antiplatelet therapy with ticagrelor for up to 1 month may be considered, given the low revascularization rates at 1 year (5.7%) and 4 years (21.1%) follow-up. Coronary Vasospasm: Long-acting calcium channel blockers (both dihydropyridine and non-dihydropyridine) are commonly used in MINOCA patients with epicardial coronary vasospasm.

Mar 25

CardioNerds co-founders Dr. Daniel Ambinder and Dr. Amit Goyal are joined by Dr. Spencer Weintraub, Chief Resident of Internal Medicine at Northwell Health, Dr. Michael Albosta, third-year Internal Medicine resident at the University of Miami, and Anna Biggins, Registered Dietitian Nutritionist at the Georgia Heart Institute. Expert commentary is provided by Dr. Zahid Ahmad, Associate Professor in the Division of Endocrinology at the University of Texas Southwestern. Together, they discuss a fascinating case involving a patient with a new diagnosis of hypertriglyceridemia. Episode audio was edited by CardioNerds Intern Student Dr. Pacey Wetstein. A woman in her 30s with type 2 diabetes, HIV, and polycystic ovarian syndrome presented with one day of sharp epigastric pain, non-bloody vomiting, and a new lower extremity rash. She was diagnosed with hypertriglyceridemia-induced pancreatitis, necessitating insulin infusion and plasmapheresis. The CardioNerds discuss the pathophysiology of hypertriglyceridemia-induced pancreatitis, potential organic and iatrogenic causes, and the cardiovascular implications of triglyceride disorders. We explore differential diagnoses for cardiac and non-cardiac causes of epigastric pain, review acute and long-term management of hypertriglyceridemia, and discuss strategies for the management of the chylomicronemia syndrome, focusing on lifestyle changes and pharmacotherapy. This episode is part of a case reports series developed in collaboration with the National Lipid Association and their Lipid Scholarship Program, with mentorship from Dr. Daniel Soffer and Dr. Eugenia Gianos. US Cardiology Review is now the official journal of CardioNerds! Submit your manuscript here. CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls - Hypertriglyceridemia Cardiac sarcoidosis can present with a variety of symptoms, including arrhythmias, heart block, heart failure, or sudden cardiac death. The acute management of hypertriglyceridemia-induced pancreatitis involves prompt recognition and initiation of therapy to lower triglyceride levels using either plasmapheresis or intravenous insulin infusion +/- heparin infusion. Insulin infusion is used more commonly, while plasmapheresis is preferred in pregnancy. Medications such as fibrates and omega-3 fatty acids can be used to maintain long-term triglyceride reduction to prevent the recurrence of pancreatitis, especially in patients with persistent triglyceride elevation despite lifestyle modifications. Statins can be used in patients for ASCVD reduction in patients with a 10-year ASCVD risk > 5%, age > 40 years old, and diabetes or diabetes with end-organ damage or known atherosclerosis. Consider preferential use of icosapent ethyl as an omega-3 fatty acid for triglyceride lowering if the patients fit the populations that appeared to benefit in the REDUCE IT trial. Apply targeted dietary interventions within the context of an overall healthy dietary pattern, such as a Mediterranean or DASH diet. Limit full-fat dairy, fatty meats, refined starches, added sugars, and alcohol. Encourage high-fiber vegetables, whole fruits, low-fat or fat-free dairy, plant proteins, lean poultry, and fish. Pay special attention to the cooking oils to ensure the patient is not using palm oil, coconut oil, or butter when cooking. Instead, use liquid non-tropical plant oils. Initiate a very low-fat diet ( 750 mg/dL. Recommend and encourage patients to exercise regularly, with a minimum goal of 150 minutes/week of moderate-intensity aerobic activity. If weight loss is required, aim for more than >225 - 250 minutes/week. Develop patient-centered and multidisciplinary strategies for preventing hypertriglyceridemia-induced pancreatitis by incorporating patient education on the importance of medication adherence, specialist follow-up, regular monitoring of triglyceride levels, and lifestyle modifications to maintain optimal lipid profiles and reduce the future risk of pancreatitis. Notes - Hypertriglyceridemia Who is at risk for hypertriglyceridemia and what are the key pathophysiological mechanisms by which elevated triglycerides may lead to pancreatitis? The exact mechanism is not clear. The proposed mechanism is that when serum triglycerides exceed 1000 mg/dL, blood flow is impaired through the capillary beds supplying the pancreas, resulting in ischemia. The ischemic injury resulting from this disruption of microcirculation disrupts the acinar structure of pancreatic cells and exposes pancreatic enzymes to triglyceride-rich particles. This results in activation of enzymatic activity with degradation of the chylomicron-triglycerides particles, which causes inflammation, subsequently leading to hemorrhage, edema, and necrosis of the pancreatic tissue. Chylomicronemia syndrome can be multifactorial or familial. Familial chylomicronemia syndrome (FCS) is often discovered very early in life, and patients have a loss of function in one of the several genes involved in regulating triglyceride metabolism. These genes include LPL, APOC2, APOA5, LMF1, and GPIHBP1. Multifactorial chylomicronemia syndrome is the most common cause of chylomicronemia syndrome. It is usually the result of a clustering of genetic variants, including heterozygosity of one of the five genes previously mentioned, as well as more frequent variants with small effects in more than 40 additional genes that have been implicated. Having a genetic variant plus an aggravating factor will often exacerbate the metabolic defect and lead to chylomicronemia syndrome. There are many potential aggravating factors, but some of the more common ones include a diet high in refined sugars, heavy alcohol consumption, obesity with or without metabolic syndrome, medications, renal disease, HIV, and pregnancy. What are the acute treatment strategies for hypertriglyceridemia-induced pancreatitis, and how are they similar and different to treating pancreatitis from other etiologies? All patients should be assessed for hemodynamic compromise, the severity of illness with or without scoring systems, and end-organ damage to determine the need for intensive care resources. Initially, patients usually require aggressive fluid resuscitation and pain management, which are standard across all types of acute pancreatitis. Delayed fluid resuscitation has been associated with worse outcomes. Multiple trials have been performed evaluating the best amount of fluid. Although there is not an exact answer to this, as all patients are different, all patients should be resuscitated until euvolemic. The WATERFALL trial showed that administration of 10 mL/kg bolus followed by 1.5 mL/kg maintenance until the patient reaches euvolemia was a superior approach to more aggressive fluid resuscitation. A patient's volume status should be reassessed every 6 hours for 24 – 48 hours, and fluids should be discontinued once euvolemia has been achieved. There is no guideline consensus on the preferred analgesic management, but it is generally recommended to administer medication to mitigate symptoms of pain and nausea for all patients. For hypertriglyceridemia-induced pancreatitis, it is key to initiate fasting to decrease chylomicron production and further increasing triglyceride levels. Although historically, this was the same approach for other causes of pancreatitis, more recent data shows that early enteral feeding reduces the risk of complications such as pancreatic necrosis. However, these studies were not performed in patients with pancreatitis from hypertriglyceridemia and should not be extrapolated to this distinct population. Currently, it is recommended that patients be kept NPO until triglycerides are below 500 mg/dL, which is the point at which LPL activity becomes saturated. When feeding is initiated, it should be with a very low-fat diet with no refined carbohydrates. Hypertriglyceridemia differs from other causes of pancreatitis as the management is centered around the rapid reduction of triglyceride content in the blood. Generally, these patients are admitted to the intensive care unit to undergo either insulin infusion +/- heparin drip or plasmapheresis. Although there has never been a clinical trial comparing these two approaches, a recent comprehensive meta-analysis showed no significant difference in mortality or clinical outcomes. Insulin infusion had a lower number of deaths, but a higher rate of acute renal failure, hypoglycemia, and hypotension, neither of which reached statistical significance. Insulin is more commonly used and generally preferred given that it is more cost-effective, less invasive, and can have utility in treating underlying diabetes exacerbation, which is common amongst these patients. Insulin infusion works by increasing the activity of lipoprotein lipase (LPL), resulting in increased clearance of chylomicron particles. Although in some countries, insulin is combined with heparin, given heparin's ability to increase LPL release, this is rarely done as heparin can deplete endothelial LPL, increase bleeding events, and potentially cause heparin-induced thrombocytopenia. Plasmapheresis, on the other hand, works by removing the triglycerides directly from the bloodstream, which can rapidly reduce levels. It does require central venous access, which is more invasive. Plasmapheresis is preferred in pregnancy as data in case series supports it reduces the risk of a systemic inflammatory response. What are the proposed mechanisms by which high triglycerides may contribute to atherosclerosis?

Mar 13

CardioNerds (Dr. Rick Ferraro and Dr. Dan Ambinder) join Dr. Sri Mandava, Dr. David Meister, and Dr. Marissa Donatelle from the Columbia University Division of Cardiology at Mount Sinai Medical Center in Miami. Expert commentary is provided by Dr. Pranav Venkataraman. They discuss the following case involving a patient with cardiac sarcoidosis presenting as STEMI. A 57-year-old man with a history of hyperlipidemia presented with sudden onset chest pain. On admission, he was vitally stable with a normal cardiorespiratory exam but appeared in acute distress and was diffusely diaphoretic. His ECG revealed sinus rhythm, a right bundle branch block (RBBB), and ST elevation in the inferior-posterior leads. He was promptly taken for emergent cardiac catheterization, which identified a complete thrombotic occlusion of the mid-left circumflex artery (LCX) and large obtuse marginal (OM) branch, with no underlying coronary atherosclerotic disease. Aspiration thrombectomy and percutaneous coronary intervention (PCI) were performed, with one drug-eluting stent placed. An echocardiogram showed a left ventricular ejection fraction (EF) of 31%, hypokinesis of the inferior, lateral, and apical regions, and an apical left ventricular thrombus. The patient was started on triple therapy. A hypercoagulable workup was negative. A cardiac MRI was obtained to further evaluate non-ischemic cardiomyopathy. In conjunction with a subsequent CT chest, the results raised suspicion for cardiac sarcoidosis with systemic involvement. In view of a reduced EF and significant late-gadolinium enhancement, electrophysiology was consulted to evaluate for ICD candidacy. A decision was made to delay ICD implantation until a definitive diagnosis of cardiac sarcoidosis could be established by tissue biopsy. The patient was started on HF-GDMT and discharged with a LifeVest. Close outpatient follow-up with cardiology and electrophysiology was arranged. US Cardiology Review is now the official journal of CardioNerds! Submit your manuscript here. CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls - Cardiac Sarcoidosis Presenting as STEMI Cardiac sarcoidosis can present with a variety of symptoms, including arrhythmias, heart block, heart failure, or sudden cardiac death. Symptoms can be subtle or mimic other cardiac conditions. Conduction abnormalities, particularly AV block or ventricular arrhythmias, are common and may be the initial indication of cardiac involvement with sarcoidosis. The additive value of Echocardiography, FDG-PET, and cardiac MR is indispensable in the diagnostic workup of suspected cardiac sarcoidosis. Specific role of MRI/PET: Both cardiac MRI and FDG-PET provide a complementary role in the diagnosis of cardiac sarcoidosis. Cardiac MRI is an effective diagnostic screening tool with fairly high sensitivity but is limited by its inability to decipher inflammatory (“active” disease) versus fibrotic myocardium. FDG-PT helps to make this discrimination, refine the diagnosis, and guide clinical management. Ultimately, these studies are most useful when interpreted in the context of other clinical information. Primary prevention of sudden cardiac death in cardiac sarcoidosis focuses on risk stratification, with ICD placement for high-risk patients. For patients awaiting definitive diagnosis, a LifeVest may be used as a temporary measure to protect from sudden arrhythmic events until an ICD is placed. Notes - Cardiac Sarcoidosis Presenting as STEMI 1. Is STEMI always a result of coronary artery disease? By definition, a STEMI is an acute S-T segment elevation myocardial infarction. This occurs when there is occlusion of a major coronary artery, which results in transmural ischemia and damage, resulting in electrical changes seen on the ECG. The most common cause of coronary artery occlusion is coronary artery disease (CAD) from plaque rupture and thrombus formation; however, many other causes of coronary artery occlusion are not related to CAD. These include vasospasm (isolated and recurrent), in-situ thrombotic occlusion, spontaneous coronary artery dissection, and supply-demand mismatch, such as in the setting of severe anemia. DDx includes other causes of injury current, such as myocarditis. It is important to keep these other differentials in mind while preparing for coronary angiography, as it may help guide intra-catheterization and post-catheterization management. 2. What are the most common causes of LV thrombus? When considering the causes of thrombus formation, think of Virchow’s triad. As with any other location, thrombus formation in the LV may be caused by injury/inflammation, systemic thrombophilia, and stasis. Acute myocardial infarction (especially anterior MI) - damaged myocardium and impaired LV function lead to blood stasis and thrombus formation. Heart failure with reduced ejection fraction (HFrEF) - severely impaired contractility increases the risk of thrombus development Non-Ischemic cardiomyopathies - dilated or hypertrophic cardiomyopathies may cause abnormal blood flow, promoting thrombus formation. Arrhythmias - although more associated with atrial thrombus, atrial fibrillation can also contribute to LVT in cases of significant LV dysfunction. Ventricular arrhythmias can also cause LV thrombus. Hypercoagulable conditions - Conditions such as antiphospholipid antibody syndrome, inherited thrombophilias, malignancy-associated hypercoagulability, polycythemia vera, hyperhomocysteinemia, nephrotic syndrome or systemic lupus erythematous may predispose to LV thrombus formation Inflammatory conditions - conditions like myocarditis or cardiac sarcoidosis can lead to inflammation along with focal stasis from aneurysmal changes, contributing to thrombus formation 3. What is the clinical presentation of cardiac sarcoidosis? Chest pain: can arise from several mechanisms such as myocardial inflammation, pericarditis, coronary artery involvement, or arrhythmias. Heart Failure: symptoms such as dyspnea, fatigue, and peripheral edema may result from left ventricular dysfunction or restrictive cardiomyopathy. Arrhythmias: palpitations, dizziness or syncope may occur due to ventricular tachycardia or ventricular fibrillation. Conduction abnormalities: Heart block, especially complete AV block, is a common early manifestation. Some studies have found that AV block is the presenting symptom in more than 40% of patients with cardiac sarcoidosis. Sudden cardiac death (SCD): sudden death can occur due to ventricular arrhythmias or severe heart block. Asymptomatic: in some cases, cardiac sarcoidosis is discovered incidentally during imaging or evaluation for systemic sarcoidosis. 4. What are the key imaging modalities used in the diagnosis of cardiac sarcoidosis? Echocardiography, FDG-PET, and cardiac MRI are the key imaging modalities used to diagnose cardiac sarcoidosis. The echocardiogram is often normal in clinically silent disease, but several key features may be seen in clinically active disease. The most specific findings are basal interventricular thinning and LV aneurysm. Other less specific findings include increased LV wall thickness, LV/RV diastolic and/or systolic dysfunction, and wall motion abnormalities (non-coronary distribution). Strain imaging is promising for use in earlier stages of disease, but this is not well established yet. FDG-PET is crucial in the initial diagnosis of cardiac sarcoidosis, allowing active inflammatory disease to be detected. There is no pathognomonic PET finding; however, focal or focal-on-diffuse FDG uptake patterns are highly suggestive of active disease. It should be noted that FDG-PET is also useful in guiding treatment or response to immunosuppressive therapy, as it can track the degree of inflammation over time. The role of cardiac MRI is discussed below. 5. What is the specific role of cardiac MRI in the diagnosis of cardiac sarcoidosis? This depends on the specific clinical setting. A patient with established extra-cardiac sarcoidosis but asymptomatic from a cardiac standpoint should be appropriately screened for cardiac involvement by clinical history, ECG, echocardiography, and cardiac monitoring (e.g. Holter monitor, etc). If any of the aforementioned “screening” tests are abnormal, a cardiac MRI is then indicated to assess for evidence of cardiac sarcoidosis. More specifically, cardiac MRI detects inflammation and edema at earlier stages of disease and scar tissue at later stages. The classical finding specific for cardiac sarcoidosis is patchy late gadolinium enhancement, with a predilection for the basal septum and basal inferolateral wall. The enhancement is either subepicardial or mid-wall and rarely transmural. It should be noted that once cardiac sarcoidosis is diagnosed, FDG-PET imaging should be utilized in conjunction with, or complementary to MRI, to assess for “active sarcoid” (i.e. myocardial inflammation). On the other hand, a patient with no known extracardiac sarcoidosis but with suggestive cardiac findings should have a cardiac MRI to assess for typical features as mentioned above, in addition to assessment for non-cardiac involvement. It should be noted that cardiac MRI can also provide significant prognostic information. The presence of LGE portends a worse prognosis due to increased CV death and ventricular arrhythmias. It should also be noted that LGE does not discriminate between active inflammation and fibrosis. Tissue characterization with T1 and T2 mapping techniques or PET imaging, as described above, can be more useful in this sense. References 1.) Cheng RK, Kittleson MM,

Mar 5

CardioNerds Cardiac Amyloidosis Series Chair Dr. Rick Ferraro and Episode Lead Dr. Anna Radakrishnan discuss the biology of transthyretin amyloid cardiomyopathy (ATTR-CM ) with Dr. Daniel Judge. Notes were drafted by Dr. Anna Radakrishnan. The audio was engineered by student Dr. Julia Marques. This episode provides a comprehensive overview of transthyretin (ATTR) cardiac amyloidosis, a complex and rapidly evolving disease process. The discussion covers the key red flags for cardiac amyloidosis, the diagnostic pathway, and the implications of hereditary versus wild-type ATTR. Importantly, the episode delves into the current and emerging therapies for ATTR, including stabilizers, gene silencers, and promising treatments like CRISPR-Cas9 and antibody-based approaches. Dr. Judge shares his insights and excitement about the rapidly advancing field, highlighting the need for early diagnosis and the potential to improve long-term outcomes for patients with this condition. Enjoy this Circulation Paths to Discovery article to learn more about the CardioNerds mission and journey. US Cardiology Review is now the official journal of CardioNerds! Submit your manuscripts here. CardioNerds Cardiac Amyloid PageCardioNerds Episode Page Pearls: - Biology of Transthyretin amyloid cardiomyopathy Maintain a high index of suspicion! Look for subtle (yet telling) signs like ventricular hypertrophy, discordant EKG findings, bilateral carpal tunnel syndrome, and spontaneous biceps tendon rupture. Utilize the right diagnostic tests. Endomyocardial biopsy remains the gold standard, but non-invasive tools like PYP scan with SPECT imaging and genetic testing are essential for accurate diagnosis. Differentiating hereditary from wild-type ATTR is critical, as genetic forms may have a more aggressive course and familial implications. Early diagnosis and intervention significantly improve prognosis, making vigilance in screening and prompt treatment initiation essential. The future is now! Cutting-edge therapies are transforming the treatment landscape, including TTR stabilizers, gene silencers, and emerging technologies like CRISPR-Cas9 and antibody-based treatments. Notes - Biology of Transthyretin amyloid cardiomyopathy What is transthyretin amyloid (aTTR) and how is it derived? Transthyretin (TTR) is a transport protein primarily synthesized by the liver, responsible for carrying thyroid hormones (thyroxine) and retinol (vitamin A) in the blood. It circulates as a tetramer, composed of four identical monomers, which is essential for its stability and function. In transthyretin amyloid (ATTR) amyloidosis, the TTR protein becomes unstable, leading to its dissociation into monomers. These monomers misfold and aggregate into insoluble amyloid fibrils, which deposit extracellularly in tissues such as the heart, nerves, and gastrointestinal tract. This progressive amyloid deposition leads to organ dysfunction, including restrictive cardiomyopathy and neuropathy. There are two main forms of ATTR amyloidosis: hereditary (variant) and wild-type (senile) ATTR. Hereditary ATTR (ATTRv) is caused by mutations in the TTR gene. These mutations destabilize the TTR tetramer, making it more prone to dissociation. This increases misfolding and amyloid fibril formation, resulting in systemic amyloid deposition. Wild-type ATTR (ATTRwt) occurs without genetic mutations and is primarily age-related. Over time, even normal TTR tetramers can become unstable, leading to gradual misfolding and amyloid deposition, particularly in the heart. ATTRwt is a common but often underdiagnosed cause of heart failure with preserved ejection fraction (HFpEF) in elderly individuals. How does aTTR lead to deleterious effects in the heart and other organ systems? Transthyretin amyloidosis leads to organ dysfunction through the deposition of misfolded TTR protein as amyloid fibrils, which accumulate extracellularly and disrupt normal tissue architecture and function. These deposits cause progressive damage by increasing stiffness, inducing oxidative stress, and impairing normal cellular function. Cardiac manifestations include amyloid deposition in the myocardial interstitium, leading to increased stiffness, diastolic dysfunction, and restrictive cardiomyopathy. As the disease progresses, systolic dysfunction may develop. Amyloid infiltration can also cause arrhythmia, conduction abnormalities such as atrioventricular block and atrial fibrillation, valvular thickening, coronary ischemia, and pericardial effusion. Disruption of transverse tubules in cardiomyocytes contributes to heart failure and arrhythmia. Systemic involvement depends on the culprit amylodogenic protein. AL amyloidosis caused by deposition of immunoglobulin light chains may deposit in and disrupt the function of any tissue/organ except for the central nevous system. ATTR amyloidosis primarily affects the heart, peripheral nerves, and the musculoskeletal system. Peripheral neuropathy can cause sensory loss, pain, and motor weakness, while autonomic dysfunction may lead to orthostatic hypotension, gastroparesis, and urinary retention. Carpal tunnel syndrome is a common early sign. Gastrointestinal amyloid deposits (specifically for AL but not ATTR) can cause gastroparesis, diarrhea, constipation, and malabsorption, leading to weight loss and malnutrition. Renal involvement (specifically for AL but not ATTR), though less common, can present as proteinuria and renal dysfunction. Amyloid deposition in soft tissues and the lungs may lead to hoarseness and musculoskeletal stiffness. As the disease progresses, continued amyloid accumulation leads to worsening organ dysfunction and failure. Early diagnosis and intervention are essential to slowing disease progression and managing symptoms effectively. When and why is aTTR cardiac amyloidosis hereditary versus obtained sporadically? Hereditary aTTR is caused by genetic mutations in the TTR gene, which are often autosomal dominant. Common mutations include V122I (more common in African Americans) and V30M (more common in certain regions like Portugal). Hereditary aTTR typically presents at an earlier age and may have a more aggressive course, with a higher likelihood of neuropathic involvement. Wild-type aTTR, or senile systemic amyloidosis, occurs sporadically and is more common in older individuals, typically without a family history. The exact reasons for the development of wild-type aTTR are not fully understood, but factors like chronic inflammation and exercise may play a role in the misfolding and aggregation of the normal TTR protein. References: Biology of Transthyretin amyloid cardiomyopathy Ruberg FL, Maurer MS. Cardiac Amyloidosis Due to Transthyretin Protein. JAMA. 2024;331(9):778-778. https://doi.org/10.1001/jama.2024.0442 Ruberg FL, Grogan M, Hanna M, Kelly JW, Maurer MS. Transthyretin Amyloid Cardiomyopathy. Journal of the American College of Cardiology. 2019;73(22):2872-2891. https://doi.org/10.1016/j.jacc.2019.04.003 ‌Maurer MS, Bokhari S, Damy T, et al. Expert Consensus Recommendations for the Suspicion and Diagnosis of Transthyretin Cardiac Amyloidosis. Circulation: Heart Failure. 2019;12(9). https://doi.org/10.1161/circheartfailure.119.006075 ‌Griffin JM, Rosenthal JL, Grodin JL, Maurer MS, Grogan M, Cheng RK. ATTR Amyloidosis: Current and Emerging Management Strategies. JACC: CardioOncology. 2021;3(4):488-505. https://doi.org/10.1016/j.jaccao.2021.06.006

Feb 24

Join CardioNerds EP Council Chair Dr. Naima Maqsood and Episode Lead Dr. Jeanne De Lavallaz as they discuss the results of the VANISH2 Trial with expert faculty Dr. Jeff Healey and Dr. Roderick Tung. Audio editing by CardioNerds academy intern, Grace Qiu. The VANISH2 trial enrolled 416 patients with ischemic cardiomyopathy, an ICD in place, and recurrent episodes of sustained monomorphic ventricular tachycardia (VT) to receive either first-line VT catheter ablation or antiarrhythmic drug therapy with the primary composite outcome of death from any cause, appropriate ICD shock, ventricular tachycardia storm (meaning at least 3 ventricular tachycardia events within 24hrs) or treated ventricular tachycardia below the detection limit of the ICD. The study population had a mean age of 68 years, with 94% being men and predominantly of white ethnicity. On average, 14 years had elapsed since their last myocardial infarction, with approximately 60% having undergone percutaneous coronary intervention at the time. The mean ejection fraction was 34%. This episode was planned in collaboration with Heart Rhythm TV with mentorship from Dr. Daniel Alyesh and Dr. Mehak Dhande. CardioNerds Journal Club PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! References - VANISH2 Trial Sapp, J. L., Tang, A. S. L., Parkash, R., Stevenson, W. G., Healey, J. S., Gula, L. J., Nair, G. M., & the VANISH2 Study Team. (2025). Catheter ablation or antiarrhythmic drugs for ventricular tachycardia. The New England Journal of Medicine, 392, 737–747.

Feb 14

CardioNerds (Dr. Colin Blumenthal and Dr. Saahil Jumkhawala) join Dr. Rohan Ganti, Dr. Nikita Mishra, and Dr. Jorge Naranjo from the Rutgers – Robert Wood Johnson program for a college basketball game, as the buzz around campus is high. They discuss the following case involving a patient with ventricular tachycardia: The case involves a 61-year-old man with a medical history of hypothyroidism, hypertension, hyperlipidemia, seizure disorder on anti-epileptic medications, and major depressive disorder, who presented to the ER following an out-of-hospital cardiac arrest. During hospitalization, he experienced refractory polymorphic ventricular tachycardia (VT), requiring 18 defibrillation shocks. Further evaluation revealed non-obstructive hypertrophic cardiomyopathy (HCM). We review the initial management of electrical storm, special ECG considerations, diagnostic approaches once ischemia has been excluded, medications implicated in polymorphic VT, the role of multi-modality imaging in diagnosing hypertrophic cardiomyopathy, and risk stratification for implantable cardioverter-defibrillator (ICD) placement in patients with HCM. Expert commentary is provided by Dr. Sabahat Bokhari. Episode audio was edited by CardioNerds Intern and student Dr. Pacey Wetstein. US Cardiology Review is now the official journal of CardioNerds! Submit your manuscript here. CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls - A Curious Case of Refractory Ventricular Tachycardia - Rutgers-Robert Wood Johnson Diagnostic Uncertainty in VT Storm: In VT storm, ischemia is a primary consideration; when coronary angiography excludes significant epicardial disease, alternative causes such as cardiomyopathies, channelopathies, myocarditis, electrolyte disturbances, or drug-induced arrhythmias must be explored. ST elevations in ECG lead aVR: ST elevations in lead aVR and diffuse ST depressions can sometimes represent post-arrest oxygen demand and myocardial mismatch rather than an acute coronary syndrome. This pattern may occur in the context of polymorphic VT (PMVT), where myocardial oxygen demands outstrip supply, especially after an arrest. While these ECG changes could suggest myocardial ischemia, caution is needed, as they might not always indicate coronary pathology. However, PMVT generally should raise suspicion for underlying coronary disease and may warrant a coronary angiogram for further evaluation. Medication Implications in PMVT and HCM: Certain medications, including psychotropic drugs (e.g., antidepressants, antipsychotics) and anti-epileptic drugs, can prolong the QT interval or interact with other drugs, thereby increasing the risk of polymorphic VT in patients with underlying conditions like HCM. Careful management of these medications is critical to avoid arrhythmic events in predisposed individuals. Multi-Modality Imaging in HCM: Cardiac MRI with late gadolinium enhancement (LGE) is invaluable in assessing myocardial fibrosis, a key predictor of arrhythmic risk, and can guide decisions regarding ICD implantation. Echocardiography and contrast-enhanced CT can provide additional insights into structural abnormalities and risk assessment. Polymorphic VT in Nonobstructive HCM: Polymorphic ventricular tachycardia (PMVT) can occur in nonobstructive hypertrophic cardiomyopathy due to myocardial fibrosis and disarray, even in the absence of significant late gadolinium enhancement and left ventricular outflow tract obstruction. ICD Risk Stratification in HCM: Risk stratification for ICD placement in HCM includes assessment of clinical features such as family history of sudden cardiac death, history of unexplained syncope, presence of nonsustained VT on ambulatory monitoring, massive left ventricular hypertrophy (wall thickness ≥30 mm), and evidence of extensive myocardial fibrosis on cardiac MRI. Notes - A Curious Case of Refractory Ventricular Tachycardia - Rutgers-Robert Wood Johnson Is there a benefit of starting antiarrhythmic medications for patients presenting with an out-of-hospital cardiac arrest with shock-refractory VT or VF? There is likely no benefit. An RCT published by Kudenchuk et al in 2016 in which patients who had a non-traumatic out-of-hospital cardiac arrest with shock-refractory VF or pulseless VT were randomly assigned to receive lidocaine, amiodarone, or saline placebo, in addition to standard care, showed that neither antiarrhythmic drug had a significantly higher rate of survival or favorable neurologic outcome compared to placebo6. What is the differential diagnosis and empiric management for a patient with polymorphic ventricular tachycardia? The differential diagnosis for ventricular tachycardia includes myocardial ischemia, electrolyte derangements, medications that may cause QT prolongation, congenital long QT syndrome, Brugada syndrome, myocarditis, dilated cardiomyopathy, arrhythmic cardiomyopathies, and infiltrative or structural heart disease. Standard BLS and ACLS measures are first-line treatment for pulseless VT. For stable patients, the 2017 AHA/ACC/HRS0 guidelines list beta-blockers as first-line antiarrhythmic therapy because they have been shown to reduce mortality and suppress ventricular arrhythmias in structurally normal hearts3. Amiodarone is also listed, though its long-term effect on survival is unclear, with most studies showing no clear benefit over placebo 3. Lidocaine and mexiletine are also commonly used, but because they are less efficacious compared to amiodarone, they are usually used as combination therapy for refractory patients4. Multiple trials have demonstrated the efficacy of procainamide as an adjunct medication in patients with ongoing ventricular arrhythmias, despite amiodarone and lidocaine4. Quinidine has also been used for patients as a salvage therapy for patients with structural heart disease for recurrent ventricular arrhythmias despite antiarrhythmic drug treatment 4. What medications can be associated with polymorphic VT? Medications that are commonly associated with QT prolongation, therefore making patients more susceptible to developing VT, include Class I and Class III antiarrhythmics; fluoroquinolone and macrolide antibiotics, as well as antifungals; tricyclic antidepressants as well as certain SSRI’s and SNRI’s; and antipsychotics, among others5. In this video, Dr. Nino Isakadze explains the proper way to measure the QT interval. How can multimodal imaging help reach a diagnosis in patients with PMVT with a relatively normal echocardiogram and no coronary artery disease? Multimodal imaging, specifically cardiac MRI, is useful for reaching a diagnosis in patients with PMVT due to improved myocardial tissue characterization. Improved definition of the myocardium allows for the detection of structural abnormalities that may not be as easily visualized on TTE, such as LV non-compaction, now called excessive trabeculation of the left ventricle, and to more accurately measure left ventricular wall thickness, which is useful for diagnosing and risk stratifying patients with hypertrophic cardiomyopathy. Improved tissue characterization by measuring T1 relaxation time, T2 relaxation time, extracellular volume, and late gadolinium enhancement (LGE) pattern is also useful for diagnosing infiltrative disease. Certain LGE patterns are associated with different cardiac conditions and play a role in determining prognosis. For example, the detection of mid-wall LGE in patients with dilated cardiomyopathy portends an increased risk of adverse events. What are the risk factors for sudden cardiac death in patients with HCM? The updated 2024 HCM guidelines have outlined several risk factors for sudden cardiac death 1 Family history of sudden cardiac death Unexplained syncope NSVT episodes on ambulatory monitoring when runs are frequent (≥ 3), longer (≥ 10 beats), and faster (≥ 200 bpm) Increased LV wall thickness, with elevated risk greater than 30 mm Other risk stratification markers include extensive LGE seen on cardiac MRI, apical aneurysm, and EF < 50% in patients without high-risk features 1 The AHA HCM SCD Calculator can be used to risk stratify patients to assist with decision-making in ICD implantation in these patients2 References Ommen SR, Ho CY, Asif IM, et al. 2024 AHA/ACC/AMSSM/HRS/PACES/SCMR Guideline for the Management of Hypertrophic Cardiomyopathy: A Report of the American Heart Association/American College of Cardiology Joint Committee on Clinical Practice Guidelines [published correction appears in Circulation. 2024 Aug 20;150(8):e198. doi: 10.1161/CIR.0000000000001277]. Circulation. 2024;149(23):e1239-e1311. doi:10.1161/CIR.0000000000001250 AHA HCM SCD Calculator Al-Khatib SM, Stevenson WG, Ackerman MJ, et al. 2017 AHA/ACC/HRS Guideline for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society [published correction appears in Circulation. 2018 Sep 25;138(13):e419-e420. doi: 10.1161/CIR.0000000000000614]. Circulation. 2018;138(13):e272-e391. doi:10.1161/CIR.0000000000000549 Larson J, Rich L, Deshmukh A, Judge EC, Liang JJ. Pharmacologic Management for Ventricular Arrhythmias: Overview of Anti-Arrhythmic Drugs. J Clin Med. 2022;11(11):3233. Published 2022 Jun 6. doi:10.3390/jcm11113233 Nachimuthu S, Assar MD, Schussler JM. Drug-induced QT interval prolongation: mechanisms and clinical management. Ther Adv Drug Saf. 2012;3(5):241-253.

Jan 31

Join CardioNerds EP Council Chair Dr. Naima Maqsood and Episode Lead Dr. Jeanne De Lavallaz as they discuss the results of the ARREST-AF Trial with expert faculty Dr. Prashanthan Sanders and Dr. Mehak Dhande. Audio editing by CardioNerds intern Bhavya Shah. The ARREST-AF trial enrolled 122 patients with a BMI of 27 kg/m2 or greater and at least one cardiovascular risk factor with either paroxysmal or persistent AF and were scheduled to undergo de novo AF ablation. They were randomized to an intensive risk factor management (RFM) program versus usual care. The RFM program addressed obesity, sleep apnea, HTN, HLD, tobacco, and alcohol abuse, whereas the usual care arm had a discussion of risk factors but without an extensive risk factor modification or follow-up program. The study population had a mean age of 60 years, a mean BMI of 33 kg/m2, and 56-60% of patients with persistent AF. A third of the study population was female. The trial showed a significant improvement in the primary endpoint of the percentage of patients free from atrial fibrillation after ablation in those receiving the intensive lifestyle RFM program. At the end of the 12.3-month follow-up period, 66% percent of patients in the RFM group were free from AF compared to 42% in the usual care group (HR 0.53, p = 0.03). The RFM group also showed significant improvement in AF symptom severity, decline in body weight, systolic blood pressure, glycemic control, and exercise capacity. On average, patients in the RFM arm lost 9 kg of weight compared to 1 kg in the control group. Similarly, systolic blood pressure decreased by 13.1 mmHg in the RFM group but increased by four mmHg in the control group. This episode was planned in collaboration with Heart Rhythm TV with mentorship from Dr. Daniel Alyesh and Dr. Mehak Dhande. CardioNerds Journal Club PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! References - The SUMMIT Trial Pathak, Rajeev K., et al. "Aggressive Risk Factor Reduction Study for Atrial Fibrillation and Implications for the Outcome of Ablation: The ARREST-AF Cohort Study." Journal of the American College of Cardiology, vol. 64, no. 21, 2014, pp. 2222–2231.

Jan 21

Join CardioNerds Heart Failure Section Chair Dr. Jenna Skowronski, episode lead Dr. Merna Hussein, and expert faculty Dr. Milton Packer as they discuss the SUMMIT trial. The SUMMIT trial randomized 731 patients with HFpEF with LVEF ≥ 50% and obesity with BMI ≥ 30 kg/m2 to receive tirzepatide or placebo for at least 52 weeks. The two co-primary endpoints were a composite of time to cardiovascular death or a worsening heart failure event and quality of life measured by the Kansas City Cardiomyopathy Questionnaire clinical summary score (KCCQ-CSS). Treatment with tirzepatide led to a lower risk of the composite of cardiovascular death or worsening heart failure as well as improved quality of life. This episode was planned in collaboration with the American College of Cardiology Section of the Prevention of Cardiovascular Disease with mentorship from Section Chair Dr. Eugenia Gianos. CardioNerds Journal Club PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! References - The SUMMIT Trial Packer, M., Zile, M. R., Kramer, C. M., Baum, S. J., Litwin, S. E., Menon, V., Ge, J., Weerakkody, G. J., Ou, Y., Bunck, M. C., Hurt, K. C., Murakami, M., Borlaug, B. A., & SUMMIT Trial Study Group. (2024). Tirzepatide for Heart Failure with Preserved Ejection Fraction and Obesity. The New England Journal of Medicine. https://doi.org/10.1056/NEJMoa2410027

Jan 16

Join CardioNerds Heart Failure Section Chair Dr. Jenna Skowronski, episode lead Dr. Apoorva Gangavelli, and expert faculty Dr. Ronald Witteles as they discuss the Nex-Z trial. This was a phase 1, open-label trial investigating nex-z, a CRISPR-Cas9-based treatment, in 36 patients with transthyretin amyloidosis with cardiomyopathy (ATTR-CM). The primary objectives were aimed at studying the safety and pharmacodynamics of this novel gene-based treatment modality. This episode dives into the nuances of the data, future directions for investigation, and future clinical implications. CardioNerds Journal Club PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! References - The Nex-Z Trial Fontana, M., Solomon, S. D., Kachadourian, J., Walsh, L., Rocha, R., Lebwohl, D., Smith, D., Täubel, J., Gane, E. J., Pilebro, B., Adams, D., Razvi, Y., Olbertz, J., Haagensen, A., Zhu, P., Xu, Y., Leung, A., Sonderfan, A., Gutstein, D. E., & Gillmore, J. D. (2024). CRISPR-Cas9 Gene Editing with Nexiguran Ziclumeran for ATTR Cardiomyopathy. The New England Journal of Medicine. https://doi.org/10.1056/NEJMoa2412309

Jan 15

Join CardioNerds co-founder Dr. Daniel Ambinder, episode lead Dr. Nidhi Patel, and expert faculty Dr. Keith Ferdinand as they discuss the BP ROAD trial. The BP ROAD trial randomized 12,821 patients 50 years of age or older with type 2 diabetes, elevated systolic blood pressure, and an increased risk of cardiovascular disease to receive intensive treatment that targeted a systolic blood pressure of less than 120 mm Hg or standard treatment that targeted a systolic blood pressure of less than 140 mm Hg for up to 5 years. Investigators found a significant reduction of major cardiovascular events with intensive blood pressure lowering. This episode dives into the nuances of the data and clinical implications. This episode was planned in collaboration with the American College of Cardiology Section of the Prevention of Cardiovascular Disease with mentorship from Section Chair Dr. Eugenia Gianos. CardioNerds Journal Club PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! References - BPROAD Trial Bi, Y., Li, M., Liu, Y., Li, T., Lu, J., Duan, P., Xu, F., Dong, Q., Wang, A., Wang, T., Zheng, R., Chen, Y., Xu, M., Wang, X., Zhang, X., Niu, Y., Kang, Z., Lu, C., Wang, J., … Wang, W. (2024). Intensive Blood-Pressure Control in Patients with Type 2 Diabetes. New England Journal of Medicine. https://doi.org/10.1056/NEJMoa2412006

Dec 13, 2024

CardioNerds (Dr. Dan Ambinder and guest host, Dr. Pooja Prasad) join Dr. Donny Mattia from Phoenix Children’s pediatric cardiology fellowship, Dr. Sri Nayak from the Mayo Clinic – Arizona adult cardiology fellowship, and Dr. Harrison VanDolah from the University of Arizona College of Medicine - Phoenix Med/Peds program for a sunrise hike of Piestewa Peak, followed by some coffee at Berdena’s in Old Town Scottsdale (before the bachelorette parties arrive), then finally a stroll through the Phoenix Desert Botanical Gardens to discuss a thought-provoking case series full of clinical cardiology pearls. Expert commentary is provided by Dr. Tabitha Moe. Episode audio was edited by Dan Ambinder. They discuss the following case: Cardiology is consulted by the OB team for a 27-year-old female G1, now P1, who has just delivered a healthy baby boy at 34 weeks gestation after going into premature labor. She is experiencing shortness of breath and is found to have a significant past cardiac history, including atrial fibrillation and preexcitation, now with a pacemaker and intracardiac defibrillator. We review the differential diagnosis for peripartum cardiomyopathy (PPCM) and then combine findings from her infant son, who is seen by our pediatric cardiology colleagues and is found to have severe hypertrophic cardiomyopathy (HCM). Genetic testing for both ultimately reveals a LAMP2 mutation consistent with Danon Disease. The case discussion focuses on the differential diagnosis for PPCM, HCM, pearls on Danon Disease and other HCM “phenocopies,” and the importance of good history. US Cardiology Review is now the official journal of CardioNerds! Submit your manuscript here. CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Case Media Pearls Peripartum cardiomyopathy is a diagnosis of exclusion – we must exclude other possible etiologies of heart failure! Be on the lookout for features of non-sarcomeric HCM – as Dr. Michelle Kittleson said in Episode 166, “LVH plus” states. HCM with preexcitation, heart block, strong family history, or extracardiac symptoms such as peripheral neuropathy, myopathy, or cognitive impairment should be evaluated for infiltrative/inherited cardiomyopathies! As an X-linked dominant disorder, Danon disease will present differently in males vs females, with males having much more severe and earlier onset disease with extracardiac features. Making the diagnosis for genetic disorders such as Danon disease is important for getting the rest of family members tested as well as the opportunity for specialized treatments such as gene therapy Up to 5% of Danon disease cases may be due to copy number variants, which may be missed in genetic testing that does not do targeted deletion/duplication analysis!). Notes What is the differential diagnosis for peripartum cardiomyopathy? Peripartum cardiomyopathy is a diagnosis of exclusion – we must exclude other possible etiologies of heart failure! First, ensure that you are not missing an acute life-threatening etiology of acute decompensated heart failure – pulmonary embolism, amniotic fluid embolism, ACS, and SCAD should all be ruled out. Second, a careful history can identify underlying heart disease or risk factors for the development of heart failure, such as substance use, high-risk behaviors that put one at risk for HIV infection, and family history that suggests an inheritable cardiomyopathy. Lastly, a careful review of echocardiographic imaging may also identify underlying etiologies that warrant a change in management. Diagnosis of peripartum cardiomyopathy is important to consider as within 7 days of onset, patients may be eligible for treatment with bromocriptine – consider referring the patient for enrollment in the ongoing RCT ReBIRTH. Check out Cardionerds Episode 113 and the great article linked below for more details on heart failure in pregnancy and postpartum! What is the differential diagnosis for hypertrophic cardiomyopathy? Though by far the most common differential diagnosis for HCM is simple LVH or athlete’s heart, as Dr. Michelle Kittleson taught us in CardioNerds Episode 166, we should “remain alert for “LVH+” states.” It is helpful to think of them in two buckets – sarcomeric mutations (classic HCM) or non-sarcomeric causes (“phenocopies”). If you see systemic signs like peripheral neuropathy, renal dysfunction, or skin changes – clues towards a systemic pathology (for adult colleagues, first think amyloidosis; for peds, colleagues, think genetic syndromes such as RASopathies like Noonan syndrome, glycogen, and lysosomal storage diseases like Fabry). Additionally, certain additional cardiac findings can point towards a non-sarcomeric HCM – recall way back in CardioNerds Episode 68 when our friends at VCU presented a man in his 60s with a history of WPW/preexcitation and HCM and was found to have a PRKAG2 mutation, which is a similar lysosomal vacuolopathy to Danon disease. Another example was seen in Episode 349 when we saw a patient with HCM and heart block who was found to have Fabry disease. What is Danon disease, and how does it present? Danon disease is a rare X-linked dominant genetic disorder due to deficiency in LAMP2, a glycoprotein involved in protecting the lysosome from its roles in endocytosis and autophagy When deficiency of LAMP2 occurs, products build up into vacuoles and lead to cardiomyocyte dysfunction and death. Interestingly, autophagy disruption is the suspected mechanism of cardiomyopathies from anthracyclines and hydroxychloroquine – Danon disease severity underscores the importance of this process! Estimated prevalence of Danon disease in adult patients with HCM is 1-4%, however when both HCM and pre-excitation are present, this rises to 17%. It is highly penetrant, meaning most patients with the mutation will show symptoms. There are several extracardiac features such as skeletal myopathy, retinopathy, and cognitive impairment – these correlated with areas in the body where LAMP2 is expressed more! Classic presentations – remember that X-linked inheritance results in differential expression between males and females!Males: young onset with severe LVH/HCM and extracardiac phenotype Females: isolated cardiomyopathy (can be either dilated or hypertrophic) with preexcitation arrhythmias with a family history suggesting X-linked dominant transmission (i.e., males more severely affected than females). When taking a family history, note that male-to-male transmission (can’t happen since males don’t pass on an X chromosome to their male children) or female-to-offspring transmission (suggests mitochondrial disease) should prompt alternate diagnosis. However, an estimated 1/3 of Danon disease cases are de novo mutations! See Episode 300 for a great in-depth overview of the pathophysiology of Danon disease How is Danon disease diagnosed? Though there are some proposed characteristic cardiac MRI findings (diffuse LGE sparing the interventricular septum), diagnosis is genetic with a loss-of-function mutation in LAMP2 paired with characteristic cardiac or extracardiac features (see below diagnostic algorithm from Hong et al. JACC 2023) LAMP2 is now included in most hypertrophic and dilated CM panels – if found, it is crucial to ensure the patient’s family members also undergo testing and potentially cardiac evaluation! (Note: up to 5% of Danon disease cases may be due to copy number variants, which may be missed in genetic testing that does not do targeted deletion/duplication analysis!) Differential DiagnosisSarcomeric HCM – the “classic” HCM, which has numerous genetic causes, all of which affect the sarcomere with age-related penetrance leading to three peaks in age at onset (infancy <1yr, teenage/early adulthood, and mid-adulthood). Progression towards massive LVH and systolic dysfunction is uncommon (<10%) and should raise suspicion of a rare genocopy such as Danon. EKG is usually mostly normal in these patients, unlike in Danon disease, which often has striking abnormalities.Pompe disease – lysosome storage disease from mutations in acid alpha-glucosidase leading to lysosomal glycogen accumulation. Autosomal recessive. It can be an infantile form with severe LVH/HCM, and the later forms can have classic skeletal myopathy as well, but usually, these patients have less severe cardiac features.RAS-opathies – genetic diseases due to mutations in the RAS/MAPkinase pathway. Classic examples are Noonan syndrome, LEOPARD syndrome, and Costello syndrome. All have classic extracardiac manifestations as well as oftentimes HCM, as well as congenital heart disease such as pulmonary valve stenosis.Fabry disease – also an X-linked recessive lysosomal disorder due to alpha-galactosidase A enzyme deficiency; however, it is rarely prominent in childhood and is usually more characterized by extracardiac manifestations. HCM is a cardiac manifestation presenting in the 30s-40s.Friedrich ataxia – autosomal recessive multisystem disease due to GAA sequence expansion in the FXN gene that encodes frataxin, a mitochondrial protein, which impairs mitochondrial oxidative phosphorylation. “HCM” is a common disease manifestation in addition to the classic severe neurologic presentation.Mitochondrial diseases – heterogenous conditions affecting mitochondrial DNA, transmitted in matrilinear pattern, with cardiac hypertrophy being a classic disease manifestation in addition to preexcitation. These may present with severe cognitive impairment than Danon disease.PRKAG2 mutations – cause dysregulation of adenosine monophosphate kinase,

Nov 18, 2024

CardioNerds (Dr. Dan Ambinder and Dr. Yoav Karpenshif – Chair of the CardioNerds Critical Care Cardiology Council) join Dr. Munim Khan, Dr. Shravani Gangidi, and Dr. Rachel Goodman from Tufts Medical Center’s general cardiology fellowship program for hot pot in China Town in Boston. They discuss a case involving a patient who presented with stress cardiomyopathy leading to cardiogenic shock. Expert commentary is provided by Dr. Michael Faulx from the Cleveland Clinic. Notes were drafted by Dr. Rachel Goodman. Audio editing by Dr. Diane Masket. A young woman presents with de novo heart-failure cardiogenic shock requiring temporary mechanical circulatory support who is found to have basal variant takotsubo cardiomyopathy. We review the definition and natural history of takotsubo cardiomyopathy, discuss initial evaluation and echocardiographic findings, and review theories regarding pathophysiology of the clinical syndrome. We also highlight complications of takotsubo cardiomyopathy, with a focus on left ventricular outflow obstruction, cardiogenic shock, and arrythmias. US Cardiology Review is now the official journal of CardioNerds! Submit your manuscript here. CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls Takotsubo cardiomyopathy is defined as a reversible systolic dysfunction with wall motion abnormalities that do not follow a coronary vascular distribution. Takotsubo cardiomyopathy is a diagnosis of exclusion; patients often undergo coronary angiography to rule out epicardial coronary artery disease given an overlap in presentation and symptoms with acute myocardial infarction. There are multiple echocardiographic variants of takotsubo. Apical ballooning is the classic finding, but mid-ventricular, basal, and biventricular variants exist as well. Patients with takotsubo cardiomyopathy generally recover, but there are important complications to be aware of. These include arrhythmia, left ventricular outflow tract (LVOT) obstruction related to a hyperdynamic base in the context of apical ballooning, and cardiogenic shock. Patients with Impella devices are at risk of clot formation and stroke. Assessing the motor current can be a clue to what is happening at the level of the motor or screw. Notes What is Takotsubo Syndrome (TTS)? TTS is a syndrome characterized by acute heart failure without epicardial CAD with regional wall motion abnormalities seen on echocardiography that do not correspond to a coronary artery territory (see below).1 TTS classically develops following an acute stressor—this can be an emotional or physical stressor.1 An important feature of TTS is that the systolic dysfunction is reversible. The time frame of reversibility is variable, though generally hours to weeks.2 Epidemiologically, TTS has a predilection for post-menopausal women, however anyone can develop this syndrome.1 TTS is a diagnosis of exclusion. Coronary artery disease (acute coronary syndrome, spontaneous coronary artery dissection, coronary embolus, etc) should be excluded when considering TTS. Myocarditis is on the differential diagnosis. What are the echocardiographic findings of takotsubo cardiomyopathy? The classic echocardiographic findings of TTS is “apical ballooning,” which is a way of descripting basal hyperkinesis with mid- and apical hypokinesis, akinesis, or dyskinesis.3 There are multiple variants of TTS. The four most common are listed below:3(1) Apical ballooning (classic TTS)(2) Mid-ventricular variant(3) Basal variant (4) Focal variant Less common variants include the biventricular variant and the isolated right ventricular variant.3 Do patients with TTS generally have EKG changes or biomarker elevation? Patients often have elevated troponin, though the severity wall motion abnormalities seen on TTE is generally out of proportion to the degree of troponin elevation.4 BNP/NTproBNP are typically elevated, especially early in the course.4 During the acute phase (defined as within the first 12 hours), patients may have ST elevation or depression, T wave inversions, new LBBB, or QT prolongation.4 What are complications of takotsubo cardiomyopathy? Heart failure2 LV outflow tract obstruction—if there is an LVOT obstruction, it is important to avoid diuretics, vasodilators such as nitroglycerin, and inotropic agents.2 Cardiogenic shock.2 Atrial and ventricular arrhythmias.2 LV thrombus—this is of particular risk in patients with the classic “apical ballooning” variant of takotsubo due to apical akinesis and therefore stagnant flow.2 References Lyon AR, Citro R, Schneider B, et al. Pathophysiology of Takotsubo Syndrome. J Am Coll Cardiol. 2021;77(7):902-921. doi:10. 1016/j.jacc.2020.10.060 Singh T, Khan H, Gamble DT, Scally C, Newby DE, Dawson D. Takotsubo Syndrome: Pathophysiology, Emerging Concepts, and Clinical Implications. Circulation. 2022;145(13):1002-1019. doi:10.1161/CIRCULATIONAHA.121.055854 Ghadri JR, Wittstein IS, Prasad A, et al. International Expert Consensus Document on Takotsubo Syndrome (Part I): Clinical Characteristics, Diagnostic Criteria, and Pathophysiology. Eur Heart J. 2018;39(22):2032-2046. doi:10.1093/eurheartj/ehy076 Current state of knowledge on Takotsubo syndrome: a Position Statement from the Taskforce on Takotsubo Syndrome of the Heart Failure Association of the European Society of Cardiology - Lyon - 2016 - European Journal of Heart Failure - Wiley Online Library

Nov 14, 2024

In this episode, CardioNerds Dr. Gurleen Kaur and Dr. Akiva Rosenzveig are joined by Cardio-Rheumatology experts, Dr. Brittany Weber and Dr. Michael Garshick to discuss treating inflammation, delving into the pathophysiology behind the inflammatory hypothesis of atherosclerotic cardiovascular disease and the evolving data on anti-inflammatory therapies for reducing ASCVD risk, with insights on real-world implementation. Show notes were drafted by. Dr. Akiva Rosenzveig. This episode was produced in collaboration with the American Society of Preventive Cardiology (ASPC) with independent medical education grant support from Agepha Pharma. CardioNerds Prevention PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls - Treating Inflammation Our understanding of the pathophysiology of atherosclerosis has undergone a few iterations from the incrustation hypothesis to the lipid hypothesis to the response-to-injury hypothesis and culminating with our current understanding of the inflammation hypothesis. Both the adaptive and innate immune systems play instrumental roles in the pathogenesis of atherosclerosis. After adequately controlling classic modifiable risk factors such as blood pressure, dyslipidemia, glucose intolerance, and obesity, systemic inflammation as assessed by CRP can be ascertained as CRP is associated with ~1.8-fold increased risk of cardiovascular events Although the most common side effect of colchicine is gastrointestinal intolerance, colchicine can induce lactose intolerance, so a lactose free diet may help ameliorate colchicine-induced GI symptoms. Anti-inflammatory therapeutics have shown promise in reducing cardiovascular risk but much more is to be learned with ongoing and future basic, translational, and clinical research. Show notes - Treating Inflammation What are the origins of the inflammatory hypothesis? The first hypothesis as to the pathogenesis of atherosclerosis was the incrustation hypothesis by Carl Von Rokitansky in 1852. He suggested that atherosclerosis begins in the intima with thrombus deposition.In 1856, Rudolf Virchow suggested the lipid hypothesis whereby high levels of cholesterol in the blood lead to atherosclerosis. He observed inflammatory changes in the arterial walls associated with atherosclerotic plaque growth, called endo-arteritis chronica deformans.In 1977, Russell Ross suggested the response-to-injury hypothesis, that atherosclerosis develops from injury to the arterial wall.In the 1990’s the role of inflammation in ASCVD became more recognized. Both the adaptive and innate immune system are critical in atherosclerosis. Lipids and inflammation are synergistic in that lipid exposure is required but they translocate through damaged endothelium which occurs by way of inflammatory cytokines, namely within the NLRP3 inflammasome (IL-1, IL-6 etc.).Smooth muscle cells are also involved. They migrate to the endothelial region and secrete collagen to create the fibrous cap. They can also transform into macrophage-like cells to take up lipids and become foam cells. T, B, and K cells are also part of this milieu. In fact, neutrophils, macrophages and monocytes make up only a small portion of the cells involved in the atherosclerotic process. What are ways to individually optimize one’s ASCVD risk?Ensure the patient is on appropriate antiplatelet therapy, lipid lowering therapy, blood pressure is well controlled, and the Hemoglobin A1c is well controlled. Smoking cessation is pivotal.If the patient has an elevated Lipoprotein (a), pursue more aggressive lipid lowering therapy. Targeted therapies may become available in the future. Assess the patient’s systemic inflammatory risk as measured by C-Reactive Protein (CRP) What is the evidence for utilizing CRP in risk stratification?CRP, initially termed Fraction C (discovered as a c polysaccharide component of the pneumococcal cell wall), was first discovered at Rockefeller University in the 1930’s. It was discovered to be an acute phase reactant in the 1940’s and noted to be synthesized in the liver in the 1960’s.Although it is not causal in atherosclerosis, elevated CRP is associated with elevated rates of cardiovascular disease. This was first noted in the landmark New England Journal of Medicine study by Ridker et al that showed elevated CRP was associated with elevated cardiovascular risk and treating with anti-inflammatory medication (aspirin) lowered CRP and CV risk.The statin trials also showed reduction in CRP levels was associated with better outcomes.High-sensitivity CRP (hsCRP) >3 mg/L has odds ratio of ~1.8 for risk of CV disease. Recent analyses of the PROMINENT, REDUCE-IT, and STRENGTH trials demonstrated that hsCRP was a more powerful determinant of recurrent CV events, CV death, and all-cause mortality than LDL-C. After effectively controlling the previously stated modifiable risk factors, what therapeutic options remain in a patient with an elevated CRP?CANTOS trial was the first proof of concept trial investigating Canakinumab (an IL-1 inhibitor) which showed a ~15% relative risk reduction in cardiovascular eventsCIRT trial investigated methotrexate in patients without autoimmune disease. It was stopped early due to it being a negative trial. This emphasized the complex role inflammation plays in ASCVD, and that both patient selection and chosen anti-inflammatory therapy are important to consider for ASCVD risk reduction.Colchicine has seen a lot of focus in this space with trials such as COLCOT, COPS, LODOCO, LODOCO 2, LODOCO MI. Overall, it appears that colchicine may be more effective in chronic stable ischemic heart disease. The CLEAR SYNERGY trial investigated colchicine in the peri-MI period and was a negative trial. However, we do not yet have the published data to further analyze it. A review article by Potere et al (referenced below) provides a useful summary of novel therapies and upcoming trials in the inflammation in ASCVD space. How do we approach inflammation in women?We know that immune response differs between men and women. Women have more robust immune response to vaccines and viruses and greater innate and adaptive immune responses.Women have slightly higher CRP than men. Studies have shown that average high sensitivity hsCRP is 1.7 for women and 1.2 for men. In the JUPITER trial, the subgroup of patients with hsCRP>7 mg/L had the highest proportion of women relative to men. Regardless, hsCRP remains a reliable predictor of CV events in both men and women. What are some practical considerations when starting colchicine?It may help with adherence, if you walk patients through what to expect with the medication.Obtain renal and liver function tests as both organs contribute to colchicine metabolism and clearance.Obtain a thorough medication reconciliation as colchicine has some notable drug-drug interactions.The most common side effects is GI intolerance; cytopenias are rare occurrences. Note that colchicine can induce lactose intolerance, a potential mechanism for causing GI intolerance, so a lactose free diet may help with adherence. What do we have to look forward to in the anti-inflammation space in CV disease? There is still a lot to be learned and discovered in this space. Some clinical trials to look out for are the ZEUS, ARTEMIS, and HERMES trials which look at Ziltivekimab, an IL-6 inhibitor, in chronic kidney disease, acute myocardial infarction, and heart failure, respectively. References - Treating Inflammation Nidorf SM, Eikelboom JW, Budgeon CA, Thompson PL. Low-dose colchicine for secondary prevention of cardiovascular disease. J Am Coll Cardiol. 2013;61(4):404-410. doi:10.1016/j.jacc.2012.10.027 Nidorf SM, Fiolet ATL, Mosterd A, et al. Colchicine in Patients with Chronic Coronary Disease. N Engl J Med. 2020;383(19):1838-1847. doi:10.1056/NEJMoa2021372 Tardif JC, Kouz S, Waters DD, et al. Efficacy and Safety of Low-Dose Colchicine after Myocardial Infarction. N Engl J Med. 2019;381(26):2497-2505. doi:10.1056/NEJMoa1912388 Hennessy T, Soh L, Bowman M, et al. The Low Dose Colchicine after Myocardial Infarction (LoDoCo-MI) study: A pilot randomized placebo controlled trial of colchicine following acute myocardial infarction. Am Heart J. 2019;215:62-69. doi:10.1016/j.ahj.2019.06.003 Tong DC, Quinn S, Nasis A, et al. Colchicine in Patients With Acute Coronary Syndrome: The Australian COPS Randomized Clinical Trial. Circulation. 2020;142(20):1890-1900. doi:10.1161/CIRCULATIONAHA.120.050771 Ridker PM, Everett BM, Thuren T, et al. Antiinflammatory Therapy with Canakinumab for Atherosclerotic Disease. N Engl J Med. 2017;377(12):1119-1131. doi:10.1056/NEJMoa1707914 Ridker PM, Everett BM, Pradhan A, et al. Low-Dose Methotrexate for the Prevention of Atherosclerotic Events. N Engl J Med. 2019;380(8):752-762. doi:10.1056/NEJMoa1809798 Potere N, Bonaventura A, Abbate A. Novel Therapeutics and Upcoming Clinical Trials Targeting Inflammation in Cardiovascular Diseases. Arterioscler Thromb Vasc Biol. Published online October 10, 2024. doi:10.1161/ATVBAHA.124.319980 Ridker PM, Cushman M, Stampfer MJ, Tracy RP, Hennekens CH. Inflammation, aspirin, and the risk of cardiovascular disease in apparently healthy men [published correction appears in N Engl J Med 1997 Jul 31;337(5):356]. N Engl J Med. 1997;336(14):973-979. doi:10.1056/NEJM199704033361401 Ridker PM, Danielson E, Fonseca FA, et al. Rosuvastatin to prevent vascular events in men and women with elevated C-reactive protein. N Engl J Med. 2008;359(21):2195-2207. doi:10.1056/NEJMoa0807646 Ridker PM, Bhatt DL, Pradhan AD, et al.

Nov 13, 2024

The following question refers to Sections 7.3.3 and 7.3.6 of the 2022 ACC/AHA/HFSA Guideline for the Management of Heart Failure.The question is asked by Palisades Medical Center medicine resident & CardioNerds Academy Fellow Dr. Maryam Barkhordarian, answered first by UTSW AHFT Cardiologist & CardioNerds FIT Ambassador Dr. Natalie Tapaskar, and then by expert faculty Dr. Robert Mentz.Dr. Mentz is associate professor of medicine and section chief for Heart Failure at Duke University, a clinical researcher at the Duke Clinical Research Institute, and editor-in-chief of the Journal of Cardiac Failure. Dr. Mentz has been a mentor for the CardioNerds Clinical Trials Network as lead principal investigator for PARAGLIDE-HF and is a series mentor for this very Decipher the Guidelines Series. For these reasons and many more, he was awarded the Master CardioNerd Award during ACC22.The Decipher the Guidelines: 2022 AHA / ACC / HFSA Guideline for The Management of Heart Failure series was developed by the CardioNerds and created in collaboration with the American Heart Association and the Heart Failure Society of America. It was created by 30 trainees spanning college through advanced fellowship under the leadership of CardioNerds Cofounders Dr. Amit Goyal and Dr. Dan Ambinder, with mentorship from Dr. Anu Lala, Dr. Robert Mentz, and Dr. Nancy Sweitzer. We thank Dr. Judy Bezanson and Dr. Elliott Antman for tremendous guidance.Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. American Heart Association’s Scientific Sessions 2024As heard in this episode, the American Heart Association’s Scientific Sessions 2024 is coming up November 16-18 in Chicago, Illinois at McCormick Place Convention Center. Come a day early for Pre-Sessions Symposia, Early Career content, QCOR programming and the International Symposium on November 15. It’s a special year you won’t want to miss for the premier event for advancements in cardiovascular science and medicine as AHA celebrates its 100th birthday. Registration is now open, secure your spot here!When registering, use code NERDS and if you’re among the first 20 to sign up, you’ll receive a free 1-year AHA Professional Membership! Question #39 Ms. Kay Lotsa is a 48-year-old woman with a history of CKD stage 2 (baseline creatinine ~1.2 mg/dL) & type 2 diabetes mellitus. She has recently noticed progressively reduced exercise tolerance, leg swelling, and trouble lying flat. This prompted a hospital admission with a new diagnosis of decompensated heart failure. A transthoracic echocardiogram reveals LVEF of 35%. Ms. Lotsa is diuresed to euvolemia, and she is started on carvedilol 25mg BID, sacubitril/valsartan 49-51mg BID, and empagliflozin 10mg daily, which she tolerates well. Her eGFR is at her baseline of 55 mL/min/1.73 m2 and serum potassium concentration is 3.9 mEq/L. Your team is anticipating she will be discharged home in the next one to two days and wants to start spironolactone. Which of the following is most important regarding her treatment with mineralocorticoid antagonists?ASpironolactone is contraindicated based on her level of renal impairment and should not be startedBSerum potassium levels and kidney function should be assessed within 1-2 weeks of starting spironolactoneCEplerenone confers a higher risk of gynecomastia than does spironolactoneDThe patient will likely not benefit from initiation of spironolactone if her cardiomyopathy is ischemic in origin Answer #39 ExplanationThe correct answer is B – after starting a mineralocorticoid receptor antagonist (MRA), it is important to closely monitor renal function and serum potassium levels.MRA (also known as aldosterone antagonists or anti-mineralocorticoids) show consistent improvements in all-cause mortality, HF hospitalizations, and SCD across a wide range of patients with HFrEF.The RALES trial of spironolactone vs. placebo in highly symptomatic HFrEF (LVEF ≤ 35%, NYHA III-IV), trial of eplerenone vs placebo post-MI in patients with LVEF ≤ 40%, and EMPHASIS-HF trial of eplerenone vs placebo in less symptomatic HFrEF (LVEF ≤ 35%, NYHA II) altogether suggest MRAs confer improvements in all-cause mortality, HF hospitalizations, and sudden cardiac death in patients with HFrEF. Importantly, these benefits have been demonstrated across a wide range of HFrEF severity and etiologies, including ischemic cardiomyopathy (Option D).Therefore, in patients with HFrEF and NYHA class II to IV symptoms, an MRA (spironolactone or eplerenone) is recommended to reduce morbidity and mortality, if eGFR is >30 mL/min/1.73 m2 and serum potassium is <5.0 mEq/L. Careful monitoring of potassium, renal function, and diuretic dosing should be performed at initiation and closely monitored thereafter to minimize risk of hyperkalemia and renal insufficiency (Class 1, LOE A). MRA therapy in this context provides high economic value. Adverse Effects of MRAsBoth spironolactone and eplerenone are excreted by the kidney and due to their inhibition of aldosterone signaling, reduce potassium excretion in the urine. For these reasons, the initiation of MRAs is contraindicated in patients with eGFR of ≤30 mL/min/1.73m2 or serum potassium levels of ≥5.0 mEq/L. After starting or intensifying MRA therapy, serum potassium levels and renal function should be rechecked at approximately 1 week, at 4 weeks, and every 6 months thereafter, provided clinical stability. Hyperkalemia can increase the risk of ventricular arrhythmias and death. Unfortunately, this often results in de-escalation or discontinuation of RAASi and a subsequent loss of long-term cardiorenal benefits of maximally tolerated GDMT. The utility of prescribing potassium binders (e.g., patiromer, sodium zirconium cyclosilicate) to improve outcomes by facilitating continuation of Patiromer and sodium zirconium cyclosilicate remove potassium by exchanging cations leading to increased fecal excretion and thereby lowering serum potassium levels. These have been FDA approved for treatment of hyperkalemia for patients receiving RAASi.Therefore, the use of potassium binders (patiromer, sodium zirconium cyclosilicate) to improve outcomes by facilitating the continuation of RAASi therapy in patients with HF who experience hyperkalemia (serum potassium level ≥5.5 mEq/L) received a Class 2b recommendation (LOE B-R), but overall utility remains uncertain. In the DIAMOND trial, patients with HFrEF and hyperkalemia were randomized to patiromer vs. control. In the run-in phase, all patients were started on patiromer, and subsequently, RAASi therapy was initiated/optimized. After this, patients were randomized to continue vs stop patiromer. Hard clinical primary endpoints of time to CV death or first CV hospitalization were changed to mean change in serum potassium due to challenges with recruitment related to the COVID-19 pandemic. There was a significant reduction in the mean change of potassium (0.03 mEq/L in the patiromer group vs. 0.13 mEq/L in the control). Additionally, 85% of the patiromer arm was able to be optimized on RAASi. Aside from hyperkalemia, troublesome side effects of MRAs include gynecomastia and vaginal bleeding. Eplerenone results in lower rates of these side effects than spironolactone given greater specificity for the aldosterone receptor (Option C). Main TakeawayMineralocorticoid receptor antagonists, like spironolactone and eplerenone, reduce all-cause mortality, HF hospitalizations, and sudden cardiac death in a wide range of patients with HFrEF. Monitoring renal function and potassium levels while on MRA therapy is imperative.Guideline Loc.Section 7.3.3 Section 7.3.6 Decipher the Guidelines: 2022 Heart Failure Guidelines PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron!

Nov 11, 2024

The following question refers to Sections 7.4 and 7.5 of the 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure.The question is asked by the Director of the CardioNerds Internship Dr. Akiva Rosenzveig, answered first by Vanderbilt AHFT cardiology fellow Dr. Jenna Skowronski, and then by expert faculty Dr. Randall Starling.Dr. Starling is Professor of Medicine and an advanced heart failure and transplant cardiologist at the Cleveland Clinic where he was formerly the Section Head of Heart Failure, Vice Chairman of Cardiovascular Medicine, and member of the Cleveland Clinic Board of Governors. Dr. Starling is also Past President of the Heart Failure Society of America in 2018-2019. Dr. Staring was among the earliest CardioNerds faculty guests and has since been a valuable source of mentorship and inspiration. Dr. Starling’s sponsorship and support was instrumental in the origins of the CardioNerds Clinical Trials Program.The Decipher the Guidelines: 2022 AHA / ACC / HFSA Guideline for The Management of Heart Failure series was developed by the CardioNerds and created in collaboration with the American Heart Association and the Heart Failure Society of America. It was created by 30 trainees spanning college through advanced fellowship under the leadership of CardioNerds Cofounders Dr. Amit Goyal and Dr. Dan Ambinder, with mentorship from Dr. Anu Lala, Dr. Robert Mentz, and Dr. Nancy Sweitzer. We thank Dr. Judy Bezanson and Dr. Elliott Antman for tremendous guidance.Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. American Heart Association’s Scientific Sessions 2024As heard in this episode, the American Heart Association’s Scientific Sessions 2024 is coming up November 16-18 in Chicago, Illinois at McCormick Place Convention Center. Come a day early for Pre-Sessions Symposia, Early Career content, QCOR programming and the International Symposium on November 15. It’s a special year you won’t want to miss for the premier event for advancements in cardiovascular science and medicine as AHA celebrates its 100th birthday. Registration is now open, secure your spot here!When registering, use code NERDS and if you’re among the first 20 to sign up, you’ll receive a free 1-year AHA Professional Membership! Question #38 Mrs. M is a 65-year-old woman with non-ischemic dilated cardiomyopathy (LVEF 40%) and moderate to severe mitral regurgitation (MR) presenting for outpatient follow-up. Despite improvement overall, she continues to experience dyspnea on exertion with two flights of stairs and occasional PND. She reports adherence with her medication regimen of sacubitril-valsartan 97-103mg twice daily, metoprolol succinate 200mg daily, spironolactone 25mg daily, empagliflozin 10mg daily, and furosemide 80mg daily. A transthoracic echocardiogram today shows an LVEF of 35%, an LVESD of 60 mm, severe MR with a regurgitant fraction of 60%, and an estimated right ventricular systolic pressure of 40 mmHg. Her EKG shows normal sinus rhythm at 65 bpm and a QRS complex width of 100 ms. What is the most appropriate recommendation for management of her heart failure?AContinue maximally tolerated GDMT; no other changesBRefer for cardiac resynchronization therapy (CRT)CRefer for transcatheter mitral valve intervention Answer #38 ExplanationChoice C is correct. The 2020 ACC/AHA Guidelines for the management of patients with valvular heart disease outline specific recommendations.In patients with chronic severe secondary MR related to LV systolic dysfunction (LVEF <50%) who have persistent symptoms (NYHA class II, III, or IV) while on optimal GDMT for HF (Stage D), M-TEER is reasonable in patients with appropriate anatomy as defined on TEE and with LVEF between 20% and 50%, LVESD ≤70 mm, and pulmonary artery systolic pressure ≤70 mmHg (Class 2a, LOE B-R).Conversely, mitral valve surgery may have a role in the following contexts:Severe secondary MR when CABG is planned (Class 2a, LOE B-NR)Chronic severe secondary MR related to atrial annular dilation with preserved LV systolic function (LVEF ≥50%) who have severe persistent symptoms (NYHA class III or IV) despite therapy for HF and therapy for associated AF or other comorbidities (Stage D) (Class 2b, LOE B-NR)Chronic severe secondary MR related to LV systolic dysfunction (LVEF <50%) who have persistent severe symptoms (NYHA class III or IV) while on optimal GDMT for HF (Stage D) (Class 2b, LOE B-NR).Choice A is incorrect. GDMT has been shown to improve MR and LV dimensions in patients with HFrEF and secondary MR, and it is a Class 1 recommendation (LOE B-R) to optimize GDMT before any intervention for secondary MR related to LV dysfunction. This includes both medical GDMT and cardiac resynchronization therapy (CRT) where appropriate. Our patient is still having symptoms despite being on the maximally tolerated doses of medical GDMT. This highlights the importance of a multidisciplinary approach to the management of valvular heart disease in patients with HF in accordance with clinical practice guidelines to prevent worsening of HF and adverse clinical outcomes (Class 1, LOE B-R). A cardiologist with expertise in the management of HF is integral in the shared decision-making for valve intervention and should guide optimization of GDMT to ensure that medical options for HF and secondary MR have been effectively applied for an appropriate time-period and exhausted before considering intervention.Choice B is incorrect. While CRT has been shown to improve MR, LV dimensions, and outcomes in patients with HFrEF and secondary MR in appropriately selected patients, our patient would not be a candidate given that her QRS duration was < 120ms (Class 3: no benefit, LOE B-R).Main TakeawayIn patients with severe secondary MR and reduced ejection fraction with persistent symptoms despite GDMT, M-TEER is reasonable in patients with appropriate anatomy as defined on TEE and with LVEF between 20% and 50%, LVESD ≤70 mm, and pulmonary artery systolic pressure ≤70 mmHg. Conversely, surgery may be appropriate for some patients. HF ad VHD should be managed in a multidisciplinary fashion. Guideline Loc.Sections 7.4-7.5Figure 10Also: Section 7.3 from “Otto, C. M., Nishimura, R. A., Bonow, R. O., Carabello, B. A., rwin, J. P., Gentile, F., Jneid, H., Krieger, ric v., Mack, M., McLeod, C., O’Gara, P. T., Rigolin, V. H., Sundt, T. M., Thompson, A., & Toly, C. (2021). 2020 ACC/AHA Guideline for the Management of Patients With Valvular Heart Disease: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. In Circulation (Vol. 143, Issue 5, pp. E72–E227). Lippincott Williams and Wilkins. https://doi.org/10.1161/CIR.0000000000000923” Decipher the Guidelines: 2022 Heart Failure Guidelines PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron!

Nov 6, 2024

In this episode, Dr. Paul Ridker, a pioneer in the field of cardiovascular inflammation, joins the CardioNerds (Dr. Gurleen Kaur, Dr. Richard Ferraro, and Dr. Nidhi Patel) to discuss the evolving landscape of inflammation as a key factor in cardiovascular risk reduction. The discussion dives into the importance of biomarkers like high-sensitivity C-reactive protein (hs-CRP) in guiding treatment strategies, the insights gleaned from landmark trials like the JUPITER and CANTOS studies, and the future of targeted anti-inflammatory therapies in cardiology. Show notes were drafted by Dr. Nidhi Patel. Audio editing by CardioNerds academy intern, Grace Qiu. This episode was produced in collaboration with the American Society of Preventive Cardiology (ASPC) with independent medical education grant support from Lexicon Pharmaceuticals. CardioNerds Prevention PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls - Targeting Inflammation for Cardiovascular Risk "If you don’t measure it, you can’t treat it”: Incorporate hs-CRP into routine practice for patients at risk of cardiovascular events, as it provides crucial information for risk stratification and management. Recognize the dual benefits of statins in lowering both LDL and inflammation, particularly in patients with elevated hs-CRP. Encourage patients to adopt heart-healthy habits, as lifestyle changes remain foundational in reducing both cholesterol and inflammatory risk. Reminder that most autoimmune or inflammatory diseases, from psoriasis to Addison’s disease to lupus to scleroderma to inflammatory bowel disease, have been shown to have elevated cardiovascular risk Ongoing randomized trials including ZEUS, HERMES, and ARTEMIS will inform whether novel targeting of IL-6 can safely lower cardiovascular event rates or slow renal progression Show notes - Targeting Inflammation for Cardiovascular Risk Why is it important to measure both LDL and hs-CRP, and what factors increase hs-CRP? Inflammation and hyperlipidemia are synergistic in promoting atherosclerosis. They interact to exacerbate plaque formation and instability, increasing the risk of cardiovascular events. Just like we measure blood pressure and LDL to know what to treat, we should measure hs-CRP to guide targeted therapy. Clinical Example: in Ms. Flame's case, despite achieving target LDL levels with statins, her elevated hs-CRP indicates ongoing inflammation and residual cardiovascular risk that should be assessed. Residual inflammatory risk should be assessed in both primary and secondary prevention. Increased BMI1, smoking2, a sedentary lifestyle3, and genetics4 (such as a higher risk of metabolic disease in South Asians) all raise hs-CRP levels. SGLTi5 and GLP-1 agonists6 have also been shown to decrease hs-CRP levels. What data do we have to support measuring hs-CRP? Women’s Health Study7: an early study showing that hs-CRP predicted risk at least as well as LDL cholesterol and that models incorporating hs-CRP in addition to lipids were significantly better at predicting risk than models based on lipids alone. JUPITER Trial8 (Primary Prevention): Among patients with normal LDL but elevated hs-CRP there was a 44% reduction in major cardiovascular events (>50% in MI and stroke) and a 20% reduction in all-cause mortality in patients treated with statins. These results led to changes in guidelines in recognizing the need to measure and treat inflammation. CANTOS Trial9 (Secondary Prevention): Randomized >10K patients with previous MI and hs-CRP ≥ 2mg/L and found that canakinumab reduced hs-CRP level from baseline in a dose-dependent manner, without reduction in the LDL, ApoB, TG, or blood pressure. What are the guidelines and supportive data on using Colchicine? Colchicine 0.5 mg is the first FDA-approved anti-inflammatory therapy indicated for reducing cardiovascular events among adults who have established ASCVD or are at risk of developing it. The use of Colchicine is supported by the LoDoCo, LoDoCo-2, and COLCOT trials, which showed a ~25-30% risk reduction in cardiovascular risk. In comparison, studies using ezetimibe10 have shown a 6-7% relative risk reduction and PCSK9 inhibitors11 ~15% risk reduction for LDL reduction.LoDoCo12- in those with stable CAD, patients who received colchicine in addition to standard of care had a significantly lower composite rate of ACS compared to those who only received standard of care at a median follow-up of 3 years.LoDoCo-213- randomized control, multicentric trial in patients with stable CAD showing group randomized to colchicine + standard of compare had reduced MACE compared to those with placebo + standard of care at a median follow-up of 2.8 years. COLCOT14- Addition of colchicine within 30 days of ACS resulted in a reduction of the primary composite outcome of cardiovascular death, resuscitated cardiac arrest, MI, stroke, or urgent hospitalization for angina What are examples of ongoing trials that will shape the future of our anti-inflammatory toolbox? ZEUS Trial15- ongoing trial that randomizes patients with ASCVD, hs-CRP ≥ 2 and CKD (eGFR between 15-60 OR EGFR ≥ 60 and urinary albumin-to-creatinine ratio ≥200) to Ziltivekimab or placebo, and assesses time to first occurrence of MACE. Hermes HFpEF16- ongoing trial that randomizes patients with HFpEF and HFmrEF to Ziltivekimab or placebo, and assesses time to first occurrence of cardiovascular death, heart failure hospitalization, or urgent heart failure visit Artemis Acute Ischemia17- ongoing trial that randomizes patients hospitalized with MI to Ziltivekimab or placebo, and assess time to MACE. Clazakizumab in patients receiving maintenance dialysis18- this study randomized adults with known cardiovascular disease and/or DM2 receiving dialysis with hs-CRP ≥ 2 to receive Clazakizumab or placebo. The primary endpoint is a reduction in hs-CRP over 12 weeks. References - Targeting Inflammation for Cardiovascular Risk Visser M, Bouter LM, McQuillan GM, Wener MH, Harris TB. Elevated C-Reactive Protein Levels in Overweight and Obese Adults. JAMA. 1999;282:2131-2135. doi: 10.1001/jama.282.22.2131 Tonstad S, Cowan JL. C-reactive protein as a predictor of disease in smokers and former smokers: a review. Int J Clin Pract. 2009;63:1634-1641. doi: 10.1111/j.1742-1241.2009.02179.x Esteghamati A, Morteza A, Khalilzadeh O, Anvari M, Noshad S, Zandieh A, Nakhjavani M. Physical inactivity is correlated with levels of quantitative C-reactive protein in serum, independent of obesity: results of the national surveillance of risk factors of non-communicable diseases in Iran. J Health Popul Nutr. 2012;30:66-72. doi: 10.3329/jhpn.v30i1.11278 Anand SS, Razak F, Yi Q, Davis B, Jacobs R, Vuksan V, Lonn E, Teo K, McQueen M, Yusuf S. C-reactive protein as a screening test for cardiovascular risk in a multiethnic population. Arterioscler Thromb Vasc Biol. 2004;24:1509-1515. doi: 10.1161/01.ATV.0000135845.95890.4e La Grotta R, de Candia P, Olivieri F, Matacchione G, Giuliani A, Rippo MR, Tagliabue E, Mancino M, Rispoli F, Ferroni S, et al. Anti-inflammatory effect of SGLT-2 inhibitors via uric acid and insulin. Cell Mol Life Sci. 2022;79:273. doi: 10.1007/s00018-022-04289-z Mazidi M, Karimi E, Rezaie P, Ferns GA. Treatment with GLP1 receptor agonists reduce serum CRP concentrations in patients with type 2 diabetes mellitus: A systematic review and meta-analysis of randomized controlled trials. J Diabetes Complications. 2017;31:1237-1242. doi: 10.1016/j.jdiacomp.2016.05.022 Ridker PM, Hennekens CH, Buring JE, Rifai N. C-reactive protein and other markers of inflammation in the prediction of cardiovascular disease in women. N Engl J Med. 2000;342:836-843. doi: 10.1056/nejm200003233421202 Ridker PM, Danielson E, Fonseca FA, Genest J, Gotto AM, Jr., Kastelein JJ, Koenig W, Libby P, Lorenzatti AJ, MacFadyen JG, et al. Rosuvastatin to prevent vascular events in men and women with elevated C-reactive protein. N Engl J Med. 2008;359:2195-2207. doi: 10.1056/NEJMoa0807646 Ridker PM, Everett BM, Thuren T, MacFadyen JG, Chang WH, Ballantyne C, Fonseca F, Nicolau J, Koenig W, Anker SD, et al. Antiinflammatory Therapy with Canakinumab for Atherosclerotic Disease. New England Journal of Medicine. 2017;377:1119-1131. doi: 10.1056/NEJMoa1707914 Cannon CP, Blazing MA, Giugliano RP, McCagg A, White JA, Theroux P, Darius H, Lewis BS, Ophuis TO, Jukema JW, et al. Ezetimibe Added to Statin Therapy after Acute Coronary Syndromes. New England Journal of Medicine. 2015;372:2387-2397. doi: 10.1056/NEJMoa1410489 Sabatine MS, Giugliano RP, Keech AC, Honarpour N, Wiviott SD, Murphy SA, Kuder JF, Wang H, Liu T, Wasserman SM, et al. Evolocumab and Clinical Outcomes in Patients with Cardiovascular Disease. New England Journal of Medicine. 2017;376:1713-1722. doi: 10.1056/NEJMoa1615664 Nidorf SM, Eikelboom JW, Budgeon CA, Thompson PL. Low-dose colchicine for secondary prevention of cardiovascular disease. J Am Coll Cardiol. 2013;61:404-410. doi: 10.1016/j.jacc.2012.10.027 Nidorf SM, Fiolet ATL, Mosterd A, Eikelboom JW, Schut A, Opstal TSJ, The SHK, Xu XF, Ireland MA, Lenderink T, et al. Colchicine in Patients with Chronic Coronary Disease. N Engl J Med. 2020;383:1838-1847. doi: 10.1056/NEJMoa2021372 Tardif JC, Kouz S, Waters DD, Bertrand OF, Diaz R, Maggioni AP, Pinto FJ, Ibrahim R, Gamra H, Kiwan GS, et al. Efficacy and Safety of Low-Dose Colchicine after Myocardial Infarction. N Engl J Med. 2019;381:2497-2505. doi: 10.1056/NEJMoa1912388 ZEUS - Effects of Ziltivekimab Versus Placebo on Cardiovascular Outcomes in Participants With Established Atherosclerotic Cardiovascular Disease, Chronic Kidney Disease and Systemic Inflammation. In; 2021.

Nov 5, 2024

The following question refers to Section 7.4 of the 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure.The question is asked by the Director of the CardioNerds Internship Dr. Akiva Rosenzveig, answered first by Vanderbilt AHFT cardiology fellow Dr. Jenna Skowronski, and then by expert faculty Dr. Clyde Yancy.Dr. Yancy is Professor of Medicine and Medical Social Sciences, Chief of Cardiology, and Vice Dean for Diversity and Inclusion at Northwestern University, and a member of the ACC/AHA Joint Committee on Clinical Practice Guidelines.The Decipher the Guidelines: 2022 AHA / ACC / HFSA Guideline for The Management of Heart Failure series was developed by the CardioNerds and created in collaboration with the American Heart Association and the Heart Failure Society of America. It was created by 30 trainees spanning college through advanced fellowship under the leadership of CardioNerds Cofounders Dr. Amit Goyal and Dr. Dan Ambinder, with mentorship from Dr. Anu Lala, Dr. Robert Mentz, and Dr. Nancy Sweitzer. We thank Dr. Judy Bezanson and Dr. Elliott Antman for tremendous guidance.Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. American Heart Association’s Scientific Sessions 2024As heard in this episode, the American Heart Association’s Scientific Sessions 2024 is coming up November 16-18 in Chicago, Illinois at McCormick Place Convention Center. Come a day early for Pre-Sessions Symposia, Early Career content, QCOR programming and the International Symposium on November 15. It’s a special year you won’t want to miss for the premier event for advancements in cardiovascular science and medicine as AHA celebrates its 100th birthday. Registration is now open, secure your spot here!When registering, use code NERDS and if you’re among the first 20 to sign up, you’ll receive a free 1-year AHA Professional Membership! Question #37 Mr. S is an 80-year-old man with a history of hypertension, type II diabetes mellitus, and hypothyroidism who had an anterior myocardial infarction (MI) treated with a drug-eluting stent to the left anterior descending artery (LAD) 45 days ago. His course was complicated by a new LVEF reduction to 30%, and left bundle branch block (LBBB) with QRS duration of 152 ms in normal sinus rhythm. He reports he is feeling well and is able to enjoy gardening without symptoms, though he experiences dyspnea while walking to his bedroom on the second floor of his house. Repeat TTE shows persistent LVEF of 30% despite initiation of goal-directed medical therapy (GDMT). What is the best next step in his management?AMonitor for LVEF improvement for a total of 60 days prior to further interventionBImplantation of a dual-chamber ICDCImplantation of a CRT-DDContinue current management as device implantation is contraindicated given his advanced age Answer #37 Explanation Choice C is correct. Implantation of a CRT-D is the best next step. In patients with nonischemic DCM or ischemic heart disease at least 40 days post-MI with LVEF ≤35% and NYHA class II or III symptoms on chronic GDMT, who have reasonable expectation of meaningful survival for >1 year,ICD therapy is recommended for primary prevention of SCD to reduce total mortality (Class 1, LOE A). A transvenous ICD provides high economic value in this setting, particularly when a patient’s risk of death from ventricular arrhythmia is deemed high and the risk of nonarrhythmic death is deemed low. In addition, for patients who have LVEF ≤35%, sinus rhythm, left bundle branch block (LBBB) with a QRS duration ≥150 ms, and NYHA class II, III, orambulatory IV symptoms on GDMT, cardiac resynchronization therapy (CRT) is indicated to reduce total mortality, reduce hospitalizations, and improve symptoms and QOL. Cardiac resynchronization provides high economic value in this setting. Mr. S therefore meets criteria for both ICD and CRT. Choice A is incorrect. All patients should be on maximally tolerated doses of GDMT prior to consideration of device implantation to allow for assessment of LVEF recovery. Patients who have experienced myocardial infarction should be reassessed 40 days after the event and after achieving maximally tolerated doses of GDMT. Choice B in incorrect. For patients in sinus rhythm with a LBBB morphology and QRS duration >150 ms with an LVEF ≤35%, there were significant improvements in 6-minute walk test performance, quality of life, NYHA classification, and LVEF after implantation of CRT. Mortality and hospitalizations were also found to be decreased in patients with CRT-P & CRT-D. Overall, CRT has been shown to have high economic value in these patients. It should be noted that CRT has the most benefit in patients with a wide QRS (>150 ms), LBBB morphology, and LVEF ≤35%, though trials have shown a modest benefit in special populations. CRT has a Class 2a recommendation (LOE B-NR) in patients with LVEF ≤35%, sinus rhythm, and NYHA Class II, III, or ambulatory IV symptoms on GDMT, with either:a) Non-LBBB pattern with a QRS duration ≥150 msb) LBBB with a QRS duration of 120 to 149 ms Choice D is incorrect. If LVEF remains ≤35% in a patient with a life expectancy >1 year, trials have shown that ICD placement for primary prevention reduces sudden cardiac death and also has a high economic value. There is no indication that this patient has a life expectancy 150 ms, CRT-D is also appropriate and cost effective.Guideline Loc.Section 7.4 Decipher the Guidelines: 2022 Heart Failure Guidelines PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron!

Oct 31, 2024

In this episode, Dr. Gurleen Kaur (Cardiology FIT at Brigham and Women’s Hospital and APD of the CardioNerds Academy) and Dr. Diane Masket (Medicine Resident at the University of Chicago Northshore and CardioNerds Academy Intern) discuss with Dr. Minnow Walsh (Medical Director of the Heart Failure and Cardiovascular programs at Ascension St. Vincent Heart Center in Indianapolis) about her personal and professional journey in Cardiology. They discuss Dr. Walsh’s authorship of the recent ACC statement on career flexibility in Cardiology, her involvement with the ACC at both the local and national levels, and her passion for making cardiology a more inclusive and welcoming field for all. Notes were drafted by Dr. Diane Masket and episode audio was engineered by student Dr. Grace Qiu. The PA-ACC & CardioNerds Narratives in Cardiology is a multimedia educational series jointly developed by the Pennsylvania Chapter ACC, the ACC Fellows in Training Section, and the CardioNerds Platform with the goal to promote diversity, equity, and inclusion in cardiology. In this series, we host inspiring faculty and fellows from various ACC chapters to discuss their areas of expertise and their individual narratives. Join us for these captivating conversations as we celebrate our differences and share our joy for practicing cardiovascular medicine. We thank our project mentors Dr. Katie Berlacher and Dr. Nosheen Reza. The PA-ACC & CardioNerds Narratives in Cardiology PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Video version - Career Flexibility in Cardiology https://youtu.be/ygNH6fcQ5ek Quoatables - Career Flexibility in Cardiology “You have to learn to live with ambivalence. You can’t do everything. You can’t do everything all at one time” “One of the most important things the College is behind and pushing, is that competency-based evaluation is what should be used in fellowship rather than this sort of cookie cutter approach where you have to do these many months of echo and this much of cath lab. So, I think flexibility moving from volume to competency is one push.” “Fellowship is daunting, and internal medicine residency is too, but I think culture is how we feel every day. And I think the more we increase flexibility the more that culture is going to shift. Notes - Career Flexibility in Cardiology Process of developing ACC Health Policy Statements These documents address issues that require ACC influence and usually involve a variety of institutions, governing bodies, and other stakeholders. ACC comes to an agreement on how they will approach this topic and shares it broadly. Most of the existing ACC health policy statements are disease-based instead of profession-based. The ACC Career Flexibility statement grew out of the diversity, equity, and inclusion task force, which is a standing committee. A variety of authors are included in health policy statements to reflect the perspectives of many different interest groups. All policy statements, including the one about career flexibility, are available online on JACC.org 1 Major Components of the ACC Career Flexibility Health Policy Statement There are 18 principles that highlight the most important aspects regarding career flexibility in cardiology.2 Flexibility allows for deceleration (decrease in work hours, responsibilities, etc.) and acceleration based on the needs of the physician. For example, during childbearing and rearing time periods, there could be a deceleration, which could accelerate when parenthood responsibilities have decreased. It does not only need to be based around parenting; physicians who are not parents also desire flexibility and enjoy spending time on activities other than their careers. These needs will be unique for each person. Individuals seeking flexibility also must understand that there will be an adjustment in their compensation as they are no longer working full-time. Career flexibility is beneficial at all stages with a desire for a safe training environment early, ability to decelerate mid-career to focus on other priorities and late career to possibly accelerate and works towards a tenure. Allowing flexibility in cardiology is a major pathway to increasing diversity in the workforce which ultimately creates a more inclusive and welcoming environment. Both men and women in cardiology are interested in flexibility. For many years there was a belief that only women wanted this flexibility; however, in recent years it has become apparent that all cardiologists seek the opportunity for a better work-life balance. References: https://www.jacc.org/guidelines 2022 ACC Health Policy Statement on Career Flexibility in Cardiology. J Am Coll Cardiol 2022;Oct 13

Oct 23, 2024

The following question refers to Sections 2.1 and 4.2 of the 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure.The question is asked by CardioNerds Academy Intern Dr. Adriana Mares, answered first by CardioNerds FIT Trialist Dr. Christabel Nyange, and then by expert faculty Dr. Shelley Zieroth. Dr. Zieroth is an advanced heart failure and transplant cardiologist, Head of the Medical Heart Failure Program, the Winnipeg Regional Health Authority Cardiac Sciences Program, and an Associate Professor in the Section of Cardiology at the University of Manitoba. Dr. Zieroth is a past president of the Canadian Heart Failure Society. She has been a PI Mentor for the CardioNerds Clinical Trials Program. The Decipher the Guidelines: 2022 AHA / ACC / HFSA Guideline for The Management of Heart Failure series was developed by the CardioNerds and created in collaboration with the American Heart Association and the Heart Failure Society of America. It was created by 30 trainees spanning college through advanced fellowship under the leadership of CardioNerds Cofounders Dr. Amit Goyal and Dr. Dan Ambinder, with mentorship from Dr. Anu Lala, Dr. Robert Mentz, and Dr. Nancy Sweitzer. We thank Dr. Judy Bezanson and Dr. Elliott Antman for tremendous guidance. Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. American Heart Association’s Scientific Sessions 2024As heard in this episode, the American Heart Association’s Scientific Sessions 2024 is coming up November 16-18 in Chicago, Illinois at McCormick Place Convention Center. Come a day early for Pre-Sessions Symposia, Early Career content, QCOR programming and the International Symposium on November 15. It’s a special year you won’t want to miss for the premier event for advancements in cardiovascular science and medicine as AHA celebrates its 100th birthday. Registration is now open, secure your spot here!When registering, use code NERDS and if you’re among the first 20 to sign up, you’ll receive a free 1-year AHA Professional Membership! Question #36 A 50-year-old woman presents to establish care. Her medical history includes COPD, prediabetes, and hypertension. She is being treated with chlorthalidone, amlodipine, lisinopril, and a tiotropium inhaler. She denies chest pain, dyspnea on exertion, or lower extremity edema. On physical exam, blood pressure is 154/88 mmHg, heart rate is 90 beats/min, and respiration rate is 22 breaths/min with an oxygen saturation of 94% breathing ambient room air. BMI is 36 kg/m2. Jugular venous pulsations are difficult to assess due to her body habitus. Breath sounds are distant, with occasional end-expiratory wheezing. Heart sounds are distant, and extra sounds or murmurs are not detected. Extremities are warm and without peripheral edema. B-type natriuretic peptide level is 28 pg/mL (28 ng/L). A chest radiograph shows increased radiolucency of the lungs, flattened diaphragms, and a narrow heart shadow consistent with COPD. An electrocardiogram shows evidence of left ventricular hypertrophy. The echocardiogram showed normal LV and RV function with no significant valvular abnormalities. In which stage of HF would this patient be classified?AStage A: At Risk for HFBStage B: Pre-HFCStage C: Symptomatic HFDStage D: Advanced HF Answer #36 Explanation The correct answer is A – Stage A or at risk for HF. This asymptomatic patient with no evidence of structural heart disease or positive cardiac biomarkers for stretch or injury would be classified as Stage A or “at risk” for HF. The ACC/AHA stages of HF emphasize the development and progression of disease with specific therapeutic interventions at each stage. Advanced stages and disease progression are associated with reduced survival. The stages were revised in this edition of guidelines to emphasize new terminologies of “at risk” for Stage A and “pre-HF” for Stage B. At Stage A, emphasis is placed on the prevention of structural heart disease by aggressive risk factor modification. Healthy lifestyle habits, including regular physical activity, maintaining a normal weight, healthy dietary habits, and avoiding smoking, help reduce the future risk of HF. For patients with established hypertension, coronary disease, or diabetes, optimal control of risk factors is crucial. For hypertension, the SPRINT trial and subsequent meta-analysis of 35 BP-lowering trials have demonstrated a substantial reduction in incident HF and mortality with aggressive BP control. For diabetes, SGLT2 inhibitors have demonstrated reductions in HF hospitalizations regardless of baseline HF status. Screening patients “at risk” for HF for disease progression may be beneficial. The STOP-HF study randomized patients with risk factors but without established LV systolic dysfunction or symptomatic HF to screening with BNP testing or usual care. Screening with BNP followed by an echocardiogram and referral to a cardiovascular specialist for those with levels ≥50 pg/mL led to a reduction in the composite endpoint of incident asymptomatic LV dysfunction with or without newly diagnosed HF. Accordingly, BNP or NT–proBNP–based screening followed by team-based care, including a cardiovascular specialist, has a Class 2a (LOE B-R) recommendation in patients at risk of developing HF to prevent the development of LV dysfunction or new-onset HF. Our patients should be counseled on healthy lifestyles, smoking cessation, and weight loss. Her anti-hypertensive regimen should be intensified for blood pressure optimization. Her ASCVD risk should be calculated, and counseling regarding statin use should be provided accordingly. If she develops overt diabetes, she should be started on an SGLT-2 inhibitor. Given her BNP level, she does not currently warrant further evaluation with an echocardiogram or referral to a specialist.Main TakeawayPatients with Stage A HF are those who are at risk for HF but are without symptoms, structural heart disease, or cardiac biomarkers of stretch or injury. At this stage, the emphasis should be on identifying and modifying risk factors.Guideline Loc.Sections 2.1 and 4.2 Decipher the Guidelines: 2022 Heart Failure Guidelines PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron!

Oct 21, 2024

CardioNerds (Dr. Dan Ambinder and Dr. Rick Ferraro) join Dr. Mansi Oberoi and Dr. Mohan Gudiwada from the University of Nebraska Medical Center discuss a case of constrictive pericarditis. Expert commentary is provided by Dr. Adam Burdorf, who serves as the Program Director for the Cardiovascular Medicine Fellowship at the University of Nebraska Medical Center. The case discussed involves a 76-year-old woman with a history of monoclonal gammopathy of undetermined significance, chronic obstructive pulmonary disease, type 2 diabetes mellitus, and squamous cell carcinoma was admitted to the hospital for worsening shortness of breath, swelling in lower extremities, hyponatremia, and urinary tract infection. CT chest to evaluate for pulmonary embolism showed incidental pericardial calcifications; the heart failure team was consulted for the management of her decompensated heart failure. Echo images were nondiagnostic. Subsequent invasive hemodynamic monitoring showed elevated right and left-sided filling pressures, diastolic equalization of LV and RV pressures, and positive RV square root sign with ventricular interdependence. Cardiac MRI showed septal flattening on deep inspiration and septal bounce, suggestive of interventricular dependence. After a heart team discussion and with shared-decision making the patient opted for medical management owing to her comorbidities and frailty. Enjoy this 2024 JACC State-of-the-Art Review to learn more about pericardial diseases and best practices for pericardiectomy (Al-Kazac et al., JACC 2024) US Cardiology Review is now the official journal of CardioNerds! Submit your manuscript here. CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Case Media - Constrictive Pericarditis Echo: Left Ventricular ejection fraction = 55-60%. Unclear septal motion in the setting of atrial fibrillation MRI: Diastolic septal flattening with deep inspiration as well as a septal bounce suggestive of interventricular dependence and constrictive physiology References Garcia, M. Constrictive Pericarditis Versus Restrictive Cardiomyopathy. Journal of the American College of Cardiology, vol. 67, no. 17, 2016, pp. 2061–2076. Pathophysiology and Diagnosis of Constrictive Pericarditis. American College of Cardiology, 2017. Geske, J., Anavekar, N., Nishimura, R., et al. Differentiation of Constriction and Restriction: Complex Cardiovascular Hemodynamics. Journal of the American College of Cardiology, vol. 68, no. 21, 2016, pp. 2329–2347. Constrictive Pericarditis. ScienceDirect. Constrictive Pericarditis. Journal of the American College of Cardiology, vol. 83, no. 12, 2024, pp. 1500-1512.

Oct 10, 2024

Dr. Amit Goyal, along with episode chair Dr. Dinu Balanescu (Mayo Clinic, Rochester), and FIT leads Dr. Sonu Abraham (University of Kentucky) and Dr. Natasha Vedage (MGH), dive into the fascinating topic of channelopathies with Dr. Michael Ackerman, a genetic cardiologist and professor of medicine, pediatrics, and pharmacology at Mayo Clinic, Rochester, Minnesota. Using a case-based approach, they review the nuances of diagnosis and treatment of channelopathies, including Brugada syndrome, catecholaminergic polymorphic ventricular tachycardia (CPVT), and long QT syndrome. Dr. Sonu Abraham drafted show notes. Audio engineering for this episode was expertly handled by CardioNerds intern, Christiana Dangas. The CardioNerds Beyond the Boards Series was inspired by the Mayo Clinic Cardiovascular Board Review Course and designed in collaboration with the course directors Dr. Amy Pollak, Dr. Jeffrey Geske, and Dr. Michael Cullen. CardioNerds Beyond the Boards SeriesCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls and Quotes - Channelopathies One cannot equate the presence of type 1 Brugada ECG pattern to the diagnosis of Brugada syndrome. Clinical history, family history, and/or genetic testing results are required to make a definitive diagnosis. The loss-of-function variants in the SCN5A gene, which encodes for the α-subunit of the NaV1.5 sodium channel, is the only Brugada susceptibility gene with sufficient evidence supporting pathogenicity. Exertional syncope is an “alarm” symptom that demands a comprehensive evaluation with 4 diagnostic tests: ECG, echocardiography, exercise treadmill test, and Holter monitor. Think of catecholaminergic polymorphic ventricular tachycardia (CPVT) in a patient with exertional syncope and normal EKG! ICD therapy is never prescribed as monotherapy in patients with CPVT. Medical therapy with a combination of nadolol plus flecainide is the current standard of care. Long QT syndrome is one of the few clinical scenarios where genetic testing clearly guides management, particularly with respect to variability in beta-blocker responsiveness. Notes - Channelopathies 1. What are the diagnostic criteria for Brugada syndrome (BrS)? Three repolarization patterns are associated with Brugada syndrome in the right precordial leads (V1-V2): Type 1: Prominent coved ST-segment elevation displaying J-point amplitude or ST-segment elevation ≥2 mm, followed by a negative T wave. Type 2/3: Saddleback ST-segment configuration with variable levels of ST-segment elevation. It is important to note that only a type 1 pattern is diagnostic for Brugada syndrome, whereas patients with type 2/3 patterns may benefit from further testing. The Shanghai score acknowledges that relying solely on induced type 1 ECG changes has limitations. Therefore, one cannot equate the presence of a type 1 Brugada ECG pattern alone to the diagnosis of Brugada syndrome. The score suggests incorporating additional information—such as clinical history, family history, and/or genetic testing results—to achieve a definitive diagnosis. 2. What is the significance of genetic testing in Brugada syndrome? There are 23 alleged Brugada syndrome susceptibility genes published with varying levels of evidence. However, only one gene mutation, the loss-of-function variants in the SCN5A gene encoding for the α-subunit of the NaV1.5 sodium channel, is considered to have sufficient evidence. The overall yield of BrS genetic testing is 20%. The presence of PR prolongation (>200 ms) along with type I EKG pattern increases the yield to 40%. On the contrary, in the presence of a normal PR interval, the likelihood of SCN5A positivity drops to 460 ms. 10. What are the three primary mutations implicated in Long QT syndrome? LQT1 (30-40% of cases) Mutation: loss of function in potassium channel gene KCNQ1 ECG: broad-based T wave Trigger: activity, adrenaline, exercise BB responsiveness: +++ (nadolol or propranolol) LQT2 (second most common) Mutation: loss of function in potassium channel gene KCNH2 ECG: notched T wave Trigger: auditory (alarm clock), post-partum BB responsiveness: ++ LQT3 Mutation: gain of function or leakiness of sodium channel SCN5A (note: BrS is due to loss of function in the same gene) ECG: normal T wave after prolonged isoelectric ST segment Trigger: none, but typically happens during rest BB responsiveness: + (propranolol); may consider combination therapy with mexiletine or mexiletine monotherapy. References - Channelopathies Charles Antzelevitch, Gan-Xin Yan, Michael J. Ackerman, Arthur A.M. Wilde et al. J-Wave syndromes expert consensus conference report: Emerging concepts and gaps in knowledge, EP Europace, Volume 19, Issue 4, April 2017, Pages 665–694 Krahn AD, Behr ER, Hamilton R, Probst V, Laksman Z, Han HC. Brugada Syndrome. JACC Clin Electrophysiol. 2022 Mar;8(3):386-405. PMID: 35331438. Chockalingam, P, Crotti, L, Girardengo, G. et al. Not All Beta-Blockers Are Equal in the Management of Long QT Syndrome Types 1 and 2: Higher Recurrence of Events Under Metoprolol. JACC. 2012 Nov, 60 (20) 2092–2099 Priori SG, Wilde AA, Tracy C et al. HRS/EHRA/APHRS expert consensus statement on the diagnosis and management of patients with inherited primary arrhythmia syndromes: document endorsed by HRS, EHRA, and APHRS in May 2013 and by ACCF, AHA, PACES, and AEPC in June 2013. Heart Rhythm. 2013 Dec;10(12):1932-63. PMID: 24011539. Viskin S, Rosovski U, Zeltser D et al. Inaccurate electrocardiographic interpretation of long QT: the majority of physicians cannot recognize a long QT when they see one. Heart Rhythm. 2005 Jun;2(6):569-74. PMID: 15922261. Horner JM, Ackerman MJ. Ventricular ectopy during treadmill exercise stress testing in the evaluation of long QT syndrome. Heart Rhythm. 2008 Dec;5(12):1690. PMID: 19084807; PMCID: PMC3281579.

Oct 2, 2024

The CardioNerds Academy is excited to present the 3rd Annual Sanjay V. Desai Lecture in Medical Education, featuring a deep dive into the evolving role of Artificial Intelligence in Medical Education. Join us as Dr. Kathryn Berlacher, Dr. Melissa McNeil, and Dr. Alfred Shoukry explore the transformative potential of AI in training future healthcare professionals and enhancing educational methodologies. Their insightful discussion sheds light on the integration of cutting-edge technologies to improve medical learning and patient care. The conversation is faciliated by Dr. Tommy Das, Program Director of the CardioNerds Academy, and CardioNerds Academy Chiefs: Dr. Callie Clark, Dr. Rachel Goodman, Dr. Ronaldo Correa Fabiano, and Dr. Claire Cambron, who bring their expertise and enthusiasm to this engaging discussion on the future of medical education. Special thanks to Pace Wetstein, CardioNerds academy intern, for his exceptional audio editing in this episode. Dr. Kathryn Berlacher is a graduate of The Ohio State University College of Medicine and completed her internal medicine residency, chief residency, and cardiology fellowship at UPMC, where she has been on faculty since 2012. She earned a master's degree in medical education from the University of Pittsburgh and has served as the Program Director of the Cardiovascular Fellowship Program since 2015. In 2021, she was appointed Associate Chief of Education for the UPMC Heart and Vascular Institute. Additionally, Dr. Berlacher is the director of the McGee Women's Heart Program and chief of medicine at McGee Women's Hospital. Nationally, she serves as the chair for the American College of Cardiology’s Annual Scientific Sessions for 2025 and 2026, regularly speaking on women's cardiology, medical education, diversity, inclusion, and health equity.Dr. Alfred Shoukry graduated from Northwestern University with dual degrees in Neurobiology and Biomedical Engineering. He completed medical school and internal medicine residency at UPMC, where he also earned a certificate in medical education. Dr. Shoukry serves as core faculty at the University of Pittsburgh School of Medicine and cares for patients at the VA in Pittsburgh. As the course director for Population Health, he teaches on topics such as patient safety, quality improvement, and bioinformatics. He is an expert on the impact of large language models in medical education, presenting locally and nationally on the subject.Dr. Melissa McNeil received her undergraduate degree from Princeton University, her MD from the University of Pittsburgh, and a Master of Public Health from the same institution. She is a professor emeritus of medicine at the University of Pittsburgh and recently joined the faculty at Brown University as a professor of medicine. Dr. McNeil serves as an academic hospitalist and senior consultant to the Women's Health Division at Brown. Her expertise lies in developing training programs to foster leaders in women's health education and research. She has been recognized nationally for her contributions, including being named the Society of General Internal Medicine Distinguished Professor of Women's Health in 2014 and receiving their Career Achievement in Medical Education award in 2016. Dr. Sanjay V Desai serves as the Chief Academic Officer, The American Medical Association and is the former Program Director of the Osler Medical Residency at The Johns Hopkins Hospital. Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. US Cardiology Review is now the official journal of CardioNerds! Submit your manuscript here. CardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron!

Oct 1, 2024

CardioNerds Drs. Jason Feinman, Gurleen Kaur, and Rick Ferraro discuss the implementation of SGLT inhibitors in clinical practice with Dr. Alison Bailey. Notes were drafted by Dr. Jason Feinman. In this episode, we discuss the implementation of SGLTi in clinical practice scenarios, including for individuals with heart failure regardless of ejection fraction, those with chronic kidney disease, and those with diabetes mellitus. The group also discusses important side effects to monitor for, as well as how to counsel patients when prescribing these medications. This episode was produced in collaboration with the American Society of Preventive Cardiology (ASPC) with independent medical education grant support from Lexicon Pharmaceuticals. CardioNerds Prevention PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls - Clinical Implementation of SGLT Inhibitors For patients with heart failure with reduced ejection fraction, SGLT inhibitors reduce the composite outcome of cardiovascular death or heart failure hospitalization by 25%. SGLT inhibitors can be safely started in patients with an eGFR as low as 20. There are ongoing trials investigating the safety of these medications in individuals with eGFR lower than 20 or those who are receiving dialysis. An eGFR decrease of 3-5 ml/min on average is expected after starting an SGLTi, but this will stabilize over time and provides protective effects of renal dysfunction in the long run. Early data that suggested an association between SGLTi and bacterial UTI development hasn’t panned out in the long run, but there is an association between SGLTi and the development of either genital mycotic infections or yeast infections. Perineal hygiene is important to prevent the development of either. A patient-centered, shared decision-making approach should guide the choice of agents for individuals with type 2 diabetes mellitus. In certain patients, it may be reasonable to choose an SGLTi as the first-line agent. Show notes - Clinical Implementation of SGLT Inhibitors What is the data supporting the use of SGLTi in HFpEF? The EMPEROR-Preserved and DELIVER trials investigated the impact of empagliflozin and dapagliflozin, respectively, on cardiovascular outcomes in patients with mildly reduced or preserved ejection fraction. The SOLOIST-WHF trial investigated a combined SGLT1/2 inhibitor, sotagliflozin, in patients with recently worsening heart failure, irrespective of ejection.SGLTi have been demonstrated to reduce the risk of cardiovascular death or worsening heart failure, including heart failure hospitalization, in these individuals. A meta-analysis of the EMPEROR-Preserved and DELIVER trials demonstrated a hazard ratio of 0.80 for cardiovascular death or first hospitalization for heart failure for empagliflozin or dapagliflozin over placebo in the setting of HFpEF. What is the data supporting the use of SGLTi in HFrEF? In addition to the SOLOIST-WHF trial that was previously discussed, the EMPEROR-HF and DAPA-HF investigated the impact of SGLTi medications in patients with HFrEF. In patients with HFrEF, SGLTi medications have been demonstrated to reduce the risk of either cardiovascular death or heart failure hospitalization. Dapagliflozin and empagliflozin had a pooled risk reduction of all-cause death of 13%, a pooled risk reduction of cardiovascular death of 14%, and a 26% reduction in the combination of CV death or first hospitalization for heart failure. What is the expected impact of SGLTi on renal function? Dapagliflozin, empagliflozin, sotagliflozin, ertugliflozin, and canagliflozin have all been studied for their impact on renal dysfunction in individuals both with and without diabetes. In the CANVAS trial, canagliflozin was associated with an initial decrease in eGFR of 3.2ml/min compared to placebo but overall decreased change from baseline in eGFR compared to placebo at trial end.In a large meta-analysis, SGLTi medications reduced the progression of kidney disease by 37%. The risk of acute kidney injury was reduced by 23%. What are the recommendations for SGLTi in patients with type 2 diabetes mellitus? ADA guidelines emphasize a patient-centered shared decision-making approach when choosing which pharmacologic agent to prescribe for an individual with diabetes mellitus. Factors in choosing which agent include the risk of cardiovascular disease, the risk of renal disease, and whether there is an emphasis on weight reduction. What side effects should be monitored for when starting an individual on an SGLTi medication? Side effects with SGLTi medications are overall rare but include DKA, genital mycotic infections, necrotizing fasciitis, and volume status derangements. In the CANVAS trial, SGLTi was associated with an increased risk of amputation, but this has not been shown to be consistent in other trials. Nevertheless, in a meta-analysis including CANVAS, SGLTi medications were associated with a 15% relative risk of amputation over placebo medications.The relative risk of DKA in the same meta-analysis was 2.12. Careful assessment of an individual's volume status and whether they are on any other diuretic medications when initiating an SGLTi medication may allow for upfront adjustment of these medications to reduce the risk of dehydration. References - Clinical Implementation of SGLT Inhibitors Solomon SD, McMurray JJV, Claggett B, et al. Dapagliflozin in Heart Failure with Mildly Reduced or Preserved Ejection Fraction. N Engl J Med. 2022;387(12):1089-1098. Anker SD, Butler J, Filippatos G, et al. Empagliflozin in Heart Failure with a Preserved Ejection Fraction. N Engl J Med. 2021;385(16):1451-1461. Bhatt DL, Szarek M, Steg PG, et al. Sotagliflozin in Patients with Diabetes and Recent Worsening Heart Failure. N Engl J Med. 2021;384(2):117-128. Vaduganathan M, Docherty KF, Claggett BL, et al. SGLT-2 inhibitors in patients with heart failure: a comprehensive meta-analysis of five randomised controlled trials. Lancet. 2022;400(10354):757-767. Packer M, Anker SD, Butler J, et al. Cardiovascular and Renal Outcomes with Empagliflozin in Heart Failure. N Engl J Med. 2020;383(15):1413-1424. McMurray JJV, Solomon SD, Inzucchi SE, et al. Dapagliflozin in Patients with Heart Failure and Reduced Ejection Fraction. N Engl J Med. 2019;381(21):1995-2008. Zannad F, Ferreira JP, Pocock SJ, et al. SGLT2 inhibitors in patients with heart failure with reduced ejection fraction: a meta-analysis of the EMPEROR-Reduced and DAPA-HF trials. Lancet. 2020;396(10254):819-829. Neal B, Perkovic V, Mahaffey KW, et al. Canagliflozin and Cardiovascular and Renal Events in Type 2 Diabetes. N Engl J Med. 2017;377(7):644-657. Nuffield Department of Population Health Renal Studies Group; SGLT2 inhibitor Meta-Analysis Cardio-Renal Trialists' Consortium. Impact of diabetes on the effects of sodium glucose co-transporter-2 inhibitors on kidney outcomes: collaborative meta-analysis of large placebo-controlled trials. Lancet. 2022;400(10365):1788-1801. American Diabetes Association Professional Practice Committee. 9. Pharmacologic Approaches to Glycemic Treatment: Standards of Care in Diabetes-2024. Diabetes Care. 2024;47(Suppl 1):S158-S178.

Sep 23, 2024

CardioNerds (Amit Goyal) join Dr. Merna Hussien, Dr. Akhil Kallur, Dr. Abhinav Saxena, and Dr. Brody Deb from the MedStar Georgetown - Washington Hospital Center in DC for a stroll around Rock Creek Park as they discuss an unusual case of cobalt cardiomyopathy. Expert commentary is provided by Dr. Nana Afari Armah. Episode audio was edited by CardioNerds Intern Christiana Dangas. The case is of a middle-aged woman with a past medical history of hypertension, hyperlipidemia, and bilateral hip replacements, who presented with subacute progressive exertional dyspnea, orthopnea, and constitutional symptoms and was found to have SCAI Stage C cardiogenic shock. Transthoracic echocardiogram showed severely reduced left ventricular ejection fraction (LVEF, 20-25%) and a moderate pericardial effusion. Cardiac catheterization revealed biventricular failure with elevated filling pressures. A cardiac MRI showed diffuse late gadolinium enhancement (LGE) in the left ventricle. Endomyocardial biopsy showed nonspecific chronic inflammation. However, the evidence of mitochondrial heavy metal toxicity and elevated cobalt levels made the diagnosis of cobalt cardiomyopathy. The patient underwent revision of hip joint implants to ceramic implants and started chelation therapy. However, due to persistent stage D heart failure despite normalization of cobalt levels, she underwent orthotropic heart transplantation. US Cardiology Review is now the official journal of CardioNerds! Submit your manuscript here. CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Case MEdia - Cobalt Cardiomyopathy Pearls - Cobalt Cardiomyopathy A good history goes a long way in diagnosing non-ischemic cardiomyopathy (NICM). Common problems can have uncommon presentations requiring a high degree of suspicion for diagnosis. Imaging features can overlap between causes of NICM. History helps in targeting further histological workup and uncovering the root cause. Multidisciplinary effort is essential in making a rare diagnosis. Taken from1 - Singh M, Krishnan M, Ghazzal A, Halushka M, Tozzi JE, Bunning RD, Rodrigo ME, Najjar SS, Molina EJ, Sheikh FH. From Hip to Heart: A Comprehensive Evaluation of an Infiltrative Cardiomyopathy. CJC Open. 2021 Nov 1;3(11):1392–5. Notes - Cobalt Cardiomyopathy How common is cobalt cardiomyopathy? When should it be suspected? Cobalt cardiomyopathy is incredibly rare, with only a handful of reported cases. 2 It is also known as beer drinkers’ cardiomyopathy, as cobalt was added to beer for fortification in Quebec 3, where it was first reported. Cobalt cardiomyopathy is characterized by its rapidly progressive nature, the presence of low voltages on EKG, and diffuse infiltration. Patients also complained of a previous history of anorexia and weight loss and were found to have polycythemia and thyroid abnormalities on labs. This syndrome was very similar to wet beriberi except for the absence of a therapeutic response to thiamine. Taken from - 2 Later, this was noted in patients with total metal hip arthroplasty 4–6, especially in patients with metal-on-metal hip arthroplasty, which led to corrosion and leakage of cobalt into the bloodstream. The syndrome in these patients was similar to those in beer drinkers from Quebec. This figure, taken from 2, shows the reports of Cobalt cardiomyopathy after cobalt alloy prostheses. [HX1] What is the pathophysiology of cobalt cardiomyopathy? Cobalt has a variety of effects on the heart, both microscopically and biochemically.Cobalt may have multiple calcium-mediated cardiac effects and may also interfere with the Krebs cycle and ATP generation by mitochondria. Histology may show modest changes with no inflammatory response on microscopy and ultrastructural changes, including vacuolar degeneration and swollen and distorted mitochondria with loss of cristae. Remarkably, cardiac dysfunction does not correlate with serum cobalt levels. 2 How does cobalt cardiomyopathy present, and how do we diagnose it? Diagnosis is made with a consistent exposure history and high index of suspicion. Patients present with anorexia and cachexia and complain of rapid onset and progression of symptoms of cardiomyopathy.Labs may show polycythemia and thyroid dysfunction. Cobalt levels should be elevated, but the severity of the disease does not correlate well with levels. Cardiac workup: EKG shows low voltage from infiltration and pericardial effusion. Echocardiogram shows systolic dysfunction and pericardial effusion. MRI shows diffuse infiltrative pathology. Native heart pathology is often diagnostic. 2 How is cobalt cardiomyopathy managed? Medical management of heart failure, including guideline directed medical therapy (GDMT), inotropic support, and mechanical circulatory support, implantable device or transplant where appropriate. Oral chelating agents should be used. The mainstay of management is the removal of the prosthesis or source of exposure. 2 What is the prognosis of Cobalt Cardiomyopathy? In the beer-drinker population, the prognosis was bad. Patients in that population had rapid clinical progression leading to cyanosis, marked elevation of cardiac and hepatic enzymes, lactic acidosis, and shock, and a high mortality rate (of 10%–40%), which was proportional to the daily intake of beer. 2 Some patients may recover function after removal of the cobalt source and normalization of the levels. However, some patients, like our patient, continue to have deterioration of function despite lower Cobalt levels requiring mechanical support and heart transplant. Infographic made by the team (Made with BioRender – license included) References - Cobalt Cardiomyopathy 1. Singh M, Krishnan M, Ghazzal A, et al. From Hip to Heart: A Comprehensive Evaluation of an Infiltrative Cardiomyopathy. CJC Open. 2021;3(11):1392-1395. https://www.ncbi.nlm.nih.gov/pubmed/34901809 2. Packer M. Cobalt Cardiomyopathy. Circ Heart Fail. 2016;9(12):e003604. https://www.ahajournals.org/doi/epub/10.1161/CIRCHEARTFAILURE.116.003604 3. Mercier G, Patry G. Quebec beer-drinkers’ cardiomyopathy: clinical signs and symptoms. Can Med Assoc J. 1967;97(15):884-888. https://pubmed.ncbi.nlm.nih.gov/6051257/ 4. Oldenburg M, Wegner R, Baur X. Severe cobalt intoxication due to prosthesis wear in repeated total hip arthroplasty. J Arthroplasty. 2009;24(5):825.e15-20. https://www.ncbi.nlm.nih.gov/pubmed/18835128 5. Tower SS. Arthroprosthetic cobaltism: neurological and cardiac manifestations in two patients with metal-on-metal arthroplasty: a case report. J Bone Joint Surg Am. 2010;92(17):2847-2851. https://www.ncbi.nlm.nih.gov/pubmed/21037026 6. Casian M, Bica R, Ionescu V, Predescu V, Țincu R, Jurcuț R. Too young for an acquired cardiomyopathy? Cobalt metallosis as a cardiac amyloidosis mimicker. ESC Heart Fail. 2024;11(2):1236-1241. https://onlinelibrary.wiley.com/doi/10.1002/ehf2.14695

Sep 19, 2024

The following question refers to Section 2.2 of the 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure.The question is asked by University of Colorado internal medicine resident Dr. Hirsh Elhence, answered first by University of Chicago advanced heart failure cardiologist and Co-Chair for the CardioNerds Critical Care Cardiology Series Dr. Mark Belkin, and then by expert faculty Dr. Mark Drazner.Dr. Drazner is an advanced heart failure and transplant cardiologist, Professor of Medicine, and Clinical Chief of Cardiology at UT Southwestern. He is the President of the Heart Failure Society of America.The Decipher the Guidelines: 2022 AHA / ACC / HFSA Guideline for The Management of Heart Failure series was developed by the CardioNerds and created in collaboration with the American Heart Association and the Heart Failure Society of America. It was created by 30 trainees spanning college through advanced fellowship under the leadership of CardioNerds Cofounders Dr. Amit Goyal and Dr. Dan Ambinder, with mentorship from Dr. Anu Lala, Dr. Robert Mentz, and Dr. Nancy Sweitzer. We thank Dr. Judy Bezanson and Dr. Elliott Antman for tremendous guidance.Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. Question #35 A 50-year-old woman with a history of congestive heart failure, hypertension, type 2 diabetes mellitus, and obstructive sleep apnea presents to the outpatient clinic to follow up on her heart failure management. One year prior, echocardiogram showed an ejection fraction of 30% with an elevated BNP, for which she was started on appropriate GDMT. Repeat echocardiogram today showed an EF of 50%. Which of the following best describes her heart failure status? A HFrEF (HF with reduced EF) B HFimpEF (HF with improved EF) C HFmrEF (HF with mildly reduced EF) D HFpEF (HF with preserved EF) Answer #35 Explanation The correct answer is B – HFimpEF, or heart failure with improved ejection fraction, best describes her current heart failure status. Left ventricular ejection fraction is an important factor in classifying heart failure given differences in prognosis, response to treatment, and use in clinical trial enrollment criteria. The classification of heart failure by EF (adopted from the Universal Definition of HF): – HFrEF (HF with reduced EF): LVEF ≤40% – HFimpEF (HF with improved EF): previous LVEF ≤40%, a ≥10% increase from baseline LVEF, and a second measurement of LVEF >40%. – HFmrEF (HF with mildly reduced EF): LVEF 41%–49%, andevidence of spontaneous or provokable increased LV filling pressures (e.g., elevated natriuretic peptide, noninvasive and invasive hemodynamic measurement) – HFpEF (HF with preserved EF): LVEF ≥50%, and evidence of spontaneous or provokable increased LV filling pressures (e.g., elevated natriuretic peptide, noninvasive and invasive hemodynamic measurement) Patients with HFmrEF are usually in a dynamic state of improving from HFrEF or deteriorating towards HFrEF. Therefore, patients with HFmrEF may benefit from follow-up evaluation of systolic function and etiology of sub-normal EF. Improvements in EF are associated with better outcomes but do not indicate full myocardial recovery or normalization of LV function. Indeed, structural and functional abnormalities such as LV dilation and systolic or diastolic dysfunction often persist. Moreover, EF may remain dynamic with fluctuations in either direction depending on factors such as GDMT adherence and re-exposure to cardiotoxic agents. As such, the term heart failure with “improved EF” was deliberately chosen over “recovered EF” and “preserved EF”. Importantly, in patients with HFimpEF while on GDMT, the EF may decrease after withdrawal of GDMT. Main Takeaway Classification of Heart failure helps direct and track management. Guideline Loc. Section 2.2 Decipher the Guidelines: 2022 Heart Failure Guidelines PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron!

Sep 18, 2024

CardioNerds Cardio-Rheumatology Series Co-Chairs Dr. Rick Ferraro, Dr. Gurleen Kaur, and and Dr. Bree Hansen discuss how to decipher cardiovascular risk in patients with rheumatological conditions with cardio-rheumatology experts Dr. Brittany Weber and Dr. Michael Garshick. In this episode, Drs. Weber and Garshick take us through the role of inflammation in patients with rheumatologic conditions and cardiovascular disease. They discuss the increased prevalence of traditional cardiac risk factors in this population and how these standard cardiac risk factors do not account for the full extent of cardiovascular risk. Dr. Bree Hansen drafted show notes. Audio editing by CardioNerds intern Christiana Dangas. CardioNerds Prevention PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls - Cardio-Rheumatology - Deciphering Cardiovascular Risk in Patients with Rheumatological Conditions Cardiovascular disease prevalence: cardiovascular disease is common in patients with autoimmune rheumatologic disease; therefore, we must take every opportunity to screen patients early. Limitations of Traditional Scores: conventional risk calculators often underestimate cardiovascular risk for autoimmune disease patients, necessitating additional methods to assess risk accurately. Integration of Disease-Specific Biomarkers: using biomarkers specific to autoimmune diseases, such as lupus, enhances risk assessment and helps in tailoring treatment strategies. Value of Imaging and Risk Enhancers: incorporating imaging (like CAC scoring and carotid ultrasound) and evaluating additional risk factors (such as lipoprotein(a) and high-sensitivity CRP) provides a more comprehensive view of cardiovascular risk and guides more effective management. Show notes - Cardio-Rheumatology - Deciphering Cardiovascular Risk in Patients with Rheumatological Conditions Show notes (Drafted by Dr. Bree Hansen): How does inflammation contribute to atherosclerosis, specifically in autoimmune rheumatologic diseases like psoriasis? Lipids need to enter the intimal space of blood vessels, which can be facilitated by endothelial damage caused by chronic cytokine stimulation, such as TNF or IL-6. Once in the intima, lipids are recognized as foreign, leading to the recruitment of monocytes that transform into macrophages to clear these lipids. However, this process often exacerbates the problem, leading to persistent inflammation and atherosclerotic plaque formation. Specifically, in psoriasis, the endothelial damage is particularly pronounced due to cytokines like TNF, IL-17, and interferons. The inflammasome pathway, which is highly active in psoriasis, also contributes to endothelial damage. Additionally, hyperactivated platelets in psoriasis can further damage the endothelium and contribute to atherosclerosis. Overall, atherosclerosis results from a combination of traditional risk factors and systemic inflammation, leading to the development of cardiovascular disease. Which traditional cardiovascular risk factors are increased in patients with rheumatologic conditions? Patients with autoimmune diseases may be up to > three times more likely to develop cardiovascular disease, similar to the risk of type 2 diabetes; therefore, it is important to screen patients with autoimmune rheumatologic disorders for cardiovascular disease Most common cardiovascular risk factors, such as smoking, diabetes, hypertension, and dyslipidemia, are also increased in patients with autoimmune rheumatologic disorders. Smoking, specifically, is highly prevalent in psoriasis and exhibits a dose-response relationship with psoriasis severity. Hyperlipidemia is another common risk factor present in patients with autoimmune rheumatologic disease; however, a “lipid paradox” also exists. The "lipid paradox," where lower LDL (low-density lipoprotein) levels are associated with higher inflammation, seems counterintuitive since lower LDL is often thought to indicate lower cardiovascular risk. This paradox is particularly well-documented in rheumatoid arthritis (RA) but may apply to various other conditions as well. In clinical practice, it's important to assess lipid levels not only during periods of high inflammation but also when the patient is in a state of disease remission or stability. This is because lipid levels can fluctuate based on the level of inflammation and the medications a patient takes, such as biologics. How can cardiovascular disease risk be estimated in patients with rheumatologic conditions beyond that of traditional risk factor calculators? Traditional cardiovascular risk scores like the Framingham Risk Score and ACC/AHA Pool Cohort Equation often underestimate risk, particularly for patients with autoimmune diseases. Risk calculators in women with RA underestimated cardiovascular risk at least 2‐fold. The Run-On Risk Score includes inflammatory markers like CRP but can still fall short in risk assessment. While some specialized calculators like The British SCORE2 system, which initially included rheumatoid arthritis (RA), and later QRISK3, which added lupus and steroid use, include these autoimmune conditions, no standard tool is universally applied for these diseases. Therefore, clinicians need to integrate multiple data sources to assess risk effectively Recent research, such as a study from Dr. Weber's group, has highlighted that incorporating lupus-specific biomarkers such as persistently positive double-stranded DNA, low complement levels, and lupus anticoagulant into risk calculators improves risk prediction for lupus patients. Thus, beyond traditional risk factors, clinicians should assess disease duration, activity biomarkers, and the impact of treatments (including medications like hydroxychloroquine that have potential cardiotoxicity). Clinicians should also use other risk enhancers, like lipoprotein(a) and high-sensitivity CRP, and consider imaging techniques like coronary artery calcium (CAC) scoring to evaluate atherosclerotic burden. Elevated lipoprotein(a) levels and high CAC scores indicate higher risk, even if traditional risk scores suggest otherwise. References - Deciphering Cardiovascular Risk in Patients with Rheumatological Conditions Conrad N, Verbeke G, Molenberghs G, et al. Autoimmune diseases and cardiovascular risk: a population‐based study on 19 autoimmune diseases and 12 cardiovascular diseases in 22 million individuals in the UK. Lancet. 2022;400:733–743. Crowson CS, Liao KP, Davis JM 3rd, et al. Rheumatoid arthritis and cardiovascular disease. Am Heart J. 2013;166(4):622-628.e1. doi:10.1016/j.ahj.2013.07.010 Garshick MS, Ward NL, Krueger JG, Berger JS. Cardiovascular Risk in Patients With Psoriasis: JACC Review Topic of the Week. J Am Coll Cardiol. 2021;77(13):1670-1680. doi:10.1016/j.jacc.2021.02.009 Weber, B, Paik, J, Aghayev, A. et al. Novel Imaging Approaches to Cardiac Manifestations of Systemic Inflammatory Diseases: JACC Scientific Statement. JACC. 2023 Nov, 82 (22) 2128–2151. https://doi.org/10.1016/j.jacc.2023.09.819 Mortensen M, Jensen J, Sand N, et al. Association of Autoimmune Diseases with Coronary Atherosclerosis Severity and Ischemic Events. JACC. 2024. Jun, 83 (25) 2643-2654. Doi: 10.1016/j.jacc.2024.04.030 Choi M, Guan H, Yoshida K, et al. Personalizing cardiovascular risk prediction for patients with systemic lupus erythematosus. Seminars in Arthritis and Rheumatism. 2024. Aug:67:152468. Doi: 10.1016/j.semarthrit.2024.152468.

Sep 6, 2024

CardioNerds Dan Ambinder and Dr. Devesh Rai join cardiology fellows and National Lipid Association lipid scholars Dr. Jelani Grant from Johns Hopkins University and Dr. Alexander Razavi from Emory University. They discuss a case involving a patient with familial hypercholesterolemia. Dr. Archna Bajaj from University of Pennsylvania provides expert commentary. Drs. Jelani Grant and Alexander Razavi drafted notes. CardioNerds Intern Pacey Wetstein engineered episode audio. This episode is part of a case reports series developed in collaboration with the National Lipid Association and their Lipid Scholarship Program, with mentorship from Dr. Daniel Soffer and Dr. Eugenia Gianos. A classic finding in patients with familial hypercholesterolemia is the presence of markedly elevated levels of total and low-density lipoprotein cholesterol (LDL-C) with an LDL-C concentration of 190 mg/dL or greater. However, severe hypercholesterolemia is not inevitably present, and many patients who carry this diagnosis may have lower LDL-C levels. This case history describes a young woman whose mother and brother met clinical and genetic criteria for heterozygous familial hypercholesterolemia but who had only a mild elevation in LDL-C, falling to 130 mg/dL after dietary intervention. Despite this finding, genetic testing revealed the presence of the same genetic variants as were noted in her mother and brother. In addition, a second genetic variant predisposing them to cholesterol gallstone formation was identified in all three family members. If genetic testing had not been performed, the diagnosis may have been missed or delayed, resulting in an increased risk for vascular complications associated with familial hypercholesterolemia. This case supports the value of genetic testing of family members of those with familial hypercholesterolemia, even when LDL-C levels are not severely elevated. US Cardiology Review is now the official journal of CardioNerds! Submit your manuscript here. CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls - Exposing an Unusual Presentation of Familial Hypercholesterolemia – National Lipid Association Familial hypercholesterolemia (FH) is among the most common autosomal co-dominant genetic conditions (approximately 1:200 to 1:300 for HeFH, 1:160,000 to 1:300,000 for HoFH). Genetic testing has a role for all first-degree relatives when a family history of FH is strongly suggestive, regardless of LDL-C level. Heterogeneity in ASCVD risk among individuals with FH is derived from background polygenic risk, clinical risk factors (e.g., timing of lipid-lowering initiation and adjacent risk factors), as well as subclinical atherosclerosis burden. In clinical or genetically confirmed FH, an LDL-C goal of 55 mg/dL is recommended. Beyond statins, FDA-approved non-statin therapies for FH include ezetimibe, PCSK9 mAb, bempedoic acid, inclisiran, evolocumab (only HoFH), lomitapide (only HoFH), and LDL apheresis. Notes - Exposing an Unusual Presentation of Familial Hypercholesterolemia – National Lipid Association What are the diagnostic criteria for FH? Dutch Lipid Clinic Network1 Variables: family history, clinical history, physical exam, LDL-C level, DNA (LDLR, APOB, PCSK9) Simon-Broome1 Variables: total or LDL-C, physical exam, DNA (LDLR, APOB, PCSK9), family history Emphasis on clinical history and physical exam reduces sensitivity U.S. Make Early Diagnosis Prevent Early Death (MEDPED) 1 Only one of the three where no genetic testing is required, may work well in cascade screening Variables: age, total cholesterol, family relative (and degree) with FH Definite, probable, possible, unlikely Emphasis on clinical history and physical exam reduces sensitivity How does FH affect CAD risk? There is about a 20-fold higher risk of premature CHD in FH without treatment2 For any CHD3As high as 100-fold greater risk in young men with FH Risk is lower in women versus men (approximate 10-year age difference in development) Up to one-half of men and one-third of women with FH will suffer fatal or non-fatal coronary events before age 50 and 60 years old, respectively 4 Despite this high risk, it is important to note heterogeneity in FH that can be attributable to:Polygenic riskTiming of lipid-lowering therapy initiationAdjacent risk factors Subclinical atherosclerosis burden 5 6 7 What is the role of genetic testing in FH? Clinical value of genetic testing:Providing prognostic informationPromotes initiation and adherence of lipid-lowering therapies Serves as a basis for more effective cascade screening Heterogeneity in FH may be attributable to other genes that regulate LDL-C, but which are not tested as part of the FH gene panel. For example, there are polygenic risk scoring systems to gauge the relative impact on LDL-C; however, this is not routinely done, but potentially impactful Provide guideline-based recommendations for treatment Beyond statins, FDA-approved non-statin therapies for FH include: ezetimibe, PCSK9 mAb, bempedoic acid, inclisiran, evinacumab (only HoFH), lomitapide (only HoFH), and LDL apheresis8. Based on the 2022 ACC Expert Consensus Decision Pathway for Non-Statin Therapy, an LDL-C goal of 190 mg/dL Inadequate reduction of LDL-C (>50% and LDL-C <70 mg/dL or non-HDL-C <100 mg/dL) Intolerance to at least two statin therapies, with an attempt to initiate FDA-approved lowest dose of statin and a trial of an alternative statin therapy regimen such as every other day dosing References Vallejo-Vaz AJ, Ray KK. Epidemiology of familial hypercholesterolaemia: Community and clinical. Atherosclerosis. 2018;277. doi:10.1016/j.atherosclerosis.2018.06.855Link to article Austin MA, Hutter CM, Zimmern RL, Humpries SE. Familial hypercholesterolemia and coronary heart disease: A HuGE association review. Am J Epidemiol. 2004;160(5). doi:10.1093/aje/kwh237Link to article Watts GF, Lewis B, Sullivan DR. Familial hypercholesterolemia: A missed opportunity in preventive medicine. Nat Clin Pract Cardiovasc Med. 2007;4(8). doi:10.1038/ncpcardio0941Link to article Marks D, Thorogood M, Neil HAW, Humphries SE. A review on the diagnosis, natural history, and treatment of familial hypercholesterolaemia. Atherosclerosis. 2003;168(1). doi:10.1016/S0021-9150(02)00330-1Link to article Mszar R, Grandhi GR, Valero-Elizondo J, et al. Absence of Coronary Artery Calcification in Middle-Aged Familial Hypercholesterolemia Patients Without Atherosclerotic Cardiovascular Disease. JACC Cardiovasc Imaging. 2020;13(4). doi:10.1016/j.jcmg.2019.11.001Link to article Miname MH, Bittencourt MS, Moraes SR, et al. Coronary Artery Calcium and Cardiovascular Events in Patients With Familial Hypercholesterolemia Receiving Standard Lipid-Lowering Therapy. JACC Cardiovasc Imaging. 2019;12(9). doi:10.1016/j.jcmg.2018.09.019Link to article Sandesara PB, Mehta A, O’Neal WT, et al. Clinical significance of zero coronary artery calcium in individuals with LDL cholesterol ≥190 mg/dL: The Multi-Ethnic Study of Atherosclerosis. Atherosclerosis. Published online 2020. doi:10.1016/j.atherosclerosis.2019.09.014Link to article Lloyd-Jones DM, Morris PB, Ballantyne CM, et al. 2022 ACC Expert Consensus Decision Pathway on the Role of Nonstatin Therapies for LDL-Cholesterol Lowering in the Management of Atherosclerotic Cardiovascular Disease Risk: A Report of the American College of Cardiology Solution Set Oversight Committee. J Am Coll Cardiol. 2022;80(14):1366-1418. doi:10.1016/j.jacc.2022.07.006Link to article

Aug 20, 2024

CardioNerds Cofounder Dr. Amit Goyal, Chair of the CardioNerds Heart Failure Committee Dr. Jenna Skowronski, and Episode FIT Lead Dr. Shazli Khan discuss iron deficiency and its impact on heart failure with Dr. Robert Mentz, Chief of Heart Failure at Duke University and principal investigator of the HEART-FID trial. In this case-based discussion, they cover the diagnostic criteria of iron deficiency in heart failure, epidemiology, and strengths and limitations of different iron formulations. They also review clinical trials examining the impact of iron deficiency on quality of life, heart failure hospitalizations, and mortality. Importantly, they stress the relevance of iron metabolism in heart failure, irrespective of the presence of anemia. They also discuss the approach to addressing outpatient management of iron in heart failure and future directions of research needed in this domain. Notes were drafted by Dr. Shazli Khan, and Dr. Daniel Ambinder engineered episode audio. Click here for CME. This episode was created in collaboration with the Cardiometabolic Health Congress and is supported by an educational grant from American Regent. Please follow the link in the show notes for free CME. All CardioNerds education is planned, produced, and reviewed by CardioNerds. Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. CardioNerds Heart Success Series PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls - Iron Deficiency in Heart Failure Think about iron deficiency in ALL patients with heart failure and send appropriate diagnostic labs, even if there is no evidence of anemia! Iron deficiency in heart failure has a specific and distinguished definition, defined as a ferritin level of <100 ng/mL, or a ferritin level between 100-300 ng/mL with a transferrin saturation of <20%. Data thus far suggests that treatment of iron deficiency in heart failure results in improved quality of life, as well as a probable reduction in heart failure hospitalizations, and that administration of intravenous iron has a favorable safety profile. Not all formulations of iron are created equal – intravenous iron formulations have been shown to be effective in this population, but oral iron therapy has not. Management of iron deficiency in the outpatient setting is an evolving area of research, but patients should typically receive surveillance labs and additional treatment with IV iron if indicated. Show notes - Iron Deficiency in Heart Failure How is iron deficiency in heart failure defined, and how prevalent is iron deficiency in this patient population? Iron deficiency is common in patients with heart failure, with an estimated prevalence of 50-60%.Iron deficiency in heart failure is associated with worse outcomes, including increased hospitalization and mortality and poorer functional status and quality of life.Iron deficiency in heart failure is defined as a ferritin level of <100 ng/mL or a ferritin level of 100-300 ng/mL plus a transferrin saturation of <20%. There is an evolving school of thought that suggests transferrin saturation alone may be the best indicator of iron deficiency in heart failure, but more data are needed. Importantly, iron deficiency in heart failure can be seen in patients with both reduced and preserved ejection fraction. Which patients should be screened for iron deficiency? There is a class I indication to send iron studies in all patients with heart failure as a part of the initial diagnostic work-up for the underlying etiology of the cardiomyopathy, as well as to assess for the presence of iron deficiency.The presence of anemia is not required to check iron studies, as many patients with iron deficiency in heart failure may not have concomitant anemia. That is, all patients with heart failure should be evaluated for iron deficiency, irrespective of the presence of anemia. What are the hypothesized mechanisms of iron deficiency in heart failure, and how does iron deficiency impact patients with heart failure? Mechanisms causing iron deficiency in heart failure are multifactorial, including reduced oral intake, reduced gut absorption, reduced iron availability due to sequestration, and increased loss due to higher rates of bleeding.Nutritional variation is one proposed mechanism, as patients living with heart failure tend to take in less iron in their diet, and the iron consumed tends to be less easily absorbed.Due to chronic inflammation, there are increased levels of iron sequestration in cells in patients with heart failure, rendering the available iron stores unable to be used.Patients with chronic heart failure also tend to be on anti-platelet agents and/or anticoagulants (due to often-occurring comorbidities), which may potentially lead to bleeding complications, consequently causing iron deficiency. Iron deficiency has been associated with decreased exercise tolerance and functional status, worse quality of life, and increased risk of heart failure hospitalizations. What are the key takeaways of the clinical trials done in patients with heart failure and iron deficiency? The FAIR-HF trial published in 2009 demonstrated that treatment with IV ferrous carboxymaltose (FCM) in patients with heart failure led to improved symptoms and quality of life with an acceptable safety profile. These benefits were verified in a follow-up study known as CONFIRM-HF, demonstrating improvement in 6MWT and functional capacity.The AFFIRM-AHF trial investigated IV FCM in patients with iron deficiency and a left ventricular ejection fraction of <50%. It was a neutral trial with no significant improvement in their primary endpoint, a composite of hospitalization and death. The trial did demonstrate the safety of FCM and decreased hospitalizations. Of note, this trial was significantly impacted by the COVID pandemic, which may have affected the results. The IRONMAN trial was similar in design to AFFIRM-AHF but used a different iron formulation (iron derisomaltose) and had similar findings. The HEART-FID trial was a larger study including 3000 patients with HFrEF investigating treatment with IV ferric carboxymaltose every six months if the patients remained iron deficient. The primary endpoint was a hierarchical composite of death within 12 months after randomization, hospitalizations for heart failure within 12 months after randomization, or change from baseline to 6 months in the 6-minute walk distance. While it was considered a neutral trial with a p=0.019 with a prespecified significance level of 0.01, it demonstrated a trend to improved mortality and six-minute walk. Which patients should we treat with iron, and with what formulation? What do the guidelines recommend? Patients who have chronic heart failure on maximally tolerated guideline-directed medical therapy with iron deficiency are candidates for intravenous iron supplementation with the goal of improving quality of life and reducing heart failure hospitalizations.Intravenous iron has been shown to be effective, but oral iron therapy has shown no benefit in trials.Per the updated 2023 ESC guidelines, there is a class IA recommendation to provide intravenous iron supplementation in symptomatic patients with heart failure with reduced and mid-range ejection fraction with iron deficiency to both alleviate HF symptoms and improve quality of life.There is a class IIA recommendation to provide supplementation to reduce heart failure hospitalizations. Surveillance labs in the outpatient setting, combined with continued treatment for persistent iron deficiency, are likely beneficial in patients with heart failure. References - Iron Deficiency in Heart Failure Packer M, Anker SD, Butler J, et al. Identification of three mechanistic pathways for iron-deficient heart failure. Eur Heart J. 2024;45(26):2281-2293. doi:10.1093/eurheartj/ehae284. https://academic.oup.com/eurheartj/article/45/26/2281/7668668 Salah HM, Savarese G, Rosano GMC, et al. Intravenous iron infusion in patients with heart failure: a systematic review and study-level meta-analysis. ESC Heart Fail. 2023;10(2):1473-1480. doi:10.1002/ehf2.14310. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10053151/ Ponikowski P, Kirwan BA, Anker SD, et al. Ferric carboxymaltose for iron deficiency at discharge after acute heart failure: a multicentre, double-blind, randomised, controlled trial. Lancet. 2020;396(10266):1895-1904. doi:10.1016/S0140-6736(20)32339-4. https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(20)32339-4/abstract Kalra PR, Cleland JGF, Petrie MC, et al; IRONMAN Study Group. Intravenous ferric derisomaltose in patients with heart failure and iron deficiency in the UK (IRONMAN): an investigator-initiated, prospective, randomised, open-label, blinded-endpoint trial. Lancet. 2022;400(10369):2199-2209. doi:10.1016/S0140-6736(22)02083 https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(22)02083-9/fulltext Mentz RJ, Garg J, Rockhold FW, et al; HEART-FID Investigators. Ferric Carboxymaltose in Heart Failure with Iron Deficiency. N Engl J Med. 2023;389(11):975-986. doi:10.1056/NEJMoa2304968. https://www.nejm.org/doi/full/10.1056/NEJMoa2304968 McDonagh TA, Metra M, Adamo M, et al; ESC Scientific Document Group. 2023 Focused Update of the 2021 ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure. Eur Heart J. 2023;44(37):3627-3639. doi:10.1093/eurheartj/ehad195. Erratum in: Eur Heart J. 2024;45(1):53. doi:10.1093/eurheartj/ehad613. https://academic.oup.com/eurheartj/article/44/37/3627/7246292?login=false Anker SD, Comin Colet J, Filippatos G, et al.

Aug 18, 2024

CardioNerds Cardio-Rheumatology Series Co-Chairs Dr. Rick Ferraro, Dr. Gurleen Kaur, and Episode Lead Dr. Ronaldo Correa discuss “The Role of Inflammation in Cardiovascular Disease” with Dr. Antonio Abbate. Join the CardioNerds as they kick off the Cardio-Rheumatology series with Dr. Antonio Abbate. In this episode, Dr. Abbate, a leading expert in cardio-immunology, discusses the role of inflammation in cardiovascular disease. We explore the molecular mechanisms linking inflammation to atherosclerosis, the impact of chronic low-grade systemic inflammation on heart disease, and potential therapeutic targets. Dr. Abbate shares insights on how genes and lifestyle factors contribute to inflammation, the use of inflammatory markers in clinical practice, and emerging anti-inflammatory therapies in atherosclerotic cardiovascular disease. Tune in for an enlightening conversation on the intersection of inflammation and cardiovascular health. Dr. Ronaldo Correa drafted the notes. Episode audio was engineered by Dr. Amit Goyal. CardioNerds Prevention PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls - Cardio-Rheumatology: The Role of Inflammation in Cardiovascular Disease Inflammation is key in the pathogenesis and progression of atherosclerosis. Estimating systemic inflammation is part of a comprehensive preventive assessment (primary/secondary). Patients with autoimmune inflammatory diseases are at a higher risk for cardiovascular events. C-reactive protein (CRP) can estimate systemic inflammation and help assess residual inflammatory risk in patients with traditional intermediate/low cardiovascular disease, guiding management consideration with lipid-lowering therapy, aspirin, and colchicine. The pharmacological management of atherosclerosis is evolving beyond primarily lipid-lowering therapies to focus on targeting the underlying residual inflammatory process. Colchicine (inflammasome blocker as an anti-mitotic drug) is approved for use in chronic stable CVD in selected cases, and interleukin pathway blockers, especially IL-1 and IL-6, are under clinical trial investigation. First things first! Prioritize treating and optimizing traditional risk factors and comorbidities and emphasize lifestyle modifications to reduce cardiovascular disease (control diabetes and hypertension, reduce or cease smoking/alcohol, lose weight, and engage in regular physical activity). They all impact inflammation directly or indirectly Show notes - Cardio-Rheumatology: The Role of Inflammation in Cardiovascular Disease Notes: Notes drafted by Dr. Ronaldo Correa. What is the link between inflammation and cardiovascular atherosclerosis? Inflammation is involved both in the pathogenesis and progression of atherosclerosis.Histopathological coronary atherosclerosis studies have demonstrated the presence of inflammatory mediators as well as a central role of factors of innate immunity such as macrophages and T cells which can interact with vascular smooth muscle cells in the progression of atherosclerotic plaque.Patients with autoimmune inflammatory conditions have earlier and higher cardiovascular event rates (accelerated atherosclerosis due to residual inflammatory risk). Elevated inflammatory markers (for example, high CRP) predict cardiovascular events. How should inflammation be considered in the context of residual cardiovascular risk? Inflammation may be the inciting factor in atherosclerosis, or it may amplify the process driven primarily by other risk factors. Therefore, treating the comorbidities and traditional CVD contributors is key to reducing the vicious inflammatory cycle.Assessing residual risk using inflammatory markers can assist in management. C-reactive protein (CRP) can estimate systemic inflammation and help assess residual inflammatory risk in patients with traditional intermediate/low cardiovascular disease, guiding management consideration with lipid-targeting therapies, aspirin, and colchicine. Optimizing traditional risk factors, emphasizing appropriate treatment for hypertension, diabetes, dyslipidemia, weight loss, obstructive sleep apnea (OSA), depression, underlying inflammatory conditions, and lifestyle modifications such as consuming a Mediterranean diet, alcohol/smoking reduction/cessation, and getting regular physical activity can help directly and indirectly reduce inflammatory contributors. How does inflammation contribute to thrombosis, and what are the implications for cardiovascular disease? Inflammation increases the expression of procoagulant factors through the inflammasome pathway, including mediators like IL-6.Proinflammatory changes in endothelial cells, leukocytes, and platelets promote thrombosis.The concept of immunothrombosis has emerged, especially highlighted by conditions like COVID-19. Inflammation-induced thrombosis has significant implications for cardiovascular disease. What are the key inflammatory pathways involved in atherosclerosis, and what therapeutic targets have emerged? The inflammatory process is complex, and we still have much to learn about it. Three inflammatory therapeutic targets are highlighted: NLRP3 inflammasome, IL-1, and IL-6.Colchicine is an NLRP3 inflammasome blocker that is FDA-approved as an add-on medication for secondary ischemic prevention in patients with stable CAD who remain at higher risk despite optimal medical therapy with aspirin and statin.The CANTOS trial showed a significant reduction in MACE and hsCRP in post-MI patients who received canakinumab (IL-1 inhibitor) as an add-on therapy. The ZEUS trial is investigating Ziltivekimab (an IL-6 inhibitor) for secondary ASCVD prevention. Rilonacept (an IL-1 inhibitor) is FDA-approved for recurrent pericarditis based on the RHAPSODY trial. Ongoing trials are further exploring inflammation-targeting therapies for the treatment of cardiovascular disease. References - Cardio-Rheumatology: The Role of Inflammation in Cardiovascular Disease Engelen SE, Robinson AJB, Zurke YX, Monaco C. Therapeutic strategies targeting inflammation and immunity in atherosclerosis: how to proceed?. Nat Rev Cardiol. 2022;19(8):522-542. doi:10.1038/s41569-021-00668-4 Kong P, Cui ZY, Huang XF, Zhang DD, Guo RJ, Han M. Inflammation and atherosclerosis: signaling pathways and therapeutic intervention. Signal Transduct Target Ther. 2022;7(1):131. Published 2022 Apr 22. doi:10.1038/s41392-022-00955-7 Saigusa R, Winkels H, Ley K. T cell subsets and functions in atherosclerosis. Nat Rev Cardiol. 2020;17(7):387-401. doi:10.1038/s41569-020-0352-5 Sage AP, Tsiantoulas D, Binder CJ, Mallat Z. The role of B cells in atherosclerosis. Nat Rev Cardiol. 2019;16(3):180-196. doi:10.1038/s41569-018-0106-9 Suero-Abreu GA, Zanni MV, Neilan TG. Atherosclerosis With Immune Checkpoint Inhibitor Therapy: Evidence, Diagnosis, and Management: JACC: CardioOncology State-of-the-Art Review. JACC CardioOncol. 2022;4(5):598-615. Published 2022 Dec 20. doi:10.1016/j.jaccao.2022.11.011 Zhao TX, Mallat Z. Targeting the Immune System in Atherosclerosis: JACC State-of-the-Art Review. J Am Coll Cardiol. 2019;73(13):1691-1706. doi:10.1016/j.jacc.2018.12.083 Geovanini GR, Libby P. Atherosclerosis and inflammation: overview and updates. Clin Sci (Lond). 2018;132(12):1243-1252. Published 2018 Jun 21. doi:10.1042/CS20180306 Fragoulis GE, Soulaidopoulos S, Sfikakis PP, Dimitroulas T, D Kitas G. Effect of Biologics on Cardiovascular Inflammation: Mechanistic Insights and Risk Reduction. J Inflamm Res. 2021;14:1915-1931. Published 2021 May 14. doi:10.2147/JIR.S282691 Giles JT, Sattar N, Gabriel S, et al. Cardiovascular Safety of Tocilizumab Versus Etanercept in Rheumatoid Arthritis: A Randomized Controlled Trial. Arthritis Rheumatol. 2020;72(1):31-40. doi:10.1002/art.41095 Del Buono MG, Bonaventura A, Vecchié A, et al. Pathogenic pathways and therapeutic targets of inflammation in heart diseases: A focus on Interleukin-1. Eur J Clin Invest. 2024;54(2):e14110. doi:10.1111/eci.14110 Abbate A, Toldo S, Marchetti C, Kron J, Van Tassell BW, Dinarello CA. Interleukin-1 and the Inflammasome as Therapeutic Targets in Cardiovascular Disease. Circ Res. 2020;126(9):1260-1280. doi:10.1161/CIRCRESAHA.120.315937 Toldo S, Abbate A. The role of the NLRP3 inflammasome and pyroptosis in cardiovascular diseases. Nat Rev Cardiol. 2024;21(4):219-237. doi:10.1038/s41569-023-00946-3

Aug 16, 2024

CardioNerds (Drs. Teodora Donisan, Jenna Skowronski, and Johnny Hourmozdi) discuss Cardiomyopathies with Dr. Steve Ommen. Through a case-based discussion, we review the diagnostic evaluation of suspected restrictive cardiomyopathy, and Dr. Ommen shares his expertise in the nuances of caring for patients with hypertrophic cardiomyopathy, from counseling to pharmacologic, device, and septal reduction therapies. We cover the foundations of diagnosis and management that will be helpful to CardioNerds preparing to encounter hypertrophic cardiomyopathy on the boards or on the wards. Dr. Johnny Hourmozdi drafted notes. The audio was engineered by Dr. Atefeh Ghorbanzadeh. The CardioNerds Beyond the Boards Series was inspired by the Mayo Clinic Cardiovascular Board Review Course and designed in collaboration with the course directors Dr. Amy Pollak, Dr. Jeffrey Geske, and Dr. Michael Cullen. CardioNerds Beyond the Boards SeriesCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls and Quotes - Cardiomyopathies The presence of an S4 and a rapid y-descent in the jugular venous pulsation on exam should clue you to the presence of a restrictive filling pattern. Restrictive filling doesn’t necessarily mean restrictive cardiomyopathy and is more commonly due to dilated or ischemic cardiomyopathy. The five main topics of counseling that every hypertrophic cardiomyopathy (HCM) patient should understand: (1) Prognosis, (2) Family Screening, (3) Risk of Sudden Death, (4) Treatments, and (5) Physical Activity. Remember 1/3: In clinical trials of cardiac myosin inhibitors for HCM (mavacamten), about a third of patients had a tremendous improvement in symptoms, another third had some improvement, and the final third had no improvement or had to discontinue the drug due to negative inotropy. When counseling patients about septal reduction therapy, consider the patient’s age. For younger patients, surgical myectomy at an experienced center offers a higher success rate and greater durability with lower rates of pacemaker placement when compared to alcohol septal ablation. Historically, the conclusion that it was higher risk to be an athlete with HCM was unfortunately generalized to mean that it was high risk to exercise for patients with HCM. “And we turned a generation of HCM patients into HCM cardiometabolic syndrome patients, which is actually a worse combination.” Notes - Cardiomyopathies What is the initial approach to evaluating a patient with new or suspected cardiomyopathy, including hypertrophic cardiomyopathy (HCM)? A history and physical exam, including a thorough past medical and family history, is always the first step and helps determine the patient’s risk for potential underlying etiologies, including genetic cardiomyopathies, hypertrophic cardiomyopathy, or those related to treatments of previous cancer. In terms of ECG findings, pay attention to QRS voltage (high or low) and the presence of any arrhythmias. TTE should be obtained in all patients and is often sufficient to diagnose many underlying cardiomyopathies, including HCM. Cardiac MRI (CMR) is helpful as an adjunct when TTE alone is inconclusive or imaging quality is poor. CMR can help provide a better idea of chamber sizes and wall thickness, and late gadolinium contrast enhancement (LGE) can also be helpful if present in a specific pattern, though often HCM patients may have non-specific patterns of LGE. Invasive hemodynamics assessment is reserved for patients with discordance between non-invasive testing and the clinical impression. It can also be useful to guide the management of heart failure, especially in advanced disease. How do you treat patients with hypertrophic obstructive cardiomyopathy (HOCM)? In patients with HCM and LVOT obstruction (defined as a resting peak LVOT gradient >30 mmHg), we want to avoid medications that increase inotropy, reduce preload (diuretics), or reduce afterload (pure vasodilators). First-line medical therapies for symptomatic HOCM include non-vasodilating beta-blockers (e.g., metoprolol) and/or non-dihydropyridine calcium channel blockers (e.g., diltiazem, verapamil). For those with symptoms despite the above first-line medications, second-line therapies include the addition of disopyramide or the newer myosin inhibitors (e.g., mavacamten). In patients who don’t respond to medical therapies, a referral should be made for septal reduction therapy at an experienced center. Surgical myectomy involves open heart surgery and has a success rate of 90-95% with a durable result. Alcohol septal ablation can be done percutaneously and offers a shorter recovery time, but it has a lower success rate of 75-85%. Septal ablation comes with a similar risk of stroke and mortality compared to surgery (<0.5%) and with a higher rate of pacemaker implantation (5-10% vs 3%). How should patients with HCM be counseled with regard to physical activity and exercise? Observational studies suggest an increased risk of sudden cardiac death among athletes with HCM as compared to those without HCM. Among patients with HCM, it is less clear whether there is an association between gradations of physical activity and risk for SCD. For patients with HCM, the safety and benefits of low to moderate-intensity exercise for cardiovascular health and fitness are established. The 2024 HCM guidelines recommend counseling patients to engage in 150-300 minutes of low-moderate intensity exercise per week in keeping with physical activity guidelines for the general population (Class 1, LOE B-R). For athletes looking to engage in vigorous exercise or competitive sport, shared decision-making with an expert in HCM is recommended. For most patients, universal restriction from this level of exercise is not indicated. What is the approach to genetic testing and family screening for HCM? All patients with a clinical diagnosis of HCM should be offered genetic testing with a gene panel test. Genetic testing results can help with family screening and may inform prognosis but do not currently impact therapy decisions for the patient. In those where a pathogenic or likely pathogenic variant is identified, cascade testing for this variant should be offered to first-degree relatives. If no variant or a variant of unknown significance (VUS) is identified, then periodic echocardiographic screening should be performed instead in all first-degree relatives. For adults, screening ECG and TTE in first-degree relatives should begin when a family member has been diagnosed with HCM and be repeated every 3-5 years. For children and adolescents, initiation of screening should be no later than the onset of puberty and be repeated every 1-2 years. Who should be offered an implantable cardiac defibrillator (ICD) for prevention of sudden cardiac death? There are “three layers of eligibility” for an ICD among patients with HCM, corresponding with the strength of the guideline recommendation based on indication (Class 1, 2a, and 2b, respectively). The “top layer” or Class 1 indication where there is broad agreement that every patient should get an ICD is when a patient has had a documented cardiac arrest or sustained ventricular tachycardia. The “second layer” or Class 2a indication are patients with one or more major risk factors for SCD, in whom it is reasonable to pursue an ICD:Massive hypertrophy (LVH of 30 mm or greater in any segment)A history of “scary” syncope that is suspected to be due to arrhythmiaA family history of sudden cardiac deathLV apical aneurysm with transmural scar LV systolic dysfunction (EF <50%) The last layer or Class 2b indication where it is of uncertain benefit but may be offered in shared decision-making is when there is extensive LGE present on CMR or frequent nonsustained VT on ambulatory monitoring in the absence of any major clinical risk factor. Using an HCM risk calculator can be helpful for estimating individual patient risk for SCD by incorporating all of the above risk factors and can help to frame a shared decision-making discussion around ICD placement. References - Cardiomyopathies 1. Ommen SR, Ho CY, et al. 2024 AHA/ACC/AMSSM/HRS/PACES/SCMR Guideline for the Management of Hypertrophic Cardiomyopathy. Journal of the American College of Cardiology. 2024;83(23):2324-2405. doi:10.1016/j.jacc.2024.02.014 2. Saberi S, Wheeler M, Bragg-Gresham J, et al. Effect of Moderate-Intensity Exercise Training on Peak Oxygen Consumption in Patients With Hypertrophic Cardiomyopathy: A Randomized Clinical Trial. JAMA. 2017;317(13):1349-1357. doi:10.1001/jama.2017.2503 3. Desai MY, Owens A, Wolski K, et al. Mavacamten in Patients With Hypertrophic Cardiomyopathy Referred for Septal Reduction: Week 56 Results From the VALOR-HCM Randomized Clinical Trial. JAMA Cardiology. 2023;8(10):968-977. doi:10.1001/jamacardio.2023.3342 4. Maron BJ, Doerer JJ, Haas TS, Tierney DM, Mueller FO. Sudden Deaths in Young Competitive Athletes. Circulation. 2009;119(8):1085-1092. doi:10.1161/CIRCULATIONAHA.108.804617

Aug 9, 2024

The following question refers to Sections 6.1 and 7.4 of the 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure. The question is asked by University of Colorado internal medicine resident Dr. Hirsh Elhence, answered first by University of Chicago advanced heart failure cardiologist and Co-Chair for the CardioNerds Critical Care Cardiology Series Dr. Mark Belkin, and then by expert faculty Dr. Mark Drazner. Dr. Drazner is an advanced heart failure and transplant cardiologist, Professor of Medicine, and Clinical Chief of Cardiology at UT Southwestern. He is the President of the Heart Failure Society of America. The Decipher the Guidelines: 2022 AHA / ACC / HFSA Guideline for The Management of Heart Failure series was developed by the CardioNerds and created in collaboration with the American Heart Association and the Heart Failure Society of America. It was created by 30 trainees spanning college through advanced fellowship under the leadership of CardioNerds Cofounders Dr. Amit Goyal and Dr. Dan Ambinder, with mentorship from Dr. Anu Lala, Dr. Robert Mentz, and Dr. Nancy Sweitzer. We thank Dr. Judy Bezanson and Dr. Elliott Antman for tremendous guidance. Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. Question #34 Question StemA 72-year-old woman with a history of hypertension, type 2 diabetes mellitus, and a recent myocardial infarction is seen in your clinic. Two months previously, she was hospitalized with a myocardial infarction and underwent successful revascularization of the left anterior descending artery with a drug-eluting stent. Following her myocardial infarction, an echocardiogram revealed an ejection fraction of 17%, and she was discharged on metoprolol succinate, lisinopril, spironolactone, and dapagliflozin with escalation to maximal tolerated doses over subsequent visits. A repeat echocardiogram performed today in your clinic reveals an ejection fraction of 26%. An electrocardiogram reveals normal sinus rhythm with a narrow QRS at a heart rate of 65 beats per minute. She is grateful for her cardiac rehabilitation program and reports no ongoing symptoms. Which of the following devices is indicated for placement at this time?Answer choicesAImplantable loop recorderBICDCCRT-DDCRT-P Answer #34 Explanation The correct answer is B.This patient suffered a myocardial infarction more than 40 days ago and has been on appropriate guideline-directed medical therapy since that time. Her left ventricular ejection fraction has improved but remains under 30%. For patients who have suffered a myocardial infarction over 40 days prior with LVEF ≤ 30% and NYHA Class I symptoms while receiving GDMT and have a reasonable expectation of meaningful survival for >1 year, an ICD is recommended for primary prevention of sudden cardiac death to reduce total mortality (Class I, LOE B-R).The MADIT-II trial enrolled 1,232 patients with a prior myocardial infarction and LVEF ≤ 30% to prophylactic ICD or medical therapy. At a median follow-up of 20 months, the trial was terminated early for reduced all-cause mortality with prophylactic ICD. The DINAMIT trial later investigated the implantation of ICD in patients with MI and an LVEF of ≤ 35% at 6 to 40 days after the initial myocardial infarction. This trial found no differences in all-cause mortality between the two groups. Therefore, the current recommendation is to wait at least 40 days with GDMT prior to re-evaluation of left ventricular ejection fraction before proceeding with ICD implantation.Cardiac resynchronization therapy entails implanted pacemakers to simultaneously pace both the RV and LV in order to improve electrical synchrony and generally provides benefit in those with systolic dysfunction and a wide left bundle branch block. Specifically, for patients who have LVEF ≤35%, sinus rhythm, left bundle branch block (LBBB) with a QRS duration ≥150 ms, and NYHA class II, III, or ambulatory IV symptoms on GDMT, CRT is indicated to reduce total mortality, reduce hospitalizations, and improve symptoms and QOL (Class I, LOE B-R). CRT implantation provides high economic value in this setting. CRT implantation carries a Class 2a recommendation for those with reduced LVEF (≤35%) and either a non-LBBB pattern with a QRS ≥150 ms or a LBBB with QRS duration 120-149ms. This patient with a narrow QRS does not have indications for CRT placement at this time.Main TakeawayICD implantation is recommended as primary prophylaxis against ventricular arrhythmias for patients with LVEF ≤30% after 40 days following myocardial infarction despite use of GDMT.Guideline Loc.Section 6.1 and 7.4 Decipher the Guidelines: 2022 Heart Failure Guidelines PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron!

Aug 7, 2024

CardioNerds Dan Ambinder and Dr. Devesh Rai join cardiology fellows and National Lipid Association lipid scholars Dr. Oby Ibe from Temple University and Dr. Elizabeth Epstein from Scripps Clinic. They discuss a case involving a patient with elevated Lp(a). Dr. Jessica Pena provides expert commentary. Drs. Oby Ibe and Elizabeth Epstein drafted notes. CardioNerds Intern Christiana Dangas engineered episode audio. This episode is part of a case reports series developed in collaboration with the National Lipid Association and their Lipid Scholarship Program, with mentorship from Dr. Daniel Soffer and Dr. Eugenia Gianos. An asymptomatic 34-year-old female presented to the cardiology clinic for cardiovascular risk assessment. Her past medical history included polycystic ovarian syndrome (PCOS) and depression. Her labs were notable for total cholesterol 189 mg/dL, LDL of 131 mg/dL, HDL 34 mg/dL, triglycerides 134 mg/dL, and Lp(a) 217 nmol/L. Her 10-year ASCVD risk by the PREVENT calculator was 0.5%, and her 30-year risk was 3.5%. She had no carotid plaque. Because her 30-year risk was significantly increased by her elevated Lp(a), intensive risk factor management was emphasized, and she was started on a low-dose statin with a plan to follow the patient to reassess the need for intensification of lipid-lowering and/or initiation of novel Lp(a)-lowering therapies over time. US Cardiology Review is now the official journal of CardioNerds! Submit your manuscript here. CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls - Little (a), Big Deal – National Lipid Association You are never too young to see a preventive cardiologist! The field of preventive cardiology is shifting focus towards the identification of early upstream risk and intervention before the development of clinical ASCVD (1,5). Patients who have a strong family history of cardiovascular disease, a personal history of CVD at an early age, multiple risk factors, or genetic disorders such as familial hypercholesterolemia especially benefit from early cardiovascular risk assessment and reduction. Female-specific risk factors to incorporate into a young woman’s cardiovascular risk assessment include polycystic ovarian syndrome, hormone contraceptive use, early menarche (age 5 pregnancies), early menopause (age <45 years old), & post-menopausal hormone therapy. Lp(a) testing for all! The most recent NLA scientific statement on the use of Lp(a) in clinical practice recommends measuring Lp(a) at least once in every adult for risk stratification. While Lp(a) has not yet been incorporated into our risk calculators, we do know that elevated Lp(a) increases 10-year risk. The European Atherosclerosis Society published a consensus statement on Lp(a), which includes a handy table to quantify the degree to which a patient’s 10-year risk increases as Lp(a) increases. Lifestyle changes are the first line and can reduce the risk of high Lp(a) by 66%. Next, we can consider the risks and benefits of LDL-lowering in a young patient and monitor closely for the development of plaque over time. Lp(a) lowering drugs such as olpasiran are on the horizon, and we can keep this patient in mind as a potential candidate for therapy in the future. Notes - Little (a), Big Deal – National Lipid Association When should patients see a preventive cardiologist? Strong family history of cardiovascular disease – A positive family history of CVD was defined as a self‐reported diagnosis of CVD in parents, siblings, or children that occurred at 60 years or younger. A positive family history of CVD is an independent predictor of both myocardial infarction and stroke. Among individuals with hypertension, family history of CVD has been shown to be independently associated with mortality by ischemic heart disease and family history of CVD mortality with incidence of overall CVD. Family history of CVD modifies future CVD risk depending on the number and age of affected first-degree relatives. Siblings of patients with CVD have about a 40% risk increase, while offspring of parents with premature CVD have a 60% to 75% risk increase. Personal history of early CVD – A personal history of cardiovascular disease at an age younger than 60 years. For young and middle-aged adults, increases in heart disease between 2020 and 2021 explain more than 4% of the most recent shortening in life expectancy. In particular, hypertensive heart disease, heart failure, and endocarditis have increased in young adults, particularly among Black individuals, through 2018. Consequently, young adults make up a growing proportion of cardiovascular disease events, with the proportion of premature myocardial infarction among adults younger than 40 years increasing by 2% every year. The increasing event rates observed among younger adults can be attributed to the increasing prevalence and onset of risk factors such as obesity and hypertension at younger ages, which exacerbate cumulative exposure and cardiovascular disease risk over near- and long-term time horizons. Multiple cardiovascular risk factors – Risk factors include hyperlipidemia, high triglycerides, elevated lp(a), diabetes mellitus, obesity, tobacco use, unhealthy diet, and lack of physical activity. Unadjusted event rates were 8-fold to 30-fold higher in persons with adverse levels of risk factor exposure during young adulthood (age 20–39 years) compared with persons with optimal levels of exposure. Familial hypercholesterolemia – In primary prevention, patients with FH had incidences of ASCVD and coronary heart disease (CHD) of 14.9/1000 and 5.8/1000 person-years, respectively, compared to 7.1/1000 and 2.1/1000 person-years in the normolipidemic group. FH conferred a hazard ratio (HR) of 7.1 and 16.7 for ASCVD and CHD, respectively, in patients younger than 35 years. In secondary prevention, patients with FH had incidences of ASCVD and CHD of 89.7/1000 and 34.5/1000 person-years, respectively, compared to 90.9/1000 and 28.2/1000 person-years in the normolipidemic group What are some female-specific risk factors for cardiovascular disease? (7) PCOS – Polycystic ovarian syndrome (PCOS) is a disorder characterized by hyperandrogenism and menstrual irregularities. Women affected by PCOS have a heightened risk of developing diabetes due to associated insulin resistance, central obesity, and hypertension. This adverse cardiovascular risk profile in women with PCOS may lead to premature atherosclerosis (8,20). Women with PCOS have been shown to have an increased risk for CVD events (21). Depression — Among 593,616 young adults (aged 18–49 years) from 2017 to 2020, depression was independently associated with CHD and suboptimal cardiovascular health (CVH), with a dose‐response relationship (CVH was determined using 7 cardiovascular risk factors: hypertension, hypercholesterolemia, overweight/obesity, current smoking, diabetes, physical inactivity, and inadequate fruit and vegetable intake) (13). Suboptimal CVH was defined as the presence of ≥2 of these 7 cardiovascular risk factors, whereas optimal CVH was 0 or 1 cardiovascular risk factor. Early menarche – Results from the Women’s Ischemia Syndrome Evaluation (WISE) study demonstrated that in comparison to women with menarche at age 12 years, there was an approximately 4-fold adjusted increased risk for major adverse cardiac events for menarche ≤ 10 years (15). African descent – Safford et al. found that among those at the highest CHD risk, Black women’s hyperlipidemia was the least likely to be treated or controlled. Lp(a) is significantly higher among Blacks versus Whites, and in both, increased Lp(a) correlates positively with LDL-C and negatively with triglycerides. Another study based on the MESA population demonstrated that Black participants showed a significant risk of CHD in those with Lp(a) levels ≥ 75 nmol/L as opposed to White and Hispanic participants who had a greater risk with Lp(a) levels ≥125 nmol/L. Elevated BMI – Obesity and higher measures of central adiposity are associated with significantly higher rates of CAD, CVD mortality, sudden cardiac death, heart failure, and arrhythmias (23). High BMI accounted for 4.0 million deaths in 2015, more than two-thirds of which were caused by cardiovascular disease. Marked increases in obesity prevalence among adolescents over the past 35 years ultimately contribute to CVD risk into young adulthood. Who should be getting an Lp(a) measured? Per the most NLA-focused update to the 2019 scientific statement on the use of Lp(a) in clinical practice, we now have sufficient evidence to support measuring Lp(a) at least once in all adults for risk stratification. What risk calculators would apply to a young adult? The American Heart Association recently released the PREVENT calculator (c-statistic 0.72) for 10- and 30-year risk estimation of total CVD (composite of atherosclerotic CVD and heart failure) in primary prevention patients (10). This improves upon the prior pooled cohort equation because it is based on newer data from a larger, more diverse sample (6,612,004 US adults 30 to 79 years of age) than the existing tool. The calculator also takes into account other health conditions, such as cardiovascular-kidney-metabolic risk factors, adjusts for competing risk of non-CVD death, and incorporates an indicator of social determinants of health. Race was not included because it is a social construct, not a biological risk factor, and could, therefore, create bias.

Jul 30, 2024

The following question refers to Section 5.1 of the 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure.The question is asked by University of Colorado internal medicine resident Dr. Hirsh Elhence, answered first by advanced heart failure faculty at the University of Chicago and Co-Chair for the CardioNerds Critical Care Cardiology Series Dr. Mark Belkin, and then by expert faculty Dr. Biykem Bozkurt.Dr. Bozkurt is the Mary and Gordon Cain Chair, Professor of Medicine, Director of the Winters Center for Heart Failure Research, and an advanced heart failure and transplant cardiologist at Baylor College of Medicine in Houston, TX. She is former President of HFSA, former senior associate editor for Circulation, and current Editor-In-Chief of JACC Heart Failure. Dr. Bozkurt was the Vice Chair of the writing committee for the 2022 Heart Failure Guidelines.The Decipher the Guidelines: 2022 AHA / ACC / HFSA Guideline for The Management of Heart Failure series was developed by the CardioNerds and created in collaboration with the American Heart Association and the Heart Failure Society of America. It was created by 30 trainees spanning college through advanced fellowship under the leadership of CardioNerds Cofounders Dr. Amit Goyal and Dr. Dan Ambinder, with mentorship from Dr. Anu Lala, Dr. Robert Mentz, and Dr. Nancy Sweitzer. We thank Dr. Judy Bezanson and Dr. Elliott Antman for tremendous guidance.Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. /*! elementor - v3.23.0 - 25-07-2024 */ .elementor-toggle{text-align:start}.elementor-toggle .elementor-tab-title{font-weight:700;line-height:1;margin:0;padding:15px;border-bottom:1px solid #d5d8dc;cursor:pointer;outline:none}.elementor-toggle .elementor-tab-title .elementor-toggle-icon{display:inline-block;width:1em}.elementor-toggle .elementor-tab-title .elementor-toggle-icon svg{margin-inline-start:-5px;width:1em;height:1em}.elementor-toggle .elementor-tab-title .elementor-toggle-icon.elementor-toggle-icon-right{float:right;text-align:right}.elementor-toggle .elementor-tab-title .elementor-toggle-icon.elementor-toggle-icon-left{float:left;text-align:left}.elementor-toggle .elementor-tab-title .elementor-toggle-icon .elementor-toggle-icon-closed{display:block}.elementor-toggle .elementor-tab-title .elementor-toggle-icon .elementor-toggle-icon-opened{display:none}.elementor-toggle .elementor-tab-title.elementor-active{border-bottom:none}.elementor-toggle .elementor-tab-title.elementor-active .elementor-toggle-icon-closed{display:none}.elementor-toggle .elementor-tab-title.elementor-active .elementor-toggle-icon-opened{display:block}.elementor-toggle .elementor-tab-content{padding:15px;border-bottom:1px solid #d5d8dc;display:none}@media (max-width:767px){.elementor-toggle .elementor-tab-title{padding:12px}.elementor-toggle .elementor-tab-content{padding:12px 10px}}.e-con-inner>.elementor-widget-toggle,.e-con>.elementor-widget-toggle{width:var(--container-widget-width);--flex-grow:var(--container-widget-flex-grow)} Question #33 A 63-year-old man with a past medical history of hypertension and type 2 diabetes mellitus presents for routine follow-up. He reports feeling in general good health and enjoys 2-mile walks daily. A review of systems is negative for any symptoms. Which of the following laboratory studies may be beneficial for screening?ANT-proBNPBCK-MBCTroponinDC-reactive proteinENone of the above Answer #33 ExplanationThe correct answer is A – NT-proBNP.This patient is at risk for HF (Stage A) given the presence of risk factors (hypertension and type 2 diabetes mellitus) but the absence of signs or symptoms of heart failure.Patients at risk for HF screened with BNP or NT-proBNP followed by collaborative care, diagnostic evaluation, and treatment in those with elevated levels can reduce combined rates of LV systolic dysfunction, diastolic dysfunction, and HF.The STOP-HF (St Vincent’s Screening to Prevent Heart Failure) study was a large single-center trial of patients at risk of HF that showed BNP-based screening reduced the composite endpoint of incident asymptomatic LV dysfunction with or without newly diagnosed HF.Therefore, for patients at risk of developing HF, natriuretic peptide biomarker-based screening followed by team-based care, including a cardiovascular specialist optimizing GDMT, can be useful toprevent the development of LV dysfunction (systolic or diastolic) or new-onset HF (Class 2a, LOE B-R).There is no indication for measuring troponin, CK-MB, or CRP at this time.Main TakeawayIn patients at risk for HF, screening for pre-HF using natriuretic peptide testing followed by team-based care may be helpful for preventing disease progression. Guideline Loc.Section 5.1 Decipher the Guidelines: 2022 Heart Failure Guidelines PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron!

Jul 28, 2024

CardioNerds Dr. Rick Ferraro, Dr. Gurleen Kaur, and Dr. Maryam Barkhordarian discuss the evidence and data supporting SGLT inhibition for cardiovascular and kidney health outcomes with expert faculty Dr. Muthu Vaduganathan. They discuss the role of SGLT inhibitors in different populations, including those with diabetes mellitus, heart failure, CKD, and myocardial infarction. Show notes and audio editing by CardioNerds Academy Fellow Dr. Maryam Barkhordarian. This episode was produced in collaboration with the American Society of Preventive Cardiology (ASPC) with independent medical education grant support from Lexicon Pharmaceuticals. CardioNerds Prevention PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls - The Data Supporting SGLT Inhibition with Dr. Muthiah Vaduganathan The benefit of SGLT inhibition extends beyond diabetes, and improves cardiovascular and kidney health outcomes independent of diabetes in appropriate patient populations. SGLT inhibition decreases cardiovascular mortality and heart failure hospitalization independent of left ventricular ejection fraction. SGLT inhibitors reduce clinically relevant events such as dialysis and transplantation in CKD patients irrespective of etiology and are now a cornerstone for the prevention of CKD progression. The introduction of polypills in heart failure can simplify GDMT implementation. Show notes - The Data Supporting SGLT Inhibition with Dr. Muthiah Vaduganathan How did SGLT inhibitors transition from “diabetes medication” to guideline-directed cardiovascular medicine? Most therapies in cardiology were developed for a particular purpose and ended up being indicated for a vastly different reason. The SGLT-2 inhibitors are no different. Cardiovascular safety concerns about diabetes medications led to a mandate to conduct cardiovascular outcomes trials for all novel diabetes medications. This federal requirement shed light on the cardiovascular benefits of SGLT inhibitors in patients with diabetes. These initial trials showed that not only are these medications safe but also, surprisingly, proved their role in preventing heart failure and delaying progression of chronic kidney disease. What are the mechanisms of action of SGLT-2 and SGLT-1/2 inhibitors? The central mechanism(s) of how these medications confer health outcomes benefits patients is/are not well understood. The main organ involved in the action of SGLT-2 inhibitors is the kidney at the level of the proximal tubule, impacting the cardiovascular system by handling salt and water and improving kidney efficiency. Conversely, SGLT-1/2 inhibitors also act at the level of the gut, the predominant location of the SGLT-1 cotransporter. Their effects on the cardiovascular system are secondary, given there is no SGLT-1 or -2 cotransporters in the myocardium. These secondary effects can be impacted through blood pressure reduction, volume regulation, improved glycemic control, etc. to overall improve cardiovascular status. Whatever the underlying mechanisms, the empirical data for their use is strong and growing. What is the role of SGLT inhibitors in preventing CKD progression? RAAS inhibitors (ACE inhibitors and ARBs) have been the cornerstone of CKD management for the past two to three decades. SGLT inhibitors have been the first add-on to this background therapy. Four trials, DAPA-CKD, EMPA-CKD, CREDENCE, and the SCORED, investigated the effects of SGLT-2 and SGLT-1/2 inhibitors in patients with CKD with or without diabetes. The outcomes of these trials include modifying the course of CKD and reducing events such as dialysis initiation and transplantation. These effects were regardless of participants’ diabetic status, CKD etiology, or individual patient profile. The addition of SGLT-2 inhibitors to ACEI or ARB can be considered as GDMT of CKD. What is the role of SGLT-2 inhibitors in combination with other medications as polypill? Polypills have been beneficial in many areas such as cardiometabolic medicine, hypertension, and diabetes mellitus. In addition, a multi-drug regimen is strongly recommended in heart failure with reduced ejection fraction. Developing polypills in HFrEF has been challenging because adjacent compounds are not available in the armamentarium of sponsored pharmaceutical companies. Investigations of various polypills are underway for the management of heart failure. References - The Data Supporting SGLT Inhibition with Dr. Muthiah Vaduganathan Heerspink HJL, Stefánsson BV, Correa-Rotter R, et al. Dapagliflozin in Patients with Chronic Kidney Disease. N Engl J Med. 2020;383(15):1436-1446. doi:10.1056/NEJMoa2024816 The EMPA-KIDNEY Collaborative Group, Herrington WG, Staplin N, et al. Empagliflozin in Patients with Chronic Kidney Disease. N Engl J Med. 2023;388(2):117-127. doi:10.1056/NEJMoa2204233 Perkovic V, Jardine MJ, Neal B, et al. Canagliflozin and Renal Outcomes in Type 2 Diabetes and Nephropathy. N Engl J Med. 2019;380(24):2295-2306. doi:10.1056/NEJMoa1811744 Bhatt DL, Szarek M, Pitt B, et al. Sotagliflozin in Patients with Diabetes and Chronic Kidney Disease. N Engl J Med. 2021;384(2):129-139. doi:10.1056/NEJMoa2030186

Jul 19, 2024

In this episode, Dr. Gurleen Kaur (Cardiology FIT at Brigham and Women’s Hospital and APD of the CardioNerds Academy) and Dr. Chelsea Amo-Tweneboah (Medicine Resident at Stonybrook and CardioNerds Academy Intern) discuss with Dr. Heval Kelli (Cardiologist at Northside Hospital Cardiovascular Institute) about his personal and professional journey in Cardiology. They discuss Dr. Kelli’s lifelong advocacy for serving those in need including refugee and immigrant communities, his character in the documentary Refuge, and fostering inclusivity within Cardiology. Audio editing and show notes were drafted by Dr. Chelsea Amo-Tweneboah. The PA-ACC & CardioNerds Narratives in Cardiology is a multimedia educational series jointly developed by the Pennsylvania Chapter ACC, the ACC Fellows in Training Section, and the CardioNerds Platform with the goal to promote diversity, equity, and inclusion in cardiology. In this series, we host inspiring faculty and fellows from various ACC chapters to discuss their areas of expertise and their individual narratives. Join us for these captivating conversations as we celebrate our differences and share our joy for practicing cardiovascular medicine. We thank our project mentors Dr. Katie Berlacher and Dr. Nosheen Reza. The PA-ACC & CardioNerds Narratives in Cardiology PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Video version - Advocacy for Refugee Health and Empowering First-Generation Cardiologists https://youtu.be/hP8bLt9q2sY Quoatables - Advocacy for Refugee Health and Empowering First-Generation Cardiologists “I have always believed that if someone opened the door for you, you have to hold the door for the next generation. Because if you just walk through the door and close it, you just close the door for many people behind you.” “Instead of making luck a matter of luck, just make an opportunity for everyone else.” “Hate makes us realize that no matter how privileged you are, you are not protected.” “It is very hard to hate something you know.” “Compassion starts with the neighbor next to you, and then you go out to the world and show it.” “Your best intern wasn’t the smartest intern. Your best intern was the person ready to go for rounds, took care of everything, sharp early in the morning, stays late, and gets the work done.” “Intelligence is relative. Hard work and dedication [are] the most important thing.” Notes - Advocacy for Refugee Health and Empowering First-Generation Cardiologists Advocacy for refugee health and empowering first-generation cardiologists Focusing on creating professionals from a given community can help increase their chances of returning to that community and helping to address health disparities. Refugees and immigrants come from countries and communities where, by and large, prevention is lacking. Seeing a healthcare provider is more appropriate in dire situations. When approaching immigrants, it is important to present medical information in ways in which they can understand and absorb properly. For many refugee families, there exists a language barrier and the children are most often the advocates for the family because they are most likely to understand the language of the community they live in. The vast number of students in the US medical school system come from privileged backgrounds; however, this same statistic is not true for the populations they end up serving. It is important to have health professionals reflect the populations they serve, and one of the methods to achieve this is through introducing as many individuals as possible to the field of medicine; one of the ways to overcome a leaky pipeline is to pack the pipeline. Strategies include encouraging medical students to serve as mentors for those junior to them. It is important to build more sustainable relationships with communities because it leads to more trust and success. Advocating for mental health in these communities is very important because they face these issues at an increased level. However, it is unfortunately under-addressed. Resource avenues such as the CDC provide substantial information regarding different refugee and immigrant profiles and the issues most pertinent to these communities. Inclusivity in Cardiology It is important to normalize people feeling comfortable in having a discourse about differences and recognizing the challenges individuals face when pursuing a career in medicine or cardiology in order to promote inclusivity in this field. This is a major goal for the CardioNerds Narratives in Cardiology program. Within Cardiology, structural racism and hate are present. It is important to place yourself in a challenging environment or one different from what you are used to and attempt to find common ground with other individuals. The Bridge Between Social Issues and Cardiology As a physician, it is important to create boundaries and choose what social issues you wish to engage in. If groups of people do not see eye to eye, steps should be taken to reach out to one another and establish and try to understand what these differences are. Physicians are the best advocates in the world because, for the most part, they are trusted by their patients. Recognizing the importance of the influence that physicians have and realizing this influence can extend beyond the medical space. Humor can be another means by which to make it easier to bring up important conversations that may otherwise be difficult. Technology to Help Bridge the Gap Technology can serve as a means of being able to communicate with refugee families because they are likely to have access to a smartphone. Refugee families most often don’t understand the information given to them in paper or pamphlet form, and often important medical advice can be lost that way. Technology provides increased access to medicine and allows patients more individuality and control in keeping on top of their health. Artificial intelligence technology is the direction that health and medicine are heading in; thus, health professionals and patients must learn how to use this technology to their advantage.

Jul 12, 2024

CardioNerds co-founder Dan Ambinder joins Dr. Lefan He, Dr. Sina Salehi Omran, and Dr. Neil Gupta from the University of Rochester Cardiovascular Disease Fellowship Program for a day sailing on Lake Ontario. Expert commentary is provided by Dr. Jeffrey Bruckel, and CV Fellowship Program Director Dr. Burr Hall shares insights on the University of Rochester fellowship. The episode audio was edited by CardioNerds intern Dr. Atefeh Ghorbanzadeh. They discuss the following case involving a patient with papillary muscle rupture. This is a 63-year-old man with hypertension, hyperlipidemia, and active tobacco smoking who presented with acute dyspnea. He was tachycardic but otherwise initially hemodynamically stable. The physical exam demonstrated warm extremities with no murmurs or peripheral edema. Chest X-ray revealed diffuse pulmonary edema, and the ECG showed sinus tachycardia with T-wave inversions in the inferior leads. A bedside echocardiogram revealed a flail anterior mitral valve leaflet. The patient was taken for cardiac catheterization that revealed nonobstructive mid-RCA atheroma with a distal RCA occlusion, which was felt to reflect embolic occlusion from recanalized plaque. PCI was not performed. Right heart catheterization then demonstrated a low cardiac index as well as elevated PCWP and PA pressures. An intra-aortic balloon pump was placed at that time. A TEE was performed soon after which showed the posteromedial papillary muscle was ruptured with flail segments of the anterior mitral leaflet as well as severe posteriorly directed mitral regurgitation. The patient ultimately underwent a successful tissue mitral valve replacement and CABG. US Cardiology Review is now the official journal of CardioNerds! Submit your manuscript here. CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! case Media Pearls - A Case of Papillary Muscle Rupture Most cases of papillary muscle rupture demonstrate only small areas of ischemia with preserved ventricular function, thus causing high shear force on the ischemic papillary muscle. The posteromedial papillary muscle has a single blood supply from the posterior descending artery, while the anterolateral papillary muscle has a dual blood supply from the LAD and the circumflex. Therefore, the posteromedial papillary muscle is more vulnerable to ischemia and, hence, rupture. A murmur may be absent in cases of papillary muscle rupture due to the rapid equalization of left atrial and left ventricular pressures caused by the acuteness of the severe MR. Papillary muscle rupture should always be on the differential for acute dyspnea when ACS is suspected. While mostly associated with STEMIs, mechanical complications of acute myocardial infarctions can also occur after NSTEMIs. Always auscultate patients carefully after a myocardial infarction! When evaluating patients with chest pain presenting with acute or rapidly progressive heart failure and a hypercontractile LVEF should raise suspicion for mechanical complications of MI. Once a papillary muscle rupture is diagnosed, cardiac surgery should be immediately contacted. Temporizing measures prior to surgery include positive pressure ventilation, IV nitroglycerin/nitroprusside, and temporary mechanical circulatory support. Notes - A Case of Papillary Muscle Rupture What is the clinical presentation of acute mitral regurgitation from papillary muscle rupture? Patients typically present 3-5 days after a transmural infarct. Roughly half of these patients present with pulmonary edema that may quickly progress to cardiogenic shock. Most cases are associated with STEMIs, but papillary muscle rupture is also possible with an NSTEMI. The classic murmur is a mid-, late-, or holosystolic murmur. However, due to the rapid equalization of pressures between the LA and LV, many patients may not present with a murmur! What is the pathophysiology of papillary muscle rupture? The most common etiology is acute occlusion of the RCA causing infarct of the posteromedial papillary muscle, which then leads to a partial or complete tear 2-7 days later. The posteromedial papillary muscle has a single blood supply from the posterior descending artery, while the anterolateral papillary muscle has a dual blood supply from the LAD and the circumflex. Therefore, the posteromedial papillary muscle is more vulnerable to ischemia and, hence, rupture. What are the echocardiographic features of acute mitral regurgitation? Typically, acute mitral regurgitation is caused by acute insult to the mitral valve or mitral valve apparatus. Examples include endocarditis with leaflet perforation, acute flail leaflet in the setting of mitral valve prolapse, and infarct-related papillary muscle rupture. Also, the LVEF can be hypercontractile. Left ventricular and left atrial dimensions tend to be normal in acute MR as the heart has not had time to remodel. This also leads to rapid equalization of the LV-LA pressure during systole, blunting both the Doppler signal and the audible murmur which may under-appreciate acute severe mitral regurgitation. Severe mitral regurgitation typically has a regurgitant volume of ≥60 mL or a regurgitant fraction of at least 50%. Additionally, an effective regurgitant orifice area of 0.4 cm^2 is typically indicative of severe mitral regurgitation. A complete multiparametric assessment is more important than any single parameter. Systolic flow reversal in the pulmonary veins is pathognomonic for severe mitral regurgitation. This may not be apparent in all pulmonary veins if the MR is eccentric, as is usually the case of papillary muscle or acute leaflet flail. How should acute mitral regurgitation due to papillary muscle rupture be managed? Afterload reduction may help, but this may be limited by hypotension in the acute setting. Temporary mechanical circulatory support may be necessary, often with an intra-aortic balloon pump which can be effective in improving forward flow. The ultimate and definitive treatment is urgent cardiac surgery along with concomitant bypass grafting as appropriate. Transcatheter edge-to-edge repair may be considered sparingly when surgery is deemed very high risk. What are the other mechanical complications of acute myocardial infarction? Ventricular septal rupture typically occur 3-5 days after an infarct but there is a bimodal distribution. The presentation can vary from an isolated systolic murmur all the way to cardiogenic shock. Echocardiography will show a left to right shunt and right heart cath will show a step-up in oxygenation between the RA and PA as well as an elevated Qp/Qs. VSRs require urgent surgical or percutaneous repair. Ventricular free wall rupture also occurs 3-5 days after an infarct and presents with elevated jugular venous distension, muffled heart sounds, and pulsus paradoxus. As blood irritates the pericardium, the patient’s ECG can show new ST-elevations. Management is emergent surgery. Pseudoaneurysms present weeks to years after an infarct. These occur when a cardiac rupture is contained by pericardial adhesions and typically involve the inferior or lateral walls. Patients may be asymptomatic, but once diagnosed, pseudoaneurysms should be urgently repaired, lest they expand or become unstable. References Damluji AA, van Diepen S, Katz JN, Menon V, Tamis-Holland JE, Bakitas M, Cohen MG, Balsam LB, Chikwe J; on behalf of the American Heart Association Council on Clinical Cardiology; Council on Arteriosclerosis, Thrombosis and Vascular Biology; Council on Cardiovascular Surgery and Anesthesia; and Council on Cardiovascular and Stroke Nursing. Mechanical complications of acute myocardial infarction: a scientific statement from the American Heart Association. Circulation. 2021;144:e16–e35. doi: 10.1161/CIR.0000000000000985 Chang C et al. Transcatheter Edge-to-Edge Repair for Acute Mitral Regurgitation due to Postinfarction Papillary Muscle Rupture. JSCAI (2022) 100431. Kilic A et al. Mitral Valve Surgery for Papillary Muscle Rupture: Outcomes in 1342 Patients From The Society of Thoracic Surgeons Database. The Annals of Thoracic Surgery Volume 110, Issue 6, December 2020, Pages 1975-1981 van Diepen S, Katz JN, Albert NM, Henry TD, Jacobs AK, Kapur NK, Kilic A, Menon V, Ohman EM, Sweitzer NK, Thiele H, Washam JB, Cohen MG; on behalf of the American Heart Association Council on Clinical Cardiology; Council on Cardiovascular and Stroke Nursing; Council on Quality of Care and Outcomes Research; and Mission: Lifeline. Contemporary management of cardiogenic shock: a scientific statement from the American Heart Association. Circulation. 2017;136:e232–e268. doi: 10.1161/CIR.0000000000000525 Zoghbi, W. A., Adams, D., Bonow, R. O., Enriquez-Sarano, M., Foster, E., Grayburn, P. A., Hahn, R. T., Han, Y., Hung, J., Lang, R. M., Little, S. H., Shah, D. J., Shernan, S., Thavendiranathan, P., Thomas, J. D., & Weissman, N. J. (2017). Recommendations for noninvasive evaluation of native valvular regurgitation. Journal of the American Society of Echocardiography, 30(4), 303–371. https://doi.org/10.1016/j.echo.2017.01.007

Jul 9, 2024

CardioNerds (Drs. Gurleen Kaur and Richard Ferraro) and episode FIT Lead Dr. Saahil Jumkhawala (Cardiology Fellow at the University of Miami) discuss SGLT inhibitors, focusing on the biology of SGLT and its inhibition, with Dr. Katherine Tuttle (Executive Director for Research at Providence Healthcare, Co-Principal Investigator of the Institute of Translational Health Sciences, and Professor of Medicine at the University of Washington). Show notes were drafted by Dr. Saahil Jumkhawala. The episode audio was engineered by CardioNerds intern Christiana Dangas. This episode was produced in collaboration with the American Society of Preventive Cardiology (ASPC) with independent medical education grant support from Lexicon Pharmaceuticals. CardioNerds Prevention PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls - The Biology of SGLT Inhibition with Dr. Katherine Tuttle SGLT inhibitors, while initially developed as antidiabetic medications, have been shown to be beneficial for cardiovascular and renal outcomes. These benefits result from their on-target glucosuric effects and additional off-target effects. The side effect profiles of SGLTis are primarily mediated by glucose reabsorption in their target tissues. The side effect profile of SGLTis must be considered when prescribing these medications and is generally favorable for SGLT2is versus SGLT1is. Once SGLTis are prescribed, patients should be given specific attention to their eGFR, serum potassium, and clinical evaluations of volume status and blood pressure. Strategies to increase implementation of and reduce clinical inertia for these important class of medication remain an area of active investigation Show notes - The Biology of SGLT Inhibition with Dr. Katherine Tuttle What should prompt consideration of starting an SGLT inhibitor? Considerations for SGLT inhibitor initiation are based on a history of heart failure, kidney disease, and diabetes status. In the EMPA-KIDNEY trial, empagliflozin improved cardiovascular and kidney outcomes in those with low GFR (regardless of level of albuminuria). What is the mechanism of action of SGLT2 inhibitors? SGLT2 inhibitors improve glycemic control by blocking SGLT2 receptor-mediated reabsorption of glucose in the proximal convoluted tubule, where 80-90% of this reuptake occurs, and increased downstream excretion of glucose and sodium chloride. SGLT2 inhibitors provide only a modest glucose-lowering effect, particularly for patients with GFR 30% should be suggestive of other issues for patients taking these medications, most commonly volume depletion or hypotension. References - The Biology of SGLT Inhibition with Dr. Katherine Tuttle Cowie M.R., Fisher M. SGLT2 inhibitors: mechanisms of cardiovascular benefit beyond glycaemic control. Nat Rev Cardiol. 2020 Dec; 17(12):761-722. Kuboto Y, Shimizu W. Clinical Benefits of Sodium-Glucose Cotransporter 2 Inhibitors and the Mechanisms Underlying their Cardiovascular Effects. JACC: Asia. 2022 Jun; 2:287-293. Lopaschuk G.D., Verma S. Mechanisms of Cardiovascular Benefits of Sodium Glucose Co-Transporter 2 (SGLT2) Inhibitors. JACC Basic Trans Sci. 2020 Jun; 5(6):632-644. Harrington J., Udell J.A., Jones W.S., Anker S.D., Bhatt D.L., Petrie M.C., & Butler J. Empagliflozin in patients post myocardial infarction: rationale and design of the EMPACT-MI trial. American Heart Journal. 2022; 253:86-98. Talha K.M., Anker S.D., & Butler J. SGLT-2 inhibitors in heart failure: a review of current evidence. International Journal of Heart Failure. 2023; 5(2):82. Tuttle K.R. Digging deep into cells to find mechanisms of kidney protection by SGLT2 inhibitors. J Clin Invest. 2023; 133(5).

Jun 26, 2024

CardioNerds cofounder, Amit Goyal joins Dr. Belal Suleiman, Dr. Nkiru Osude, and Dr. David Elliott from Duke University. They discuss a case of severe mitral paravalvular regurgitation complicated by hemolytic anemia. Expert commentary is provided by Dr. Andrew Wang. Audio editing by CardioNerds Academy Intern, student doctor Adriana Mares. US Cardiology Review is now the official journal of CardioNerds! Submit your manuscript here. CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Case Media - Severe Mitral Paravalvular Regurgitation Complicated by Hemolytic Anemia - Duke University

Jun 24, 2024

CardioNerds Co-Founder Dr. Daniel Ambinder, Series Co-Chair Dr. Giselle Suero Abreu (FIT at MGH), and Episode Lead Dr. Iva Minga (FIT at the University of Chicago) discuss the use of multi-modality cardiovascular imaging in cardio-oncology with expert faculty Dr. Nausheen Akhter (Northwestern University). Show notes were drafted by Dr. Sukriti Banthiya and episode audio was edited by CardioNerds Intern and student Dr. Diane Masket. They use illustrative cases to discuss: Recommendations on the use of multimodality imaging, including advanced echocardiographic techniques and cardiac MRI, in patients receiving cardiotoxic therapies and long-term surveillance. Role of nuclear imaging (MUGA scan) in monitoring left ventricular ejection fraction. Use of computed tomography to identify and/or monitor coronary disease. Imaging diagnosis of cardiac amyloidosis. This episode is supported by a grant from Pfizer Inc. This CardioNerds Cardio-Oncology series is a multi-institutional collaboration made possible by contributions of stellar fellow leads and expert faculty from several programs, led by series co-chairs, Dr. Giselle Suero Abreu, Dr. Dinu Balanescu, and Dr. Teodora Donisan. CardioNerds Cardio-Oncology PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! References - Multi-modality Imaging in Cardio-Oncology Baldassarre L, Ganatra S, Lopez-Mattei J, et al. Advances in Multimodality Imaging in Cardio-Oncology. J Am Coll Cardiol. 2022 Oct, 80 (16) 1560–1578.

Jun 21, 2024

CardioNerds cofounders, Dan Ambinder joins Drs. Aishwarya Pastapur, Oyinkansola Osobamiro, and Rafik Issa from the University of Michigan for drinks in Ann Arbor. They discuss the following case of pericardial decompression syndrome. Expert commentary is provided by Dr. Brett Wanamaker. Notes were drafted by Dr. Aishwarya Pastapur and Dr. Rafik Issa. The episode audio was engineered by CardioNerds Intern student Dr. Atefeh Ghorbanzadeh. A woman in her 50s with a past medical history of stage IV lung cancer (with metastatic involvement of the liver, bone, and brain), previous saddle pulmonary emboli, pericardial effusion, and malignant pleural effusions presents with dyspnea. She was found to have a pericardial effusion with tamponade physiology relieved by pericardiocentesis. We discuss the management of cardiac tamponade, indications for pericardiocentesis, how to monitor for post-pericardiocentesis complications, and what to keep on your differential diagnosis for decompensation after pericardiocentesis. We discuss the epidemiology, pathophysiology, diagnosis, and management of pericardial decompression syndrome. US Cardiology Review is now the official journal of CardioNerds! Submit your manuscript here. CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Case Media - Pericardial Decompression Syndrome Pearls - Pericardial Decompression Syndrome Diminished heart sounds, a low-voltage EKG with electrical alternans, elevated jugular venous pressure/pulsations (JVP), and the presence of pulses paradoxes are important findings that could suggest tamponade. McConnell sign is strongly concerning for right ventricular failure and pulmonary hypertension, potentially due to acute pulmonary embolism. Mechanical thrombectomy for pulmonary embolism is not feasible if the emboli are diffusely scattered without a central lesion to target. For patients who experience decompensation following pericardiocentesis, consider perforation, tamponade re-accumulation, or pericardial decompression syndrome (PDS). When possible, avoid draining more than 1L of pericardial fluid at once to minimize the risk of PDS. Notes - Pericardial Decompression Syndrome What is Pericardial Decompression Syndrome (PDS), and how does it present? Pericardial decompression syndrome is a rare, life-threatening syndrome occurring in about 5-10% of cases with paradoxical worsening of hemodynamics after pericardial drainage. The clinical presentation ranges from pulmonary edema to cardiogenic shock to death, occurring a few hours to days after a successful pericardiocentesis. What is the underlying mechanism for PDS? The pathophysiology behind PDS is debated, but there are three proposed mechanisms: Paradoxical Hemodynamic Derangement: After pericardiocentesis, venous return to the RV rapidly increases, resulting in RV expansion and potentially septal deviation towards the LV. Subsequently, the LV experiences decreased preload while still facing increased afterload as a compensatory response to obstructive shock, leading to decompensation.Myocardial Ischemia: Increased intrapericardial pressure may impair coronary perfusion, leading to myocardial ischemia. Upon pericardiocentesis, there is myocardial stunning with increased demand due to increased venous return and cardiac output Sympathetic Withdrawal: Withdrawal of sympathetic activation after drainage of pericardial fluid can trigger cardiovascular collapse What are the risk factors for developing PDS, and how can we mitigate those risks for prevention? Generally, patients with long-standing pericardial effusion with chronic compression of the heart, such as those with malignant pericardial effusions, are more vulnerable to developing PDS after pericardiocentesis. Additionally, rapid fluid removal increases the risk. In terms of prevention, removing fluid to normalize CVP and MAP and letting the rest of the fluid drain slowly may mitigate the risk. How do we manage a patient with PDS? The management of PDS is supportive, focusing on addressing hemodynamic and respiratory derangements. The underlying pathophysiology should resolve in 24-48 hours. What is the prevalence and prognosis of PDS? PDS affects 5-10% of pericardiocentesis procedures, although the exact frequency is difficult to ascertain.It is a self-resolving process as the heart re-adapts to the new hemodynamics. However, during the episode of PDS, mortality can be as high as 30% per some studies. References - Pericardial Decompression Syndrome Schnur M. Understanding Pulsus Paradoxus. Accessed February 27, 2024. https://nursingcenter.com/ncblog/august-2021/understanding-pulsus-paradoxus Carlini’ ’Caterina Chiara De, Maggiolini’ ’Stefano. Pericardiocentesis in cardiac tamponade: indications and practical aspects. Accessed February 27, 2024. https://www.escardio.org/Journals/E-Journal-of-Cardiology-Practice/Volume-15/Pericardiocentesis-in-cardiac-tamponade-indications-and-practical-aspects Angouras DC, Dosios T. Pericardial Decompression Syndrome: A Term for a Well-Defined but Rather Underreported Complication of Pericardial Drainage. The Annals of Thoracic Surgery. 2010;89(5):1702-1703. doi:10.1016/j.athoracsur.2009.11.073 Imazio M. Pericardial decompression syndrome: A rare but potentially fatal complication of pericardial drainage to be recognized and prevented. European Heart Journal Acute Cardiovascular Care. 2015;4(2):121-123. doi:10.1177/2048872614557771 Prabhakar Y, Goyal A, Khalid N, et al. Pericardial decompression syndrome: A comprehensive review. World Journal of Cardiology. 2019;11(12):282-291. doi:10.4330/wjc.v11.i12.282 Sobieski C, Herner M, Goyal N, et al. Pericardial Decompression Syndrome After Drainage of Chronic Pericardial Effusions. JACC: Case Reports. 2022;4(22):1515-1521. doi:10.1016/j.jaccas.2022.08.023 Chhabra L. Pericardial Decompression Syndrome. American College of Cardiology. Accessed February 27, 2024. https://www.acc.org/Latest-in-Cardiology/Articles/2020/04/13/09/05/http%3a%2f%2fwww.acc.org%2fLatest-in-Cardiology%2fArticles%2f2020%2f04%2f13%2f09%2f05%2fPericardial-Decompression-Syndrome Pradhan R, Okabe T, Yoshida K, Angouras DC, DeCaro MV, Marhefka GD. Patient characteristics and predictors of mortality associated with pericardial decompression syndrome: a comprehensive analysis of published cases. European Heart Journal Acute Cardiovascular Care. 2015;4(2):113-120. doi:10.1177/2048872614547975 Amro A, Mansoor K, Amro M, et al. A Comprehensive Systemic Literature Review of Pericardial Decompression Syndrome: Often Unrecognized and Potentially Fatal Syndrome. Current Cardiology Reviews. 17(1):101-110.

Jun 6, 2024

CardioNerds (Amit Goyal and Dan Ambinder), Dr. Jaya Kanduri, and Dr. Jason Feinman discuss foundations of cardiovascular prevention with Dr. Stephen Kopecky. In this episode, the CardioNerds and topic expert Dr. Stephen Kopecky tackle cardiovascular prevention. They focus on how to identify patients at risk for cardiovascular disease by using the pooled cohort equation and discuss how to incorporate additional risk-enhancing factors in risk estimation. Later, they discuss the role of non-invasive imaging and testing for further patient risk stratification. Last, they discuss the appropriate pharmacologic interventions for patient care, how to determine what LDL-c to target for each patient, and how to modify your treatment modalities in response to side effects or the need for further lipid-lowering therapies. Notes were drafted by Dr. Jason Feinman. Audio was engineered by CardioNerds Intern Christiana Dangas. The CardioNerds Beyond the Boards Series was inspired by the Mayo Clinic Cardiovascular Board Review Course and designed in collaboration with the course directors Dr. Amy Pollak, Dr. Jeffrey Geske, and Dr. Michael Cullen. CardioNerds Beyond the Boards SeriesCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls and Quotes - Foundations of Cardiovascular Prevention The 2018 cardiovascular prevention guidelines indicate that a single equation, like the pooled risk equation, does not fit everyone. There are additional risk enhancers that are not factored into the pooled risk equation that can impact an individual’s risk These factors are often conditions that increase inflammation but can also include family history, ethnicity, chronic kidney disease, metabolic syndrome, premature menopause or gestational diabetes, and rheumatologic conditions Data from Get With The Guidelines demonstrates that the average LDL at the time of the first myocardial infarction is 105 mg/dL. Coronary artery calcium scores or a carotid ultrasound can be used to further risk stratify patients. However, CAC is likely to be negative in young women. A CAC of zero can be used to “de-risk” some patients but should not be used to guide therapy in the setting of tobacco usage, diabetes mellitus, or familial hypercholesterolemia. Strategies to mitigate risk include healthy lifestyle habits and selectively targeting key risk factors including LDL, hypertriglyceridemia, inflammation, and the GLP1-pathway. Upcoming medications may address elevated Lp(a). Notes - Foundations of Cardiovascular Prevention Notes: Notes drafted by Dr. Jason Feinman. How do you assess an individual's risk for cardiovascular disease? The paramount role of primary prevention is the assessment and mitigation of an individual’s risk for ASCVD event.1 The 10-year ASCVD risk calculator is a commonly used tool to assess an individual’s risk and to guide shared decision-making conversations and recommendations.2 Individuals can be characterized as having low (less than 5%), borderline (5%-7.5%), intermediate (7.5%-20%), or high (greater than 20%) risk.2 The 10-year ASCVD risk calculator has varying validation in ethnic minorities, and other risk calculators, such as the Framingham CVD risk score, may be considered in those groups.3-5 Additional risk enhancers may be used to guide recommendations for individuals at borderline or intermediate risk.1 What additional imaging testing may be beneficial in the assessment of an individual’s risk? Individuals with intermediate or borderline risk may benefit from further non-invasive imaging to help guide therapeutic recommendations.2 Coronary artery calcification is a marker of underlying atherosclerosis, which can help to reclassify patients to be at higher risk for ASCVD events and support interventions to help lower this risk.6 Conversely, a score of zero can help to reclassify individuals into lower-risk groups A score of zero should be used with caution in young women who are more likely to have non-calcified plaque and should not be used as a marker of low risk in individuals with other risk factors, including diabetes mellitus and tobacco usage.1 What non-pharmacological interventions may be considered to lower an individual’s ASCVD risk? The 2019 guidelines give a class I recommendation for a diet of vegetables, fruits, nuts, whole grains, and fish to lower ASCVD risk factors.1 Increased intake of sugar has been demonstrated to correlate with increased rates of type 2 diabetes mellitus and subsequent increased risk for cardiovascular events.7 At least 150 minutes per week of moderate-intensity or 75 minutes of vigorous intensive is recommended to reduce the risk of ASCVD events.1 What pharmacological interventions can be considered for individuals with prior ASCVD events or at high risk for ASCVD? A moderate-intensity statin is recommended for individuals at intermediate risk of ASCVD events with risk enhancers with a goal reduction in LDL-c of 30% or more.1 For individuals at a high 10-year risk for ASCVD events, a 50% reduction in LDL-C is recommended.1 A doubling of a statin dose can be predicted to lead to a 6% further reduction in LDL-C Ezetimibe can be considered as adjunct therapy for individuals receiving statin therapy who do not reach their target LDL-C.2 How do you determine the goal LDL-c? LDL goal is based on a history of prior ASCVD events and the risk of future ASCVD events. For secondary prevention, especially for individuals at high risk for ASCVD events, an LDL goal of at least less than 70 mg/dL is recommended2 References - Foundations of Cardiovascular Prevention Arnett DK, Blumenthal RS, Albert MA, et al. 2019 ACC/AHA Guideline on the Primary Prevention of Cardiovascular Disease: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines [published correction appears in Circulation. 2019 Sep 10;140(11):e649-e650] [published correction appears in Circulation. 2020 Jan 28;141(4):e60] [published correction appears in Circulation. 2020 Apr 21;141(16):e774]. Circulation. 2019;140(11):e596-e646. doi:10.1161/CIR.0000000000000678 Grundy SM, Stone NJ, Bailey AL, et al. 2018 AHA/ACC/AACVPR/AAPA/ABC/ACPM/ADA/AGS/APhA/ASPC/NLA/PCNA Guideline on the Management of Blood Cholesterol: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines [published correction appears in Circulation. 2019 Jun 18;139(25):e1182-e1186] [published correction appears in Circulation. 2023 Aug 15;148(7):e5]. Circulation. 2019;139(25):e1082-e1143. doi:10.1161/CIR.0000000000000625 Yang X, Li J, Hu D, et al. Predicting the 10-Year Risks of Atherosclerotic Cardiovascular Disease in Chinese Population: The China-PAR Project (Prediction for ASCVD Risk in China). Circulation. 2016;134(19):1430-1440. doi:10.1161/CIRCULATIONAHA.116.022367 Jung KJ, Jang Y, Oh DJ, et al. The ACC/AHA 2013 pooled cohort equations compared to a Korean Risk Prediction Model for atherosclerotic cardiovascular disease. Atherosclerosis. 2015;242(1):367-375. doi:10.1016/j.atherosclerosis.2015.07.033 D'Agostino RB Sr, Vasan RS, Pencina MJ, et al. General cardiovascular risk profile for use in primary care: the Framingham Heart Study. Circulation. 2008;117(6):743-753. doi:10.1161/CIRCULATIONAHA.107.699579 DeFilippis AP, Young R, Carrubba CJ, et al. An analysis of calibration and discrimination among multiple cardiovascular risk scores in a modern multiethnic cohort. Ann Intern Med. 2015;162(4):266-275. doi:10.7326/M14-1281 Löfvenborg JE, Andersson T, Carlsson PO, et al. Sweetened beverage intake and risk of latent autoimmune diabetes in adults (LADA) and type 2 diabetes. Eur J Endocrinol. 2016;175(6):605-614. doi:10.1530/EJE-16-0376

May 31, 2024

This case report explores the intricacies of familial hypercholesterolemia (FH), delving into its genetic basis, atherosclerotic cascade, and early-onset cardiovascular complications. It examines established diagnostic criteria and emphasizes personalized management, including statins, novel therapies, and lifestyle modifications. CardioNerds cofounders (Drs. Amit Goyal and Danial Ambinder) join Dr. Irfan Shafi, Dr. Preeya Prakash, and Dr. Rebecca Theisen from the Wayne State University/DMC and Central Michigan University at Campus Martius in Downtown Detroit for some holiday ice-skating! They discuss an interesting pediatric case (see case synopsis below). Dr. Luis C Afonso provides the Expert CardioNerd Perspectives & Review segment for this episode. Audio editing by CardioNerds academy intern, Pace Wetstein. US Cardiology Review is now the official journal of CardioNerds! Submit your manuscript here. CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Case Synopsis FH, a 9-year-old female with no previous medical history, recently moved back to the US from Iraq. She presented to establish care and discuss new-onset chest pain and dyspnea. A systolic ejection murmur was noted during her initial visit to the pediatrician, prompting cholesterol testing and a cardiology referral. Testing revealed, alarming cholesterol levels (Total Cholesterol: 802 mg/dL, LDL: 731 mg/dL, Triglycerides: 123 mg/dL) prompted concern for cardiac involvement. Due to persistent symptoms, FH was transferred to Children's Hospital of Michigan. Despite normal findings on EKG and chest x-ray, a 2/6 systolic murmur was noted. She was discharged with a cardiology clinic follow-up. However, two days later, FH experienced severe chest pain at rest, sweating, and difficulty breathing. She was transported to Children's Hospital again, and her troponin level measured 3000, and her total cholesterol was 695 mg/dL. An echocardiogram revealed valvar and supravalvar aortic stenosis, necessitating collaboration between Pediatric and Adult cardiology teams. CTA thorax revealed severe supravalvular stenosis, a hypoplastic right coronary artery, and significant coronary artery obstructions. Diagnostic cardiac catheterization confirmed severe aortic stenosis and coronary artery disease, leading to the decision for surgical intervention. FH underwent the Ross operation, left main coronary artery augmentation, and right coronary artery reimplantation. Intraoperatively, atherosclerotic plaques were observed in multiple cardiac structures. FH's recovery was uneventful, discharged on a regimen including Atorvastatin, Ezetimibe, evolocumab, and antiplatelet therapy. Persistent high LDL levels required regular plasmapheresis. Plans for evaluations in Genetics, Lipid Clinic, Endocrine, and Gastroenterology were made, potentially leading to a liver transplant assessment. Given the severity of her condition, a heart/liver transplant might be considered in the future. Conclusion: This case of FH highlights the complex presentation of severe aortic stenosis and coronary artery disease in a pediatric patient. Urgent diagnosis, interdisciplinary collaboration, and aggressive management were crucial. The case underscores the importance of comprehensive care for pediatric patients with rare cardiac conditions, emphasizing collaboration between specialties for optimal outcomes and long-term well-being. Case Media Pearls - Familial Hypercholesterolemia Mutations in LDLR, ApoB, or PCSK9 genes disrupt LDL-C clearance, leading to a cascade of events culminating in accelerated atherosclerosis and early-onset cardiovascular complications (e.g., CAD, aortic stenosis, PAD, stroke). Diagnosis of familial hypercholesterolemia relies on a combination of clinical features (xanthomas, corneal arcus, high LDL-C), family history, and genetic testing guided by established criteria like DCLN or NLA recommendations. Supravalvular aortic stenosis, while common in many congenital cases, should raise suspicion of homozygous familial hypercholesterolemia in the setting of extensively elevated LDL and unexpected coronary artery disease. A multidisciplinary approach, including involvement of pediatric and adult cardiology teams, lipid specialists and cardiothoracic surgeons, should be involved in the overall evaluation and management of these patients, both at initiation of diagnosis, and in an outpatient setting. In patients with FH, it is important to delineate between homozygous and heterozygous manifestations, as this can have extensive implications on treatment, management and the overall clinical prognosis and further disease sequelae that the patient may experience. References - Familial Hypercholesterolemia Shah, N. (2020). Familial hypercholesterolemia: Early diagnosis and treatment is key for cardiovascular prevention.Cleveland Clinic Journal of Medicine, 87(5), 109-120. https://pubmed.ncbi.nlm.nih.gov/23469913/ Turgeon, R. D., Barry, A. R., & Pearson, G. J. (2023). Familial hypercholesterolemia: Review of diagnosis,screening, and treatment. American Journal of Health-System Pharmacy, 80(11), 917-929.https://pubmed.ncbi.nlm.nih.gov/26796832/ Collins, R. T. (2018). Cardiovascular disease in Williams syndrome. Current Opinion in Pediatrics, 30(5), 609-615. https://www.ncbi.nlm.nih.gov/books/NBK544278/ Collins, R. T., Kaplan, P., Somes, G. W., & Rome, J. J. (2010). Long-term outcomes of patients with cardiovascular abnormalities and Williams syndrome. American Journal of Cardiology, 105(6), 874-878.https://pubmed.ncbi.nlm.nih.gov/30045083/ Honjo, R. S., Monteleone, V. F., Aiello, V. D., Wagenfuhr, J., Issa, V. S., Pomerantzeff, P. M. A., Furusawa, E. A.,Zanardo, E. A., Kulikowski, L. D., Bertola, D. R., & Kim, C. A. (2022). Cardiovascular findings in Williams-Beuren Syndrome: Experience of a single center with 127 cases. American Journal of Medical Genetics. Part A,188(3), 676-682. https://www.ncbi.nlm.nih.gov/books/NBK544278/ Pham, P. P., Moller, J. H., Hills, C., Larson, V., & Pyles, L. (2009). Cardiac catheterization and operative outcomes from a multicenter consortium for children with Williams syndrome. Pediatric Cardiology, 30(1), 9-14.https://pubmed.ncbi.nlm.nih.gov/19052807/ Olsen, M., Fahy, C. J., Costi, D. A., Kelly, A. J., & Burgoyne, L. L. (2014). Anaesthesia-related haemodynamic complications in Williams syndrome patients: A review of one institution's experience. Anaesthesia and Intensive Care, 42(6), 619-624. https://pubmed.ncbi.nlm.nih.gov/25233176/ Harada-Shiba, M., Arai, H., Ishigaki, Y., Ishibashi, S., Okamura, T., Ogura, M., Dobashi, K., Nohara, A., Bujo, H.,Miyauchi, K., Yamashita, S., & Yokote, K. (2018). Guidelines for diagnosis and treatment of familial hypercholesterolemia 2017. Journal of Atherosclerosis and Thrombosis, 25(8), 751-770.https://pubmed.ncbi.nlm.nih.gov/29877295/ Alnouri, F., & Santos, R. D. (2022). New trends and therapies for familial hypercholesterolemia. Journal of Clinical Medicine, 11(22), 6638. https://pubmed.ncbi.nlm.nih.gov/36431115/

May 30, 2024

In this episode, Dr. Katie Fell (General Cardiology Fellow at University of Michigan and CardioNerds Academy Fellow) and Dr. Gurleen Kaur (incoming General Cardiology fellow at Brigham and Women’s Hospital and Director of CardioNerds Internship) discuss with Dr. James Arrighi (General Cardiologist and CEO of ACGME-International) about developing as a clinician educator and the concept of competency-based education. The PA-ACC & CardioNerds Narratives in Cardiology is a multimedia educational series jointly developed by the Pennsylvania Chapter ACC, the ACC Fellows in Training Section, and the CardioNerds Platform with the goal to promote diversity, equity, and inclusion in cardiology. In this series, we host inspiring faculty and fellows from various ACC chapters to discuss their areas of expertise and their individual narratives. Join us for these captivating conversations as we celebrate our differences and share our joy for practicing cardiovascular medicine. We thank our project mentors Dr. Katie Berlacher and Dr. Nosheen Reza. The PA-ACC & CardioNerds Narratives in Cardiology PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Video version - Becoming a “Big E” Medical Educator as a Cardiologist with Dr. James Arrighi https://youtu.be/xcrwnz6_9Qg Quoatables - Becoming a “Big E” Medical Educator as a Cardiologist with Dr. James Arrighi “You really have to have a passion or a love for what you do...that’s probably responsible for most of the success one has in life” (time 4:43) “Sub-subspecialty societies in Cardiology represent [a] great opportunity for junior faculty or even trainees to get involved, even before getting involved in ACC.” (time 5:30) “Competency-based medical education and time variable training are not synonymous.” (time 16:43) “As Cardiology evolves into more and more subspecialties...it begs the question... ‘Is Cardiology a primary specialty?’” (time 27:30) “We need to think about [a] more efficient ways for training.” (time 31:55) “As a clinician educator, there’s variety, there’s innovation!” (time 41:22) Notes - Becoming a “Big E” Medical Educator as a Cardiologist with Dr. James Arrighi How might one develop as a clinician educator on a national level? Junior faculty and trainees should consider taking advantage of education opportunities in various Cardiology sub-specialty societies (ex: American Society of Nuclear Cardiology, ASNC). This may include involvement in different committees. These opportunities are great ways to build connections and establish a reputation on a national level. This can help lead to other opportunities with larger national organizations (ex: ACC, AHA). Cardiology Training Oversight The Accreditation Council for Graduate Medical Education (ACGME) and American Board of Internal Medicine (ABIM) both have regulatory power over Cardiology training, providing the minimum clinical experience standards for Cardiology fellowship training programs.The ACGME oversees accreditation for Cardiology fellowships.The ABIM defines the requirements for eligibility for certification of individuals. Over time, the ACGME has transitioned to placing an emphasis on quality improvement, with a particular focus on continuous programmatic improvement. The American College of Cardiology (ACC) helps define more granular recommendations for Cardiology training programs and their curriculum.Periodically the ACC releases training guidelines for Cardiology fellowship programs, called Core Cardiovascular Training Statements, or COCATS. This document provides more contemporary, detailed, and specialty-specific recommendations for Cardiology training as compared to ACGME.While ACC has no regulatory authority over Cardiology training programs, COCATS documents provide a roadmap for program directors on how to structure training. The most recent version of the document, COCATS 4, incorporated in the concept of competency-based education (CBME). What is Competency-Based Education (CBME)? Medical education has evolved to focus more on outcome-based assessments of trainees structured around competency evaluations.In 2002, the ACGME defined competencies by which training programs should evaluate their trainees. As a result, training shifted from a time-based structure to one in which trainees must demonstrate specific competencies within a specific time frame.ACC further defined competencies for Cardiology training in the Core Cardiovascular Training Statement 4 (COCATS 4). This is the first COCATs document introducing aspects of CBME, including defining competencies, milestones, and tools to assess a Cardiology trainee’s performance.Each of these documents focuses on optimizing fellow time while in training, targeting education to the learner’s goals and their future career trajectory. Moving to a competency-based, time-variable training program in the U.S. would be challenging and would require significant restructuring of our current GME training system, including Medicare funding. What is ACGME-International (ACGME-I)? Group within the ACGME dedicated to improving health care internationally by assessing and advancing the quality of resident physicians’ education through accreditation.The organization is currently present in 12 countries at 23 sponsoring institutions (as of April 2024). ACGME-I provides postgraduate medical education programs with standardized frameworks on how to improve the quality of teaching, learning, research, and clinical practice for their trainees. References Weissman G, Auseon AJ, Arrighi JA, et al. Perceptions and Utilization of the U.S. Core Cardiovascular Training Statement. J Am Coll Cardiol. 2019;73(22):2896-2899. Halperin JL, Williams ES, Fuster V. COCATS 4 Introduction. J Am Coll Cardiol. 2015;65(17):1724-1733. Arrighi JA, Kilic S, Haines PG. Perspectives on Current Training Guidelines for Cardiac Imaging and Recommendations for the Future. Curr Cardiol Rep. 2018;20(6):43. Published 2018 Apr 23. ACGME Program Requirements for Graduate Medical Education in Cardiovascular Disease. Accessed February 2, 2024. Mendes LA, Weissman G, Berlacher K, et al. Competency-Based Alternative Training Pathway in Cardiovascular Disease and Clinical Cardiac Electrophysiology. J Am Coll Cardiol. 2022;79(25):2540-2542. Production Team Dr. Gurleen Kaur Amit Goyal, MD Daniel Ambinder, MD

May 23, 2024

CardioNerds (Dr. Jessie Holtzman, Chair for the CardioNerds Women’s Heart Disease Committee, and Dr. Naima Maqsood, Chair for the CardioNerds Electrophysiology Committee) join Dr. Ritika Gadodia, Dr. Namratha Meda, and Dr. Tsion Aberra from the Medstar Washington Hospital Center/Georgetown University Program for the National Cherry Blossom Festival. They discuss involving a patient with Chagas cardiomyopathy. Dr. Rachel Marcus provides the Expert CardioNerd Perspectives & Review segment for this episode. Episode audio was edited by Dr. Diane Masket. A 79-year-old male with a history of cardiomyopathy presented with recurrent ventricular tachycardia (VT) post-CRT-D placement. On arrival, the patient was in cardiogenic shock. Initial treatment with amiodarone and milrinone failed, necessitating the addition of mexiletine. Imaging was suggestive of a left ventricular ejection fraction of 20-25% with severe global hypokinesis. Prior coronary angiogram had shown nonobstructive coronary artery disease. Further non-ischemic cardiomyopathy evaluation was unrevealing. Given his El Salvadorian origins, Chagas serology results revealed Chronic Chagas Cardiomyopathy (CCM) confirmed by CDC testing. This case underscores the importance of suspecting CCM in patients with risk factors. An early diagnosis of CCM, can prevent catastrophic events (heart blocks, ventricular arrhythmias, thromboembolic events). In summary, this case takes the learner through the journey of a patient with non-ischemic cardiomyopathy and emphasizes the importance of approaching it with a wide range of differentials. US Cardiology Review is now the official journal of CardioNerds! Submit your manuscript here. CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Case Media Pearls - Chronic Chagas Cardiomyopathy with Recurrent Ventricular Tachyarrhythmia Always consider Chagas cardiomyopathy when you have a patient from Latin America who presents with non-ischemic cardiomyopathy. Chagas cardiomyopathy is associated with an unfavorable prognosis and serves as an independent predictor of mortality. Chagas cardiomyopathy is arrhythmogenic and requires consideration for ICD and, when appropriate, catheter based ventricular tachycardia ablation. It is crucial to treat patients with nifurtimox and benznidazole when appropriate. Provide screening for first-degree family members or close relatives who may have lived in the same environment. Show Notes - Chronic Chagas Cardiomyopathy with Recurrent Ventricular Tachyarrhythmia What is the disease progression in Chagas disease5? Acute Stage:Initial infection occurs through contact with infected triatomine bug feces or contaminated blood products.Symptoms may be mild or absent but can include fever, fatigue, body aches, and swelling at the injection site (chagoma). Parasitemia is high during this stage. Intermediate/Indeterminate Stage:The infection becomes chronic if left untreated.Many individuals enter this stage with no noticeable symptoms.Parasitemia levels decrease, but the parasite remains in the body, mainly in muscle and cardiac tissue. This stage can last for years to decades. Chronic Stage:Some individuals will remain asymptomatic throughout their lives.Cardiac complications (chronic Chagas cardiomyopathy) can lead to arrhythmias, congestive heart failure, and sudden death. Digestive complications can result in enlarged esophagus (megaesophagus) and colon (megacolon), leading to difficulties in swallowing and digestion. When do we suspect, and who do we screen, for Chagas disease? The seroprevalence of CCM in the USA is as high as 19%16. Among patients with LVEF<50%, the rate of positive serology was 28%. Similarly, the seropositivity among patients who reported recognizing the reduviid bug was 31%. Individuals who have lived in endemic countries of Mexico, Central and South America, excluding the Caribbean islands. T. cruzi seroprevalence is highest in Bolivia, Argentina, Paraguay, Ecuador, El Salvador, and Guatemala6. Close relatives and those born to women from endemic countries7. Persons with a history of bite/exposure to the vector responsible for transmission. EKG abnormalities suggestive of infection even in the absence of symptoms. TTE changes: regional wall motion abnormalities (particularly basal inferolateral, apical aneurysm)4 What diagnostic tests can confirm the diagnosis of chronic Chagas cardiomyopathy? Serologic testing: no available assay has sufficient sensitivity and specificity to be used alone. Two serologic tests based on different antigens and/or techniques (e.g., ELISA and IFA) are used in parallel to increase the accuracy of the diagnosis8. EKG: RBBB, LAFB, AV block, atrial fibrillation, ventricular tachycardias TTE: dilated cardiomyopathy, reduced ejection fracture, regional wall motion abnormalities, left ventricular apical aneurysm Cardiac MRI: myocardial fibrosis is a striking feature of CCM and LGE is used to detect and qualify the extent. Myocardial fibrosis also plays a role in risk stratification of CCM9. What are the indications for treatment of Chagas disease? Acute phase. Early chronic phase, including women of childbearing age. Reactivated infection (e.g., after immunosuppression). Adults <50 years of age who do not have advanced cardiomyopathy (stage B1)10. In all other cases, the potential benefit of medication in delaying the development of Chagas disease should be weighed against potential adverse reactions- benznidazole and nifurtimox should not be taken by pregnant women or people with kidney or liver failure. What are the benefits of screening and early diagnosis? Effective treatment, particularly in the acute phase. The BENEFIT trial showed that Trypanocidal therapy with benznidazole in patients with CCM did not significantly reduce cardiac deterioration11. Screening of family members/friends who grew up in the same environment. Reduction of transmission due to blood transfusions and congenital transmission. Early initiation of GDMT (guideline-directed medical therapy) for clinical heart failure 2/2 CCM. Ongoing surveillance for cardiomyopathy can prevent catastrophic events (heart blocks, ventricular arrhythmias, thromboembolic events). Cost effectiveness: Early diagnosis and treatment may reduce healthcare costs compared to the treatment of complications that arise from the chronic phase of the disease. Early diagnosis may also reduce the number of endomyocardial biopsies. How is the management of VT unique in chronic Chagas cardiomyopathy? In comparison to cardiomyopathies of other etiologies, CCM is associated with a higher risk of life-threatening ventricular arrhythmias and an unfavorable prognosis12,14. Per ESC guidelines, the greatest benefit of ICD in CCM is in patients with an LVEF ≤40%15. Per Gali et al, most patients with an ICD received appropriate ICD shocks/therapies regardless of their LV systolic function13. Ablation of VT requires extensive mapping because multiple discrete circuits are typically present. The most common site of origin is the LV basal inferolateral wall. However, 1/3rd of the foci is located on the epicardial surface. This necessitates epicardial mapping to achieve successful ablation6. References - Chronic Chagas Cardiomyopathy with Recurrent Ventricular Tachyarrhythmia Ghzally Y, Mahajan K. Implantable Defibrillator. In: StatPearls. StatPearls Publishing; 2023. Accessed October 7, 2023. http://www.ncbi.nlm.nih.gov/books/NBK459196/ Vrettos A, Panoulas V. Diagnosing STEMI in the presence of paced rhythm: dispelling the myth of the ‘uninterpretable paced ECG.’ BMJ Case Rep. 2021;14(7):e242546. doi:10.1136/bcr-2021-242546 3. Bozkurt B, Colvin M, Cook J, et al. Current Diagnostic and Treatment Strategies for Specific Dilated Cardiomyopathies: A Scientific Statement From the American Heart Association. Circulation. 2016;134(23). doi:10.1161/CIR.0000000000000455 Forsyth CJ, Manne-Goehler J, Bern C, et al. Recommendations for Screening and Diagnosis of Chagas Disease in the United States. The Journal of Infectious Diseases. 2022;225(9):1601-1610. doi:10.1093/infdis/jiab513 CDC - Chagas Disease - Disease. Accessed October 7, 2023. https://www.cdc.gov/parasites/chagas/disease.html Chagas Cardiomyopathy: An Update of Current Clinical Knowledge and Management: A Scientific Statement From the American Heart Association | Circulation. Accessed October 7, 2023. https://www.ahajournals.org/doi/10.1161/CIR.0000000000000599 Montgomery SP, Parise ME, Dotson EM, Bialek SR. What Do We Know About Chagas Disease in the United States? The American Journal of Tropical Medicine and Hygiene. 2016;95(6):1225-1227. doi:10.4269/ajtmh.16-0213 Malone CJ. A Rapid Review on the Efficacy and Safety. Pan American Health Organization (PAHO) and the World Health Organization (WHO); 2021. Nunes MCP, Badano LP, Marin-Neto JA, et al. Multimodality imaging evaluation of Chagas disease: an expert consensus of Brazilian Cardiovascular Imaging Department (DIC) and the European Association of Cardiovascular Imaging (EACVI). European Heart Journal - Cardiovascular Imaging. 2018;19(4):459-460n. doi:10.1093/ehjci/jex154 10. Prevention CC for DC and. CDC - Chagas Disease - Resources for Health Professionals - Antiparasitic Treatment. Published April 11, 2022. Accessed October 7, 2023. https://www.cdc.gov/parasites/chagas/health_professionals/tx.html 11. Morillo CA, Marin-Neto JA, Avezum A, et al. Randomized Trial of Benznidazole for Chronic Chagas’ Cardiomyopathy. N Engl J Med. 2015;373(14):1295-1306. doi:10.1056/NEJMoa1507574 12.

May 14, 2024

CardioNerds Dr. Josh Saef and Dr. Tommy Das join Dr. Omkar Betageri, Dr. Andrew Geissler, Dr. Philip Lacombe, and Dr. Cashel O’Brien from the Maine Medical Center in Portland, Maine to enjoy an afternoon by the famous Portland headlight. They discuss a case of a patient who presents with obstructive cardiogenic shock. Dr. Bram Geller and Dr. Jon Donnelly provide the Expert CardioNerd Perspectives & Review segment for this episode. Dr. Maxwell Afari, the Maine Medical Center cardiology fellowship program director highlights the fellowship program. Audio editing by CardioNerds Academy Intern, student doctor Tina Reddy. This is the case of a 42 year-old woman born with complicated Tetralogy of Fallot repair culminating in a 29mm Edwards Sapiens (ES) S3 valve placement within a pulmonary homograft for graft failure who was admitted to the cardiac ICU for progressive cardiogenic shock requiring vasopressors and inotropic support. Initial workup showed lactic acidosis, acute kidney injury, elevated NT-proBNP, and negative blood cultures. TTE showed at least moderate biventricular systolic dysfunction. She was placed on furosemide infusion, blood cultures were drawn and empiric antibiotics initiated. Right heart catheterization demonstrated elevated right sided filling pressures, blunted PA pressures with low PCWP, low cardiac index, and low pulmonary artery pulsatility index. Intracardiac echocardiography (ICE) showed a large mass within the ES valve apparatus causing restrictive valve motion with a low gradient across the pulmonic valve in the setting of poor RV function. Angiography revealed a large filling defect and balloon valvuloplasty was performed with immediate hemodynamic improvement. Blood cultures remained negative, she was gradually weaned off of inotropic and vasopressor support, and discharged. Despite empiric treatment for culture negative endocarditis and ongoing anticoagulation, she was readmitted for recurrent shock one month later at which time the pulmonic mass was revisualized on ICE. A valve-in-valve transcatheter pulmonary valve (29mm ES S3) was placed to compress what was likely pannus, with an excellent hemodynamic result and no visible mass on ICE. US Cardiology Review is now the official journal of CardioNerds! Submit your manuscript here. CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Case Media Pearls - Obstructive Cardiogenic ShocK Tetralogy of Fallot is the most common cyanotic defect and can lead to long term complications after surgical repair including chronic pulmonary insufficiency, RV dysfunction, residual RVOT obstruction and branch pulmonary artery stenoses. Chronic RV failure may be more indicative of a structural defect and therefore require interventional or surgical management. Valve thrombosis, infective endocarditis and obstructive pannus formation should be considered in the differential of a patient with obstructive shock with a prosthetic valve. Bioprosthetic pulmonic valve obstruction may be effectively managed with balloon valvuloplasty in patients who present in acute extremis but TCPV will likely provide a more lasting result. While valvular gradients are typically assessed via echocardiography, invasive hemodynamics can serve as a critical adjunctive tool in its characterization. Show Notes - Obstructive Cardiogenic ShocK Notes were drafted by Drs. Omkar Betageri, Philip Lacombe, Cashel O’Brien, and Andrew Geissler. What are the common therapies and management for Tetralogy of Fallot? Tetralogy of Fallot is the most common cyanotic defect in children beyond the age of one year Anatomic Abnormalities: Anterior and Superior deviation of the conal septum creating a SubAo VSD and encroachment on the RVOT. The Ao follows the conal septum anteriorly to override the VSD and RVH is a consequence of an RV chamber that is at systemic pressure. The need for medical intervention is dependent on the degree of RVOT obstruction, pulmonary regurgitation, and/or peripheral pulmonary artery obstruction. Many patients are minimally cyanotic in newborn period and clinical follow-up with elective surgical correction between 3 months and 6 months of age is a preferred approach. Total surgical correction typically involves placing patients on cardiopulmonary bypass, relieving right sided obstruction (sometimes utilizing trans-annular patch), and connecting left ventricular blood flow with aortic, with VSD closure. Hypercyanotic “Tet” spells can occur in the neonatal period when there is an acute muscular spasm in the RVOT, fall in SVR or increase in PVR to facilitate right to left shunting at the VSD. It is managed medically with a stepwise approach placing the patient in knee-chest position, administer oxygen, IV fluids and a dose of narcotics, IV beta blocker, IV phenylephrine, ECMO Long term complications post-surgical repair include chronic pulmonary insufficiency, RV dysfunction, residual RVOT obstruction, peripheral PA obstruction, aortic root dilation, endocarditis, arrhythmias, and sudden cardiac death. How should we approach the management of chronic right ventricular failure? Briefly, RV failure can result in chamber dilatation, bowing of the interventricular septum to the LV, impairing LV stroke volume, and ultimately causing hemodynamic collapse. This is the frequently referenced “RV spiral” The primary step in management of RV cardiogenic shock should be to identify and reverse the primary etiology While patients in acute RV failure may respond well to therapies such as fluid resuscitation, inotropes and vasopressors, or inhaled nitric oxide, patients with chronic RV failure (such as in our case) are more likely to have structural defects driving their decompensation Chronic RV failure can result from etiologies related to preload (ASD, tricuspid and pulmonic insufficiency), afterload (pulmonic or pulmonary artery stenosis, pulmonary vascular disease, and left heart disease) or contractility (RV myopathy or ARVC).VSD is not volume loading to RV and Eisenmenger’s would be a pressure load b/c of increased PVR and actually volume unload the RV with R to L VSD shunting. In acute stabilization, it is reasonable to utilize methods used to manage acute RV failure, with the understanding that interventional/surgical management will ultimately be necessary for definitive management When should bioprosthetic valve obstruction be suspected and what is the differential for this? What is the initial workup? Obstruction should be suspected in any patient with a history of prosthetic valve placement who presents with a new murmur, new history of exercise intolerance, syncope/presyncope, or evidence of heart failure on exam. Differential diagnosis includes pannus ingrowth, thrombus, and vegetation. The anterior location of a surgically replaced RVOT/PV also makes it susceptible to compressive forces from the chest wall anteriorly and dilated Ao posteriorly, particularly in growing children. For bioprosthetic valves pannus is more common than acute thrombosis. Age of the valve, risk factors for infection, and anticoagulation status are clinical signs that may help differentiate. Diagnosis is typically made by transthoracic echocardiology (TTE): Increased gradients across the PV, RV hypertrophy, dilatation or dysfunction, increasing TR volume with elevated gradients from RV to RA. Cardiac CT or CMRI can also be helpful in characterizing the stenosis (discreet or long-segment, singular or stenoses in series). Invasive hemodynamic assessment in the catheterization laboratory can be especially helpful to more specifically characterize the degree and location of the obstruction as well as perform intervention (balloon, stent placement, TCPV) to relieve the obstruction. It is not uncommon that distal pulmonary artery stenting is required at the time of ballooning of the valve or valve-in-valve TCPVR. Lab testing sometimes performed includes INR, hemoglobin level, hemolysis labs, NT-BNP. If acute thrombosis of the bioprosthetic valve is diagnosed, a hypercoaguable work-up to include familial thrombophilia should be performed FDG PET may be an adjunctive tool to help evaluate for prosthetic valve endocarditis by detection of acute inflammation. What are the indications for management of valve obstruction? What are the primary management strategies? As previously discussed the differential diagnosis of bioprosthetic valve obstruction includes BPVT, pannus, and vegetation. Valve intervention is indicated for symptomatic severe stenosis and treatment strategy depends on the underlying cause. BPVT: If stable, can trial anticoagulation therapy. If unstable immediate therapy is required which requires surgery or fibrinolytics. Pannus: Severe stenosis caused by soft tissue overgrowth with degeneration and calcium requires stenting open the obstructive valve in the catheterization laboratory followed by a valve-in-valve TCPV placement. It is increasingly rare that an obstructed bioprosthetic PV cannot be managed in this fashion and surgical PVR is needed. Medical therapy is ineffective in treating the underlying cause although can treat consequences from heart failure. Vegetation: Endocarditis with vegetation causing severe stenosis is usually treated with surgical intervention. Decisions regarding surgical indications for endocarditis are complex and a trial of medical therapy is reasonable in less severe disease. For native pulmonic valve obstruction many patients are amenable to balloon valvuloplasty and recurrent stenosis is rare. Patients are usually left with some degree of pulmonic insufficiency.

May 13, 2024

CardioNerds Co-Founder Dr. Daniel Ambinder, Episode Chair Dr. Dinu Balanescu, and FIT Lead Dr. Natalie Tapaskar discuss advanced heart failure in CardioOncology with expert Dr. Richard Cheng. Audio editing by CardioNerds Academy Intern, Dr. Akiva Rosenzveig. In this episode, we discuss the spectrum of advanced heart failure in patients with a history of cancer. We dissect cancer therapy-related cardiac dysfunction (CTRCD) cases and the imaging and biomarker tools available for risk stratification and disease monitoring. We delve into the data on the use of guideline-directed medical therapy (GDMT) and cardiac resynchronization therapy (CRT) in these patients. We discuss the risk of prior radiation and chemotherapy during cardiac surgery. Finally, we learn about the post-transplant risk of rejection, recurrent malignancy, and de-novo malignancies, as well as treatment strategies we can employ for these patients. This episode is supported by a grant from Pfizer Inc. This CardioNerds Cardio-Oncology series is a multi-institutional collaboration made possible by contributions of stellar fellow leads and expert faculty from several programs, led by series co-chairs, Dr. Giselle Suero Abreu, Dr. Dinu Balanescu, and Dr. Teodora Donisan. CardioNerds Cardio-Oncology PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls and Quotes - Advanced Heart Failure in CardioOncology Use the HFA-ICOS risk tool to understand the baseline risk of developing cancer therapy-related cardiac dysfunction (CTRCD). Key factors are type of cancer therapy, baseline CV risk factors, and age. A relative change in global longitudinal strain of more than 15% from baseline is a marker of early cardiac dysfunction and predicts the subsequent risk for systolic dysfunction in patients undergoing cardiotoxic chemotherapy. Statins may be useful in prevention of cardiovascular dysfunction in patients receiving anthracycline chemotherapy. There is limited data on the 4 pillars of GDMT in prevention of CTRCD, but should be started early once CRTCD is suspected or diagnosed! Mediastinal radiation causes adhesions and scarring which increase the risk of bleeding during cardiac surgery, lead to longer operative times, and can lead to RV failure and poor wound healing. Patients with a pre-transplant history of malignancy have a higher risk of mortality due to post-transplant malignancy. And patients with active cancer should not be considered for heart transplant. Post-transplant malignancy risk can be mitigated by utilizing an mTOR based, CNI free immunosuppression regimen. Show notes - Advanced Heart Failure in CardioOncology How do cardio-oncology and advanced heart failure intersect? There are 3 basic populations of patients to consider:Patients with advanced heart failure who develop cancer.Patients with pre-existing chemotherapy and radiation exposure for cancer treatment who later develop advanced heart failureHeart transplant recipients who, in the long term are at very high risk of developing cancer Cardio-oncologists must consider risk assessment and mitigation, long-term prognosis, and treatment strategies for each of these unique populations. How can we assess the risk of developing cardiovascular disease during cancer treatment (CTRCD)? There are many proposed risk tools. However, the majority are not well-validated. One of the most used tools is the HFA-ICOS risk tool.1You can select the planned cancer therapy for the patient (anthracyclines, HER-2, VEGF, RAF/MEK inhibitors, Kinase inhibitors, multiple myeloma therapies) and then calculate their risk of developing CV disease during cancer treatment based on baseline variables:1) previous history of CV disease,2) biomarkers – troponin and NT-proBNP3)age,4) CV risk factors -HTN, DM, CKD,5) previous cardio-toxic treatments,6) lifestyle risk factors- smoking, obesity The risk tool will then give you a ranking of very high, high, medium, or low risks. How should we use imaging to evaluate cardiac dysfunction in patients undergoing cancer treatments? Echo with global longitudinal strainA relative change in global longitudinal strain of more than 15% from baseline is a marker of early cardiac dysfunction and predicts the subsequent risk for systolic dysfunction.Data are mixed on the benefit of intervening on drops in GLS without a concomitant drop in LVEF. Current vendor software has improved the consistency in GLS measurements across vendors, which used to be quite problematic.Echo LVEFSome centers prefer to use 3D LVEF to track patients over time.For asymptomatic high-risk patients, we should obtain echocardiograms at 1, 3, and 5 years post-cancer therapies and then every 5 years thereafter.But surveillance should occur on a case-by-case basis. CPETCan be used to risk stratify patients with lung or colon cancer before starting cancer treatment.You can trend peak VO2 over time after cancer treatments. However, this is generally a data-sparse zone! Can we use serum biomarkers such as troponin or NT-proBNP in monitoring for the development of CTRCD? Elevations in BNP during cancer treatment are associated with subsequent cardiovascular disease.Elevations in troponin and myeloperoxidase in breast cancer patients receiving anthracyclines can predict the risk of cardiotoxicity. Novel biomarkers – data-free zoneCRP is a marker of inflammation and may be helpful in patients undergoing radiation therapy.Immunoglobulins- baseline elevated IgE levels have a lower risk for cardiotoxicity. Cell-free DNA – may be the future? What is the role of cardiovascular medications and devices in preventing and treating CTRCD? Prevention:Statins – The STOP-CA trial showed that use of atorvastatin 40 mg/day in patients with lymphoma receiving anthracycline chemotherapy reduced the incidence of cardiac systolic dysfunction compared to placebo.2SGLT2i – limited retrospective data in patients with diabetes and anthracycline chemotherapy. May have lower rates of cardiac events on SGLT2i.Currently there is not enough data to recommend routine use of SGLT2i, ARNI, and BB for cardioprotection before cancer therapies. Treatment: Treat these patients similarly to other heart failure patients. The four pillars of GDMT work! Early recognition is critical to confer better long-term outcomes. CRT-D: MADIT-CHIC3 showed that CRT therapy improved LVEF at 6 months in patients with chemotherapy-induced cardiomyopathy.Only consider ICD if life expectancy is >1 year.There is a risk of device reset for radiation directly over the device. ICDs are more sensitive to ionizing radiation, leading to inappropriate shocks. Can consider moving the device to a non-radiation field. What do we need to consider when patients with a history of cancer are being evaluated for heart transplant and left ventricular assist device (LVAD)? Heart transplantPatients with chemo-induced cardiomyopathy have no differences in post-transplant outcomes compared to patients with other causes of cardiomyopathy.Patients with a pre-transplant history of malignancy have a higher risk of mortality due to post-transplant malignancy, particularly in those with a history of hematologic malignancy.Patients with active cancer should not be considered for heart transplant.The duration and interval of waiting after active cancer before a heart transplant depends on the type and stage of cancer. LVADPatients with chemotherapy-induced cardiomyopathy have similar outcomes and rates of post-LVAD RV dysfunction as patients with other etiologies of cardiomyopathy. Limited data on performing LVAD in patients with active cancer. What risk does prior mediastinal radiation pose to cardiac surgery? Mediastinal radiationIncreases adhesions and scarring, increasing the risk of bleeding during cardiac surgery. Longer operative times may also increase the risk of RV failure. There can also be atrophy of sternal muscles, which can lead to poor wound healing What do the post-heart transplant rejection and malignancy profiles look like for patients with a history of chemotherapy-induced cardiomyopathy? Patients with prior chemotherapy have depressed immunosurveillance from their innate immune system and, thus, may have a lower risk of rejection. But there is limited data here. Patients with a history of pre-transplant malignancy are at increased risk of recurrence and PTLD. You can consider decreasing immunosuppression or switching to mTOR inhibitor-based regimen to reduce the risk. What must we know about de-novo malignancy post-heart transplant? Risk factors: history of prior malignancy, heavier immunosuppression, older recipient age, smoking history, radiation exposure, genetic variants.Treatment: reduce immunosuppression as much as possible and switch to an mTOR-based regimen. What about immune checkpoint inhibitors post-transplant? These work by upregulating T cell activity, which counteracts our transplant immunosuppression. High risk of rejection, but some successful case reports of use. References - Advanced Heart Failure in CardioOncology Lyon AR, Dent S, Stanway S, et al. Baseline cardiovascular risk assessment in cancer patients scheduled to receive cardiotoxic cancer therapies: a position statement and new risk assessment tools from the C ardio‐ O ncology S tudy G roup of the H eart F ailure A ssociation of the E uropean S ociety of C ardiology in collaboration with the I nternational C ardio‐ O ncology S ociety. Eur J Heart Fail. 2020;22(11):1945-1960. doi:10.1002/ejhf.1920 Neilan TG, Quinaglia T, Onoue T, et al. Atorvastatin for Anthracycline-Associated Cardiac Dysfunction: The STOP-CA Randomized Clinical Trial. JAMA. 2023;330(6):528. doi:10.1001/jama.

May 7, 2024

CardioNerds, Dr. Richard Ferraro and Dr. Dan ambinder join Dr. Li Pang, Dr. Emily Hendricks, and Dr. Bei Jiang from West Virginia University to discuss the following case that features apical obliteration with biventricular thrombus. Dr. Christopher Bianco provides the Expert CardioNerd Perspectives & Review (E-CPR) for this episode. Audio editing by CardioNerds Academy Intern, student doctor Tina Reddy. A 37-year-old Caucasian man with a history of tobacco smoking and hypertension who presented with chest pain and elevated troponin was admitted for non-ST elevation myocardial infarction (NSTEMI). Ischemic evaluation with an invasive coronary angiogram was negative. He was treated as NSTEMI and scheduled for outpatient cardiac MRI (CMR). The patient came back 2 months later with right arm weakness and confusion and was found to have an embolic stroke. Labs showed positive troponin with a flat trend and hypereosinophilia. Transthoracic echocardiogram (TTE) showed obliteration of LV and RV apex with thrombus and reduced LV systolic function. CMR was consistent with myocarditis with biventricular thrombus. The patient was started on corticosteroids and warfarin. Hypereosinophilia workup was positive for PDGFRA alpha rearrangement. He was diagnosed with primary hypereosinophila syndrome. Imatinib was initiated. The patient was followed up with the hematology clinic, achieved a complete hematologic response with normalized cell count, and remained free from any cardiovascular event at the 8-month follow-up. US Cardiology Review is now the official journal of CardioNerds! Submit your manuscript here. CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Case Media Pearls - Apical Obliteration with Biventricular Thrombus Cardiac MRI is a valuable test for patients presenting with myocardial infarction with non-obstructive coronary arteries (MINOCA). Obliterated apex with apical thrombus on TTE with hypereosinophilia should raise high suspicion for eosinophilic myocarditis. Initiation of corticosteroids is the first-line treatment for eosinophilic myocarditis, which is associated with lower mortality in patients with myocarditis. For other potential complications, such as heart failure, intracardiac thrombus, arrhythmia, and pericardial effusion, the standard of care for each disorder is recommended. Hypereosinophilia can be seen in parasitic infections, vasculitis, asthma, allergy, hematological malignancies, and as a primary disorder. Show Notes - Apical Obliteration with Biventricular Thrombus What is the differential diagnosis for patients with elevated troponin and nonobstructive CAD? The occurrence of acute myocardial infarction (AMI) without significant CAD was reported 80 years ago. However, the term MINOCA (myocardial infarction with non-obstructive coronary arteries) has only been used recently to describe these patients. It involves ischemic and nonischemic etiologies. First, overlooked ischemic etiologies need to be ruled out by reconciling the angiogram images such as spontaneous coronary artery dissection (SCAD) and plaque disruption. Intracoronary imaging, such as intravascular ultrasound (IVUS) or optical coherence tomography (OCT), may be applied to evaluate for SCAD and subtypes of plaque disruption when indicated. The investigation continues with nonischemic causes such as stress cardiomyopathy, myocarditis, pulmonary embolism, demand ischemia from sepsis, anemia, chest trauma, heart failure exacerbation, arrhythmia, and stroke. The diagnosis of MINOCA is established when it fulfills the following criteria: First, it is AMI by the Fourth Universal Definition; Second, less than 50% of stenotic lesion on angiogram; Third, there is no alternate diagnosis. MINOCA etiologies include coronary artery spasms and microvascular dysfunction. It is recommended to perform CMR in all MINOCA patients without an obvious underlying cause. What are the common causes of LV thrombus? The incidence of LV thrombus has been reported between 4-39% after anterior MI. The temporal incidence has been decreasing. It is also commonly seen in dilated cardiomyopathy with an incidence of 2-36%. The pathophysiology of intracardiac thrombus formation obeys Virchow’s triad rule, which states that endocardial injury, hypercoagulability/inflammation, and stasis lead to thrombogenesis. Other etiologies of LV thrombus include eosinophilic myocarditis and LV noncompaction. What are the characteristic echocardiographic and CMR findings of eosinophilic myocarditis (EM)? During the acute necrotic stage, there is increased subendocardial echogenicity, wall thickening, impaired regional wall motion, and pericardial effusion; there is edema without fibrosis on CMR. During the thrombotic stage, intracardiac thrombus is often detected in the ventricles on TTE; on CMR, there is endomyocardial involvement and intracardiac thrombus. During the fibrotic stage, in addition to the cumulative findings from previous stages, restrictive physiology, valvular thickening, and restricted motion can occur on TTE; on CMR, endomyocardial fibrosis with LGE is present. What is the management for eosinophilic myocarditis (EM)? Two aspects must be considered in the treatment of eosinophilic myocarditis: the management of acute cardiac conditions and the treatment of underlying causes. Corticosteroids are the first-line treatment for EM. A meta-analysis of 179 cases showed that steroid use is associated with a lower mortality rate. No clinical trial data are available for the treatment of eosinophilic myocarditis. The dose and duration of corticosteroids in each individual case can be different. For intracardiac thrombus, vitamin K antagonists (VKAs) are the drugs of choice. Complete gradual resolution of intracardiac thrombus with VKA in eosinophilic myocarditis was reported at the 18-month follow-up. The INR target was 2-3. Emerging data showed the noninferiority of using DOAC for LV thrombus compared to warfarin as an alternative for stroke prevention. There is an increased risk of stroke in patients on VKA but with subtherapeutic INR levels. The guidelines recommend DOAC as a reasonable alternative to VKA to treat LV thrombus. For other potential complications such as heart failure, intracardiac thrombus, arrhythmia, and pericardial effusion, the standard of care for each complication is recommended. There is no large data to suggest a specific approach in eosinophilic myocarditis. It has been reported to achieve full recovery with GDMT in addition to treating the underlying cause in a case report of eosinophilic myocarditis with severely reduced LV systolic function. What is hypereosinophilic syndrome (HES)? HES is pleomorphic in clinical presentation and can be idiopathic or associated with a variety of underlying conditions, including allergic, rheumatologic, infectious, and neoplastic disorders. There are 4 groups. In primary HES, the hypereosinophilia is driven by a clonal process in stem cell or myeloid lineage. Patients usually present with a myeloid neoplasm and myeloid proliferative disorder. Besides eosinophilia, they may have other cytopenias, blasts, or dysplastic cells in peripheral blood. They can present with constitutional symptoms or hepatosplenomegaly. Some of these patients have disease-defining mutations or chromosome translocation. They require treatment for their underlying hematologic condition. Secondary HES usually have polyclonal eosinophilia secondary to some stimulus. The stimulus may be infections, rheumatology conditions, solid tumors, and lymphoid neoplasm. The underlying condition increases eosinophilic cytokines leading to an increase in eosinophil production. The third group is familial HES results from certain genetic factors. If no cause of HES can be identified, they fall into the category of idiopathic HES. Patients with HES secondary to myeloid and lymphoid disorders need to follow up with a hematology specialist. References - Apical Obliteration with Biventricular Thrombus Bondue A, Carpentier C, Roufosse F. Hypereosinophilic syndrome: considerations for the cardiologist. Heart 2022;108:164-171. Merlo M, Gagno G, Baritussio A et al. Clinical application of CMR in cardiomyopathies: evolving concepts and techniques : A position paper of myocardial and pericardial diseases and cardiac magnetic resonance working groups of Italian society of cardiology. Heart Fail Rev 2023;28:77-95. Murthy SB. Troponin Elevation After Ischemic Stroke and Future Cardiovascular Risk: Is the Heart in the Right Place? Journal of the American Heart Association 2021;10:e021474. Dhaliwal JSS, Ansari SA, Ghosh S, Chitkara A, Khizer U. Duet of Death: Biventricular Thrombus in a Methamphetamine User. Cureus 2023;15:e39917. Levine GN, McEvoy JW, Fang JC et al. Management of Patients at Risk for and With Left Ventricular Thrombus: A Scientific Statement From the American Heart Association. Circulation 2022;146:e205-e223. Parrillo JE. Heart Disease and the Eosinophil. New England Journal of Medicine 1990;323:1560-1561. Wright BL, Leiferman KM, Gleich GJ. Eosinophil Granule Protein Localization in Eosinophilic Endomyocardial Disease. New England Journal of Medicine 2011;365:187-188. Polte CL, Bobbio E, Bollano E et al. Cardiovascular Magnetic Resonance in Myocarditis. Diagnostics 2022;12:399. Ammirati E, Frigerio M, Adler ED et al. Management of Acute Myocarditis and Chronic Inflammatory Cardiomyopathy: An Expert Consensus Document. Circ Heart Fail 2020;13:e007405. Ito S, Isotani A, Yamaji K, Ando K. Follow-up magnetic resonance imaging of Löffler endocarditis: a case report.

May 5, 2024

CardioNerds (Drs. Richard Ferraro, Gurleen Kaur, and Rupan Bose) discuss the growing epidemic of obesity and dive into the role of its procedural management with Dr. Steve Nissen, Chief Academic Officer at the Cleveland Clinic HVTI and past president of the American College of Cardiology. This is an exciting topic that reflects a major inflection point in cardiovascular care. In this episode, we discuss the importance of addressing obesity in cardiovascular care, as it is a major driver of cardiovascular disease and the progression of associated cardiovascular comorbidities. We look at the role of bariatric surgery and its ability to produce sustained weight loss. Finally, we look into the emerging role of new medical therapies such as GLP1 and GIP agonist medications. Notes were drafted by Dr. Rupan Bose and episode audio was edited by CardioNerds Intern Dr. Atefeh Ghorbanzadeh. This episode was produced in collaboration with the American Society of Preventive Cardiology (ASPC) with independent medical education grant support from Novo Nordisk. See below for continuing medical education credit. Claim CME for this episode HERE. CardioNerds Prevention PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls and Quotes - Procedural Management of Obesity with Dr. Steve Nissen Obesity is associated with adverse cardiovascular outcomes. Returning to a healthy weight can largely prevent the downstream consequences of obesity. Regarding lifestyle modifications, diet alone is insufficient in sustaining prolonged weight loss. It is associated with short-term weight loss, but it is generally necessary to supplement with exercise and activity to ensure sustained weight loss. Bariatric surgery should be considered for patients with BMI ≥40 kg/m2 or BMI ≥35 kg/m2 with obesity-related comorbid conditions who are motivated to lose weight and who have not responded to behavioral treatment with or without pharmacotherapy. New emerging medications, including GLP1 receptor agonists, GIP receptor agonists, and glucagon receptor agonists, are beginning to approach weight loss levels that were previously only seen with bariatric surgery. Further research in this dynamic area is ongoing. Show notes - Procedural Management of Obesity with Dr. Steve Nissen Notes drafted by Dr. Rupan Bose. What is the role of obesity in the burden of cardiovascular disease, and why is it so important for CardioNerds to address it? According to the AHA, approximately 2.8 to 3.5 billion people worldwide are either overweight or obese. It is estimated that by 2030, 30% of people in the US will have a BMI greater than 30. Adipose tissue is associated with cytokine release. Cytokines, in turn, can activate and increase levels of IL-1 beta, IL-6, and CRP, leading to an increased inflammatory state. This pro-inflammatory state then accelerates the rate of cardiovascular disease. Obesity is also associated with significant joint and orthopedic diseases, which further impact patients’ quality of life and morbidity. Additionally, obesity is associated with NASH cirrhosis. These adverse liver outcomes hold additional significant systemic implications and morbidity. How do you determine one’s goal weight and goal BMI? Is BMI a good standard for measuring obesity? BMI is a variable of both weight and height. However, it cannot differentiate those whose weight is from adipose tissue versus from muscle mass. Therefore, BMI measurements can sometimes be misleading. Waist circumference may be a better measurement standard for obesity and risk assessment. The “apple shape” body type, with more abdominal fat, is associated with higher inflammation and cardiovascular risk than the “pear-shaped” body type, which is where there is more fat deposition in the buttocks and thighs. A fat distribution that is more centralized corresponds with greater cardiovascular risk. “Normal” BMI and “normal” waist circumference can differ based on ethnicity. For example, a BMI of 22.6 in South Asians carries a similar risk to a BMI of 30 in White European patients. Therefore, providers must remain cognizant of these differences when making individual patient recommendations. Does childhood obesity correlate with obesity at later ages? At what age should we start screening for and addressing obesity? Childhood obesity, or obesity at a young age, often correlates with continued obesity later in life. But it is interesting that if one can return to a healthy body weight at some point in their life, one can largely prevent the downstream consequences of obesity The USPSTF recommends clinicians screen for obesity in children and adolescents age 6 and older and offer behavioral interventions to promote improvements in weight status (grade B recommendation) What procedures or surgeries are available to patients with obesity? Bariatric surgery is an excellent option with great outcomes if done for the right patient. The 2013 AHA/ACC/TOS guidelines for the management of overweight and obesity in adults recommend bariatric surgery for patients with BMI ≥40 kg/m2 or BMI ≥35 kg/m2 with obesity-related comorbid conditions who are motivated to lose weight and who have not responded to behavioral treatment with or without pharmacotherapy. Several studies have shown that patients with bariatric surgery had a huge reduction in myocardial infarction, stroke, kidney disease, and death. Bariatric surgery can help address other cardiovascular comorbidities. For example, the STAMPEDE trial (Schauer, R et al.) demonstrated that bariatric surgery plus intensive medical therapy was more effective than intensive medical therapy alone in decreasing or, in some cases, resolving hyperglycemia. Additionally, the magnitude of weight loss from bariatric surgery is often greater than the absolute magnitude of weight loss through medical therapy alone. Therefore, for patients with a very high BMI, bariatric surgery may be better suited to achieve the necessary weight loss. What emerging medications are available to patients with obesity? And what medications are just around the corner? GLP1 agonists, or dual GIP-GLP1 receptor agonists, drugs are associated with approximately 20% reduction in body weight. In the SELECT trial, semaglutide was associated with a 9.3% reduction in body weight (Please see GLP1 series for additional details!). In the SURMOUNT-1 trial, tirzepatide was associated with a 22% reduction in body weight. Future trials will look at triple agonists that combine GLP1, GIP, and glucagon agonist properties. One such drug is retatrutide, which previously demonstrated a 24% (and approximately 28.5% in females) reduction in body weight. These medications are approaching similar weight loss magnitudes to bariatric surgery (a Roux en Y procedure achieves approximately 25% weight loss on average), though additional studies are ongoing. What other strategies can one use to lower body weight and maintain that weight loss? Diet alone is not sustainable in reducing weight and keeping weight off. Unfortunately, the body subconsciously activates adaptive responses that down-regulate metabolism, which in turn burns fewer calories. Therefore, exercise and activity play a key role in continuing to burn calories, allowing for sustained weight loss. All patients should, therefore, be counseled on both diet and exercise strategies to address obesity and weight loss. Discussing weight and body image is often a sensitive subject and can carry a stigma for some patients. What are some recommendations on how we can address these topics in a safe and supportive manner? It is important to create a safe, supportive, and non-judgmental space when discussing weight with patients. We should also make an effort to understand the specific drivers of each individual patient’s weight gain. Some drivers include emotional stress, socio-economic factors, lifestyle barriers, etc. By understanding each specific driver, we can be more targeted in our approach and build more individualized plans with our patients. We can also recruit other clinical team members to assist the patient in their weight loss journey. Some such teammembers include dieticians, psychiatrists, social workers, etc. References - Procedural Management of Obesity with Dr. Steve Nissen Jastreboff, A. M., Aronne, L. J., Ahmad, N. N., Wharton, S., Connery, L., Alves, B., ... & Stefanski, A. (2022). Tirzepatide once weekly for the treatment of obesity. New England Journal of Medicine, 387(3), 205-216. https://www.nejm.org/doi/full/10.1056/NEJMoa2206038 Lincoff, A. M., Brown-Frandsen, K., Colhoun, H. M., Deanfield, J., Emerson, S. S., Esbjerg, S., ... & Ryan, D. H. (2023). Semaglutide and cardiovascular outcomes in obesity without diabetes. New England Journal of Medicine. https://www.nejm.org/doi/full/10.1056/NEJMoa2307563 Schauer, P. R., Bhatt, D. L., Kirwan, J. P., Wolski, K., Aminian, A., Brethauer, S. A., ... & Kashyap, S. R. (2017). Bariatric surgery versus intensive medical therapy for diabetes—5-year outcomes. New England Journal of Medicine, 376(7), 641-651. https://www.nejm.org/doi/full/10.1056/nejmoa1600869 Jensen, M. D., Ryan, D. H., Apovian, C. M., Ard, J. D., Comuzzie, A. G., Donato, K. A., ... & Yanovski, S. Z. (2014). 2013 AHA/ACC/TOS guideline for the management of overweight and obesity in adults: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and The Obesity Society. Journal of the American college of cardiology, 63(25 Part B), 2985-3023. Powell-Wiley, T. M., Poirier, P., Burke, L. E., Després, J. P., Gordon-Larsen, P., Lavie, C. J., ...

May 3, 2024

CardioNerds (Drs. Gurleen Kaur and Richard Ferraro) and episode FIT Lead Dr. Spencer Carter (Cardiology Fellow at UT Southwestern) discuss the clinical implementation of GLP-1 receptor agonists with Dr. Neha Pagidapati (Faculty at Duke University School of Medicine). In this episode of the CardioNerds Cardiovascular Prevention Series, we discuss the clinical implementation of glucagon-like peptide-1 (GLP-1) receptor agonists. We cover the clinical indications, metabolic and cardiovascular benefits, and potential limitations of these emerging and exciting therapies. Show notes were drafted by Dr. Spencer Carter. Audio editing was performed by CardioNerds Academy Intern, student Dr. Pacey Wetstein. This episode was produced in collaboration with the American Society of Preventive Cardiology (ASPC) with independent medical education grant support from Novo Nordisk. See below for continuing medical education credit. Claim CME for this episode HERE. CardioNerds Prevention PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls and Quotes - Clinical Implementation of GLP-1 Receptor Agonists GLP-1 agonists work through a variety of mechanisms to counteract metabolic disease. They increase insulin secretion, inhibit glucagon secretion, slow gastric motility, and increase satiety to limit excess energy intake. Patients with type II diabetes and an elevated risk for atherosclerotic cardiovascular disease should be considered for GLP-1 agonist therapy regardless of hemoglobin A1c. GLP-1 agonists offer significant ASCVD risk reduction even in the absence of diabetes. Newer data suggest a significant reduction in cardiovascular events with GLP-1 agonist therapy in patients who are overweight or obese and have a prior history of heart disease. GLP-1 agonists should generally be avoided in patients with a history of medullary thyroid cancer or MEN2. As these medications slow gastric emptying, relative contraindications include history of recurrent pancreatitis and gastroparesis. GLP-1 agonists should be initially prescribed at the lowest dose and slowly uptitrated to avoid gastrointestinal side effects. Show notes - Clinical Implementation of GLP-1 Receptor Agonists What were the groundbreaking findings of the STEP1 and SURMOUNT-1 trials and how these impact cardiovascular wellness? The STEP1 and SURMOUNT trials demonstrated sustained clinically relevant reduction in body weight with semaglutide and tripeptide, respectively, in patients with overweight and obesity. As obesity is an important risk factor for the development of cardiovascular disease, weight reduction meaningfully contributes to cardiovascular wellness. What were the findings of the LEADER trial and their implications for patients with type II diabetes and high cardiovascular risk? The LEADER trial demonstrated a significant reduction in the rate of cardiovascular death, nonfatal MI, or nonfatal stroke in patients with type II diabetes treated with liraglutide. GLP-1 receptor agonist therapy should be considered in all patients with type II diabetes and elevated ASCVD risk regardless of A1c or current hyperglycemic therapy. What are current indications for GLP1 agonists in the context of cardiometabolic disease. GLP-1 receptor agonists should be considered in patients with type II diabetes and high ASCVD risk OR patients without diabetes who are overweight/obese and have a history of cardiovascular disease. What are important side effects or contraindications to GLP1 agents when used for cardiovascular risk reduction and wellness? GLP-1 receptor agonists should be avoided in patients with a history of medullary thyroid cancer or MEN2. Relative contraindications include recurrent pancreatitis, gastroparesis, or ongoing unexplained gastrointestinal symptoms. What are practical concerns associated with GLP-1 use, and how can these be overcome? Affordability and availability remain the leading practical limitations for GLP-1 receptor agonist therapies. Many insurance companies will cover semaglutide and tirzepatide for patients with diabetes. Obtaining coverage may be difficult otherwise, but this is an evolving field as more clinical trial data emerge. Beware of unauthentic/alternate formulations of these medications, as they tend not to be FDA-regulated and can pose health risks. Some patients express concern about injectable therapies, but GLP-1 injectors are typically very well tolerated and easy to use. References - Clinical Implementation of GLP-1 Receptor Agonists Brown, E., Heerspink, H. J., Cuthbertson, D. J., & Wilding, J. P. (2021). SGLT2 inhibitors and GLP-1 receptor agonists: established and emerging indications. The Lancet, 398(10296), 262-276. https://www.sciencedirect.com/science/article/pii/S0140673621005365 Wilding, J. P., Batterham, R. L., Calanna, S., Davies, M., Van Gaal, L. F., Lingvay, I., ... & Kushner, R. F. (2021). Once-weekly semaglutide in adults with overweight or obesity. New England Journal of Medicine. https://www.nejm.org/doi/full/10.1056/NEJMoa2032183 Müller, T. D., Blüher, M., Tschöp, M. H., & DiMarchi, R. D. (2022). Anti-obesity drug discovery: advances and challenges. Nature Reviews Drug Discovery, 21(3), 201-223. https://www.nature.com/articles/s41573-021-00337-8 Jastreboff, A. M., Aronne, L. J., Ahmad, N. N., Wharton, S., Connery, L., Alves, B., ... & Stefanski, A. (2022). Tirzepatide once weekly for the treatment of obesity. New England Journal of Medicine, 387(3), 205-216. https://www.nejm.org/doi/full/10.1056/NEJMoa2206038 Lincoff, M, Brown-Frandsen K, Colhoun H, et al. Semaglutide and Cardiovascular Outcomes in Obesity without Diabetes. (2023). 389(24):2221-2232. https://www.nejm.org/doi/full/10.1056/NEJMoa2307563 Eberly, L, Yang L, Essien U, et al. (2021). Racial, ethnic, and socioeconomic inequities in glucagon-like-peptide-1 receptor agonist use among patients with diabetes in the US; 2(12):e214182. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8796881/

Apr 25, 2024

CardioNerds (Dr. Dan Ambinder), Dr. Nino Isakadze (EP Fellow at Johns Hopkins Hospital), and Dr. Karan Desai (Cardiology Faculty at Johns Hopkins Hospital) join Digital Health Experts, Dr. Alexis Beatty (Cardiologist and associate professor in the department of epidemiology and biostatistics at UCSF) and Dr. Seth Martin (Director of the Johns Hopkins Center for Mobile Technologies to Achieve Equity in Cardiovascular Health (mTECH), which is part of the American Heart Association (AHA) Strategically Focused Research Networks on Health Technology & Innovation) for another installment of the Digital Health Series. In this specific episode, we discuss pearls, pitfalls, and everything in between for emerging digital health innovators. This series is supported by an ACC Chapter Grant in collaboration with Corrie Health. Audio editing by CardioNerds Academy Intern, student doctor Shivani Reddy. In this series, supported by an ACC Chapter Grant and in collaboration with Corrie Health, we hope to provide all CardioNerds out there a primer on the role of digital heath in cardiovascular medicine. Use of versatile hardware and software devices is skyrocketing in everyday life. This provides unique platforms to support healthcare management outside the walls of the hospital for patients with or at risk for cardiovascular disease. In addition, evolution of artificial intelligence, machine learning, and telemedicine is augmenting clinical decision making at a new level fueling a revolution in cardiovascular disease care delivery. Digital health has the potential to bridge the gap in healthcare access, lower costs of healthcare and promote equitable delivery of evidence-based care to patients. This CardioNerds Digital Health series is made possible by contributions of stellar fellow leads and expert faculty from several programs, led by series co-chairs, Dr. Nino Isakadze and Dr. Karan Desai. Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. CardioNerds Digital Health Series PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron!

Apr 22, 2024

Immunotherapy is a type of novel cancer therapy that leverages the body’s own immune system to target cancer cells. In this episode, we focused on the most common type of immunotherapy: immune checkpoint inhibitors or ICIs. ICIs are monoclonal antibodies targeting immune “checkpoints” or brakes to enhance T-cell recognition against tumors. ICI has become a pillar in cancer care, with over 100 approvals and 5,000 ongoing trials. ICIs can lead to non-specific activation of the immune system, causing off-target adverse events such as cardiotoxicities. ICI-related myocarditis, though less common, can be fatal in 30% of cases. Clinical manifestations vary but can include chest pain, dyspnea, palpitations, heart failure symptoms, and arrhythmias. Diagnosis involves echocardiography, cardiac MRI, and endomyocardial biopsy. Treatment includes high-dose corticosteroids with potential additional immunosuppressants. Baseline EKG and troponin are recommended before ICI initiation, but routine surveillance is not advised. Subclinical myocarditis is a challenge, with unclear management implications. So let’s dive in and learn about cardiotoxicity of novel immunotherapies with Drs. Giselle Suero (series co-chair), Evelyn Song (episode FIT lead), Daniel Ambinder (CardioNerds co-founder), and Tomas Neilan (faculty expert). Audio editing by CardioNerds Academy Intern, Dr. Maryam Barkhordarian. This episode is supported by a grant from Pfizer Inc. This CardioNerds Cardio-Oncology series is a multi-institutional collaboration made possible by contributions of stellar fellow leads and expert faculty from several programs, led by series co-chairs, Dr. Giselle Suero Abreu, Dr. Dinu Balanescu, and Dr. Teodora Donisan. CardioNerds Cardio-Oncology PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls and Quotes - Cardiotoxicity of Novel Immunotherapies Immune checkpoint inhibitors (ICI) play a crucial role in current oncology treatment by enhancing T-cell recognition against tumors. ICI-related cardiac immune-related adverse events (iRAEs) include myocarditis, heart failure, stress-cardiomyopathy, conduction abnormalities, venous thrombosis, pericardial disease, vasculitis, and atherosclerotic-related events. ICI myocarditis can be fatal; thus, prompt recognition and treatment is crucial. Management includes cessation of the ICI and treatment with corticosteroids and potentially other immunosuppressants. Close monitoring and collaboration with cardiology and oncology are crucial. Rechallenging patients with immunotherapies after developing an iRAE is controversial and requires careful consideration of risks and benefits, typically with the involvement of a multidisciplinary team. Show notes - Cardiotoxicity of Novel Immunotherapies What are immune checkpoint inhibitors (ICIs)? ICIs are monoclonal antibodies used to enhance the body’s immune response against cancer cells. Currently, there are four main classes of FDA-approved ICIs: monoclonal antibodies blocking cytotoxic T lymphocyte antigen-4 (CTLA-4), programed cell death protein-1 (PD-1), lymphocyte-activation gene 3 (LAG3), and programmed cell death ligand-1 (PD-L1). ICIs can lead to non-specific activation of the immune system, potentially causing off-target adverse events in various organs, including the heart, leading to myocarditis. The mechanisms of cardiac iRAEs are not fully understood, but they are believed to involve T-cell activation against cardiac antigens, which leads to inflammation and tissue damage. What are the cardiotoxicities related to ICI therapies? ICI-related cardiac immune-related adverse events (iRAEs) include myocarditis, heart failure, stress-cardiomyopathy, conduction abnormalities, venous thrombosis, pericardial disease, vasculitis, and atherosclerotic-related events. ICI-related myocarditis is considered rare compared to other systemic IRAEs. While the incidence rate of ICI-myocarditis is around 0.7-2.0%, it can be fatal in 30% of cases. Clinical manifestations vary but can include chest pain, dyspnea, palpitations, heart failure symptoms, and arrhythmias. Severe cases of ICI myocarditis can present as cardiogenic shock or complete heart block (a fulminant myocarditis picture). The timing of adverse events is typically within the first three months of starting immunotherapy, with the majority occurring early on; however, some cases may present after three months. Increased clinical suspicion is key for early recognition and prompt diagnosis and treatment. What is the general approach to the diagnosis of ICI-myocarditis? Diagnosis is based on clinical history and presentation, elevated troponin, and imaging findings. Echocardiography (with global longitudinal strain) and cardiac MRI (with T1 and T2 mapping as per the modified Lake Louise Criteria) are key diagnostic tools. If cardiac MRI is not diagnostic but suspicion remains high, an endomyocardial biopsy is the next diagnostic step. Baseline cardiac tests, such as ECG and troponin, are important before initiating ICIs in every patient to serve as a reference standard for comparison in case of troponin elevation during therapy. However, routine surveillance of asymptomatic patients on ICIs is not recommended. How do endomyocardial biopsy findings for ICI-myocarditis compare to other types of autoimmune-mediated conditions such as transplant rejection? ICI-myocarditis is pathologically almost identical to transplant rejection; therefore, a similar grading system used for transplant rejection is applied to ICI-myocarditis to determine the severity and provide guidance on the intensity of immunosuppression. What are the treatment strategies for ICI-myocarditis? In general, all patients with suspected ICI-myocarditis should have their immunotherapy held temporarily until the diagnosis is confirmed. Next, patients should be typically admitted to an inpatient unit with telemetry capabilities, given the risk of progression to complete heart block and cardiogenic shock. High-dose corticosteroids are the first-line pharmacological treatment, but the optimal dose varies between guidelines. An approach for severe life-threatening cases based on the NCCN and SITC guideline recommendations is a pulse of high-dose corticosteroids (consider 1000 mg methylprednisolone IV daily for 3–5 days until troponin normalizes) followed by a taper of 1–2 mg/kg methylprednisolone or oral prednisone for 4–6 weeks. For patients who do not respond to high-dose corticosteroids, additional immunosuppressive therapies can be considered, including intravenous immunoglobulin (IVIG), mycophenolate mofetil, anti-thymocyte globulin (ATG), alemtuzumab (monoclonal antibody to CD52), abatacept (CTLA-4 agonist), or plasmapheresis. This is an area where more data is needed to support guidelines for patient treatment. Currently, there are ongoing studies in this area, such as a phase 3 clinical of Abatacept for immune checkpoint inhibitor-associated myocarditis (ATRIUM, NCT053359280) High doses of corticosteroids used to treat ICI-associated myocarditis may adversely impact cancer outcomes. Further research is needed to understand the impact of cardiac toxicities and immunosuppressive treatments on cancer outcomes Can patients be re-treated after an episode of ICI myocarditis? Patients who develop ICI-associated adverse events, including myocarditis, may have a second chance and be rechallenged with ICIs after resolution of the adverse event, but this decision should be made carefully considering the risks and benefits. References - Cardiotoxicity of Novel Immunotherapies Zhang L, Reynolds KL, Lyon AR, Palaskas N, Neilan TG. The Evolving Immunotherapy Landscape and the Epidemiology, Diagnosis, and Management of Cardiotoxicity: JACC: CardioOncology Primer. JACC CardioOncology. 2021;3(1):35-47. doi:10.1016/J.JACCAO.2020.11.012 Drobni ZD, Alvi RM, Taron J, et al. Association Between Immune Checkpoint Inhibitors With Cardiovascular Events and Atherosclerotic Plaque. Circulation. 2020;142(24):2299-2311. doi:10.1161/CIRCULATIONAHA.120.049981 Stein-Merlob AF, Rothberg M V., Holman P, Yang EH. Immunotherapy-Associated Cardiotoxicity of Immune Checkpoint Inhibitors and Chimeric Antigen Receptor T Cell Therapy: Diagnostic and Management Challenges and Strategies. Curr Cardiol Rep. 2021;23(3):1-11. doi:10.1007/s11886-021-01440-3 Suero-Abreu GA, Zanni MV, Neilan TG. Atherosclerosis With Immune Checkpoint Inhibitor Therapy: Evidence, Diagnosis, and Management: JACC: CardioOncology State-of-the-Art Review. JACC CardioOncol. 2022 Dec 20;4(5):598-615. doi: 10.1016/j.jaccao.2022.11.011. PMID: 36636438; PMCID: PMC9830225.

Mar 14, 2024

CardioNerds join Dr. Inbar Raber and Dr. Susan Mcilvaine from the Beth Israel Deaconess Medical Center for a Fenway game. They discuss the following case: A 72-year-old man presents with two weeks of progressive dyspnea, orthopnea, nausea, vomiting, diarrhea, and right upper quadrant pain. He has a history of essential thrombocytosis, Barrett’s esophagus, basal cell skin cancer, and hypertension treated with hydralazine. He is found to have bilateral pleural effusions and a pericardial effusion. He undergoes a work-up, including pericardial cytology, which is negative, and blood tests reveal a positive ANA and positive anti-histone antibody. He is diagnosed with drug-induced lupus due to hydralazine and starts treatment with intravenous steroids, resulting in an improvement in his symptoms. Expert commentary is provided by UT Southwestern internal medicine residency program director Dr. Salahuddin (“Dino”) Kazi. US Cardiology Review is now the official journal of CardioNerds! Submit your manuscript here. CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Case Media Pearls - A Drug's Adverse Effect Unleashes the Wolf The differential diagnosis for pericardial effusion includes metabolic, malignant, medication-induced, traumatic, rheumatologic, and infectious etiologies. While pericardial cytology can aid in securing a diagnosis of cancer in patients with malignant pericardial effusions, the sensitivity of the test is limited at around 50%. Common symptoms of drug-induced lupus include fever, arthralgias, myalgias, rash, and/or serositis. Anti-histone antibodies are typically present in drug-induced lupus, while anti-dsDNA antibodies are typically absent (unlike in systemic lupus erythematosus, SLE). Hydralazine-induced lupus has a prevalence of 5-10%, with a higher risk for patients on higher doses or longer durations of drug exposure. Onset is usually months to years after drug initiation. Show Notes - A Drug's Adverse Effect Unleashes the Wolf There is a broad differential diagnosis for pericardial effusion which includes metabolic, malignant, medication-induced, traumatic, rheumatologic, and infectious etiologies. Metabolic etiologies include renal failure and thyroid disease. Certain malignancies are more likely to cause pericardial effusions, including lung cancer, lymphoma, breast cancer, sarcoma, and melanoma. Radiation therapy to treat chest malignancies can also result in a pericardial effusion. Medications can cause pericardial effusion, including immune checkpoint inhibitors, which can cause myocarditis or pericarditis, and medications associated with drug-induced lupus, such as procainamide, hydralazine, phenytoin, minoxidil, or isoniazid. Trauma can cause pericardial effusions, including blunt chest trauma, cardiac surgery, or cardiac catheterization. Rheumatologic etiologies include lupus, rheumatoid arthritis, systemic sclerosis, sarcoid, and vasculitis. Many different types of infections can cause pericardial effusions, including viruses (e.g., coxsackievirus, echovirus, adenovirus, human immunodeficiency virus, and influenza), bacteria (TB, staphylococcus, streptococcus, and pneumococcus), and fungi. Other must-not-miss etiologies include emergencies like type A aortic dissection and myocardial infarction. In a retrospective study of all patients who presented with a hemodynamically significant pericardial effusion and underwent pericardiocentesis, 33% of patients were found to have an underlying malignancy(Ben-Horin et al). Bloody effusion and frank tamponade were significantly more common among patients with malignant effusion, but the overlap was significant, and no epidemiologic or clinical parameter was found useful to differentiate between cancerous and noncancerous effusions. Although this patient’s pericardial fluid cytology was negative, cytology is typically only positive in around 50% of malignant effusions (Ben-Horin et al). The risk of drug-induced lupus (DIL) with hydralazine is high, approaching 10% of all treated patients. Another more commonly implicated cardiovascular drug is procainamide, with an incidence of 15-20%. Anti-histone antibodies are typically positive in DIL caused by hydralazine or procainamide, whereas anti-double stranded DNA antibodies are typically absent (in contrast to systemic lupus erythematosus). The most common symptoms of DIL include fever, arthralgias, myalgias, rash, and/or serositis with onset after months to years of drug exposure. If serositis is present, it is more often pleuritis, +/- pericarditis. In addition to stopping the offending medication, treatment is extrapolated from the treatment of idiopathic systemic lupus and can include NSAIDs, hydroxychloroquine, and/or systemic steroids, depending on disease severity. References - A Drug's Adverse Effect Unleashes the Wolf Ben-Horin, Bank, Guetta, & Livneh, A. (2006). Large symptomatic pericardial effusion as the presentation of unrecognized cancer - A study in 173 consecutive patients undergoing pericardiocentesis. Medicine (Baltimore), 85(1), 49–53. Borchers, A.T., Keen, C.L. and Gershwin, M.E. (2007), Drug-Induced Lupus. Annals of the New York Academy of Sciences, 1108: 166-182. Feng, Glockner, J., et al. (2011). Cardiac Magnetic Resonance Imaging Pericardial Late Gadolinium Enhancement and Elevated Inflammatory Markers Can Predict the Reversibility of Constrictive Pericarditis After Antiinflammatory Medical Therapy A Pilot Study. Circulation (New York, N.Y.), 124(17), 1830–1837

Mar 12, 2024

Welcome back to the CardioNerds Cardiovascular Prevention Series, where we are continuing our discussion of Glucagon-like Peptide-1 Receptor Agonists (GLP-1 RAs). This class of medications is becoming a household name, not only for their implications for weight loss but also for their effect on cardiovascular disease. CardioNerds Dr. Ty Sweeney (CardioNerds Academy Faculty Member and incoming Cardiology Fellow at Boston Medical Center), Dr. Rick Ferraro (CardioNerds Academy House Faculty and Cardiology Fellow at Johns Hopkins Hospital), and special guest Dr. Franck Azobou (Cardiology Fellow at UT Southwestern) sat down with Dr. Darren McGuire (Cardiologist at UT Southwestern and Senior Editor of Diabetes and Vascular Disease Research) to discuss important trial data on GLP-1 RAs in patients with heart disease, as well as recent professional society guidelines on their use. Show notes were drafted by Dr. Ty Sweeney. Audio editing was performed by CardioNerds Intern student Dr. Diane Masket. If you haven’t already, be sure to check out CardioNerds episode #350 where we discuss the basics and mechanism of action of GLP-1 RAs with Dr. Dennis Bruemmer. This episode was produced in collaboration with the American Society of Preventive Cardiology (ASPC) with independent medical education grant support from Novo Nordisk. See below for continuing medical education credit. Claim CME for this episode HERE. CardioNerds Prevention PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls and Quotes - GLP-1 Agonists: Diving into the Data Patients with diabetes and clinical atherosclerotic cardiovascular disease (ASCVD) or who are at high risk of ASCVD benefit from treatment with a GLP-1 RA. For persons with sufficient ASCVD risk and type 2 diabetes, GLP-1 RAs and SGLT2 inhibitors can, and often should, be used in combination. "Just like we don’t consider ‘and/or’ for the four pillars of guideline-directed medical therapy for heart failure with reduced ejection fraction, we shouldn’t parcel out these two therapeutic options...it should be both.” Setting expectations with your patients regarding injection practices, side effects, and expected benefits can go a long way toward improving the patient experience with GLP-1 RAs. Utilize a multidisciplinary approach when caring for patients on GLP-1 RAs. Build a team with your patient’s primary care provider, endocrinologist, clinical pharmacist, and nurse. “This is really a cardiologist issue. These are no longer endocrinology or primary care drugs. We need to be prescribing them ourselves just like we did back in the nineties when we took over the statin prescriptions from the endocrinology domain...we need to lead the way.” Show notes - GLP-1 Agonists: Diving into the Data For which patients are GLP-1 RAs recommended to reduce the risk of major cardiac events? For patients with type 2 diabetes and ASCVD, starting a GLP-1 RA carries a Class 1, Level of Evidence A recommendation in the most recent ESC and ACC guidelines. For patients without diabetes or clinical ASCVD with an estimated 10-year risk of CVD exceeding 10%, consideration of starting a GLP-1 RA carries a Class 2b, Level of Evidence C recommendation to reduce CV risk. The STEP-HFpEF trial showed that among patients with obesity and HFpEF, once-weekly semaglutide may be beneficial in terms of weight loss and quality of life. The results of the FIGHT and LIVE trials question the utility and safety of liraglutide in treating patients with advanced HFrEF. Of the over 17,000 patients enrolled in the SELECT trial, about 25% had heart failure, of which about one-third had HFrEF. Stay tuned for sub-analyses from that trial for more info! Can we still prescribe GLP-1 Ras in patients with well-controlled T2DM? The recommendation to start GLP-1 RAs for cardiovascular benefit in eligible patients is made irrespective of HbA1C. If A1c is very low, or if the patient is experiencing episodes of hypoglycemia, consider backing off background diabetes therapy, especially if they don’t confer CV benefit. Note, the recent ESC guidelines recommending SGLT2i and GLP-1RA therapy do so irrespective of background metformin therapy. This is supported by the ADA Standards of Care in Diabetes. Is there evidence to suggest oral vs injectable GLP-1 RAs with respect to cardiac outcomes? The PIONEER-6 trial suggests cardiovascular benefit of oral semaglutide in patients with diabetes compared to placebo; however, the trial was only powered to assess safety. The ongoing SOUL trial is examining cardiovascular outcomes among patients being treated with oral semaglutide vs placebo with the primary outcome of time from randomization to the first occurrence of a major adverse CV event. Stay tuned! It is crucial that oral semaglutide be taken on an empty stomach, given its unique absorption and pharmacokinetics. What side effects can patients expect when initiating GLP-1 RAs? Nausea is common after starting these medications, but this generally ameliorates after 1-2 weeks of therapy. Setting expectations with your patients ahead of time can go a long way to improving adherence. We do not have dose-response data to say whether sub-maximal doses of GLP-1 RAs (for example, in patients who do not want or cannot tolerate the full dose) are effective. That said, the SELECT trial suggests the benefits of starting GLP-1 RAs begin early, even at introductory doses. Therefore, if a patient truly cannot tolerate higher doses, it may be reasonable to titrate slowly or hold at a lower dose. What does the literature say regarding the combined use of SGLT2 inhibitors and GLP-1 RAs? Sub-analyses examining the effect of background therapy when patients are randomized to receive the other vs. placebo suggest patients enjoy at least as good, if not better, outcomes from the combination of therapies. One of the first planned sub-analyses of SOUL will look at the potential additive effects of oral semaglutide alongside background SGLT2 inhibitor therapy. References - GLP-1 Agonists: Diving into the Data Marx N, Federici M, Schütt K, et al. 2023 ESC Guidelines for the management of cardiovascular disease in patients with diabetes: Developed by the task force on the management of cardiovascular disease in patients with diabetes of the European Society of Cardiology (ESC). European Heart Journal. 2023;44(39):4043-4140. https://academic.oup.com/eurheartj/article/44/39/4043/7238227?login=false Virani SS, Newby LK, Arnold SV, et al. 2023 AHA/ACC/ACCP/ASPC/NLA/PCNA Guideline for the Management of Patients With Chronic Coronary Disease: A Report of the American Heart Association/American College of Cardiology Joint Committee on Clinical Practice Guidelines. Circulation. 2023;148(9):e9-e119. https://www.ahajournals.org/doi/10.1161/CIR.0000000000001168 ElSayed NA, Aleppo G, Aroda VR, et al. 10. Cardiovascular Disease and Risk Management: Standards of Care in Diabetes—2023. Diabetes Care. 2022;46(Supplement_1):S158-S190. https://diabetesjournals.org/care/article/46/Supplement_1/S158/148038/10-Cardiovascular-Disease-and-Risk-Management Husain M, Birkenfeld AL, Donsmark M, et al. Oral Semaglutide and Cardiovascular Outcomes in Patients with Type 2 Diabetes. New England Journal of Medicine. 2019;381(9):841-851. https://www.nejm.org/doi/full/10.1056/NEJMoa1901118 McGuire DK, Busui RP, Deanfield J, et al. Effects of oral semaglutide on cardiovascular outcomes in individuals with type 2 diabetes and established atherosclerotic cardiovascular disease and/or chronic kidney disease: Design and baseline characteristics of SOUL, a randomized trial. Diabetes Obes Metab. 2023;25(7):1932-1941. https://pubmed.ncbi.nlm.nih.gov/36945734/ Kosiborod MN, Abildstrøm SZ, Borlaug BA, et al. Semaglutide in Patients with Heart Failure with Preserved Ejection Fraction and Obesity. N Engl J Med. 2023;389(12):1069-1084. https://pubmed.ncbi.nlm.nih.gov/37622681/ Jorsal A, Kistorp C, Holmager P, et al. Effect of liraglutide, a glucagon-like peptide-1 analogue, on left ventricular function in stable chronic heart failure patients with and without diabetes (LIVE)-a multicentre, double-blind, randomised, placebo-controlled trial. Eur J Heart Fail. 2017;19(1):69-77. https://pubmed.ncbi.nlm.nih.gov/27790809/ Margulies KB, Hernandez AF, Redfield MM, et al. Effects of Liraglutide on Clinical Stability Among Patients With Advanced Heart Failure and Reduced Ejection Fraction: A Randomized Clinical Trial. JAMA. 2016;316(5):500-508. https://jamanetwork.com/journals/jama/article-abstract/2540402

Mar 10, 2024

The following question refers to Section 13 of the 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure.The question is asked by Western Michigan University medical student and CardioNerds Intern Shivani Reddy, answered first by Mayo Clinic Cardiology Fellow and CardioNerds Academy Faculty Dr. Dinu Balanescu, and then by expert faculty Dr. Harriette Van Spall.Dr. Van Spall is an Associate Professor of Medicine, cardiologist, and Director of E-Health at McMaster University. Dr Van Spall is a Canadian Institutes of Health Research-funded clinical trialist and researcher with a focus on heart failure, health services, and health disparities.The Decipher the Guidelines: 2022 AHA / ACC / HFSA Guideline for The Management of Heart Failure series was developed by the CardioNerds and created in collaboration with the American Heart Association and the Heart Failure Society of America. It was created by 30 trainees spanning college through advanced fellowship under the leadership of CardioNerds Cofounders Dr. Amit Goyal and Dr. Dan Ambinder, with mentorship from Dr. Anu Lala, Dr. Robert Mentz, and Dr. Nancy Sweitzer. We thank Dr. Judy Bezanson and Dr. Elliott Antman for tremendous guidance.Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. Question #32 Palliative and supportive care has a role for patients with heart failure only in the end stages of their disease. TRUE FALSE Answer #32 Explanation The correct answer is False Palliative care is patient- and family-centered care that optimizes health-related quality of life by anticipating, preventing, and treating suffering and should be integrated into the management of all stages of heart failure throughout the course of illness. The wholistic model of palliative care includes high-quality communication, estimation of prognosis, anticipatory guidance, addressing uncertainty, shared decision-making about medically reasonable treatment options, advance care planning; attention to physical, emotional, spiritual, and psychological distress; relief of suffering; and inclusion of family caregivers in patient care and attention to their needs during bereavement. As such, for all patients with HF, palliative and supportive care—including high-quality communication, conveyance of prognosis, clarifying goals of care, shared decision-making, symptom management, and caregiver support—should be provided to improve QOL and relieve suffering (Class 1, LOE C-LD). For conveyance of prognosis, objective risk models can be incorporated along with discussion of uncertainty since patients may overestimate survival and the benefits of specific treatments – “hope for the best, plan for the worst.” For clarifying goals of care, the exploration of each patient’s values and concerns through shared decision-making is essential in important management decisions such as when to discontinue treatments, when to initiate palliative treatments that may hasten death but provide symptom management, planning the location of death, and the incorporation of home services or hospice. It is a Class I indication that for patients with HF being considered for, or treated with life-extending therapies, the option for discontinuation should be anticipated and discussed through the continuum of care, including at the time of initiation, and reassessed with changing medical conditions and shifting goals of care (LOE C-LD). Caregiver support should also be offered to family members even beyond death to help them cope with the grieving process. A formal palliative care consult is not needed for each patient, but the primary team should exercise the above domains to improve processes of care and patient outcomes. Specialist palliative care consultation can be useful to improve QOL and relieve suffering for patients with heart failure—particularly those with stage D HF who are being evaluated for advanced therapies, patients requiring inotropic support or temporary mechanical support, patients experiencing uncontrolled symptoms, major medical decisions, or multimorbidity, frailty, and cognitive impairment (Class 2a, LOE B). Studies have been mixed on if the palliative team itself improves quality of life and well-being so these interventions should be tailored to each patient and caregiver. For patients with HF, execution of advanced directives can be useful to improve documentation of treatment preferences, delivery of patient-centered care, and dying in a preferred place (Class 2a, LOE C-LD). In patients with advanced HF with expected survival < 6 months, timely referral to hospice can be useful to improve QOL (Class 2a, LOE C-LD) Main Takeaway In summary, the core principles of palliative care that include communication, transparency on prognosis, clarification of goals of care, shared decision-making, symptom management, and caregiver support should be integrated into each patient’s treatment plan regardless of the stage of heart failure Guideline Loc. Section 13, Figure 15, Table 32 Decipher the Guidelines: 2022 Heart Failure Guidelines PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron!

Mar 5, 2024

CardioNerds cofounder Dr. Dan Ambinder joins Dr. Angie Molina, Dr. Cullen Soares, and Dr. Andrew Lutz from the University of Maryland Medical Center for some beers and history by Fort McHenry. They discuss a case of disseminated haemophilus influenzapresumed fulminant bacterial myocarditis with mixed septic/cardiogenic shock. Expert commentary is provided by Dr. Stanley Liu (Assistant Professor, Division of Cardiovascular Medicine, University of Maryland School of Medicine). Episode audio was edited by Dr. Chelsea Amo-Tweneboah. A woman in her twenties with a history of intravenous drug use presented with acute onset fevers and sore throat, subsequently developed respiratory distress and cardiac arrest, and was noted to have epiglottic edema on intubation. She developed shock and multiorgan failure. ECG showed diffuse ST elevations, TTE revealed biventricular dysfunction, and pleural fluid culture grew Haemophilus influenza. Right heart catheterization showed evidence of cardiogenic shock. She improved with supportive care and antibiotics. US Cardiology Review is now the official journal of CardioNerds! Submit your manuscript here. CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls - Sore Throat, Fever, and Myocarditis - It’s not always COVID-19 The post-cardiac arrest ECG provides helpful information for diagnosing the underlying etiology.​ Be aware of diagnostic biases - availability and anchoring biases are particularly common during respiratory viral (such as COVID-19, RSV) surges. Consider a broad differential diagnosis in evaluating myocarditis, including non-viral etiologies. Right heart catheterization provides crucial information for diagnosis and management of undifferentiated shock​. When assessing the need for mechanical circulatory support, consider the current hemodynamics, type of support needed, and risks associated with each type. Show Notes - Sore Throat, Fever, and Myocarditis - It’s not always COVID-19 ECG findings consistent with pericarditis include diffuse concave-up ST elevations and downsloping T-P segment (Spodick’s sign) as well as PR depression (lead II), and PR elevation (lead aVR). In contrast, regional ST elevations with “reciprocal” ST depressions and/or Q-waves should raise concern for myocardial ischemia as the etiology. Biventricular dysfunction and elevated troponin are commonly seen post-cardiac arrest and may be secondary findings. However, an elevation in troponin that is out of proportion to expected demand ischemia, ECG changes (pericarditis, ischemic ST elevations), and cardiogenic shock suggest a primary cardiac etiology for cardiac arrest. The differential diagnosis of infectious myopericarditis includes, most commonly, viral infection (respiratory viruses) and, more rarely, bacterial, fungal, or parasitic. Noninfectious myopericarditis may be autoimmune (such as lupus, sarcoidosis, checkpoint inhibitors), toxin-induced (alcohol, cocaine), and medication-induced (anthracyclines and others). Right heart catheterization can help diagnose the etiology of undifferentiated shock, including distinguishing between septic and cardiogenic shock, by providing right and left-sided filling pressures, pulmonary and systemic vascular resistance, and cardiac output. Mechanical circulatory support (MCS) is indicated for patients in cardiogenic shock with worsening end-organ perfusion despite inotropic and pressor support. MCS includes intra-aortic balloon pump, percutaneous VAD, TandemHeart, and VA-ECMO. The decision to use specific types of MCS should be individualized to each patient with their comorbidities and hemodynamic profile. Shock teams are vital to guide decision-making. References Witting MD, Hu KM, Westreich AA, Tewelde S, Farzad A, Mattu A. Evaluation of Spodick's Sign and Other Electrocardiographic Findings as Indicators of STEMI and Pericarditis. J Emerg Med. 2020;58(4):562-569. doi:10.1016/j.jemermed.2020.01.017 Ferrero P, Piazza I, Lorini LF, Senni M. Epidemiologic and clinical profiles of bacterial myocarditis. Report of two cases and data from a pooled analysis. Indian Heart J. 2020;72(2):82-92. doi:10.1016/j.ihj.2020.04.005 Pollack A, Kontorovich AR, Fuster V, Dec GW. Viral myocarditis--diagnosis, treatment options, and current controversies. Nat Rev Cardiol. 2015;12(11):670-680. doi:10.1038/nrcardio.2015.108 Hsu S, Fang JC, Borlaug BA. Hemodynamics for the Heart Failure Clinician: A State-of-the-Art Review. J Card Fail. 2022;28(1):133-148. doi:10.1016/j.cardfail.2021.07.012 Korabathina R., Heffernan K.S., Paruchuri V., Patel A.R., Mudd J.O., Prutkin J.M., et al: The pulmonary artery pulsatility index identifies severe right ventricular dysfunction in acute inferior myocardial infarction. Catheter Cardiovasc Interv 2012; 80: pp. 593-600. https://pubmed.ncbi.nlm.nih.gov/21954053/ Drazner MH, Velez-Martinez M, Ayers CR, et al. Relationship of right- to left-sided ventricular filling pressures in advanced heart failure: insights from the ESCAPE trial. Circ Heart Fail. 2013;6(2):264-270. doi:10.1161/CIRCHEARTFAILURE.112.000204

Feb 19, 2024

CardioNerds Dr. Rick Ferraro (CardioNerds Academy House Faculty and Cardiology Fellow at JHH), Dr. Gurleen Kaur (Director of the CardioNerds Internship and Internal Medicine resident at BWH), and Dr. Alli Bigeh (Cardiology Fellow at the Ohio State) as they discuss the growing obesity epidemic and how it relates to cardiovascular disease with Dr. Ambarish Pandey (Cardiologist at UT Southwestern Medical Center). Show notes were drafted by Dr. Alli Bigeh. CardioNerds Academy Intern and student Dr. Shivani Reddy performed audio editing. Obesity is an important modifiable risk factor for cardiovascular disease, and it is on the rise! Here, we discuss how to identify patients with obesity and develop an approach to address current lifestyle recommendations. We also discuss the spectrum of pharmacologic treatment options available, management strategies, and some therapy options that are on the horizon. This episode was produced in collaboration with the American Society of Preventive Cardiology (ASPC) with independent medical education grant support from Novo Nordisk. See below for continuing medical education credit. Claim CME for this episode HERE. CardioNerds Prevention PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls and Quotes - Lifestyle & Pharmacologic Management of Obesity Identify obese patients not just using BMI, but also using anthropometric measurements such as waist circumference (central adiposity). Lifestyle modifications are our first line of defense against obesity! Current recommendations emphasize caloric restriction of at least 500kcal/day, plant-based and Mediterranean diets, and getting at least 150 minutes of moderate-intensity weekly exercise. Dive into the root cause of eating and lifestyle behaviors. It is crucial to address adverse social determinants of health with patients to identify the driving behaviors, particularly among those individuals of low socioeconomic status. Newer weight loss agents are most effective at achieving and maintaining substantial weight loss, in particular Semaglutide (GLP-1) and Tirzepatide (GLP-1/GIP). Initiate at a low dose and titrate up slowly. Obesity is a risk factor and potential driver for HFpEF. Targeted treatment options for obese patients with HFpEF include SGLT-2 inhibitors and semaglutide, which recently showed improvement in quality of life and exercise capacity in the STEP-HFpEF trial. Show notes - Lifestyle & Pharmacologic Management of Obesity How do we identify and define obesity? The traditional definition of obesity is based on body mass index (BMI), defined as BMI greater than or equal to 30.0 kg/m2 (weight in kg/height in meters).Recognize that BMI may not tell the whole story. A limitation of BMI is it does not reflect differences in body composition and distribution of fat.Certain patients may not meet the BMI cutoff for obesity but have elevated cardiovascular risk based on increased central adiposity, specifically those that are categorized as overweight.The devil lies in the details of anthropometric parameters. Include waist circumference measurements as part of an obesity assessment of visceral adiposity. A waist circumference greater than 40 inches for men and greater than 35 inches for women is considered elevated. What are some current lifestyle recommendations for obese patients? Lifestyle recommendations are the first line of defense against obesity.Current ACC/AHA guidelines suggest a target of reducing caloric intake by 500 kcal per day. For patients with severe obesity, this number may be higher.Emphasis on hypocaloric plant-based and Mediterranean dietsReduce total carbohydrate intake to 50-130 grams per day.Focus on a low-fat diet with less than 30% of total energy coming from fat with a high-protein diet to maintain lean mass and promote satiety.The overarching theme of prevailing lifestyle recommendations is incorporating whole grains, vegetables, fruit, nuts, and fiber-rich foods while minimizing saturated fats, salt, and sugar intake. ACC/AHA recommendations include 150 minutes of moderate-intensity exercise per week. What are some tips for addressing lifestyle modifications with patients? Tailor the approach to each individual patient. Get to the root cause and identify barriers to addressing the behaviors.Consider getting a psychosocial assessment and focus on behavior modification strategies. Eating behaviors can be associated with other behavioral disorders.Patients with severe obesity have a higher risk of adverse cardiovascular events. A risk-based approach for these patients mandates a greater emphasis on weight reduction and caloric restriction. Consider access to nutrient-dense food, socioeconomic status, cost of healthy foods, access to exercise resources, and safety of neighborhoods when making recommendations. What are the current pharmacologic options for weight loss? Which are the most effective? Consider pharmacological agents once lifestyle modifications and social determinants of health have been addressed. We should not get hung up on lifestyle modifications and fail to progress to using pharmacotherapies or surgical therapies in patients with morbid obesity or cardiovascular disease. Pharmacological therapy can be considered in patients with BMI >30 or BMI >27 with comorbidities. There are a variety of agents such as Orlistat, Phentermine/Topiramate, Bupropion/Naltrexone, GLP-1 receptor agonists (Liraglutide, Semaglutide) and Tirzepatide (GLP-1/GIP). Tirzepatide has the highest amount of reported weight loss, with patients achieving 23% weight loss or up to 50 pounds of weight loss based on the latest SURMOUNT trial. Semaglutide can achieve 16% weight loss based on trial data. The remaining agents have reported weight loss between 6-10%. Bariatric surgery should also be considered, especially in patients with severe obesity (BMI >40). Compare and contrast the GLP-1 agents, specifically semaglutide and liraglutide. GLP-1 receptor agonists activate GLP-1 receptors in the pancreas, which increases insulin release, slows gastric emptying, and reduces appetite.Semaglutide has a greater weight reduction of up to 16% total weight loss compared to 6% for liraglutide.There have been higher reported adverse effects with liraglutide as well. In the STEP-8 trial, the proportion of participants discontinuing treatment for any reason was 13.5% with semaglutide versus 27.6% with liraglutide. Gastrointestinal adverse events were the most common and reported by 84.1% with semaglutide and 82.7% with liraglutide. The SELECT trial in patients with preexisting cardiovascular disease and overweight or obesity but without diabetes, weekly subcutaneous semaglutide at a dose of 2.4 mg reduced the incidence of death from cardiovascular causes, nonfatal myocardial infarction, or nonfatal stroke by approximately 20%. Liraglutide has been shown to reduce cardiovascular outcomes in patients with established cardiovascular disease but only in patients with diabetes thus far. What other newer agents are on the horizon for treatment of obesity? An oral formulation of semaglutide 50mg is currently being tested, with phase 3 results showing up to 15% weight reduction in participants. Retatrutide is a new triple-hormone-receptor agonist (an agonist of the glucose-dependent insulinotropic polypeptide [GIP], glucagon-like peptide 1, and glucagon receptors). Phase 2 trial was recently published, reporting up to 25% weight loss in patients. Discuss some strategies to mitigate the GI side effects when using GLP-1 receptor agonists. Most importantly- keep a close eye on patient’s symptoms and prepare them for potential side effects along with the mechanism through which they work (i.e., inducing early satiety).Expect some degree of gastrointestinal discomfort so patients know what to expect. Side effects often dissipate with continued use of the medication. This can help minimize discontinuation.Counsel on diet and nutrition. Patients should eat small food portions for better tolerability, given the effect of the medication to slow gastric emptying.Providers should focus on starting at a low dose and titrating up slowly. If side effects become intolerable, providers can consider using the last tolerated dose or switching medication classes (i.e. Tirzepatide). References - Lifestyle & Pharmacologic Management of Obesity Chakhtoura M, Haber R, Malak G, Caline R, Raya T, Mantzoros CS. Pharmacotherapy of obesity: an update on the available medications and drugs under investigation. Pharmacotherapy of obesity: an update on the available medications and drugs under investigation. 2023;58:101882-101882. doi:https://doi.org/10.1016/j.eclinm.2023.101882 Després JP, Carpentier AC, Tchernof A, Neeland IJ, Poirier P. Management of Obesity in Cardiovascular Practice. Journal of the American College of Cardiology. 2021;78(5):513-531. doi:https://doi.org/10.1016/j.jacc.2021.05.035 ‌Dominguez LJ, Veronese N, Di Bella G, et al. Mediterranean diet in the management and prevention of obesity. Experimental Gerontology. 2023;174:112121. doi:https://doi.org/10.1016/j.exger.2023.112121 Jastreboff AM, Aronne LJ, Ahmad NN, et al. Tirzepatide Once Weekly for the Treatment of Obesity. New England Journal of Medicine. 2022;387(3). doi:https://doi.org/10.1056/nejmoa2206038 Jensen MD, Ryan DH, Apovian CM, et al. 2013 AHA/ACC/TOS Guideline for the Management of Overweight and Obesity in Adults. Circulation. 2013;129(25 suppl 2):S102-S138. doi:https://doi.org/10.1161/01.cir.0000437739.71477.ee Kosiborod M, Abildstrøm SZ, Borlaug BA, et al. Semaglutide in Patients with Heart Failure with Preserved Ejection Fraction and Obesity.

Feb 12, 2024

CardioNerds join Dr. Ethan Fraser and Dr. Austin Culver from the MedStar Georgetown University Hospital internal medicine and cardiology programs in our nation’s capital. They discuss the following case involving an unusual case of rapidly progressive heart failure. Episode audio was edited by CardioNerds Academy Intern and student Dr. Pacey Wetstein. Expert commentary was provided by advanced heart failure cardiologist Dr. Richa Gupta. A 55-year-old male comes to the clinic (and eventually into the hospital) for what appears to be a straightforward decompensation of his underlying cardiac disease. However, things aren’t as simple as they might appear. In this episode, we will discuss the outpatient workup for non-ischemic cardiomyopathy and discuss the clinical indicators that we as clinicians should be aware of in these sick patients. Furthermore, we will discuss the differential for NICM, the management of patients with this rare disease, and how this disease can mimic other cardiomyopathies. US Cardiology Review is now the official journal of CardioNerds! Submit your manuscript here. CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Case Media - Rapidly Progressive Heart Failure Pearls - Rapidly Progressive Heart Failure The non-ischemic cardiomyopathy workup should incorporate targeted multimodal imaging, thorough history taking, broad laboratory testing, genetic testing if suspicion exists for a hereditary cause, and a deep understanding of which populations are at higher risk for certain disease states. Key Point: Always challenge and question the etiology of an unknown cardiomyopathy – do not assume an etiology based on history/patient story alone. Unexplained conduction disease in either a young or middle-aged individual in the setting of a known cardiomyopathy should raise suspicion for an infiltrative cardiomyopathy and set off a referral to an advanced heart failure program. Key Point: Consider early/more aggressive imaging for these patients and early electrophysiology referral for primary/secondary prevention. Giant Cell Myocarditis is a rapidly progressive cardiomyopathy characterized by high mortality (70% in the first year), conduction disease, and classically presents in young/middle-aged men. Key Point: If you have a younger male with rapidly progressive cardiomyopathy (anywhere as quickly as 1-2 months, weeks in some cases) and conduction disease, consider early endomyocardial biopsy, even before other advanced imaging modalities. The Diagnosis of Giant Cell Myocarditis is time-sensitive - early identification and treatment are essential to survival. Key Point: The median timeframe from the time the disease is diagnosed to the time of death is approximately 6 months. 90% of patients are either deceased by the end of 1 year or have received a heart transplant. The treatment of Giant Cell Myocarditis is still governed largely by expert opinion, but the key components include high-dose steroids and cyclosporine, largely as a bridge to transplantation or advanced heart failure therapies. Key Point: Multi-disciplinary care is essential in delivering excellent care in the diagnostic/pre-transplant period, including involvement by cardiology, cardiac surgery, radiology, critical care, allergy/immunology, case management, advanced heart failure, and shock teams if necessary. There remains significant clinical overlap between Giant Cell Myocarditis and sarcoidosis, making managing equivocal cases challenging. Key Point: Consider early FDG-PET imaging in equivocal cases, as management during the pre-transplant period and evaluation of transplant candidacy can vary drastically between the two. Show Notes - Rapidly Progressive Heart Failure 1. What is Giant Cell Myocarditis? Giant cell myocarditis is a rare and rapidly progressive cause of heart failure due to T-cell lymphocyte mediated myocardial inflammation. The pathogenesis of GCM is incompletely understood – histologically, there is infiltration of the myocardium by T-lymphocytes and macrophages, and there is typically evidence of upregulation of IL-17 and TNF-a. Classically, the disease state is associated with electrical (e.g., ventricular tachycardia, high-grade AV block) and hemodynamic instability – all of which typically progresses rapidly over a period of weeks to months. This male-predominant disease tends to occur in young and middle-aged patients – with a mean age between 42 and 60 based on several registries. While a rare disease, a high index of suspicion is necessary when patients present with rapidly progressive or fulminant heart failure, as a missed diagnosis of giant cell myocarditis is invariably fatal. Early and rapid identification of this uniquely high-risk group of heart failure patients and prompt initiation of therapy targeted towards the underlying autoimmune process, as well as management at a center with advanced heart failure and cardiovascular ICU support, is necessary. 2. How is Giant Cell Myocarditis Diagnosed? Establishing a diagnosis requires an endomyocardial biopsy (EMB), although EMB has imperfect sensitivity for GCM. Cardiac biomarkers and imaging serve an adjunct role in diagnosis; TTE findings can be variable, with either normal or dilated LV cavity size and increased wall thickness, which may be related to acute edema and inflammation. Worse LVEF on presentation has been shown to correlate with shorter transplant-free survival time. Troponin levels may be elevated, but case series have shown a lack of correlation between prognosis and troponin elevation in GCM, and importantly, in some cases, troponin values have been negative in patients later found to have GCM by biopsy. Advanced imaging is not always practical as these patients are often hemodynamically unstable, but CMR can demonstrate findings typical of myocarditis (i.e. the 2018 Lake Louise criteria). 3. What is the treatment for Giant Cell Myocarditis, and what are the future steps for disease management? Cyclosporine-based combination immunosuppressive therapy, in addition to standard heart failure guideline-directed medical and procedural therapy and management of arrhythmias, can improve outcomes in these patients. Typical regimens include cyclosporine, high-dose steroids as the mainstay, and azathioprine or alemtuzumab (an anti-CD52 monoclonal antibody) as adjunctive agents. Patients are often co-managed by advanced heart failure, cardiac intensivists, and rheumatology. As the disease progresses, patients often develop sustained or symptomatic ventricular tachycardia, conduction abnormalities refractory HF with a dilated LV phenotype and many require mechanical circulatory support and/or cardiac transplantation. GCM can remit and relapse, sometimes many years after initial diagnosis; an advanced heart failure team should follow these patients and should continue some immunosuppression (usually a calcineurin inhibitor) for at least 2 years. Overall, our understanding of the mechanism and management of GCM continues to evolve; high-grade evidence such as randomized controlled trials are extremely difficult to perform due to the rarity and high acuity of these presentations, therefore enrolling these patients in shared multicenter registries where able is essential to shrinking our knowledge gaps of this rare disease state. 4. What else should one consider in presumed cases of Giant Cell Myocarditis? There exists a significant clinical overlap between Giant Cell Myocarditis and Cardiac Sarcoidosis, so much so that some argue the two diseases exist on opposite ends of one disease spectrum. Both notably present with significant arrhythmia burden and advanced heart failure symptoms, although they are both treated quite differently and present with different time courses (mean time to onset of symptoms 0.3 months for GCM, 7 months for CS). Furthermore, data from Nordenswan et al. from Finland reveals that the diagnosis of GCM on histology was recategorized to CS in 62% of their studies reviewed upon secondary pathology review. To this end, it is important that clinicians consider further advanced imaging modalities (i.e., FDG-PET) in equivocal cases and consider expert pathology evaluation of endomyocardial biopsy samples as proper escalation of care and rapid identification can prevent significant treatment delays. References - Rapidly Progressive Heart Failure Amancherla, Kaushik, Juan Qin, Yu Wang, Margaret L. Axelrod, Justin M. Balko, Kelly H. Schlendorf, Robert D. Hoffman, Yaomin Xu, JoAnn Lindenfeld, and Javid Moslehi. “RNA-Sequencing Reveals a Distinct Transcriptomic Signature for Giant Cell Myocarditis and Identifies Novel Druggable Targets.” Circulation Research 129, no. 3 (2021): 451–53. https://doi.org/10.1161/CIRCRESAHA.121.319317. Bang, Vigyan, Sarju Ganatra, Sachin P. Shah, Sourbha S. Dani, Tomas G. Neilan, Paaladinesh Thavendiranathan, Frederic S. Resnic, et al. “Management of Patients With Giant Cell Myocarditis.” Journal of the American College of Cardiology 77, no. 8 (2021): 1122–34. https://doi.org/10.1016/j.jacc.2020.11.074. Birnie, David H., Vidhya Nair, and John P. Veinot. “Cardiac Sarcoidosis and Giant Cell Myocarditis: Actually, 2 Ends of the Same Disease?” Journal of the American Heart Association 10, no. 6 (2021): e020542. https://doi.org/10.1161/JAHA.121.020542. Bobbio, Emanuele, Marie Björkenstam, Bright I. Nwaru, Francesco Giallauria, Eva Hessman, Niklas Bergh, Christian L. Polte, Jukka Lehtonen, Kristjan Karason, and Entela Bollano. “Short- and Long-Term Outcomes after Heart Transplantation in Cardiac Sarcoidosis and Giant-Cell Myocarditis: A Systematic Review and Meta-Analysis.

Feb 9, 2024

The following question refers to Section 9.5 of the 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure. The question is asked by Keck School of Medicine USC medical student & former CardioNerds Intern Hirsh Elhence, answered first by Vanderbilt Cardiology Fellow and CardioNerds Academy Faculty Dr. Breana Hansen, and then by expert faculty Dr. Javed Butler. Dr. Butler is an advanced heart failure and transplant cardiologist, President of the Baylor Scott and White Research Institute, Senior Vice President for the Baylor Scott and White Health, and Distinguished Professor of Medicine at the University of Mississippi The Decipher the Guidelines: 2022 AHA / ACC / HFSA Guideline for The Management of Heart Failure series was developed by the CardioNerds and created in collaboration with the American Heart Association and the Heart Failure Society of America. It was created by 30 trainees spanning college through advanced fellowship under the leadership of CardioNerds Cofounders Dr. Amit Goyal and Dr. Dan Ambinder, with mentorship from Dr. Anu Lala, Dr. Robert Mentz, and Dr. Nancy Sweitzer. We thank Dr. Judy Bezanson and Dr. Elliott Antman for tremendous guidance. Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. Question #31 Mrs. Hart is a 70-year-old woman who was admitted to the CICU two days ago for signs and symptoms consistent with cardiogenic shock. Since her admission, she has been on maximal diuretics, requiring greater doses of intravenous dobutamine. Unfortunately, her liver and renal function continue to worsen, and urine output is decreasing. A right heart catheterization reveals elevated biventricular filling pressures with a cardiac index of 1.7 L/min/m2 by the Fick method. What is the next best step? A Continue current measures and monitor for improvement B Switch from dobutamine to norepinephrine C Place an intra-aortic balloon pump (IABP) D Resume guideline directed medical therapy Answer #31 Explanation The Correct answer is C – Place an intra-aortic balloon pump. This patient is between the SCAI Shock Stages C and D with elevated venous pressures, decreased urine output, and worsening signs of hypoperfusion. She has been started on appropriate therapies, including diuresis and inotropic support. The relevant Class 2a recommendation is that in patients with cardiogenic shock, temporary MCS is reasonable when end-organ function cannot be maintained by pharmacologic means to support cardiac function (LOE B-NR). Thus, the next best step is a form of temporary MCS. IABP is appropriate to help increase coronary perfusion and offload the left ventricle. In fact, for patients who are not rapidly responding to initial shock measures, triage to centers that can provide temporary MCS may be considered to optimize management (Class 2b, LOE C-LD). The guidelines further state that in patients presenting with cardiogenic shock, placement of a pulmonary arterial line may be considered to define hemodynamic subsets and appropriate management strategies (Class 2B, LOE B-NR). And so, if time allows escalation to MCS should be guided by invasively obtained hemodynamic data via PA catheterization. Several observational experiences have associated PA catheterization use with improved outcomes, particularly in conjunction with short-term MCS. Additionally, PA catheterization is useful when there is diagnostic uncertainty as to the cause of hypotension or end-organ dysfunction, particularly when the patient in shock is not responding to empiric initial measures, such as in this patient. There are additional appropriate measures at this time that are more institution-dependent. An institutional shock team would be very helpful here as they often comprise multidisciplinary teams of heart failure and critical care specialists, interventional cardiologists, surgeons, and palliative care specialists. As such, there is a Class 2a recommendation that in patients with cardiogenic shock, management by a multidisciplinary team experienced in shock is reasonable (LOE B-NR). Most documented experiences have suggested outcomes improve after shock teams are instituted. For instance, in one such experience, using a shock team was associated with improved 30-day all-cause mortality (HR, 0.61; 95% CI, 0.41–0.93) and reduced in-hospital mortality (61.0% vs. 47.9%; P=0.041). Choice A – Continue current measures and monitor for improvement – is incorrect. This patient has been deteriorating on current measures since admission and is at higher risk for SCAI Shock Stage E – extremis, refractory hypotension/hypoperfusion, and cardiac arrest and, therefore requires escalation of therapy Choice B- Switch from dobutamine to norepinephrine – is incorrect. The Class 1 LOE B-NR recommendation is that in patients with cardiogenic shock, intravenous inotropic support should be used to maintain systemic perfusion and maintain end-organ performance. Dobutamine is a more potent inotropic agent than norepinephrine. Stopping dobutamine in the setting of her low cardiac index would be incorrect. Choice D – Resume guideline-directed medical therapy – is incorrect. This patient’s shock is getting worse. The Class 1 LOE B-NR recommendation is that in patients with HFrEF, GDMT should be initiated during hospitalization after clinical stability is achieved. Restarting medications now would be premature. Main Takeaway In patients with cardiogenic shock, temporary MCS is reasonable when end-organ function cannot be maintained by pharmacologic means to support cardiac function. Guideline Loc. Section 9.5 Decipher the Guidelines: 2022 Heart Failure Guidelines PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron!

Feb 8, 2024

CardioNerds co-founder Dr. Dan Ambinder, series chair Dr. Teodora Donisan, and Dr. Sukriti Banthiya discuss cardiac tumors with Dr. Juan Lopez-Mattei, a nationally recognized expert in the fields of cardio-oncology and the director of cardiac imaging at the Lee Health Heart Institute. Here, we explore the topic of cardiac tumors, with a focus on distinguishing between primary and secondary tumors. We delve into the symptoms, diagnostic methods, and treatment options. Show notes were drafted by Dr. Sukriti Banthiya and episode audio was edited by CardioNerds Intern and student Dr. Diane Masket. This episode is supported by a grant from Pfizer Inc. This CardioNerds Cardio-Oncology series is a multi-institutional collaboration made possible by contributions of stellar fellow leads and expert faculty from several programs, led by series co-chairs, Dr. Giselle Suero Abreu, Dr. Dinu Balanescu, and Dr. Teodora Donisan. CardioNerds Cardio-Oncology PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls and Quotes - Cardiac Tumors Keep it simple when approaching an intracardiac mass; start with transthoracic echocardiography (TTE) and use transesophageal echocardiography (TEE) or cardiac magnetic resonance (CMR) based on the clinical context. Use TEE when suspecting valvular vegetations or thrombi & CMR for intracavitary cardiac masses. Cardiac tumors can manifest with a variety of symptoms; however, they are more commonly diagnosed as an incidental finding! When faced with the dilemma of selecting the most suitable imaging modality for evaluating a cardiac mass, consider the following hierarchy: begin with TTE as the first choice, followed by CMR. If the patient cannot undergo CMR, the next step is cardiac computed tomography (CT) or Fluorodeoxyglucose F18 positron emission tomography (FDG-PET). TEE is especially useful for the evaluation of small, highly mobile cardiac masses! Imaging cannot substitute a tissue diagnosis of cardiac masses. However, in cases of advanced malignancy, it may not always be necessary. Show notes - Cardiac Tumors Segment One: A big “picture” Approach to Cardiac Tumors Let’s start with an overview of cardiac masses Neoplastic vs non-neoplasticNeoplastic lesions can be further classified into Primary Cardiac Tumors (PCT’s) & Secondary Cardiac Tumor (SCT’s)A majority of PCTs are benign (up to 90%!); however, rarely, they may be malignant. SCTs are more common than PCTs, and, by definition, they are malignant tumors. Now, let’s look at the tools you can use to aid with the diagnosis of cardiac masses… Step 1: Investigate the cardiac mass initially with TTE. Step 2: Collect clues through history-taking & examination.If suspecting valvular vegetations (as in infective endocarditis!) or left atrial appendage thrombus, characterize the mass further with TEE.Consider the possibility of metastatic cardiac tumors in patients with a known malignancy, as they are more common than primary cardiac tumors. In cases where it is uncertain if the mass is a cardiac tumor or thrombus, use CMR to differentiate the two entities. Some findings on TTE that support the presence of a thrombus include left ventricular dysfunction with segmental wall motion abnormalities and/or apical aneurysm as these result in local pockets of stasis (think: Virchow’s triad) Step 3: Put it all together! Think about whether a tissue biopsy will be needed. If yes, determine whether a negative margin or open biopsy will be required. Segment Two: Symptoms, Symptoms, Symptoms! Cardiac tumors may be symptomatic and present in the 3 key ways as outlined below (Think COD 🐟). However, they are more commonly identified as incidental findings! Constitutional symptoms (fever, arthralgias, weight loss, malaise/fatigue) Obstruction - Interfering with blood outflow, arrhythmias, interference with valves causing regurgitation, pericardial effusion +/- tamponade (presyncope, syncope, dyspnea, chest discomfort) Distal embolization (pulmonary or systemic thromboembolic phenomenon) When a metastatic tumor is present, distinguishing symptoms originating from the heart becomes challenging due to potential overlap with symptoms caused by the primary malignancy. This stands in contrast to cases of primary cardiac tumors like myxomas, where symptom localization to the heart is more straightforward. Segment Three: Multimodality Imaging Imaging modalityBest used forAdvantagesDisadvantagesTTEInitial diagnostic modality Masses arising from valvesGood spatial resolution Understanding of hemodynamic significance of massLack of tissue characterization Poor acoustic window in select casesTEESmall highly mobile valvular lesions (<1cm) Visualization of structures with greater accuracy compared to TTE Use of enhancing agents can help differentiate vascular tumors from non-vascular & thrombusLack of tissue characterizationCMRDifferentiates tumor from thrombus. Identifies non-tumor masses or “pseudo-masses,” e.g. cysts, lipomasTissue characterization w/ T1, T2 weighted imaging and gadolinium enhancementLower temporal resolution Limited availability Interference from implanted electrical devicesCT & FDG-PETDifferentiates benign from malignant tumorsAlternative to CMR in pts. w/ claustrophobia & older generation cardiac devicesCT with limited soft tissue & temporal resolution compared to CMR Dietary preparation before FDG Segment Four: The Issue With Tissue! Tissue diagnosis is essential for the diagnosis of primary cardiac tumors; however, it may be less important for metastatic tumors to the heart in cases of known advanced-stage malignancies such as melanoma, breast, and lung. An overview of a rare primary cardiac malignancy: Carney Complex! A complex hereditary syndrome that affects multiple organs, including the heart, skin & endocrine organs. Epidemiology:Autosomal dominant Young age groups in both sexes Clinical presentationIntra-cardiac/extra-cardiac myxomas; intra-cardiac myxomas are multiple, bilateral (atrial and ventricular) & multicentric.Skin findings commonly include lentigines and blue nevi. Endocrine abnormalities include Cushing syndrome, pituitary & adrenal adenomas, thyroid dysfunction. Diagnosis Clues on CMRSSFP (dteady-state free precession) cine imaging, an association of punctiform areas of high & low signal intensity consistent with “Blackberry appearance”Hypoperfused enhancement pattern at first-pass perfusion imaging High signal T2-imaging, iso-intense on T1-weighted imaging TreatmentSurgical resectionAnnual surveillance for Carney complex as they frequently recur (compared with surveillance every 3-5 years for non-Carney myxomas) Genetic testing for PRKAR1 mutations in 1st degree family members Segment Five: “Secondary” to None Secondary cardiac tumors (SCT’s) Epidemiology: Cardiac metastasis is 20-40 times more common than primary cardiac tumors. Etiology:Routes of spread: hematogenous, lymphatic, transvenous, direct invasion Most common malignancies to metastasize to heart include melanomas, carcinomas of breast, lung and esophageal. Clinical PresentationPericardial effusion, tamponadeArrhythmias - “resistant” to antiarrhythmic drugsHeart failure due to myocardial infiltration Valvular dysfunction due to intracavitary masses that impede blood flow. DiagnosisEchocardiography is the initial test of choice.MRIMost malignancies exhibit low signal on T1-weighted imaging & high signal intensity on T2-weighted imaging.Exception, metastaticmelanoma, which appears hyperintense on T1-weighted imaging due to paramagnetic T1 shortening effects of melanin. FDG-PET/CTIn cardiac metastasis, the myocardium has high metabolic activity and can mimic FDG uptake seen in a tumor. Ensure adequate dietary preparation to suppress glucose uptake of normal healthy myocardium. Multi-disciplinary approach to managementTissue diagnosis is necessary.Referral to an interventional cardiologist for transvenous biopsy, orReferral to a cardiac surgeon for minimally invasive surgeryNote – tissue diagnosis can come from another metastatic site.Pathologist to confirm the malignant nature of the tumor. Cardio-oncologist to facilitate multidisciplinary team discussion involving oncologist and cardiac surgeon on the best approach to treatment. Neoadjuvant chemotherapy or radiotherapy vs. cardiac surgery References - Cardiac Tumors Tyebally, Sara, Daniel Chen, Sanjeev Bhattacharyya, Abdallah Mughrabi, Zeeshan Hussain, Charlotte Manisty, Mark Westwood, Arjun K. Ghosh, and Avirup Guha. “Cardiac Tumors: JACC CardioOncology State-of-the-Art Review.” JACC. CardioOncology 2, no. 2 (June 2020): 293–311. https://doi.org/10.1016/j.jaccao.2020.05.009. Basson, Craig T., and H. Thomas Aretz. “Case 11-2002: A 27-Year-Old Woman with Two Intracardiac Masses and a History of Endocrinopathy.” Edited by Richard C. Cabot, Nancy Lee Harris, William F. McNeely, Jo-Anne O. Shepard, Sally H. Ebeling, Stacey M. Ellender, and Christine C. Peters. New England Journal of Medicine 346, no. 15 (April 11, 2002): 1152–58. https://doi.org/10.1056/NEJMcpc010057. Colin, Geoffrey C., Bernhard L. Gerber, Mihaela Amzulescu, and Jan Bogaert. “Cardiac Myxoma: A Contemporary Multimodality Imaging Review.” The International Journal of Cardiovascular Imaging 34, no. 11 (November 2018): 1789–1808. https://doi.org/10.1007/s10554-018-1396-z.

Jan 23, 2024

CardioNerds Atrial Fibrillation Series Co-Chairs Dr. Colin Blumenthal (University of Pennsylvania Cardiology fellow) and Dr. Kelly Arps (Duke University Electrophysiology Fellow) join the 2023 atrial fibrillation guideline writing committee Chair Dr. José Joglar (UT Southwestern) and Vice Chair Dr. Mina Chung (Cleveland Clinic). They review the key takeaways from the 2023 ACC/AHA/ACCP/HRS Guideline for the Diagnosis and Management of Atrial Fibrillation. Audio editing by CardioNerds academy intern, student doctor Pace Wetstein. This podcast was developed in collaboration with the American Heart Association. For more on these guidelines, access the AHA Science News AF Guideline landing page. CardioNerds Atrial Fibrillation PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron!

Jan 16, 2024

CardioNerds nerd out with Drs. Karishma Rahman (Mount Siani Vascular Medicine fellow), Shu Min Lao (Mount Sinai Rheumatology fellow), and Constantine Troupes (Mount Sinai Vascular Surgery fellow). They discuss the following case: A 20-year-old woman with a history of hypertension (HTN), initially thought to be secondary to a mid-aortic syndrome that resolved after aortic stenting, presents with a re-occurrence of HTN. The case will go through the differential diagnosis of early onset HTN focusing on structural etiologies of HTN, including mid-aortic syndrome and aortitis. We will also discuss the multi-modality imaging used for diagnosis and surveillance, indications and types of procedural intervention, and how to diagnose and treat an underlying inflammatory disorder leading to aortitis. The expert commentary was provided by Dr. Daniella Kadian-Dodov, Associate Professor of Medicine and Vascular Medicine specialist at the Icahn School of Medicine at Mount Sinai. Audo editing was performed by Dr. Chelsea Amo-Tweneboah, CardioNerds Academy Intern and medicine resident at Stony Brook University Hospital. US Cardiology Review is now the official journal of CardioNerds! Submit your manuscript here. CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Case Media - Hypertension With a Twist Pearls - Hypertension With a Twist Early onset hypertension (HTN) and lower extremity claudication should raise suspicion for aortic stenosis (including mid-aortic syndrome). Initial evaluation should include arterial duplex ultrasound and cross-sectional imaging such as CT or MR angiogram of the chest, abdomen, and pelvis to assess for arterial stenosis involving the aorta and/or branching vessels. Mid-aortic syndrome can have multiple underlying etiologies. Concentric aortic wall thickening should raise suspicion for an underlying inflammatory disorder. Initial evaluation should include inflammatory markers such as ESR, CRP, and IL-6, but normal values do not exclude underlying aortitis. While Takayasu arteritis is the most common inflammatory disorder associated with mid-aortic syndrome, IgG4-RD should also be a part of the differential diagnosis. IgG subclass panel can detect IgG4-RD with elevated serum IgG4 levels, but some cases can require pathology for diagnosis. Catheter based intervention is a safe and effective treatment of aortic stenosis for both primary aortic stenosis and post-procedural re-stenosis. Multi-modality imaging, including cross-sectional imaging and duplex ultrasound, plays a central role for the diagnosis, management, and post-procedural surveillance of aortic disease. A multi-disciplinary team (as exemplified by the participants of this podcast!) is essential for the management of complex aortopathy cases to optimize clinical outcomes. Show Notes - Hypertension With a Twist 1. Early onset HTN can have multiple etiologies – aortic stenosis (including but not limited to secondary to congenital aortic coarctation and mid–aortic syndrome, as well as in stent re-stenosis if there is a history of aortic stenting), thrombosis, infection, inflammatory/autoimmune disorders, renovascular disease, polycystic kidney disease, and endocrine disorders. 2. Mid-aortic syndrome is characterized by segmental or diffuse narrowing of the abdominal and/or distal descending aorta with involvement of the branches of the proximal abdominal aorta (renal artery, celiac artery, superior mesenteric artery) and represents approximately 0.5 to 2% of all cases of aortic narrowing. Underlying etiologies include genetic syndromes, inflammatory, non-inflammatory, and idiopathic. It is important to have a high suspicion of underlying inflammatory disorders if cross-sectional imaging reveals concentric aortic wall thickening1,2. 3. The current treatment options for aortic stenosis (of the aorta here…not the aortic valve) include balloon angioplasty, aortic stenting, and surgical repair. While studies show the efficacy of balloon angioplasty and aortic stenting, data is limited as studies were mostly done in children3,4. 4. Aortitis5-16 can have multiple etiologies including infectious (such as TB, syphilis, HIV, bacterial, fungal), inflammatory disorders (such as large vessel vasculitis, IgG4-RD, Behcet syndrome, relapsing polychondritis, spondyloarthritis, SLE, and rheumatoid arthritis), and idiopathic. Sometimes, hereditary connective tissue disorders (such Marfan syndrome,, Ehlers-Danlos syndrome, and Loeys-Dietz syndrome) are included in the differential diagnosis, however, they would present as an aortic intramural hematoma (IMH) that typically would appears as eccentric wall thickening (rather than concentric wall thickening more consistent with aortitis). 5. While Takayasu arteritis is the most common inflammatory disorder associated with mid-aortic syndrome, IgG4-RD should also be a part of the differential diagnosis. IgG4-RD is characterized by lymphoplasmacytic infiltrates featuring IgG4 positive plasma cells. It presents in predominantly males between ages 40-70 years of age. The rate of vascular involvement is approximately 8% for aortitis and 20-36% periaortitis. It can be diagnosed with elevated serum IgG4 levels or from tissue biopsy where pathology would show dense lymphoplasmacytic infiltrates in a storiform fibrosis pattern with obliterative phlebitis and >40% plasma calls and >10 positive plasma cells/high power field. It is treated initially treated with high dose steroids with transition to steroid sparing agents such as Rituximab (RTX), azathioprine, mycophenolate, and methotrexate with RTX being the preferred agent10,14. 6. In cases of re-stenosis after initial balloon angioplasty and stenting, indications for re-intervention include hypertension in the setting of imaging evidence of re-stenosis (e.g. > 50% percent aortic narrowing relative to the aortic diameter at the diaphragm level) and pressure gradient across the coarctation > 20 mmHg. The timing of re-intervention in cases of aortitis secondary to underlying inflammatory disorders will require a multi-disciplinary discussion to determine when underlying inflammatory disorder is sufficiently controlled for re-intervention. References - Hypertension With a Twist Bacha E, Hijazi ZM. Management of Coarctation of the Aorta. U: UpToDate, Fulton DR ed UpToDate [Internet] Waltham, MA: UpToDate. 2020. Lazea C, Al-Khzouz C, Sufana C, et al. Diagnosis and management of genetic causes of middle aortic syndrome in children: a comprehensive literature review. Therapeutics and Clinical Risk Management. 2022:233-248. Rodés-Cabau J, Miró J, Dancea A, et al. Comparison of surgical and transcatheter treatment for native coarctation of the aorta in patients≥ 1 year old. The Quebec Native Coarctation of the Aorta Study. American heart journal. 2007;154(1):186-192. Meadows J, Minahan M, McElhinney DB, McEnaney K, Ringel R. Intermediate outcomes in the prospective, multicenter Coarctation of the Aorta Stent Trial (COAST). Circulation. 2015;131(19):1656-1664. Nikiphorou E, Galloway J, Fragoulis GE. Overview of IgG4-related aortitis and periaortitis. A decade since their first description. Autoimmunity reviews. 2020;19(12):102694. Kadian-Dodov D, Seo P, Robson PM, Fayad ZA, Olin JW. Inflammatory Diseases of the Aorta: JACC Focus Seminar, Part 2. Journal of the American College of Cardiology. 2022;80(8):832-844. Sohrabi B, Jamshidi P, Yaghoubi A, et al. Comparison between covered and bare Cheatham-Platinum stents for endovascular treatment of patients with native post-ductal aortic coarctation: immediate and intermediate-term results. JACC: Cardiovascular Interventions. 2014;7(4):416-423. Marvisi C, Buttini EA, Vaglio A. Aortitis and periaortitis: the puzzling spectrum of inflammatory aortic diseases. La Presse Médicale. 2020;49(1):104018. Bossone E, Pluchinotta FR, Andreas M, et al. Aortitis. Vascular pharmacology. 2016;80:1-10. Carruthers MN, Topazian MD, Khosroshahi A, et al. Rituximab for IgG4-related disease: a prospective, open-label trial. Annals of the rheumatic diseases. 2015;74(6):1171-1177. Wallace ZS, Perugino C, Matza M, Deshpande V, Sharma A, Stone JH. Immunoglobulin G4–related disease. Clinics in chest medicine. 2019;40(3):583-597. Wallace ZS, Naden RP, Chari S, et al. The 2019 American College of Rheumatology/European league against rheumatism classification criteria for IgG4‐related disease. Arthritis & Rheumatology. 2020;72(1):7-19. Onen F, Akkoc N. Epidemiology of Takayasu arteritis. La Presse Médicale. 2017;46(7-8):e197-e203. Ebbo M, Grados A, Samson M, et al. Long-term efficacy and safety of rituximab in IgG4-related disease: data from a French nationwide study of thirty-three patients. PLoS One. 2017;12(9):e0183844. Maz M, Chung SA, Abril A, et al. 2021 American College of Rheumatology/Vasculitis Foundation guideline for the management of giant cell arteritis and Takayasu arteritis. Arthritis Care & Research. 2021;73(8):1071-1087. Lupi-Herrera E, Sanchez-Torres G, Marcushamer J, Mispireta J, Horwitz S, Vela JE. Takayasu's arteritis. Clinical study of 107 cases. American heart journal. 1977;93(1):94-103.

Jan 9, 2024

CardioNerds Dr. Rick Ferraro (cardiology fellow at Johns Hopkins Hospital) and Dr. Eunice Dugan (cardiology fellow at the Cleveland Clinic) join episode lead Dr. Tiffany Brazile (cardiology fellow at the University of Texas Southwestern Medical Center and postdoctoral fellow at the Institute for Exercise and Environmental Medicine) to discuss the impact of obesity on cardiovascular disease risk, differential risk in specific populations, and effective strategies for counseling patients. They are joined by expert Dr. Jaime Almandoz, Medical Director of the Weight Wellness Program and an Associate Professor of Medicine at the University of Texas Southwestern Medical Center. Audio editing was performed by CardioNerds Academy Intern, student Dr. Tina Reddy. This episode was produced in collaboration with the American Society of Preventive Cardiology (ASPC) with independent medical education grant support from Novo Nordisk. See below for continuing medical education credit. Claim CME for this episode HERE. CardioNerds Prevention PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls and Quotes - Obesity & Cardiovascular Disease Risk The durability of metabolically healthy obesity (i.e., normal A1c, lipids, LFTs, BMP, normotensive) is limited. Within 5 years, a third of adults with “metabolically healthy” obesity will develop a cardiometabolic complication. The biomechanical and psychosocial complications of obesity are just as important as the cardiometabolic complications. Biomechanical and psychosocial complications, including obstructive sleep apnea, joint pain, and mood disorders also influence cardiovascular disease risk. Weight loss is not always the patient’s goal. Meet patients where they are and understand their challenges, concerns, and long-term goals with respect to their cardiovascular health and obesity. This information provides an opportunity to frame the conversation in a supportive and engaging way that allows for patient education. Body mass index (BMI) is a screening tool for obesity, but is not sufficient for providing individualized care. Obesity management methods that result in rapid weight loss may not be appropriate for all patients. These methods, such as bariatric surgery and GLP1-receptor agonists, require regular monitoring, follow-up, and multidisciplinary care (e.g., nutritionist, exercise physiologist, endocrinologist, cardiologist, psychologist, etc.). Show notes - Obesity & Cardiovascular Disease Risk Is it possible to be healthy at any size? Whether an individual can be healthy at any size depends on the definition of health and its durability.Approximately 10-15% of adults with obesity are metabolically healthy.The risk for developing cardiometabolic disease is higher in obese versus non-obese adults. One in three adults with metabolically healthy obesity will develop cardiometabolic complications (i.e., insulin resistance/diabetes, hyperlipidemia, hypertension) within five years. Thus, metabolically healthy obesity may represent a transient phenotype with adverse long-term consequences. Consider non-metabolic health consequences of obesity that also influence cardiovascular disease risk. Obstructive sleep apnea, joint pain leading to decreased physical activity, and mood disorders are key considerations here and encompass the biomechanical and psychosocial consequences of obesity. Does large, rapid weight loss result in poorer long-term weight loss than slower, gradual weight loss? When approaches to weight loss are not sustainable, such as extremely low-calorie diets or extreme fitness regimens, the results and associated health benefits are less likely to be durable. Rapid, large-magnitude weight loss is appropriate for some adults with obesity and can be achieved through bariatric surgery and/or anti-obesity medications. Safety and sustainability are supported by regular follow-up, monitoring, and multidisciplinary care to incorporate nutritional and physical activity recommendations. Obesity management must be individualized to meet patient needs and goals while accounting for comorbid conditions (e.g., frailty, fall risk, disordered eating, etc.) What are some best practices for incorporating the diagnosis of obesity into a patient’s assessment, including cardiovascular disease risk? Seek to understand what the patient wants to achieve during the office visit. Inquire about the patient’s health journey, goals, concerns, and challenges. In addition to addressing the patient’s expressed goals, frame the conversation in terms of concerns you have about the patient’s health. Incorporate objective measures, such as body composition, waist circumference, cardiorespiratory fitness, and biomarkers that can help support your concerns and management goals. Does obesity impact men and women differently? Prevalence: of adults with obesity, women are more likely than men to have severe obesity. Obesity is also more prevalent in women of certain racial/ethnic minorities as compared to men. Fat distribution: men tend to have more visceral or central adiposity, which is associated with increased cardiometabolic risk. Earlier in adulthood, women tend to have more body fat in the gluteofemoral region. With advancing age and menopause, the distribution of excess adipose tissue in women often shifts to the visceral/central region and may enhance cardiometabolic risk. What are the practical methods for evaluating and measuring obesity during a patient visit? BMI is a screening tool for obesity. It is blind to body composition and fat distribution. Cut points for BMI and the association with cardiovascular disease risk vary by race/ethnicity. Consideration of different BMI cut points for patients of various racial/ethnic backgrounds is important when evaluating candidacy for bariatric surgery or anti-obesity medications. Waist circumference is a useful measure to estimate visceral/central adiposity. Cut points for men and women have been established that are associated with increased cardiovascular disease risk across multiple studies. Measures of body composition provide valuable information about fat and lean body masses. DEXA scans and MRIs also provide data on fat distribution; however, they are impractical and expensive for regular use in the clinical setting. Bioelectrical impedance can provide body composition data efficiently during a clinic visit. What are alternative validated tools beyond the Pooled Cohort Equation that can be used to estimate ASCVD risk in various ethnic/racial groups? The QRISK3 calculator is an alternative assessment tool for 10-year ASCVD risk that has been validated in 9 different ethnic groups. The calculator includes novel variables, such as chronic kidney disease, history of migraines, severe mental illness, erectile dysfunction, and family history of premature ASCVD. https://www.qrisk.org/ What are the mechanisms by which obesity impacts the development of cardiovascular disease? Obesity and lipotoxicity can impact cardiovascular disease development through multiple mechanisms, including inflammation that can lead to a prothrombotic state, insulin resistance, and alterations in lipid metabolism that can promote atherosclerosis. The distribution of body fat is highly heterogeneous and is partially driven by genetics. Brown adipose tissue has a high mitochondrial load and is involved in adaptive thermogenesis. White adipose tissue is considered more of a storage form of adipose tissue that also functions as an endocrine organ and provides insulation/protection for vital organs. Ectopic fat depots, such as hepatic steatosis or epicardial adipose tissue, are metabolically active and can influence adjacent tissues through humoral and neurohormonal signals. These fat depots may also exert mechanical effects on the organs they surround. The ways in which individuals accrue fat in these different locations, the specific mechanisms by which they may increase cardiovascular disease development, and whether targeted therapies to reduce specific fat depots are incompletely understood. References - Obesity & Cardiovascular Disease Risk Wilding JPH, Batterham RL, Calanna S, et al. Once-Weekly Semaglutide in Adults with Overweight or Obesity. N Engl J Med. 2021;384(11):989-1002. doi:10.1056/NEJMoa2032183 https://pubmed.ncbi.nlm.nih.gov/33567185/ Marso SP, Daniels GH, Brown-Frandsen K, et al. Liraglutide and Cardiovascular Outcomes in Type 2 Diabetes. N Engl J Med. 2016;375(4):311-322. doi:10.1056/NEJMoa1603827 https://pubmed.ncbi.nlm.nih.gov/27295427/ Marso SP, Bain SC, Consoli A, et al. Semaglutide and Cardiovascular Outcomes in Patients with Type 2 Diabetes. N Engl J Med. 2016;375(19):1834-1844. doi:10.1056/NEJMoa1607141 https://pubmed.ncbi.nlm.nih.gov/27633186/ Gerstein HC, Colhoun HM, Dagenais GR, et al. Dulaglutide and cardiovascular outcomes in type 2 diabetes (REWIND): a double-blind, randomised placebo-controlled trial. Lancet. 2019;394(10193):121-130. doi:10.1016/S0140-6736(19)31149-3 https://pubmed.ncbi.nlm.nih.gov/31189511/

Dec 29, 2023

CardioNerds co-founder Dr. Amit Goyal, series co-chair Dr. Colin Blumenthal, and episode lead Dr. Anushka Tandon to discuss pharmacologic anticoagulation options in atrial fibrillation with Drs. Ashley Lochman and Chris Domenico. The case-based review helps clarify some key concepts, such as when warfarin is preferred for anticoagulation, who may be a good DOAC (direct-acting oral anticoagulant) candidate, how to choose an appropriate DOAC agent, and how to manage anticoagulation therapy in patients already on antiplatelet therapies. Notes were drafted by Dr. Anushka Tandon. The episode audio was edited by student Dr. Shivani Reddy. This CardioNerds Atrial Fibrillation series is a multi-institutional collaboration made possible by contributions of stellar fellow leads and expert faculty from several programs, led by series co-chairs, Dr. Kelly Arps and Dr. Colin Blumenthal. This episode was planned and recorded prior to the release of the 2023 ACC/AHA/ACCP/HRS Guideline for the Diagnosis and Management of Atrial Fibrillation. Please refer to this guideline document for the most updated recommendations. We have collaborated with VCU Health to provide CME. Claim free CME here! CardioNerds Atrial Fibrillation PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls and Quotes - Anticoagulation Pharmacology Avoid potentially fatal errors with this terminology tip for correctly referencing non-warfarin oral anticoagulant agents: it’s DOAC (like, please DO use AntiCoagulation), not NOAC (imagine someone interpreting that as “NO AntiCoagulation for this patient” at discharge – yikes)! Sometimes, an oldie really is a goodie – warfarin is recommended over DOACs for patients with mechanical heart valves, moderate-to-severe mitral stenosis, anti-phospholipid antibody syndrome (APLS), left ventricular (LV) thrombus, higher INR goals, or DOAC failure. Patient preference and medication costs should also be considered – at the end of the day, “the best drug is the drug that a patient is willing to take!” Standard-dose rivaroxaban or apixaban may be considered for use in patients weighing >120kg or with BMI >40; use of other DOACs should be limited to pts weighing =/ 120kg or with a BMI >40. However, ISTH updated their guidance in 2021 [6] to support using rivaroxaban and apixaban for VTE treatment or prevention “regardless of body weight and BMI”; these DOACs are often used in patients with obesity for non-VTE indications (e.g., thromboprophylaxis in atrial fibrillation). Data to support this include a post-hoc analysis of the ARISTOTLE trial (apixaban in atrial fibrillation), which showed that patients weighing >120kg (~5% of the study population) had similar results to the overall study population. It’s important to use adjusted body weight when calculating CrCl to estimate renal function and determine DOAC dosing in obese patients. Other DOACs should be avoided in pts >120kg/with BMI >40 due to limited or unconvincing data at this time.Hepatic impairment: DOACs have varying hepatic metabolism (apixaban is the most hepatically cleared and dabigatran the least), but limited data exist for DOAC dose adjustments in patients with hepatic impairment. DOACs should NOT be used in Child-Pugh Class C/severe hepatic disease, while rivaroxaban (and betrixaban)[GU1] should also NOT be used in moderate/CP Class B patients. DOACs should be avoided in patients with decompensated/unstable cirrhosis. Aside from these caveats, DOACs may be considered for use in mild-moderate (Class A/B) hepatic impairment (with exceptions as above).Renal impairment: DOACs may be used in stable CKD with appropriate renal dose adjustments; DOAC therapies should be held in the context of AKI. Dabigatran is the most renally cleared and generally avoided for this reason. Apixaban is the least renally cleared and is generally the preferred agent in patients with renal impairment, including ESRD (in the context of which apixaban use is supported by data, including that from a 2022 cohort study [7] vs. warfarin).Drug Interactions: rivaroxaban, apixaban, edoxaban, and dabigatran are all P-gp substrates that will be affected by P-gp inducers or inhibitors (e.g., dronedarone, amiodarone, digoxin, diltiazem, verapamil, antiepileptics, antifungals, chemotherapy agents, and St. John’s Wort). Rivaroxaban and apixaban are substrates of CYP450 enzymes, prominently 3A4, 3A5, and 2J2. Apixaban is also metabolized by 1A2 and 2C 8/9/19 to a lesser degree. Some DOACs may interact with atorvastatin or ticagrelor, but these interactions are not typically a barrier to concurrent therapy if clinically indicated. Running a drug interaction report or consulting a pharmacist to help evaluate and safely navigate drug interactions is extremely helpful in these scenarios. *In addition to DOAC package inserts, the AHA guide to DOAC use [8] is a great resource that summarizes renal/hepatic dosing considerations, drug interactions, and anticoagulant transition recommendations. What safety profile and bleeding risk considerations exist for warfarin versus DOACs? Warfarin has been studied versus individual DOACs; generally, DOACs are preferred from a safety standpoint due to lower risk of bleeding. The RE-LY trial [9] showed no difference in major bleeding but less intracranial hemorrhage (ICH) with dabigatran when compared to warfarin. The ROCKET-AF [10] trial showed a greater Hgb drop/need for transfusion with rivaroxaban but higher critical/fatal bleeding (including ICH) incidence with warfarin. In the ARISTOTLE [11] trial, apixaban was associated with significantly lower bleeding outcomes than warfarin, except for GI bleeding (for which there was no significant difference between groups). Edoxaban had a lower incidence of overall GI bleed (upper and lower GI bleeding combined), but not individual upper or lower GI bleeding, than warfarin in the ENGAGE [12] trial.There are no direct head-to-head trials comparing DOACs, though some data suggest apixaban is associated with a lower bleeding risk than rivaroxaban (no difference in ICH), and that rivaroxaban may be associated with a higher risk of hemorrhagic stroke. In older adults, DOACs can be used without safety concerns over warfarin, though avoiding dabigatran may be suggested due to a signal for increased bleeding outcomes in older adult patients. The ELDERCARE-AF [13] trial from Japan showed no difference in major bleeding, but higher rates of GI bleeding and all bleeding, with edoxaban vs. placebo in adults >/= 80 years. Overall, apixaban is generally considered safe to use/the preferred DOAC option in patients with a history of GI bleeding.

Dec 27, 2023

CardioNerds (Dr. Amit Goyal) join Dr. Anureet Malhotra, Dr. John Fritzlen, and Dr. Tarun Dalia from the University of Kansas School of Medicine for some of Kansas City’s famous barbeque. They discuss a case of Hydroxychloroquine induced cardiomyopathy. Notes were drafted by Dr. Anureet Malhotra, Dr. John Fritzlen, and Dr. Tarun Dalia. Expert commentary was provided by Dr. Pradeep Mammen. The episode audio was edited by Dr. Akiva Rosenzveig. Drug-induced cardiomyopathy remains an important and under-recognized etiology of cardiomyopathy and heart failure. Hydroxychloroquine is a disease-modifying antirheumatic drug used for various rheumatological conditions, and its long-term use is well-known to have toxic effects on cardiac muscle cells. Multiple cardiac manifestations of these drugs have been identified, the most prominent being electrophysiological disturbances. In this episode, we discuss a biopsy-proven case of hydroxychloroquine-induced cardiotoxicity with detailed histopathological and imaging findings. We develop a roadmap for the diagnosis of hydroxychloroquine-induced cardiomyopathy and discuss the various differentials of drug-induced cardiomyopathy. We highlight the importance of clinical monitoring and early consideration of drug-induced toxicities as a culprit for heart failure. US Cardiology Review is now the official journal of CardioNerds! Submit your manuscript here. CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Case Media - Hydroxychloroquine induced cardiomyopathy Pearls - Hydroxychloroquine induced cardiomyopathy Continued decline in left ventricular systolic function despite appropriate guideline directed medical therapy should prompt a thorough evaluation for unrecognized etiologies and warrants an early referral to advanced heart failure specialists. Transthoracic echocardiogram is a valuable non-invasive screening tool for suspected pulmonary hypertension, but right heart catheterization is required for definitive diagnosis. Cardiac MRI can be used for better characterization of myocardial tissue and can aid in the evaluation of patients with non-ischemic cardiomyopathy. Hydroxychloroquine (HCQ) is a commonly used DMARD that remains an underrecognized etiology of cardiomyopathy and heart failure. In addition to ophthalmological screening, annual ECG, as well as echocardiography screening for patients on long-term HCQ therapy, should be considered in patients at risk for cardiovascular toxicity, including those with pre-existing cardiovascular disease, older age, female sex, longer duration of therapy, and renal impairment. Management of hydroxychloroquine-associated cardiomyopathy consists of discontinuing hydroxychloroquine and standard guideline-directed medical therapy for heart failure. HCQ cardiomyopathy may persist despite medical therapy, and advanced therapy options may have to be considered in those with refractory heart failure. Show Notes - Hydroxychloroquine induced cardiomyopathy What are the various cardiotoxic effects of hydroxychloroquine (HCQ) and the mechanism of HCQ-mediated cardiomyopathy? One of the most frequently prescribed disease-modifying antirheumatic drugs (DMARDs), HCQ is an immunomodulatory and anti-inflammatory agent that remains an integral part of treatment for a myriad of rheumatological conditions. Its efficacy is linked to inhibiting lysosomal antigen processing, MHC-II antigen presentation, and TLR functions.8 The known cardiac manifestations of HCQ-induced toxicity include conduction abnormalities, ventricular hypertrophy, hypokinesia, and lastly, cardiomyopathy. Conduction Abnormalities - by binding to and inhibiting the human ether-à-go-go-related gene (hERG) voltage-gated potassium channel, also known as Ikr channel, HCQ can lead to prolongation of corrected QT (QTc) interval. This can lead to an increased risk of drug-induced Torsades de pointes and other lethal ventricular arrhythmias. Cardiomyopathy - HCQ is a lipophilic drug that easily permeates myocytes and binds to lysosomal phospholipids, leading to lysosomal accumulation of phospholipids. Furthermore, by increasing the pH of the lysosome, HCQ inhibits lysosomal enzymes, which interferes with lysosomal function and exocytosis, leading to an acquired lysosomal storage disorder. This results in myofibrillar disorganization, atrophy, and fibrosis, which may lead to cardiomyopathy. Risk factors for the development of cardiotoxicity are thought to be pre-existing cardiovascular disease, older age, female sex, longer duration of therapy, and renal impairment. 8 Extracardiac side effects – With long term use, HCQ can also lead to ocular toxicity, neuropathy, and myopathy with similar pathogenesis as cardiotoxicity, i.e., acquired lysosomal storage disorder. What are the histopathological findings of HCQ induced Cardiomyopathy? HCQ causes an acquired lysosomal storage disorder due to the inhibition of constitutive autophagy present in normal cardiac myocytes. On histopathology, this presents itself as cytoplasmic vacuoles, lamellar bodies and curvilinear inclusion bodies in cytoplasm that can be visualized with electron microscopy. Of these findings, curvilinear bodies are thought to be pathognomonic for HCQ induced cardiotoxicity. On histopathology, these findings can resemble inherited lysosomal storage disorders including Anderson- Fabry disease except for the presence of curvilinear bodies. 9 What is the differential diagnosis for HCQ induced cardiomyopathy? Differentials of HCQ mediated cardiomyopathy include storage disorders like Fabry disease, adult-onset Pompe disease (acid maltase deficiency), and Danon disease. Many drug-induced myopathies such as amiodarone, rituximab, prednisone, cocaine, cobalt, and several chemotherapeutic agents can also resemble HCQ mediated cardiotoxicity. Furthermore, amyloidosis, sarcoidosis and myocarditis also merit consideration as they can lead to restrictive physiology and present similar echocardiographic findings. They can be differentiated using advanced cardiac imaging such as cardiac MRI and histopathological findings on endomyocardial biopsy. How can Cardiac MRI (CMR) assist in the work up of non-ischemic cardiomyopathy? CMR can enhance visualization of cardiac structures that may be poorly seen on echocardiogram due to location or poor acoustic windows. CMR also uniquely provides detailed tissue characterization. CMR can be used for assessing many pathologies, including aortic disease, coronary artery disease, cardiomyopathies, pericardial disease, and congenital heart disease. 4 CMR is also considered the gold standard for assessing cardiac function and can be used to assess valvular pathologies with flow assessment. Late gadolinium enhancement (LGE) refers to the discrimination of regions of scar, necrosis, or inflammation from normal tissue by the prolonged retention of gadolinium-based contrast agents. The pattern of LGE, as well as T1 and T2 mapping, aid in tissue characterization and accurate diagnosis. Key take-home points are as follows: The presence of LGE in a coronary distribution can support the diagnosis of prior myocardial infarction and aid in the assessment of myocardial viability. LGE in the mid-wall and sub-epicardium of the LV is characteristic of viral myocarditis. In addition, T1 mapping helps estimate the extracellular volume, and T2 weighted imaging can show myocardial edema in patients with myocarditis. In amyloidosis, the classic CMR findings include thick LV walls, valves, and interatrial septum and the presence of a pericardial effusion. They may also have the existence of amyloid protein in the myocardial interstitium associated with characteristic patterns of circumferential subendocardial LGE. What is the management of HCQ induced cardiomyopathy? Diagnosis – HCQ cardiomyopathy diagnosis requires a high level of suspicion. A detailed history is an essential first step. CMR can aid in tissue characterization and is a helpful non-invasive tool. Definitive diagnosis can be established by obtaining an endomyocardial biopsy, given its distinctive histopathological findings, and ruling out close mimics of HCQ-induced cardiotoxicity. Treatment – the potentially reversible nature of HCQ cardiomyopathy makes early diagnosis and discontinuation of the offending drug the mainstays of treatment along with guideline directed medical therapy for heart failure. Recovery is variable and may take months or even years for LV function to improve. In some cases, there may be partial or no recovery, requiring advanced therapies evaluations. References - Hydroxychloroquine induced cardiomyopathy Greiner S, Jud A, Aurich M, et al. Reliability of Noninvasive Assessment of Systolic Pulmonary Artery Pressure by Doppler Echocardiography Compared to Right Heart Catheterization: Analysis in a Large Patient Population. Journal of the American Heart Association.2014;3(4).10.1161/JAHA.114.001103 Augustine DX, Coates-Bradshaw LD, Willis J, et al. Echocardiographic assessment of pulmonary hypertension: a guideline protocol from the British Society of Echocardiography. Echo research and practice. 2018;5(3):G11-G24. 10.1530/ERP-17-0071 Page RL, O’Bryant CL, Cheng D, et al. Drugs That May Cause or Exacerbate Heart Failure. Circulation. 2016;134(6).https://doi.org/10.1161/CIR.0000000000000426 Kramer CM. Role of Cardiac MR Imaging in Cardiomyopathies. Journal of Nuclear Medicine. 2015;56(Supplement_4):39S45S.10.2967/jnumed.114.142729. Joyce E, Fabre A, Mahon N.

Dec 20, 2023

CardioNerds meet with fellows from The Christ Hospital, Drs. Hanad Bashir, Hyunsoo Chung, and Dalia Aziz to discuss the following case that highlights angioleiomyoma: A 60-year-old woman with a past medical history significant for breast cancer (on tamoxifen) presented as a transfer to our facility for a clot-in-transit. She had initially presented to the outside hospital after progressive dyspnea on exertion and recent syncope. She was found on an echocardiogram to have a right atrial mass spanning into the right ventricle. CTA of the chest and abdomen/pelvis demonstrated extensive thrombus burden spanning from the IVC into the right ventricle. She was transferred to our facility for intervention. Endovascular attempts were unsuccessful, at which point she underwent surgical thrombectomy. Gross examination of the mass revealed a cylindrical shape, homogeneous tan color, rubbery soft tissue, measuring 25.5 cm in length and 2.3 cm in diameter. Histology confirmed the presence of angioleiomyoma. A second, smaller mass (5.2cm long and 4mm in diameter) was removed from under the tricuspid valve, with histology consistent with leiomyoma. Estrogen receptor and progesterone receptor staining were strongly positive, leading to the discontinuation of tamoxifen. Given the presence of uterine fibroids identified on the CT scan, there was concern about a uterine origin. A hysterectomy is planned for her in the near future. Expert commentary is provided by Dr. Wojciech Mazur. Episode audio was edited by student Dr. Adriana Mares. US Cardiology Review is now the official journal of CardioNerds! Submit your manuscript here. CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Case Media - The Tall Tail Heart: Angioleiomyoma – The Christ Hospital Pearls - The Tall Tail Heart: Angioleiomyoma – The Christ Hospital Although evaluation of cardiac mass by echocardiography can provide information such as size, location, and morphology, adjunctive cross-sectional imaging may be used depending on the need for further temporal resolution (CT) or tissue characterization via cardiac MRI (CMR). If suspicious for elevated metabolic activity, there should be consideration of FDG-PET. Tamoxifen (a selective estrogen receptor modulator) is an agent used for breast cancer therapy. However, its use has been associated with endometrial hyperplasia, uterine fibroids, endometrial and uterine malignancy. Increased risk of malignancy has been seen more often in post-menopausal women and is dose and time-dependent. Clot in transient is a mobile thrombus, typically within the right heart structures. It is estimated to occur in 4-18% of patients with pulmonary embolism and is associated with elevated morbidity and mortality. Treatment includes surgical embolectomy, endovascular embolectomy, systemic thrombolysis, catheter-directed thrombolysis, or systemic anticoagulation. Angioleiomyoma is a rare benign pericystic tumor that most commonly affects the extremities. There are case reports of other affected sites, including the uterus. Invasion into the cardiac structures is exceedingly rare. The only established treatment for angioleiomyoma is surgical resection. Show Notes - The Tall Tail Heart: Angioleiomyoma – The Christ Hospital Syncope Syncope is a transient loss of consciousness secondary to reduced blood flow to the brain. Often, certain presentations are mislabeled as syncope, such as seizure disorders, posttraumatic loss of consciousness, and cataplexy. An organized diagnostic approach should be used to reduce hospital admissions and medical costs and increase diagnostic accuracy. Syncope can be divided into five general subgroups. 1) Neurally mediated reflex syncope (carotid sinus syndrome, vasovagal) 2) Orthostatic syncope 3) Cardiac arrhythmias 4) Structural cardiac and pulmonary causes 5) Cerebrovascular disorders. Initial evaluation should include thorough H&P, including orthostatic vitals and ECG. If diagnosis remains uncertain after initial evaluation, patients’ syncope should be risk stratified into three groups: high, intermediate, and low risk. Additionally, the 2017 ACC/AHA/HRS guidelines stratify patient risk based on short-term ( 30 days) morbidity and mortality based on initial examination and history. Patients presenting with high-risk and short-term syncope features should be immediately hospitalized for further diagnostic testing and treatment. High-risk features are usually indicative of underlying cardiovascular causes that could lead to sudden death; this includes but is not limited to life-threatening arrhythmias and acute coronary syndrome. Risk stratification also determines the selection of diagnostic tests. When underlying cardiac etiology is suspected, diagnostic tests such as echocardiography, CT angiography, cardiac magnetic resonance, electrophysiology study, exercise stress testing, and coronary angiography may be valuable in establishing timely diagnosis in high-risk patients. Choice of study modality varies greatly based on patient presentation and risk factors. In contrast to patients presenting with high-risk syncope, low-risk patients are discharged home with re-assurance and follow-up. Strategy for Intracardiac Masses First, take into account the patient's age at the time of presentation, as certain medical conditions like rhabdomyomas and fibromas are more commonly observed among pediatric patients. Second, assess the likelihood from an epidemiological perspective and consider the clinical probability. For instance, if a patient has recently experienced an anterior wall myocardial infarction and exhibits an akinetic ventricular apex, the presence of a cardiac mass during echocardiography could indicate the possibility of an intracardiac thrombus. Third, factor in the location of the tumor. If the mass is detected on the valves, potential diagnoses to consider include thrombus or vegetation. While masses within the heart chambers might still indicate thrombus, it's also important to contemplate other possibilities, such as myxomas, lymphomas, and metastases. Fourth, delve into the tissue characteristics of the mass using additional diagnostic imaging methods like cardiac magnetic resonance imaging. Imaging Modalities for Intracardiac Masses Transthoracic echocardiography (TTE) is readily available and non-invasive. Transesophageal echocardiography (TEE) offers insights into size, shape, attachment site, extension, and hemodynamic effects. Ultrasound-enhancing agents in echocardiography help differentiate various masses. Thrombi and benign tumors display a non or low-enhancing pattern. Malignancies and highly vascular tumors display a hyperenhancing pattern. Doppler velocities aid in assessing the hemodynamic impact. Cardiac MRI (CMR) is invaluable in the assessment of cardiac masses. In addition to anatomy, dimensions, and mass consistency, using different signal sequences like T1, T2, early and late gadolinium enhancement differentiate tissue characteristics and unveil fatty presence, necrosis, bleeding, inflammation, and vascularity within a mass. Cardiac CT provides high spatial and temporal resolution, multiplanar image reconstruction, and rapid acquisition. The broad field of view allows for the evaluation of the chest, lung tissue, vascular structures, and potential masses within the chest. Cardiac CT can be used to detect calcifications within the mass, although it has less soft tissue resolution compared with CMR. FDG-PET/CT can help gauge tumors' metabolic activity. When CT alone doesn't decisively determine benign or malignant nature, PET/CT steps in, aiding in malignancy diagnosis and guiding biopsy locations, staging, and cancer therapy planning. Cardiac tumors Cardiac tumors can be categorized into primary and secondary tumors. Secondary tumors, arising from metastasis, are more prevalent and often stem from cancers like melanoma, breast, or lung cancer. Secondary tumors can lead to issues like pericardial effusion with or without cardiac tamponade, myocardial infiltration, obstruction, or embolization. Primary tumors include benign (about 80%) and malignant (about 20%) types. Malignant tumors are mainly sarcomas, such as angiosarcomas and rhabdomyosarcomas. Benign tumors encompass myxomas, gelatinous masses with scattered myxoma cells; papillary fibroelastomas, frond-like masses typically on valves; lipomas, composed of fat cells; fibromas, containing fibroblasts and mostly found in the left ventricle; and rhabdomyomas, made of maldeveloped cardiac myocytes and often seen in ventricles. Other rare tumors include Purkinje cell tumors. However, the latter three mentioned are more common in children. Clot-in-transit Clot-in-transit (CIT) is the presence of mobile echogenic material in the right atrium or ventricle as seen on ultrasound. Right heart clots are classified into three types based on their morphology:Type A (common and carries a high risk of pulmonary embolization)Type B (assumed to originate from the atrium or ventricle) Type C (rare and migratory, resembling cardiac myxomas) Intervention options for CIT include catheter-based thrombolysis, systemic (IV) thrombolysis, surgical/endovascular embolectomy, and anticoagulation therapy. Catheter-based thrombolysis involves high-frequency ultrasound exposure, catheter-directed thrombolysis, mechanical thrombectomy, and endovascular clot suction. It has a high success rate but may not work for bulky thrombi.

Dec 19, 2023

Calling all those with a passion for cardiovascular prevention! In this episode of the CardioNerds Cardiovascular Prevention Series, we take a deep dive into the world of glucagon-like peptide-1 (GLP-1) receptor agonists. Along the way, you’ll hear about the biology of the GLP-1 molecule and its related peptides, learn more about how GLP-1 agonists promote glycemic control, weight loss, and cardiometabolic health, and explore the current body of literature supporting the individualized application of these medications to patients with diabetes, obesity, and/or ASCVD. Join Dr. Christian Faaborg-Andersen (CardioNerds Academy Fellow and Internal Medicine Resident at MGH), Dr. Gurleen Kaur (Director of the CardioNerds Internship, Chief of House Einthoven, and Internal Medicine resident at BWH), and Dr. Rick Ferraro (CardioNerds Academy House Faculty and Cardiology Fellow at JHH) for a wide-ranging discussion on GLP-1 and GIP agonists with Dr. Dennis Bruemmer (Cardiologist and Director of the Center for Cardiometabolic Health in the section of Preventive Cardiology at the Cleveland Clinic). Show notes were drafted by Dr. Christian Faaborg-Andersen. Audio editing was performed by CardioNerds Academy Intern, student Dr. Tina Reddy. This episode was produced in collaboration with the American Society of Preventive Cardiology (ASPC) with independent medical education grant support from Novo Nordisk. See below for continuing medical education credit. Claim CME for this episode HERE. CardioNerds Prevention PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls and Quotes - GLP-1 Agonists: Mechanisms to Applications The selection and dosing of GLP-1 and GIP agonists (GLP-1s and GIPs) depends on their intended use as an anti-glycemic or anti-obesity agent. The cardiovascular benefits of GLP-1s and GIPs may be independent of improvements in glycemic control, and in part be driven by reduction in inflammation, a key driver of arterial plaque formation. In patients with comorbid coronary artery disease, obesity, and diabetes, GLP-1 agonists and SGLT-2 inhibitors should be used as first-line agents, over metformin. Tirzepatide is a dual agonist that activates GIP and GLP-1 receptors. GIP is highly expressed in the brain, which may mediate satiety, promote energy expenditure, and enhance peripheral glucose metabolism. Caution should be used with GLP-1 agonists in patients with long-standing diabetes complicated by gastroparesis, as well as incompletely treated diabetic retinopathy. GI upset is not uncommon with GLP-1/GIP agonists, and switching to a different agonist is unlikely to help. Show notes - GLP-1 Agonists: Mechanisms to Applications What are the mechanisms of action by which GLP-1 and GIP controls blood sugar and body weight? Glucagon-like peptide-1 (GLP-1) is an endogenous hormone that is secreted in response to an oral glucose load. It promotes insulin release, inhibits glucagon secretion, and slows gastric emptying via the brain-intestine axis, leading to satiety. GLP-1 agonists are medications that mimic the effect of this hormone and, on average, lower hemoglobin A1C by 0.8% to 1.5%. These medications include semaglutide, liraglutide, and dulaglutide. Glucose-dependent insulinotropic polypeptide (GIP) is also an endogenous hormone, similarly secreted by the body in response to an oral glucose load such as a meal. GIP is highly expressed in the arcuate nucleus and hypothalamus, which may mediate satiety, promote energy expenditure, and enhance peripheral glucose metabolism. Tirzepatide is a dual GLP-1/GIP agonist. What is the role of GLP-1/GIP agonists in patients with overweight/obesity and/or type 2 diabetes? How does the dosing of GLP-1/GIP medications change with their intended disease target? The STEP-1 trial showed that once-weekly semaglutide led to a net 15% weight loss in non-diabetic, obese/overweight patients. The SELECT trial builds on these results, showing that once-weekly semaglutide resulted in a 20% reduction in the primary composite endpoint of cardiovascular death, nonfatal myocardial infarction, or nonfatal stroke in patients with pre-existing cardiovascular disease and BMI ≥ 27kg/m2. Other notable trials in this space include the LEADER trial (liraglutide), the SUSTAIN-6 trial (semaglutide), and the REWIND trial (dulaglutide). The dosing of GLP-1 agonists depends on their intended use as either an anti-glycemic or anti-obesity agent. For weight management, the current FDA-approved therapies are semaglutide 2.4mg weekly and liraglutide 3mg daily. For diabetes, the approved medications are semaglutide 2mg weekly, dulaglutide 4.5mg weekly, and tirzepadite 15mg weekly. What are the cardiometabolic benefits of GLP-1/GIP agonist therapy, beyond glycemic control and/or weight loss? When are GLP-1/GIP agonists considered first-line therapy? The cardiovascular benefits of GLP-1s may be independent of improvements in glycemic control, and in part be driven by reductions in inflammation and cytokine response driving plaque formation in the arterial wall. In the SELECT trial, once weekly 2.4mg semaglutide led to a 20% reduction in MACE in non-diabetic, obese/overweight patients with established ASCVD. In patients with comorbid coronary artery disease, obesity, and diabetes, national guidelines recommend GLP-1 agonists and SGLT-2 inhibitors as first-line agents, over metformin. How does tirzepatide differ from GLP-1 agonists? Tirzepetide is a dual GLP-1/GIP agonist. GIP is highly expressed in the arcuate nucleus and hypothalamus, which may mediate satiety, promote energy expenditure, and enhance peripheral glucose metabolism. The SURMOUNT trial showed 20% net weight loss with tirzepatide in patients with overweight/obesity, nearly as effective as metabolic surgery. What are the absolute and relative contraindications to GLP-1/GIP agonist therapy? GLP-1/GIP agonists are contraindicated in patients with a personal or family history of medullary thyroid cancer. Caution should be used in patients with long-standing diabetes with neuropathy and gastroparesis, as well as incompletely treated diabetic retinopathy. Gallstone pancreatitis should not be considered a contraindication to GLP-1/GIP therapy after cholecystectomy, though a history of recent pancreatitis should give one pause in prescribing a GLP-1/GIP agonist. GLP-1 agonists should not be prescribed for type 1 diabetes, during pregnancy, or with breastfeeding. What are the most common side effects of GLP-1 agonists? GI upset is the most common side effect with GLP-1/GIP agonist therapy, and the incidence of these side effects is similar between tirzepadite and semaglutide in randomized control trials. References - GLP-1 Agonists: Mechanisms to Applications Wilding JPH, Batterham RL, Calanna S, et al. Once-Weekly Semaglutide in Adults with Overweight or Obesity. N Engl J Med. 2021;384(11):989-1002. doi:10.1056/NEJMoa2032183 https://pubmed.ncbi.nlm.nih.gov/33567185/ Marso SP, Daniels GH, Brown-Frandsen K, et al. Liraglutide and Cardiovascular Outcomes in Type 2 Diabetes. N Engl J Med. 2016;375(4):311-322. doi:10.1056/NEJMoa1603827 https://pubmed.ncbi.nlm.nih.gov/27295427/ Marso SP, Bain SC, Consoli A, et al. Semaglutide and Cardiovascular Outcomes in Patients with Type 2 Diabetes. N Engl J Med. 2016;375(19):1834-1844. doi:10.1056/NEJMoa1607141 https://pubmed.ncbi.nlm.nih.gov/27633186/ Gerstein HC, Colhoun HM, Dagenais GR, et al. Dulaglutide and cardiovascular outcomes in type 2 diabetes (REWIND): a double-blind, randomised placebo-controlled trial. Lancet. 2019;394(10193):121-130. doi:10.1016/S0140-6736(19)31149-3 https://pubmed.ncbi.nlm.nih.gov/31189511/

Dec 17, 2023

CardioNerds cofounder Dr. Amit Goyal and cardiology fellows from the Cleveland Clinic (Drs. Alejandro Duran Crane, Gary Parizher, and Simrat Kaur) discuss the following case: A 61-year-old man presented with symptoms of heart failure and left ventricular hypertrophy. He was given a diagnosis of obstructive hypertrophic cardiomyopathy. He eventually underwent septal myectomy, mitral valve replacement, aortic aneurysm repair, and aortic valve replacement with findings of Fabry’s disease on surgical pathology. The case discussion focuses on the differential diagnosis for LVH and covers Fabry disease as an HCM mimic. Expert commentary was provided by Dr. Angelika Ewrin. The episode audio was edited by student Dr. Diane Masket. US Cardiology Review is now the official journal of CardioNerds! Submit your manuscript here. CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Case Media - An Unusual Cause of Hypertrophic Cardiomyopathy – Cleveland Clinic Pearls - An Unusual Cause of Hypertrophic Cardiomyopathy – Cleveland Clinic Left ventricular hypertrophy is a cardiac manifestation of several different systemic and cardiac processes, and its etiology should be clarified to avoid missed diagnosis and treatment opportunities. Fabry disease is a rare, X-linked inherited disease that can present cardiac and extra-cardiac manifestations, the former of which include hypertrophic cardiomyopathy, conduction defects, coronary artery disease, conduction abnormalities, arrhythmias, and heart failure. The diagnosis of Fabry disease includes measurement of alpha-galactosidase enzyme activity as well as genetic testing to evaluate for pathogenic variants or variants of unknown significance in the GLA gene. Family members of patients diagnosed with Fabry disease should be screened based on the inheritance pattern. Multimodality imaging can be helpful in the diagnosis of Fabry disease. Echocardiography can show left ventricular hypertrophy (LVH), reduced global strain, aortic and mitral valve thickening, and aortic root dilation with associated mild to moderate aortic regurgitation. Cardiac MRI can show hypertrophy of papillary muscles, mid-wall late gadolinium enhancement and low-native T1 signal. The treatment of Fabry disease involves a multi-disciplinary approach with geneticists, nephrologists, cardiologists, nephrologists, and primary care doctors. Enzyme replacement therapy can delay the progression of cardiac disease. Show Notes - An Unusual Cause of Hypertrophic Cardiomyopathy – Cleveland Clinic What are the causes of left ventricular hypertrophy? LVH is extremely common. It is present in 15-20% of the general population, and is more common in Black individuals, the elderly, obese or hypertensive individuals, with most cases being secondary to hypertension and aortic valve stenosis. In general terms, it is helpful to divide the causes of LVH into three main groups: high afterload states, obstruction to LV ejection, and intrinsic myocardial problems. Increased afterload states include both primary and secondary hypertension and renal artery stenosis. Mechanical obstruction includes aortic stenosis, subaortic stenosis, and coarctation of the aorta. Lastly, several intrinsic problems of the myocardium can cause LV hypertrophy, such as athletic heart with physiological LVH, hypertrophic cardiomyopathy with or without outflow obstruction, and infiltrative or storage diseases such as cardiac amyloidosis, Fabry’s disease, or Danon disease, among others. How does Fabry disease present? Fabry disease is present in all races and is an X-linked lysosomal storage disorder caused by pathogenic variants in the GLA gene that result in reduced alpha-galactosidase enzyme activity, leading to accumulation of lysosomal globotriaosylceramide (Gb3) globotriaosylsphingosine (lyso-Gb3) in affected tissues, including the heart, kidneys, vasculature, and peripheral nervous system. The reported incidence of this disease is said to be between 1 in 40,000 and 1 in 117,000 individuals, but screening in newborns suggests that this incidence may be underestimated, as it is present in up to 1 in 8,800 newborns. Depending on the variant of the mutation or the presence of mosaicism in females, the disease can have variable expression with early-onset presentations in the classical form or late-onset presentations in individuals who have residual a-galactosidase enzyme activity. Fabry disease can have multiple cardiac and extracardiac manifestations. Accumulation of Gb3 occurs in all cell types of the heart, including smooth muscle cells of the endothelium, myocytes, conduction cells, and valvular fibroblasts. Accumulation of glycosphingolipids also leads to biochemical changes in cell function that lead to apoptosis, cellular necrosis, inflammation, and altered membrane ion channel properties that may lead to increased conduction velocities. In the myocardium, cell damage produces LVH and diastolic dysfunction. Damage to endothelial cells leads to coronary artery disease and myocardial ischemia. Together, these changes may eventually lead to myocardial fibrosis and systolic dysfunction. Involvement of the conduction cells can manifest as conduction abnormalities and ventricular arrhythmias. Other electrocardiographic findings are a short PQ interval or chronotropic incompetence. Aortic remodeling in FD has been well described and often presents as sinus of Valsalva dilatation or ascending aortic aneurysm, which in turn may lead to secondary aortic regurgitation. Extracardiac manifestations of Fabry disease include neuropathy, gastrointestinal symptoms, angiokeratomas, cornea verticillata (golden-brown or gray discoloration of the corneal epithelium), hypohidrosis and exercise intolerance, proteinuria and renal failure, juvenile or cryptogenic stroke, hearing loss, chronic white matter hyperintensities in brain MRI, and lymphedema. How is Fabry disease diagnosed? Diagnosis of Fabry disease should be suspected in patients with unexplained LVH, especially when there are any extracardiac red flags. LVH presents in more than half of men and more than a third of women after the third decade of life. Other electrocardiographic findings besides high QRS voltages may include inferolateral negative T-waves, short PQ intervals, and a reduced P wave duration. The diagnosis is confirmed through genetic testing that may identify pathogenic variants as well as variants of unknown significance. Enzymatic level activities should be measured as well for confirmation. Absent or reduced alpha-galactosidase activity levels coupled with pathogenic variants in genetic testing confirm a diagnosis of FD. Variants of uncertain significance might require confirmation by endomyocardial biopsy and by lyso-Gb3 level assessment. What is the role of cardiovascular imaging in the diagnosis of Fabry disease? Multimodality imaging may be helpful in the diagnosis and staging of FD. Echocardiography typically reveals LVH with disproportionate hypertrophy of the papillary muscles, loss of base-to-apex circumferential strain gradient, and right-ventricular hypertrophy with normal systolic function. There may also be abnormal thickening of the aortic and mitral valves. Global longitudinal strain and speckle tracking may allow for early detection of cardiac involvement in patients with pathogenic variants. Cardiac MRI (CMR) may help with tissue characterization. Typical CMR findings of FD include late gadolinium enhancement (LGE), initially in the basal inferolateral wall, and low native T1 signal intensity, likely reflecting glycosphingolipid myocardial storage and occurring before the development of significant LVH. Tissue characterization by CMR also allows for staging of FD cardiomyopathy in different and progressive stages of accumulation, with progressive lowering of T1 signal intensity; inflammation and hypertrophy, with low T1, initial LVH, and T2 mapping showing inflammation in the basal inferolateral segment associated with LGE; and fibrosis, with increasing T1 values or pseudo-normalization and LGE with wall thinning in the basal inferolateral segment. What is the management for Fabry disease? The main objective in the treatment of FD is prevention of disease progression and end-organ damage. The mainstay of therapy is enzyme replacement therapy (ERT) with agalsidase-alfa or beta intravenous injections every other week. Agalsidase-alfa is produced in human cell lines, while the beta form of the enzyme is produced by recombinant DNA technology using mammalian cells. ERT is indicated in patients with late-onset FD who have the presence of laboratory, histological, or imaging evidence of injury to the heart, kidney, or central nervous system. It can delay the progression of cardiac disease and reduce the cardiovascular event rate in patients with FD. Another available pharmacological agent is the chaperone agent migalastat, which can be helpful for specific genetic variants of FD by stabilizing the translated form of alpha-galactosidase. This chaperone agent is given in oral tablets every other day. There is ongoing development of novel therapies for FD with second-generation ERTs, substrate reduction therapies, and gene and mRNA therapies. References - An Unusual Cause of Hypertrophic Cardiomyopathy – Cleveland Clinic Weidemann F, Strotmann JM, Niemann M, et al. Heart Valve Involvement in Fabry Cardiomyopathy. Ultrasound in Medicine and Biology. 2009;35(5):730-735. doi:10.1016/j.ultrasmedbio.2008.10.010 Pieroni M, Moon JC, Arbustini E, et al. Cardiac Involvement in Fabry Disease: JACC Review Topic of the Week. Journal of the American College of Cardiology.

Dec 8, 2023

CardioNerds (Daniel Ambinder) joins Dr. Priyanka Ghosh and Dr. Ahmad Lone from the Guthrie Robert Packer Hospital for a day in the Finger Lakes region of New York. They discuss the following case. A 35-year-old man with nonspecific symptoms of headache, fatigue, and chest wall pain was found to have elevated troponin levels, elevated inflammatory markers, EKG with inferior and anterolateral ST depressions, and no obstructive coronary artery disease on cardiac catheterization. His peripheral eosinophilia, cardiac MRI results, and bone marrow biopsy revealed eosinophilic myocarditis from acute leukemia with eosinophilia. This episode discusses this rare type of myocardial inflammation, its potential causes, and the diagnostic workup with the mention of how this patient was ultimately treated for his acute leukemia and myocarditis. Expert commentary is provided by Dr. Saurabh Sharma. Audio editing by CardioNerds academy intern, student doctor Pace Wetstein. US Cardiology Review is now the official journal of CardioNerds! Submit your manuscript here. CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Case Media - Guthrie Robert Packer Hospital Pearls - Guthrie Robert Packer Hospital Myocarditis, especially eosinophilic myocarditis, requires a high level of clinical suspicion. Eosinophilic myocarditis should be considered in a patient presenting with chest pain, normal coronary arteries, and pronounced eosinophilia levels. Causes of eosinophilic myocarditis can vary, and diagnosis requires a thorough, detailed history, which cannot be determined many times. Treatment of eosinophilic myocarditis focuses on the underlying etiology, acute management, and therapy for concomitant heart failure or cardiomyopathy. Consider the whole-patient and cardiac manifestations of non-cardiac illnesses. Show Notes - Guthrie Robert Packer Hospital What is eosinophilic myocarditis? Eosinophilic myocarditis is a type of myocardial inflammation involving eosinophilic cell infiltration and an entity that is likely under-recognized. It requires a high level of suspicion as, many times, patients may not initially present with peripheral eosinophilia, which may develop over the course of their disease process. The presentation can vary from mild cardiac injury to fulminant cardiogenic shock depending on the degree of infiltration and concurrent other organ involvement. The presentation can include heart failure symptoms as well as electrical conduction abnormalities. How is eosinophilic myocarditis diagnosed? Eosinophilic myocarditis is diagnosed by a thorough history including new medications, exposures, travel, prior allergy history, physical exam, lab work including a complete blood count differential, inflammatory markers, cardiac biomarkers, and cardiac diagnostics which should include a 12-lead ECG and transthoracic echocardiogram as well as potentially cardiac MRI and/or endomyocardial biopsy. What are the causes of eosinophilic myocarditis? The causes of eosinophilic myocarditis include medication-induced, hypersensitivity reactions, infections, malignancy, and immune-mediated disorders such as eosinophilic granulomatosis with polyangiitis and hypereosinophilic syndromes. The hypersensitivity subtype has been reported to be the most common cause. Potential offending medications can include antibiotics, sulfonamides, anticonvulsants, anti-inflammatory medications, and diuretics. What is the treatment for eosinophilic myocarditis? Treatment for eosinophilic myocarditis is multi-faceted, including focusing on the etiology and withdrawal of any potential offending agents, management of the acute clinical presentation, and treatment of any concomitant heart failure or cardiomyopathy. Immunosuppressive therapy has been controversial; however, many case reports have successfully used methylprednisolone, and some patients with cardiogenic shock from eosinophilic myocarditis have received therapy with azathioprine. References Al Ali AM, Straatman LP, Allard MF, Ignaszewski AP. Eosinophilic myocarditis: case series and review of literature. Can J Cardiol. 2006 Dec;22(14):1233-7. doi: 10.1016/s0828-282x(06)70965-5. PMID: 17151774; PMCID: PMC2569073. Takkenberg JJ, Czer LS, Fishbein MC, Luthringer DJ, Quartel AW, Mirocha J, Queral CA, Blanche C, Trento A. Eosinophilic myocarditis in patients awaiting heart transplantation. Crit Care Med. 2004 Mar;32(3):714-21. doi: 10.1097/01.ccm.0000114818.58877.06. PMID: 15090952. Morimoto S, Kubo N, Hiramitsu S, Uemura A, Ohtsuki M, Kato S, Kato Y, Sugiura A, Miyagishima K, Mori N, Yoshida Y, Hishida H. Changes in the peripheral eosinophil count in patients with acute eosinophilic myocarditis. Heart Vessels. 2003 Sep;18(4):193-6. doi: 10.1007/s00380-003-0721-0. PMID: 14520487. Burke AP, Saenger J, Mullick F, Virmani R. Hypersensitivity myocarditis. Arch Pathol Lab Med. 1991 Aug;115(8):764-9. PMID: 1863186. Fozing T, Zouri N, Tost A, Breit R, Seeck G, Koch C, Oezbek C. Management of a patient with eosinophilic myocarditis and normal peripheral eosinophil count: case report and literature review. Circ Heart Fail. 2014 Jul;7(4):692-4. doi: 10.1161/CIRCHEARTFAILURE.114.001130. PMID: 25028351. Brambatti M, Matassini MV, Adler ED, Klingel K, Camici PG, Ammirati E. Eosinophilic Myocarditis: Characteristics, Treatment, and Outcomes. J Am Coll Cardiol. 2017 Nov 7;70(19):2363-2375. doi: 10.1016/j.jacc.2017.09.023. PMID: 29096807. Cheung CC, Constantine M, Ahmadi A, Shiau C, Chen LYC. Eosinophilic Myocarditis. Am J Med Sci. 2017 Nov;354(5):486-492. doi: 10.1016/j.amjms.2017.04.002. Epub 2017 Apr 6. PMID: 29173361. Aggarwal A, Bergin P, Jessup P, Kaye D. Hypersensitivity myocarditis presenting as cardiogenic shock. J Heart Lung Transplant. 2001 Nov;20(11):1241-4. doi: 10.1016/s1053-2498(01)00313-8. PMID: 11704488. Kounis NG, Zavras GM, Soufras GD, Kitrou MP. Hypersensitivity myocarditis. Ann Allergy. 1989 Feb;62(2):71-4. PMID: 2645814. Li H, Dai Z, Wang B, Huang W. A case report of eosinophilic myocarditis and a review of the relevant literature. BMC Cardiovasc Disord. 2015 Feb 26;15:15. doi: 10.1186/s12872-015-0003-7. PMID: 25887327; PMCID: PMC4359588.

Nov 30, 2023

CardioNerds (Dr. Josh Saef and Dr. Sumeet Vaikunth) join Dr. Sheng Fu, Dr. Payton Kendsersky, and Dr. Aniqa Shahrier from the Medical University of South Carolina for some off-shore fishing. They discuss the following featuring a patient with D-TGA and Eisenmenger’s syndrome treated with a Heartmate 3. Expert commentary was provided by Dr. Brian Houston. The episode audio was edited by student Dr. Adriana Mares. A 39-year-old woman with a history of D-transposition of the great arteries (D-TGA) with prior atrial switch repair (Mustard) was admitted from the clinic with cardiogenic shock. She underwent right heart catheterization which demonstrated elevated biventricular filling pressures and low cardiac index. An intra-aortic balloon pump was placed, and the patient was evaluated for advanced therapies. A liver biopsy showed grade 3 fibrosis, which, in combination with her shock state, made her a high-risk candidate for isolated heart or combined heart-liver transplantation. After a multi-disciplinary discussion, the patient underwent a Heartmate III left ventricular assist device (LVAD) implant in her systemic right ventricle. Although she did well post-operatively, she was admitted after a month with recurrent cardiogenic shock, with imaging showing her inflow cannula had become perpendicular to the septum. The patient and family eventually decided to pursue comfort measures, and the patient passed. US Cardiology Review is now the official journal of CardioNerds! Submit your manuscript here. CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Case Media - D-TGA and Eisenmenger’s syndrome treated with a Heartmate 3 Pearls - D-TGA and Eisenmenger’s syndrome treated with a Heartmate 3 Early diagnosis of cyanotic congenital heart disease is paramount for treatment and prevention of future complications. Adult congenital heart disease requires a multi-disciplinary team for management in consultation with an adult congenital cardiology specialist. Eisenmenger syndrome is related to multiple systemic complications and has a high rate of mortality. Advancement in PAH medical management can offer noninvasive treatment options for some patients. Transthoracic echocardiography is the cornerstone for diagnosis. Other modalities (e.g. cardiac CT, cardiac MRI, invasive catheterization) can aid in diagnosis and management. Pearls - D-TGA and Eisenmenger’s syndrome treated with a Heartmate 3 While advances in pediatric surgery have allowed many patients born with congenital heart disease to survive into adulthood, adult congenital heart disease (ACHD) patients are complex and prone to numerous adverse sequalae including arrhythmias, heart failure, valvular disease, and non-cardiac organ dysfunction. Heart failure can be a challenging presentation in ACHD patients due to a longstanding history of clinical compensation. Their unique and complex anatomy, as well as highly variable clinical presentation, present unique challenges when it comes to advanced heart failure options such as durable left ventricular assist devices (LVAD) or transplantation. While durable LVAD implantation is possible in patients with systemic right ventricles, anatomic compatibility is paramount and poses ongoing challenges in their management. Goals of care discussions should be had early, as options for treatment may be limited. Show Notes - D-TGA and Eisenmenger’s syndrome treated with a Heartmate 3 What are some common sequelae in ACHD patients? ACHD patients are a heterogeneous population, but atrial tachycardias are extremely frequent in this patient population, often due to re-entrant pathways around surgical suture lines. These can often be treated with radiofrequency ablation while paying close attention to their challenging anatomy. Heart failure is also extremely common (up to 40% incidence) but has variable incidence dependent on the specific anatomy. Valvular heart disease, including infective endocarditis as well as non-cardiac organ dysfunction, are also important contributors to the overall prognosis of ACHD patients. How does heart failure present in ACHD patients? Heart failure presentations in ACHD patients tend to be subacute and insidious, as patients often have become accustomed to their symptoms. They are often unable to identify clear exercise limitations due to the slow, subacute nature of symptoms. However, acute presentations and shock can also be seen. Heart failure is the leading cause of death in ACHD patients. What are the challenges for advanced therapies in the ACHD population? First and foremost, risk stratification for these patients is often difficult due to often unreliable self-reporting of symptoms. Thus, early recognition becomes key, but even then, may not be enough. Several anatomic and physiological challenges remain. ACHD patients have often undergone multiple cardiac surgeries, increasing the surgical risk of redo sternotomies with severe adhesions. Due to the longstanding nature of their disease, ACHD patients often develop irreversible pulmonary hypertension (making transplant prohibitive) or end-organ dysfunction secondary to right heart failure (necessitating dual organ transplant). Is durable LVAD a feasible option for patients with systemic right ventricles? Isolated case reports demonstrate the feasibility of the off-label use of durable LVADs in systemic right ventricles. The complex anatomy of these patients has led to reports of alternative implant sites for the inflow cannula to minimize obstruction. Alternative surgical approaches, such as lateral thoracotomy, have also been described to try to avoid the adhesions that are often seen in these patients as a result of multiple prior cardiac surgeries. While the surgery is technically feasible, long-term data is not available, and this remains a “bail-out” therapy with current-generation LVAD designs. What is the role of goals of care discussions in ACHD patients? Advanced care planning is rarely discussed in routine clinic visits, and most providers wait until the condition has deteriorated significantly. Most ACHD patients want to discuss advanced care early before the disease progresses, but some do not, so it is important to ask about patient preferences. The majority of ACHD patients prefer to have advanced care discussions with their ACHD provider due to an already established and trusting relationship. References Gatzoulis MA, Webb GD, F. DPE, Hornung T, O'Donnell C. Transposition of the Great Arteries. In: Diagnosis and Management of Adult Congenital Heart Disease: Expert Consult - Online and Print. 3rd ed. Elsevier; 2018:513-527. Stout KK, Daniels CJ, Aboulhosn JA, et al. 2018 AHA/ACC guideline for the management of adults with congenital heart disease: A report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines. Circulation. 2019;139(14). Schwerzmann M, Goossens E, Gallego P, et al. Recommendations for advance care planning in adults with congenital heart disease: A position paper from the ESC Working Group of adult congenital heart disease, the Association of Cardiovascular Nursing and Allied Professions (ACNAP), the European Association for Palliative Care (EAPC), and the International Society for Adult Congenital Heart Disease (ISACHD). European Heart Journal. 2020;41(43):4200-4210. doi:10.1093/eurheartj/ehaa614 Khairy P, Clair M, Fernandes SM, et al. Cardiovascular outcomes after the arterial switch operation for D-transposition of the great arteries. Circulation. Jan 22 2013;127(3):331-9. doi:10.1161/CIRCULATIONAHA.112.135046 Piran S, Veldtman G, Siu S, Webb GD, Liu PP. Heart failure and ventricular dysfunction in patients with single or systemic right ventricles. Circulation. Mar 12 2002;105(10):1189-94. doi:10.1161/hc1002.105182 Zandstra TE, Palmen M, Hazekamp MG, Meyns B, Beeres SLMA, Holman ER, Kiès P, Jongbloed MRM, Vliegen HW, Egorova AD, Schalij MJ, Tops LF. Ventricular assist device implantation in patients with a failing systemic right ventricle: a call to expand current practice. Neth Heart J. 2019 Dec;27(12):590-593. Burchill LJ. Heart transplantation in adult congenital heart disease. Heart. 2016;102:1871–1877. doi: 10.1136/heartjnl-2015-309074.

Nov 26, 2023

CardioNerds co-founder Dr. Dan Ambinder, series chair Dr. Giselle Suero Abreu, and episode FIT Lead Dr. Rachel Ohman discuss disparities in cardiooncology with Dr. Javier Gomez Valencia, the Director of Cardio-Oncology services at John H. Stronger Jr. Hospital of Cook County. Dr. Rachel Ohman drafted show notes. Audio editing by student doctor Shivani Reddy. A disproportionate burden of both cancer and cardiovascular disease affects racial and ethnic minority groups as well as lower-income communities. Similar patterns of vulnerability exist among cancer survivors with cardiovascular disease, although further investigation in these subpopulations is needed. We discuss a comprehensive approach to the cardio-oncology patient, our current understanding of the social and structural determinants of disparities in cardio-oncology populations, and other contributions to inequity in the field. Given the growing population of cancer survivors and limited accessibility to cardio-oncology specialists, these topics are of critical importance to anyone caring for cancer patients who have or are at risk for cardiovascular disease. This episode is supported by a grant from Pfizer Inc. This CardioNerds Cardio-Oncology series is a multi-institutional collaboration made possible by contributions of stellar fellow leads and expert faculty from several programs, led by series co-chairs, Dr. Giselle Suero Abreu, Dr. Dinu Balanescu, and Dr. Teodora Donisan. CardioNerds Cardio-Oncology PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls and Quotes - Disparities in CardioOncology Social and structural determinants of health are drivers of cardiovascular and cancer disparities. Existing data on cardiotoxicity outcomes suggests these determinants also contribute to disparities in cardio-oncology. Assessing social and structural determinants of health should be a routine part of evaluating a patient with an active or prior history of cancer. Customs, country of origin, and immigration status matter. Differential risk profiles among Hispanic/Latinx sub-populations require further investigation. Black patients, particularly black women with breast cancer, have elevated morbidity and mortality from cardiotoxicity. Data suggest contributions from social determinants of health. Representation in clinical trials must be diversified for applicability to our diverse patient populations. Concerted efforts should be made to recruit diverse clinical trial participants and help patients from diverse communities effectively participate in the research process, contributing to the advancement of science. Show notes - Disparities in CardioOncology How do you approach the evaluation of a new patient in cardio-oncology? How do social and structural determinants of health impact treatment-associated cardiotoxicity? The evaluation of a new patient should include an assessment of a patient’s intrinsic risk factors, risks associated with cancer treatment, and consideration of cardioprotective therapeutic strategies Social and structural vulnerabilities should also be assessed routinely as a part of risk stratification. Providers should take stock of a patient’s demographic (e.g., race/ethnicity, gender), socioeconomic (e.g., occupation, insurance status, food security, housing security), environmental (e.g., transportation, proximity to health resources, neighborhood safety), and sociocultural (e.g., psychosocial stressors, discrimination, acculturation) determinants that are in turn modulated by larger systemic forces like structural racism. This comprehensive risk assessment can guide the strategies to mitigate cardiovascular risk before, during, and after cancer treatment. What barriers to cardio-oncology care are unique to the Hispanic/Latinx population? The Hispanic/Latinx population now comprises 19% of the US population. A disproportionate fraction of the Hispanic/Latinx population is uninsured (about 20%). In addition to insurance barriers, some members of this population can face difficulties from language barriers and limited access to preventative care. Existing data suggest differential risk profiles for sub-populations of Hispanic/Latinx patients based on country of origin, customs, and immigration status. Further research is needed to investigate disparities among different sub-populations. What disparities are faced by Black patients with cancer? Black patients have an elevated risk of morbidity and mortality from cancer and are more likely to develop cardiotoxicity than their White counterparts. Black patients with breast cancer who receive anthracycline or HER2-directed therapy have a two- to three-fold risk of cardiotoxicity when compared to their White counterparts. Black patients with HER2+ breast cancer treated with trastuzumab are more likely to develop LV dysfunction than White counterparts, even after controlling for age, disease state, and cardiovascular risk factors. This suggests a role for social determinants of health that have yet to be elucidated. How can patients’ sexual orientation and gender identity influence disparities in cardio-oncology, particularly for LGBTQIA+ patients? Some of the barriers this population faces are related to social stigmatization as well as structural discrimination (e.g., lack of providers with appropriate expertise). Difficulties with accessing trusted providers can impair patients’ ability to have longitudinal care and optimal cardiotoxicity surveillance. What other areas of cardio-oncology might contribute to ongoing outcomes disparities, and how should we approach those disparities? Underrepresentation of minority groups in clinical trials is an ongoing issue. It results in our extrapolating data from homogenous populations and applying it to more diverse populations not represented adequately. Clinical trial enrollment requires more diverse and inclusive recruitment and visibility. However, we also should help patients and communities feel included in the research process, particularly given historical examples of medical exploitation. The landscape of cardiology providers also requires diversification. A diverse workforce benefits patients as well as providers. Cardiologists and healthcare providers also need to engage in political advocacy to help advocate for underrepresented vulnerable groups to combat socioeconomic disparities and public health crises that create barriers to optimal care. References - Disparities in CardioOncology Addison D, Branch M, Baik AH, et al. Equity in Cardio-Oncology Care and Research: A Scientific Statement From the American Heart Association. Circulation. 2023;148(3):297-308. doi:10.1161/CIR.0000000000001158. Ahmad J, Muthyala A, Kumar A, Dani SS, Ganatra S. Disparities in Cardio-oncology: Effects On Outcomes and Opportunities for Improvement. Curr Cardiol Rep. 2022 Sep;24(9):1117-1127. doi: 10.1007/s11886-022-01732-2. Epub 2022 Jun 27. PMID: 35759170; PMCID: PMC9244335. Branch B and Cosway D. Health Insurance Coverage by Race and Hispanic Origin: 2021. American Community Survey Briefs. 2022 Nov 22. https://www.census.gov/content/dam/Census/library/publications/2022/acs/acsbr-012.pdf. Ohman RE, Yang EH, Abel ML. Inequity in Cardio-Oncology: Identifying Disparities in Cardiotoxicity and Links to Cardiac and Cancer Outcomes. J Am Heart Assoc. 2021 Dec 21;10(24):e023852. doi: 10.1161/JAHA.121.023852. Epub 2021 Dec 16. PMID: 34913366; PMCID: PMC9075267. Sirufo MM, Magnanimi LM, Ginaldi L, De Martinis M. Overcoming LGBTQI+ Disparities in Cardio-Oncology: A Call to Action. JACC CardioOncol. 2023 Mar 7;5(2):267-270. doi: 10.1016/j.jaccao.2022.11.017. PMID: 37144105; PMCID: PMC10152199. Suero-Abreu GA, Patel S, Duma N. Disparities in Cardio-Oncology Care in the Hispanic/Latinx Population. JCO Oncol Pract. 2022 May;18(5):404-409. doi: 10.1200/OP.22.00045. PMID: 35544659.

Nov 22, 2023

CardioNerds (Dr. Josh Saef, Dr. Agnes Koczo) join Dr. Iva Minga, Dr. Kifah Hussain, and Dr. Kevin Lee from the University of Chicago - NorthShore to discuss a case of unrepaired congenital heart disease that involves D-TGA complicated by Eisenmenger syndrome. The ECPR was provided by Dr. Michael Earing. Audio editing by Dr. Akiva Rosenzveig. A 25-year-old woman with an unknown congenital heart disease that was diagnosed in infancy in Pakistan presents to the hospital for abdominal pain and weakness. She is found to be profoundly hypoxemic, and an echocardiogram revealed D-transposition of the great arteries (D-TGA) with a large VSD. As this was not repaired in childhood, she has unfortunately developed Eisenmenger syndrome with elevated pulmonary vascular resistance. She is stabilized and treated medically for her cyanotic heart disease. Unfortunately given the severity and late presentation of her disease, she has limited long-term options for care. CardioNerds discuss the diagnosis of D-TGA and Eisenmenger’s syndrome, as well as long-term management and complications associated with this entity. US Cardiology Review is now the official journal of CardioNerds! Submit your manuscript here. CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Case Media - Unrepaired Congenital Heart Disease Pearls - Unrepaired Congenital Heart Disease Early diagnosis of cyanotic congenital heart disease is paramount for treatment and prevention of future complications. Adult congenital heart disease requires a multi-disciplinary team for management in consultation with an adult congenital cardiology specialist. Eisenmenger syndrome is related to multiple systemic complications and has a high rate of mortality. Advancement in PAH medical management can offer noninvasive treatment options for some patients. Transthoracic echocardiography is the cornerstone for diagnosis. Other modalities (e.g. cardiac CT, cardiac MRI, invasive catheterization) can aid in diagnosis and management. Show Notes - Unrepaired Congenital Heart Disease Cyanotic congenital heart disease is often diagnosed in infancy and timely treatment is paramount. As these diseases progress over time, pulmonary over-circulation often pulmonary hypertension (PH), elevated pulmonary vascular resistance, and Eisenmenger syndrome will develop, which preclude definitive treatment. For D-TGA, before PH develops, there are surgical options such as the arterial switch procedure that can treat the disease. Unfortunately, once Eisenmenger syndrome develops, there are multiple systemic complications including hyperviscosity, thrombosis, bleeding, kidney disease, iron deficiency, arrhythmias, etc. that can occur. Management requires a multi-disciplinary team including an adult congenital cardiology specialist, but mortality rates remain high, with median survival reduced by 20 years, worse with complex cardiac defects. Bosentan is a first line treatment for patients with Eisenmenger syndrome, with PDE-5 inhibitors as a second line either by themselves or in combination with bosentan. Data are currently limited for latest-generation PH treatments in Eisenmenger syndrome and further study is still underway. References Ferencz C. Transposition of the great vessels. Pathophysiologic considerations based upon a study of the lungs. Circulation. 1966 Feb;33(2):232-41. Arvanitaki A, Gatzoulis MA, Opotowsky AR, Khairy P, Dimopoulos K, Diller GP, Giannakoulas G, Brida M, Griselli M, Grünig E, Montanaro C, Alexander PD, Ameduri R, Mulder BJM, D'Alto M. Eisenmenger Syndrome: JACC State-of-the-Art Review. J Am Coll Cardiol. 2022 Mar 29;79(12):1183-1198. Earing MG, Webb GD. Congenital heart disease and pregnancy: maternal and fetal risks. Clin Perinatol. 2005 Dec;32(4):913-9, viii-ix Østergaard L, Valeur N, Ihlemann N, Bundgaard H, Gislason G, Torp-Pedersen C, Bruun NE, Søndergaard L, Køber L, Fosbøl EL. Incidence of infective endocarditis among patients considered at high risk. Eur Heart J. 2018 Feb 14;39(7):623-629 Opotowsky AR, Moko LE, Ginns J, Rosenbaum M, Greutmann M, Aboulhosn J, Hageman A, Kim Y, Deng LX, Grewal J, Zaidi AN, Almansoori G, Oechslin E, Earing M, Landzberg MJ, Singh MN, Wu F, Vaidya A. Pheochromocytoma and paraganglioma in cyanotic congenital heart disease. J Clin Endocrinol Metab. 2015 Apr;100(4):1325-34. Jaïs X, D'Armini AM, Jansa P, Torbicki A, Delcroix M, Ghofrani HA, Hoeper MM, Lang IM, Mayer E, Pepke-Zaba J, Perchenet L, Morganti A, Simonneau G, Rubin LJ; Bosentan Effects in iNopErable Forms of chronIc Thromboembolic pulmonary hypertension Study Group. Bosentan for treatment of inoperable chronic thromboembolic pulmonary hypertension: BENEFiT (Bosentan Effects in iNopErable Forms of chronIc Thromboembolic pulmonary hypertension), a randomized, placebo-controlled trial. J Am Coll Cardiol. 2008 Dec 16;52(25):2127-34. Gatzoulis MA, Landzberg M, Beghetti M, Berger RM, Efficace M, Gesang S, He J, Papadakis K, Pulido T, Galiè N; MAESTRO Study Investigators. Evaluation of Macitentan in Patients With Eisenmenger Syndrome. Circulation. 2019 Jan 2;139(1):51-63. McLaughlin VV, Gaine SP, Howard LS, Leuchte HH, Mathier MA, Mehta S, Palazzini M, Park MH, Tapson VF, Sitbon O. Treatment goals of pulmonary hypertension. J Am Coll Cardiol. 2013 Dec 24;62(25 Suppl):D73-81. Stoica SC, McNeil KD, Perreas K, Sharples LD, Satchithananda DK, Tsui SS, Large SR, Wallwork J. Heart-lung transplantation for Eisenmenger syndrome: early and long-term results. Ann Thorac Surg. 2001 Dec;72(6):1887-91.

Nov 17, 2023

CardioNerds (Drs. Amit Goyal, Jason Feinman, and Tiffany Dong) discuss Beyond the Boards: Diseases of the Peripheral Arteries with Dr. Amy Pollak. We review common presentations of peripheral vascular disease, ranging from aortic disease to the more distal vessels in an engaging case-based discussion. Dr. Pollack talks us through these cases, including the diagnosis and management of peripheral vascular diseases. Show notes were drafted by Dr. Matt Delfiner and episode audio was edited by student doctor Tina Reddy. The CardioNerds Beyond the Boards Series was inspired by the Mayo Clinic Cardiovascular Board Review Course and designed in collaboration with the course directors Dr. Amy Pollak, Dr. Jeffrey Geske, and Dr. Michael Cullen. CardioNerds Beyond the Boards SeriesCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls and Quotes - Disease of the Peripheral Arteries Risk factors for abdominal aortic aneurysm include traditional atherosclerotic risk factors such as age, hypertension, hyperlipidemia, and tobacco use. Screening for AAA should be for men over the age of 65 years with a history of tobacco use. If present, medical management includes blood pressure and lipid lowering therapies to decrease the risk of expansion. Decision for surgical intervention relies on size and rate of growth of AAA, with clear indications if it grows> 10 mm in a year or diameter of 5.5 cm in men and 5.0 cm in women. When diagnosis of PAD is not straightforward (presence of symptoms but ABI is normal), an exercise ankle-brachial index (ABI) test can be useful. An exercise-induced decrease in ABI by 20% or in ankle pressure by 30 mmHg is consistent with PAD. For PAD, treatment with low dose rivaroxaban and aspirin yields lower event rates than with antiplatelet therapy alone. This in combination with lifestyle therapies (diet + exercise) and risk factor management (hypertension and hyperlipidemia) are the cornerstones of therapy. Revascularization is indicated for continued PAD symptoms despite conservative therapy. Acute limb ischemia is an “acute leg attack” and is a life-threatening emergency. Common symptoms include pain, pallor, pulselesess, parasthesias, cold temperature (poikilothermia), and paralysis. Restoration of blood flow is paramount, and emergent or urgent revascularization is the first line therapy for those with symptoms 1.3 consistent with calcified and non-compressible vessels. Toe brachial index (TBI) cutoff is 0.7. If there is strong clinical suspicion but normal ABI, then performing the test after a period of exercise (calf raises, treadmill) can be clinically useful. An exercise induced decrease in ankle pressure by 30 mm or change in ABI by 20% is consistent with PAD. Therapy for PAD includes supervised exercise training, lifestyle changes (e.g., tobacco cessation) and risk factor modification (blood pressure/lipids/glucose). Additionally, low dose rivaroxaban (2.5 mg twice daily) plus aspirin has been shown to decrease events compared to aspirin alone. If there are continued symptoms despite the above therapy, then invasive management can be considered. This includes percutaneous or surgical revascularization. This would be proceeded with CTA imaging for further guidance. Invasive angiography is reasonable for someone with a higher likelihood of a single lesion amenable to percutaneous repair. Discrete and singular lesions are usually repaired percutaneously while more diffuse or multivessel disease, then surgical management may be indicated. Acute Limb Ischemia ALI can present with the 6 Ps: pain, pallor, pulselessness, parasthesias, poikilothermia, and paralysis. Limbs may (rarely) remain viable, with signs being a clear Doppler-able pulse without sensory or muscle loss. Otherwise, a limb is salvageable if there is a faint arterial Doppler signal. If there is muscle weakness, then the limb is considered threatened. If an arterial Doppler signal is completely lost, then the limb is considered non-viable. ALI is an “acute leg attack.” The initial therapy is systemic anticoagulation with unfractionated heparin. If symptoms have been present for less than two weeks, then endovascular therapy with either thrombectomy or catheter-directed lysis are indicated. Major contraindications to lytic therapy include recent surgery, any history of intracranial bleeding or neoplasm, or if they are otherwise at a high bleeding risk. Non-viable limbs may better be served with amputation rather than revascularization. References - Disease of the Peripheral Arteries 1. Eikelboom JW, Connolly SJ, Bosch J, et al. Rivaroxaban with or without Aspirin in Stable Cardiovascular Disease. N Engl J Med. 2017;377(14):1319-1330. doi:10.1056/NEJMoa1709118 https://www.nejm.org/doi/full/10.1056/NEJMoa1709118 2. Criqui MH, Matsushita K, Aboyans V, et al. Lower Extremity Peripheral Artery Disease: Contemporary Epidemiology, Management Gaps, and Future Directions: A Scientific Statement From the American Heart Association Circulation. 2021;144(9):e171-e191. doi:10.1161/CIR.0000000000001005 https://www.ahajournals.org/doi/full/10.1161/CIR.0000000000001005?rfr_dat=cr_pub++0pubmed&url_ver=Z39.88-2003&rfr_id=ori%3Arid%3Acrossref.org 3. Lanzi S, Belch J, Brodmann M, et al. Supervised exercise training in patients with lower extremity peripheral artery disease. Vasa. 2022;51(5):267-274. doi:10.1024/0301-1526/a001024 https://econtent.hogrefe.com/doi/full/10.1024/0301-1526/a001024 4. Sabouret P, Cacoub P, Dallongeville J, et al. REACH: international prospective observational registry in patients at risk of atherothrombotic events. Results for the French arm at baseline and one year. Arch Cardiovasc Dis. 2008;101(2):81-88. doi:10.1016/s1875-2136(08)70263-8 https://www.sciencedirect.com/science/article/pii/S1875213608702638?via%3Dihub 5. Zucker EJ, Misono AS, Prabhakar AM. Abdominal Aortic Aneurysm Screening Practices: Impact of the 2014 U.S. Preventive Services Task Force Recommendations. J Am Coll Radiol. 2017;14(7):868-874. doi:10.1016/j.jacr.2017.02.020 https://www.jacr.org/article/S1546-1440(17)30200-4/fulltext 5. Hensley SE, Upchurch GR Jr. Repair of Abdominal Aortic Aneurysms: JACC Focus Seminar, Part 1. J Am Coll Cardiol. 2022;80(8):821-831. doi:10.1016/j.jacc.2022.04.066 https://www.jacc.org/doi/abs/10.1016/j.jacc.2022.04.066 6. Shishehbor MH, White CJ, Gray BH, et al. Critical Limb Ischemia: An Expert Statement. J Am Coll Cardiol. 2016;68(18):2002-2015. doi:10.1016/j.jacc.2016.04.071 https://www.jacc.org/doi/full/10.1016/j.jacc.2016.04.071 7. Kinlay S. Management of Critical Limb Ischemia. Circ Cardiovasc Interv. 2016;9(2):e001946. doi:10.1161/CIRCINTERVENTIONS.115.001946 https://www.ahajournals.org/doi/full/10.1161/CIRCINTERVENTIONS.115.001946 8. Gerhard-Herman MD, Gornik HL, Barrett C, et al. 2016 AHA/ACC Guideline on the Management of Patients With Lower Extremity Peripheral Artery Disease: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines [published correction appears in Circulation. 2017 Mar 21;135(12 ):e791-e792]. Circulation. 2017;135(12):e726-e779. doi:10.1161/CIR.0000000000000471 https://www.ahajournals.org/doi/10.1161/CIR.0000000000000471?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub%20%200pubmed

Nov 1, 2023

CardioNerds (Dr. Daniel Ambinder, Dr. Giselle Suero Abreu, Dr. Kahtan Fadah, and Dr. Colin Blumenthal) discuss arrhythmias in CardioOncology with Dr. Michael Fradley. In this episode, Dr. Michael Fradley joins us in the CardioNerds CardioOncology clinic where he uses his unique dual training in cardio-oncology and electrophysiology to walk us through the complex interplay and management of these disorders. We discuss the incidence and pathophysiology of these arrhythmias, including the link with various cancer treatments, screening and detection, and complex management including rate vs rhythm control in atrial fibrillation, need for anticoagulation, effects on the QTc and so much more. Given the unique challenges with this population we also delve into how this affects their oncology care and how to approach changes to their cancer treatment. Show notes were drafted by Dr. Kahtan Fadah and episode audio was edited by student Dr. Tina Reddy. This episode is supported by a grant from Pfizer Inc. This CardioNerds Cardio-Oncology series is a multi-institutional collaboration made possible by contributions of stellar fellow leads and expert faculty from several programs, led by series co-chairs, Dr. Giselle Suero Abreu, Dr. Dinu Balanescu, and Dr. Teodora Donisan. CardioNerds Cardio-Oncology PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls and Quotes - Arrhythmias in CardioOncology Arrhythmias are common in cancer patients due to shared risk factors and bi-directional risk between cardiac and oncologic disorders. Many cancer therapeutics can be directly arrhythmogenic or lead to cardiotoxicities that pre-dispose to arrhythmias. Though incidence of arrhythmia can be significant increased with some cancer therapeutics (e.g. ibrutinib), there is not specific data to support proactive ambulatory monitoring for arrhythmia without evidence of clear symptoms. Atrial fibrillation is the most common arrhythmia in cancer patients and management of atrial fibrillation, as well as other tachyarrhythmias, is unchanged from management in non-cancer patients. General principles of when to start anticoagulation or rate vs rhythm control are not significantly different (e.g. still use CHA2DS2-VAsC, monitor for symptoms etc), but providers should be more mindful of drug-drug interactions with cancer therapeutics. Cancer therapeutics as well as common medications used to treat side effects or complications (e.g. antiemetics, antibiotics, etc) can prolong the QT interval and increase risk of Torsades de pointes (TdP). The QTc should be monitored with an ECG for patients on these medications. If a patient does develop a serious arrhythmia like TdP, management is similar to that in non-cancer patients. The goal of arrhythmia management in cardio-oncology is to prevent cardiovascular disease from becoming a barrier to appropriate cancer therapy. Though cancer therapeutics should be temporarily or permanently discontinued in potentially fatal events (e.g TdP from QTc prolonging meds), the overall goal is to manage the arrhythmias appropriately to allow cancer therapeutics to be continued or restarted. Show notes - Arrhythmias in CardioOncology What is the prevalence of arrhythmias in patients with cancer? Arrhythmias are common in patients with cancer due to a multitude of factors. Atrial fibrillation is the most common arrhythmia in this population and occurs in approximately 5% of patients with cancer. The driving forces are multifactorial and include the direct arrhythmogenic effects of cancer therapeutics and cardiotoxicities of cancer therapeutics that make arrhythmogenesis more likely. Additionally, there is a bi-directional link between cancer and cardiac disorders. For example, not only is atrial fibrillation more common in patients with cancer, but there is also a higher incidence of cancer in patients with atrial fibrillation, likely due to shared risk factors. Risk factors in patients with cancer that make arrhythmias more likely include advanced age, metabolic disturbances, electrolyte abnormalities, and elevated levels of inflammation and catecholamines. (How) Do cancer therapeutics increase the risk of arrhythmias? Many cancer therapies are either directly or indirectly arrhythmogenic. Though therapies like the BTK inhibitor ibrutinib have a direct link to an increase incidence of atrial fibrillation, other medications like immune checkpoint inhibitors can cause myocarditis, reduce cardiac function, and predispose to arrhythmias. The following table includes broad categories of cancer therapeutics that are linked to arrhythmia: What is the appropriate arrhythmia monitoring strategy for patients receiving cancer therapy? Though there is a clear increased risk of arrhythmia in many patients with cancer receiving specific therapeutics, there is not specific data to support proactive monitoring in these patients. One meta-analysis showed that when compared to alternative regimens, ibrutinib increased the risk of incident AF compared to alternative therapies (RR 3.9, 95% CI 2.0-7.5, P 2 for men and >3 for women warrant anticoagulation. Many patients with cancer are anemic, thrombocytopenic, or prone to bleeding, which should also be taken into account when prescribing anticoagulation. Left atrial appendage closure may be a consideration for select patients. As for medications that cause QT prolongation, malignant arrhythmias are quite rare and mostly occur in patients with QTc > 500 ms. This can be multifactorial as many patients with cancer may have episodic metabolic or electrolyte abnormalities in addition to cancer therapeutics or symptom/complication management medications (e.g. antiemetics, antibiotics, etc) which can prolong the QTc or lower the threshold for arrhythmogenesis. Life threatening arrhythmias like Torsades de pointes (TdP) are treated similar to that in non-cancer patients, which can include magnesium, increasing HR with isoproterenol or transvenous pacing, anti-arrhythmic drugs, or cardioversion in addition to addressing the underlying cause. Balancing arrhythmia risk with cancer therapeutics An important goal in cardio-oncology is to prevent cardiovascular disease from becoming a barrier for a patient to receive appropriate cancer therapy. The goal is to facilitate the treatment plan that the oncologist thinks is optimal for their cancer, not to protect the heart at the expense of appropriate oncologic care. This is a difficult balancing act and, in the case of serious or potentially fatal events (e.g. Torsades from QTc prolonging meds, vasospasm with ischemia from 5FU, severe myocarditis from immune checkpoint inhibitors etc.), it is often necessary to discontinue the cancer therapeutic temporarily or permanently. Ideally, the arrhythmia should be treated and controlled allowing the patient to continue therapy while minimizing the cardiac symptoms and side effects. References - Arrhythmias in CardioOncology Leiva O, AbdelHameid D, Connors JM, Cannon CP, Bhatt DL. Common Pathophysiology in Cancer, Atrial Fibrillation, Atherosclerosis, and Thrombosis: JACC: CardioOncology State-of-the-Art Review. JACC CardioOncol. 2021;3(5):619-634. doi:10.1016/j.jaccao.2021.08.011 Fradley MG, Beckie TM, Brown SA, et al. Recognition, Prevention, and Management of Arrhythmias and Autonomic Disorders in Cardio-Oncology: A Scientific Statement From the American Heart Association. Circulation. 2021;144(3):e41-e55. doi:10.1161/CIR.0000000000000986 Leong DP, Caron F, Hillis C, et al. The risk of atrial fibrillation with ibrutinib use: a systematic review and meta-analysis. Blood. 2016;128(1):138-140. doi:10.1182/blood-2016-05-712828

Oct 30, 2023

CardioNerds join Dr. Tony Li Yi Wei, Dr. Rodney Soh Yu Hang, and Dr. Zan Ng Zhe Yan from the National University Heart Centre Singapore for a cocktail drink on the top of marina bay sands. They discuss the following case featuring a young woman with recurrent ACS ultimately found to have Takayasu Arteritis. The ECPR for this episode is provided by Dr. Teng Gim Gee and Professor Tan Huay Cheem. Episode audio was edited by student Dr. Shivani Reddy. A 37-year-old woman presents with chest pain. She has a background history of Hashimoto thyroiditis, gestational diabetes, and anemia of chronic disease and possible iron deficiency. Her significant medical history includes ischemic heart disease with prior coronary angiogram showing triple vessel coronary artery disease for which she underwent coronary artery bypass graft surgery (CABG) with LIMA-LAD, SVG-OM, SVG-RCA. After CABG, she had recurrent admissions in the subsequent year with acute coronary syndromes where she underwent percutaneous coronary intervention (PCI) to SVG-OM, RI, proximal LAD, and distal LAD. She was a non-smoker and had been compliant with her medications. For her current presentation, she underwent myocardial perfusion imaging which showed a large sized area of inducible ischemia in the LCx territory. Repeat coronary evaluation showed occluded SVG-OM, occluded LIMA-LAD where she underwent PCI. Clinically, she was noted to have weak brachial and radial pulses on the left side with systolic blood pressure difference between both arms. CT Thoracic Angiogram demonstrated concern for underlying large vessel vasculitis such as Takayasu arteritis. ESR was elevated at 34. Rheumatology was consulted and she was diagnosed with Takayasu arteritis and started on prednisolone and azathioprine. Given her young age, absence of traditional atherosclerotic risk factors, and progressive coronary disease, Takayasu arteritis was deemed the underlying etiology of her coronary disease. US Cardiology Review is now the official journal of CardioNerds! Submit your manuscript here. CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Case Media - Recurrent ACS Pearls - Recurrent ACS Approach to accelerated CAD and/or CAD in the young: Causes of MI in young patients can be divided into four groups, although a considerable overlap exists between all groups. (1) atheromatous CAD, (2) non-atheromatous process such as spontaneous coronary artery dissection, vasculitides such as Takayasu disease, (3) hypercoagulable states leading to recurrent arterial and venous thrombosis and/or thromboembolism, and (4) recreational drug use. Clinical Presentation of Takayasu and prevalence of cardiac involvement: Takayasu’s arteritis is classified as a large-vessel vasculitis because it primarily affects the aorta and its primary branches. It has a worldwide distribution; however, the greatest prevalence is seen in Asia. Women are affected in 80 to 90 percent of cases, with an age of onset that is usually between 10 and 40 years. Management of Takayasu arteritis: As for systemic anti-inflammatory therapy, the mainstay of treatment would be systemic glucocorticoids guided by the care of a rheumatologist. A steroid sparing agent may be given in conjunction for long term suppressive therapy to achieve longer-term disease control. The choice of additional agents depends on several factors including considerations regarding comorbidities, a patient's plans for conceiving a child, cost of treatments, and availability of specific agents. Options include methotrexate, azathioprine as well as mycophenolate. There are also growing studies into anti-TNF-alpha agents such as etanercept or infliximab. Show Notes - Recurrent ACS Focusing on young patients presenting with myocardial infarction (MI), the definition is often arbitrary, with most studies using an age cut off of around 40-45 years. As we know, the risk factor profile of the younger population is different with lower prevalence of traditional cardiovascular risk factors, and women of this age group are generally premenopausal. Causes of MI among such patients can be divided into four groups, although a considerable overlap exists between all groups. The first etiology is that of atheromatous CAD, which is linked to conventional risk factors in older patients that we are familiar with. This includes smoking, lipid abnormalities including familial hyperlipidemia, insulin resistance, hypertension, and obesity. Other more novel risk factors include hyperhomocysteinemia and elevated lipoprotein (a). Secondly, there are non-atheromatous coronary pathologies. These include conditions such as spontaneous coronary artery dissection especially prevalent in peripartum females. Other considerations include vasculitides with coronary artery involvement such as Kawasaki disease with coronary artery aneurysms as well as Takayasu disease, coronary vasospasm, and microvascular dysfunction The third etiology is that of hypercoagulable states leading to recurrent arterial and venous thrombosis. Examples include antiphospholipid syndrome and Factor V Leiden mutations. Acquired hypercoagulable states like nephrotic syndrome, thrombotic thrombocytopenic purpura, solid organ malignancy, and myeloproliferative disorders have possible associations with arterial disease in the form of MI (REF). Embolic phenomenon may also cause coronary obstruction (from thrombi, infective vegetations, cardiac masses, etc). Finally, recreational drug use must be considered, although it is the least common etiology in Singapore because of strict laws prohibiting it. Cocaine use is associated with MI by inducing coronary vasospasm as well as hypercoagulability, and long term cocaine use also leads to accelerated atherosclerosis as well as nonischemic cardiomyopathy. Takayasu’s arteritis is classified as a large-vessel vasculitis because it primarily affects the aorta and its primary branches. It has a worldwide distribution; however the greatest prevalence is seen in Asia. Women are affected in 80-90% of cases, with an age of onset that is usually between 10 and 40 years. The onset of symptoms in Takayasu arteritis (TAK) tends to be subacute and diagnosis is often only made at the point where there is significant vascular disease leading to symptoms due to resultant ischemia in the affected vascular territory. Physical examination is what led to the clinical suspicion of a large vessel vasculitis in our patient. Measurement of BP should be done in all four extremities to evaluate for arterial stenoses. Many patients with TAK will have partial or complete occlusion of one or both subclavian, axillary, or brachial arteries, or the brachiocephalic artery, leading to low-pressure readings in the ipsilateral arm. Similarly, femoral or more distal arterial stenoses will lower leg blood pressures and stenosis of the aorta may lead to bilateral low blood pressure readings. Bruits may be heard over the bilateral carotid, subclavian, axillary, renal, and femoral arteries, as well as the abdominal aorta. Cardiac auscultation may reveal signs of aortic valvular disease, pulmonary hypertension, or heart failure. Pulses should be felt for and evaluated at bilateral temporal, carotid, brachial, femoral, and dorsal pedal arteries, and any arterial tenderness should also be noted. Signs of limb ischemia should be sought. In most cases, a clinical diagnosis of Takayasu arteritis can be made in a patient with both suggestive clinical findings (eg, constitutional symptoms, hypertension, diminished or absent pulses, and/or arterial bruits) and imaging showing narrowing of the aorta and/or its primary branches. There are no specific diagnostic laboratory tests for TAK. As a disease with systemic inflammatory process, the erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) may be elevated but normal values do not exclude Takayasu arteritis. Patients with suspected TAK should undergo imaging of the arterial tree by MR or CT angiogram to evaluate the arterial lumen, looking out for smoothly tapered luminal narrowing or occlusion that is sometimes accompanied by thickening of the wall of the vessel. 18 F-FDG - Positron emission tomography (PET), often in combination with CT (PET-CT) or MR (PET-MR) is an increasingly utilized test to evaluate for possible large-vessel vasculitis. The finding of "hot" segments (ie, those with increased standardized uptake values of fludeoxyglucose-F18) in the right clinical setting may be suggestive of large-vessel vasculitis. There is increasing use of PET to aid in the diagnosis of TAK. Although definitive, getting a histological diagnosis via biopsy of the large arteries is impractical and rarely done. However, occasionally arterial tissue may become available after a revascularization procedure or aneurysm repair American College of Rheumatology classification criteria were developed to help distinguish one form of vasculitis from another, however they are limited in terms of their use in clinical practice. The criteria are Age at disease onset ≤ 40 years Claudication of the extremities Decreased pulsation of one or both brachial arteries Difference of at least 10 mmHg in systolic blood pressure between the arms Bruit over one or both subclavian arteries or the abdominal aorta Arteriographic narrowing or occlusion of the entire aorta, its primary branches, or large arteries in the proximal upper or lower extremities, not due to arteriosclerosis, fibromuscular dysplasia, or other causes Patients are said to have TAK if at least three of the six criteria are present.

Oct 26, 2023

The following question refers to Section 4.9 of the 2021 ESC CV Prevention Guidelines. The question is asked by Dr. Christian Faaborg-Andersen, answered first by UCSD fellow Dr. Patrick Azcarate, and then by expert faculty Dr. Melissa Tracy. Dr. Tracy is a preventive cardiologist, former Director of the Echocardiography Lab, Director of Cardiac Rehabilitation, and solid organ transplant cardiologist at Rush University. The CardioNerds Decipher The Guidelines Series for the 2021 ESC CV Prevention Guidelines represents a collaboration with the ACC Prevention of CVD Section, the National Lipid Association, and Preventive Cardiovascular Nurses Association. Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. Question #35 In patients with a low risk of cardiovascular disease, which of the following is true?AAspirin does not affect the risk of ischemic strokeBAspirin increases the risk of fatal bleeding.CAspirin reduces the risk of non-fatal MI.DAspirin reduces cardiovascular mortality Answer #35 ExplanationIn 2019, an updated meta-analysis of aspirin for primary prevention of cardiovascular events found that patients with a low risk of CVD taking aspirin did not have a reduction in all-cause or cardiovascular mortality. There was a lower risk of non-fatal MI (RR 0.82) and ischemic stroke (RR 0.87). However, aspirin was also associated with a higher risk of major bleeding (RR 1.50), intracranial bleeding (RR 1.32), and major GI bleeding (RR 1.52). There was no difference in the risk of fatal bleeding (RR 1.09).Accordingly, the ESC does not recommend antiplatelet therapy in individuals with low/moderate CV risk due to the increased risk of major bleeding (Class III, LOE A).Although aspirin should not be given routinely to patients without established ASCVD, we cannot exclude that in some patients at high or very high CVD risk, the benefits may outweigh the risks.Main TakeawayIn patients with low/moderate risk of CVD, aspirin for primary prevention is not recommended due to the higher risk of bleeding. For those at higher risk of CVD, low-dose aspirin may be considered for prevention in the absence of contraindications.Guideline Loc.Section 4.9.1, Page 3291 CardioNerds Decipher the Guidelines - 2021 ESC Prevention SeriesCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor RollCardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron!

Oct 25, 2023

The following question refers to Section 8.5 of the 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure. The question is asked by Western Michigan University medical student & CardioNerds Intern Shivani Reddy, answered first by University of Southern California cardiology fellow and CardioNerds FIT Trialist Dr. Michael Francke, and then by expert faculty Dr. Shashank Sinha. Dr. Sinha is an Assistant Professor of Medical Education at the University of Virginia School of Medicine and an advanced heart failure, MCS, and transplant cardiologist at Inova Fairfax Medical Campus. He currently serves as both the Director of the Cardiac Intensive Care Unit and Cardiovascular Critical Care Research Program at Inova Fairfax. He is also a Steering Committee member for the multicenter Cardiogenic Shock Working Group and Critical Care Cardiology Trials Network and an Associate Editor for the Journal of Cardiac Failure, the official Journal of the Heart Failure Society of America. The Decipher the Guidelines: 2022 AHA / ACC / HFSA Guideline for The Management of Heart Failure series was developed by the CardioNerds and created in collaboration with the American Heart Association and the Heart Failure Society of America. It was created by 30 trainees spanning college through advanced fellowship under the leadership of CardioNerds Cofounders Dr. Amit Goyal and Dr. Dan Ambinder, with mentorship from Dr. Anu Lala, Dr. Robert Mentz, and Dr. Nancy Sweitzer. We thank Dr. Judy Bezanson and Dr. Elliott Antman for tremendous guidance. Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. Question #30 Ms. V. Tea is a 55-year-old woman with a history of cardiac sarcoidosis, heart failure with mildly reduced ejection fraction (HFmrEF – EF 40%), and ventricular tachycardia with CRT-D who presents with recurrent VT. She has undergone several attempts at catheter ablation of VT in the past and previously had been trialed on amiodarone which was discontinued due to hepatotoxicity. She now continues to have episodic VT requiring anti-tachycardia pacing and ICD shocks despite medical therapy with mexiletine, metoprolol, and sotalol. Her most recent PET scan showed no active areas of inflammation. Currently, her vital signs are stable, and labs are unremarkable. What is the best next step for this patient? A Evaluation for heart transplant B Evaluation for LVAD C Dobutamine D Prednisone E None of the above Answer #30 Explanation The correct answer is A – evaluation for heart transplant. For selected patients with advanced heart failure despite GDMT, cardiac transplantation is indicated to improve survival and quality of life (Class 1, LOE C-LD). Heart transplantation, in this context, provides intermediate economic value. Clinical indicators include refractory or recurrent ventricular arrhythmias with frequent ICD shocks. Patient selection for heart transplant includes assessment of comorbidities, goals of care, and various other factors. The United Network of Organ Sharing Heart Transplant Allocation Policy was revised in 2018 with a 6-tiered system to better prioritize unstable patients and minimize waitlist mortality. VT puts the patient as a Status 2 on the transplant list. There was a contemporary analysis of patients with end-stage cardiomyopathy due to cardiac sarcoidosis, published in Journal of Cardiac Failure, in 2018 that demonstrated similar 1-year and 5-year survival after heart transplant between patients with and without cardiac sarcoidosis. Choice B (evaluation for LVAD) is incorrect. While bridge to transplant with LVAD is definitely a potential next step in patients with cardiac sarcoidosis, it is not recommended in patients presenting primarily with refractory ventricular arrhythmias due to granuloma-induced scarring. In this situation, patients benefit from direct heart transplant rather than bridge to transplant LVAD approach. The same study, described before in the Journal of Cardiac Failure, also showed similar 1-year and 5-year survival after bridge-to-transplant mechanical circulatory support between patients with and without cardiac sarcoidosis. Since cardiac sarcoidosis is not just limited to the left ventricle, patients being considered for LVAD need hemodynamic assessment to determine the risk of post-LVAD RV failure. Choice C (dobutamine) is incorrect. The patient is currently not decompensated in terms of contractility nor is showing signs of cardiogenic shock. Further, dobutamine may worsen arrhythmia burden. Choice D (prednisone) is incorrect as there is no sign of active inflammation on the PET scan. The recurrent ventricular arrhythmias are being driven by granuloma-induced scar. Main Takeaway Cardiac transplantation has a Class 1 (LOE C-LD) recommendation for eligible patients with advanced HF despite GDMT to improve survival and quality of life. Specifically, direct heart transplantation is the best next step in patients with cardiac sarcoidosis and refractory ventricular arrhythmias rather than a bridge-to-transplant approach. Guideline Loc. Section 8.5 Decipher the Guidelines: 2022 Heart Failure Guidelines Page CardioNerds Episode Page CardioNerds Academy Cardionerds Healy Honor Roll CardioNerds Journal Club Subscribe to The Heartbeat Newsletter! Check out CardioNerds SWAG! Become a CardioNerds Patron!

Oct 25, 2023

CardioNerds (Amit Goyal and Daniel Ambider) ACHD series co-chair Dr. Daniel Clark (Vanderbilt University), cardiology FIT lead Dr. Stephanie Fuentes (Houston Methodist Hospital), and Dr. Frank Fish, a Pediatric Electrophysiologist and the Director of the Pediatric Electrophysiology (EP) Lab at Monroe Carrell Jr Children’s Hospital at Vanderbilt University. He is a board certified Adult Congenital Heart Disease (ACHD) physician and has a wealth of experience performing EP procedures in adults living with congenital heart disease. Audio editing was performed by student Dr. Shivani Reddy. In this episode, we discuss key concepts and management of electrophysiologic issues that we can encounter when caring for adults with congenital heart disease. Arrythmias in adults with congenital heart disease can be intrinsic due to the defect itself or as a consequence of the interventions that they have undergone to palliate and/or repair these defects. The complex anatomy of these patients and the years of pressure and volume load make them not only exquisitely hemodynamically sensitive to arrhythmias (that may otherwise not be of much consequence to the general population) but they also make interventions (catheter ablation or device implant) complex. We therefore embark in a case-based discussion of patients with ACHD (Fontan circulation, Ebstein’s anomaly and Tetralogy of Fallot) in an effort to highlight the presentation of arrythmias and the management strategy in this very important group of patients. The CardioNerds Adult Congenital Heart Disease (ACHD) series provides a comprehensive curriculum to dive deep into the labyrinthine world of congenital heart disease with the aim of empowering every CardioNerd to help improve the lives of people living with congenital heart disease. This series is multi-institutional collaborative project made possible by contributions of stellar fellow leads and expert faculty from several programs, led by series co-chairs, Dr. Josh Saef, Dr. Agnes Koczo, and Dr. Dan Clark. The CardioNerds Adult Congenital Heart Disease Series is developed in collaboration with the Adult Congenital Heart Association, The CHiP Network, and Heart University. See more CardioNerds Adult Congenital Heart Disease PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls - Electrophysiology in ACHD Patients with Fontan circulation have a high risk of developing atrial (and ventricular) arrhythmias and they are highly sensitive to the hemodynamic consequences that these arrythmias ensue. The goal of therapy then should be to achieve sinus or atrial paced rhythm. Rate control should NOT the goal. Patients with Ebstein’s anomaly have high arrhythmic potential. They can have multiple accessory pathways (especially right sided) which can in turn be associated with sudden cardiac death. We should have low threshold for EPS +/- catheter ablation in patients with WPW pattern. Patients with Tetralogy of Fallot have a unique risk for SCD that warrant ICD implant apart from the standard criteria (LVEF 180 ms) and surgical repair approach. Patient’s anatomy is the major consideration when implanting devices (PPM/ICD). We ought to assess for residual intracardiac shunt at the atrial level and consider closing if feasible prior to placing a device. CRT has merit in systemic LV but less so in systemic RV. Notes- Electrophysiology in ACHD What should we know about atrial arrhythmias in a Fontan patient? Intraatrial re-entrant tachycardia (IART) is slower than typical atrial flutter with atrial rates generally

Oct 23, 2023

Join CardioNerds Co-Founder Dr. Dan Ambinder, Dr. Nino Isakadze (EP Fellow at Johns Hopkins Hospital), Dr. Karan Desai (Cardiology Faculty at Johns Hopkins Hospital and Johns Hopkins Bayview) join Digital Health Experts, Dr. Francoise Marvel (Co-Founder of Corrie Health and Co-Director of Johns Hopkins Digital Health Lab) and Dr. David Cho (Chair of the ACC Health Care Innovation Council) for another installment of the Digital Health Series. In this specific episode, we discuss pearls, pitfalls and everything in between for the emerging digital health innovator. This series is supported by an ACC Chapter Grant in collaboration with Corrie Health. Notes were drafted by Dr. Karan Desai. Audio editing was performed by student Dr. Shivani Reddy. In this series, supported by an ACC Chapter Grant and in collaboration with Corrie Health, we hope to provide all CardioNerds out there a primer on the role of digital heath in cardiovascular medicine. Use of versatile hardware and software devices is skyrocketing in everyday life. This provides unique platforms to support healthcare management outside the walls of the hospital for patients with or at risk for cardiovascular disease. In addition, evolution of artificial intelligence, machine learning, and telemedicine is augmenting clinical decision making at a new level fueling a revolution in cardiovascular disease care delivery. Digital health has the potential to bridge the gap in healthcare access, lower costs of healthcare and promote equitable delivery of evidence-based care to patients. This CardioNerds Digital Health series is made possible by contributions of stellar fellow leads and expert faculty from several programs, led by series co-chairs, Dr. Nino Isakadze and Dr. Karan Desai. Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. CardioNerds Digital Health Series PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls and Quotes - Tips for the Digital Health Innovator A critical first step in developing a digital health intervention is defining the clinical problem rather than developing the technology itself. Most digital transformations – whether in medicine or other industries – require several iterations for the technology to develop and demonstrate value. A key aspect of this iterative process was human-centered design: involving patients, their families, and other end-users early in the development of the digital health intervention. Dr. Marvel and colleagues have developed a 6-step process for innovators to consider in taking a concept to product. Notes - Tips for the Digital Health Innovator In this episode, we discussed with Dr. Marvel and Dr. Cho some general concepts on how to develop digital health interventions (DHI). DHIs have a broad definition, including any software or hardware application used to improve access, quality, efficacy or efficiency and they exist in various modalities (e.g., text message, mobile apps, wearables). Dr. Marvel has previously authored a roadmap for digital health intervention that provides guidance for an interdisciplinary approach to developing effective and evidence-based DHIs. As discussed on the episode, a critical first step is defining the clinical problem an innovator is attempting to solve instead of attempting to develop the technology solution first and then adapting it to the problem. Drs. Marvel and Cho emphasized that most digital transformations – whether in medicine or other industry – require several iterations for the technology to develop and demonstrate value. Frequent assessment in a structured manner will help the intervention mature over time. Dr. Marvel noted that a key aspect of this iterative process was human-centered design: involving patients, their families, and other end-users early in the development of the DHI. For instance, with Corrie Health, Dr. Marvel noted that patients who had suffered acute myocardial infarction were involved in a Patient Advisory Board, demonstrations were held for the Patient Advisory board, and patients invited to participate on the research team. Our experts also noted there is a wealth of literature on the common barriers in DHI adoption, including regulatory and cost requirements. Data security and interoperability are other major concerns for digital health innovators. An understanding of the healthcare ecosystem can help innovators recognize these barriers early in the design process. In the aforementioned article, Dr. Marvel and colleagues define a stepwise process to help innovators bring their concept to product: Early multidisciplinary accelerators compromised of a variety of stakeholders Establishment of institutional navigators who can provide a pathway through institutional roadblocks and operational factors Encouraging mentorship and championship from faculty-level and administration Devotion of administrative/business/finance leadership to create sustainable business models to address the reimbursement and policy landscapes Creation of expedited IRB pathways for low-risk DHIs The design of systematic processes to access patient evaluations of new technologies and consumer-centered design. References - Tips for the Digital Health Innovator Marvel FA, Wang J, Martin SS. Digital Health Innovation: A Toolkit to Navigate From Concept to Clinical Testing. JMIR Cardio. 2018 Jan 18;2(1):e2. doi: 10.2196/cardio.7586 Glaser J and Shaw S. Digital Transformation Success: What Can Health Care Providers Learn from Other Industries. NEJM Catalyst. 2022 Mar 22. doi: 10.1056/CAT.21.0434

Oct 17, 2023

CardioNerds (Drs. Amit Goyal, Matthew Delfiner, and Tiffany Dong) discuss infective endocarditis with distinguished clinician-educator Dr. Michael Cullen. We dive into the nuances of infective endocarditis, including native valve endocarditis, prosthetic valve endocarditis, and right-sided endocarditis. Notes were drafted by Dr. Tiffany Dong, and audio editing was performed by student Dr. Adriana Mares. The CardioNerds Beyond the Boards Series was inspired by the Mayo Clinic Cardiovascular Board Review Course and designed in collaboration with the course directors Dr. Amy Pollak, Dr. Jeffrey Geske, and Dr. Michael Cullen. CardioNerds Beyond the Boards SeriesCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls and Quotes The physical exam is crucial in the evaluation of infective endocarditis and includes cardiac auscultation and a search for sequelae of endocarditis, such as immunologic and embolic phenomena. The modified Duke Criteria categorizes the diagnosis of infective endocarditis into four different buckets: definite endocarditis by pathology, definite endocarditis by clinical criteria, possible endocarditis, and rejected. The diagnosis of endocarditis may involve several different imaging modalities, including transthoracic echocardiogram, transesophageal echocardiogram, 4D CT, and nuclear imaging. For left-sided endocarditis, indications to operate include endocarditis due to S. aureus or fungi, heart failure, evidence of perivalvular complications, persistent bacteremia, and large vegetations. The management of endocarditis often involves multiple teams, including cardiology, infectious disease, addiction medicine, neurology, anesthesiology, and cardiothoracic surgery. Notes What signs/complications of endocarditis are apparent on physical exam and labs? A new or worsening cardiac murmur with possible signs of volume overload. Vascular phenomena encompass splinter hemorrhages, conjunctival hemorrhages, Janeway lesions, mycotic aneurysms, and TIA/strokes. Immunologic phenomena include glomerulonephritis, Roth spots, and Osler nodes. Positive blood cultures with 2-3 samples collected. Elevated inflammatory markers. How does the modified Duke criteria assist in the diagnosis of infective endocarditis? The modified Duke criteria separate the diagnosis of endocarditis into four categories: definite endocarditis by pathology, definite endocarditis by clinical criteria, possible endocarditis, and rejected endocarditis. Definitive endocarditis by pathology requires pathologic confirmation of “bugs under the microscope.” Definitive endocarditis by clinical criteria requires two major criteria, one major and two minor criteria, or all five minor criteria. Possible endocarditis requires one major and one minor or three minor criteria. Major criteria:Positive blood culture for typical organism Evidence of endocardial involvement (e.g., vegetation on echo) Minor CriteriaPredisposing clinical factors (e.g., intravenous drug use, known valvulopathy)FeverImmunologic phenomenaVascular phenomena Blood culture for atypical organism What is the role of TTE compared to TEE in endocarditis? TTE and TEE both have their roles in the workup for endocarditis. TTE can provide a baseline screen and yield a better understanding of ventricular size and function than transesophageal. The strength of TEE is the ability to visualize smaller vegetations along with perivalvular complications that may be missed on TTE. If clinical suspicion is high for endocarditis, repeat echocardiography is warranted. What are other tools to evaluate for endocarditis in prosthetic valves? TTE and TEE remain important and should be commonly utilized for the diagnosis of endocarditis. FDG-PET can detect inflammation that could be suggestive of endocarditis. Patients should be at least six weeks after valve implantation; otherwise, FDG PET may detect normal postsurgical inflammation. Gated 4D CT can also screen for perivalvular involvement and aid with surgical planning, especially in these patients who may undergo redo surgery. What are the indications for surgery in infective endocarditis? It is important to separate left-sided and right-sided endocarditis because the indications are different. For left-sided endocarditis, indications for surgery include persistent bacteremia/fevers despite appropriate antibiotic therapy, S. aureus or fungal endocarditis, heart failure symptoms, perivalvular complications, and vegetations >20mm. For right-sided endocarditis, indications for surgery include infection with a fungal organism, heart failure due to severe tricuspid regurgitation, vegetations >10mm with embolic phenomenon, persistent bacteremia despite appropriate therapy, and perivalvular involvement. Often, medical therapy alone for right-sided endocarditis will be sufficient. What is the role of multidisciplinary teams for endocarditis? Endocarditis teams can involve cardiology, infectious disease, cardiothoracic surgery, neurology, anesthesiology, and addiction medicine. Addiction medicine is a very important group, particularly in cases where endocarditis is related to IVDU. It is a class 1 indication to consult addiction medicine to give the patient the best long-term outcome. Even if surgery is not warranted at initial hospitalization, it may be appropriate to have cardiac surgery weigh in and follow up with the patient in case there arises an indication for surgery. References Habib G, Lancellotti P, Antunes MJ, et al. 2015 ESC Guidelines for the management of infective endocarditis: The Task Force for the Management of Infective Endocarditis of the European Society of Cardiology (ESC). Endorsed by: European Association for Cardio-Thoracic Surgery (EACTS), the European Association of Nuclear Medicine (EANM). European heart journal. Nov 21 2015;36(44):3075-3128. doi:10.1093/eurheartj/ehv319 https://academic.oup.com/eurheartj/article/36/44/3075/2293384 Otto CM, Nishimura RA, Bonow RO, et al. 2020 ACC/AHA Guideline for the Management of Patients With Valvular Heart Disease: Executive Summary: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. Circulation. Feb 2 2021;143(5):e35-e71. doi:10.1161/cir.0000000000000932https://www.ahajournals.org/doi/10.1161/CIR.0000000000000923#d1e11386 Baddour LM, Wilson WR, Bayer AS, et al. Infective Endocarditis in Adults: Diagnosis, Antimicrobial Therapy, and Management of Complications: A Scientific Statement for Healthcare Professionals From the American Heart Association. Circulation. Oct 13 2015;132(15):1435-86. doi:10.1161/cir.0000000000000296https://www.ahajournals.org/doi/pdf/10.1161/CIR.0000000000000296

Oct 10, 2023

The following question refers to Section 4.7 of the 2021 ESC CV Prevention Guidelines. The question is asked by student Dr. Shivani Reddy, answered first by NP Carol Patrick, and then by expert faculty Dr. Eileen Handberg.Dr. Handberg is an Adult Nurse Practitioner, Professor of Medicine, and Director of the Cardiovascular Clinical Trials Program in the Division of Cardiovascular Medicine at the University of Florida. She has served as Chair of the Cardiovascular Team Section and the Board of Trustees with the ACC and is the President Elect for the PCNA.The CardioNerds Decipher The Guidelines Series for the 2021 ESC CV Prevention Guidelines represents a collaboration with the ACC Prevention of CVD Section, the National Lipid Association, and Preventive Cardiovascular Nurses Association.Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. Question #34 Ms. BW presents after her best friend was diagnosed with hypertension and is interested in measuring her own blood pressure. According to the ESC Guidelines, what BP screening approach is recommended for making a diagnosis of hypertension? ARepeated measurements in one visitBA single measurement in a single visitCRepeated measurements in more than one visit DReported patient history Answer #34 Explanation The correct answer is C – Repeated measurements in more than one visit.It is recommended to base the diagnosis of hypertension on repeated office BP measurements on more than one visit except when hypertension is severe (e.g., Grade 3—defined as SBP > 180 and/ or DBP >110mmHg—and especially in high-risk patients) (Class I, LOE C). In addition to recommending repeat measurements across visits, the guidelines provide a number of considerations for appropriately measuring blood pressure, such as taking measurements when seated in a quiet environment for 5 minutes and measuring in both arms at the first visit and using the higher-level value arm for visits thereafter (see Table 14 on page 3283).Additionally, home blood pressure monitoring is recommended as an alternative to repeated office measurements. Blood pressure measurements are taken with a semiautomated, validated cuff for 3 consecutive days – and 6-7 days being preferred – in the morning and at night, averaged over that period. Notably, home blood pressure thresholds for the diagnosis of hypertension are lower than for that of in-office measurements, with a daytime systolic of 135mmHg or diastolic of 85mmHg given as the level at which hypertension is diagnosed, as opposed to 140mmHg and 90mmHg for systolic and diastolic levels, respectively, given for in-office diagnosis.Main TakeawayWith the exception of those with severely elevated blood pressures, the diagnosis of hypertension requires repeated measurements across multiple office visits.Guideline Loc.Sections 4.7.1 and 4.7.2, Table 13 and 14, Figure 14 CardioNerds Decipher the Guidelines - 2021 ESC Prevention SeriesCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor RollCardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron!

Oct 5, 2023

The following question refers to Section 7.8 of the 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure.The question is asked by Stony Brook University Hospital medicine resident and CardioNerds Intern Dr. Chelsea Tweneboah, answered first by Mayo Clinic Cardiology Fellow and CardioNerds Academy Chief Dr. Teodora Donisan, and then by expert faculty Dr. Michelle Kittleson.The Decipher the Guidelines: 2022 AHA / ACC / HFSA Guideline for The Management of Heart Failure series was developed by the CardioNerds and created in collaboration with the American Heart Association and the Heart Failure Society of America. It was created by 30 trainees spanning college through advanced fellowship under the leadership of CardioNerds Cofounders Dr. Amit Goyal and Dr. Dan Ambinder, with mentorship from Dr. Anu Lala, Dr. Robert Mentz, and Dr. Nancy Sweitzer. We thank Dr. Judy Bezanson and Dr. Elliott Antman for tremendous guidance.Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. Question #29 A 69-year-old man was referred to the cardiology clinic after being found to have a reduced left ventricular ejection fraction and left ventricular hypertrophy. For the last several months he has been experiencing progressively worsening fatigue and shortness of breath while getting to the 2nd floor in his house. He has a history of bilateral carpal tunnel syndrome and chronic low back pain. He takes no medications. On exam, his heart rate is 82 bpm, blood pressure is 86/60 mmHg, O2 saturation is 97% breathing ambient air, and BMI is 29 kg/m2. He has a regular rate and rhythm with normal S1 and S2, bibasilar pulmonary rales, and 1+ pitting edema in both legs. EKG shows normal sinus rhythm with a first-degree AV delay and low voltages. Transthoracic echocardiogram shows a moderately depressed LVEF of 35-39%, severe concentric hypertrophy with a left ventricular posterior wall thickness of 1.5 cm and strain imaging showing globally reduced longitudinal strain with apical sparring. There is also biatrial enlargement and a small pericardial effusion. A pharmacologic nuclear stress test did not reveal any perfusion defects. A gammopathy panel including SPEP, UPEP, serum and urine immunofixation studies, and serum free light chains are unrevealing. A 99mTc-Pyrophosphate scan was positive with grade 3 uptake. In addition to starting diuretics, what is the next most appropriate step for managing for this patient? A Start metoprolol succinate B Start sacubitril/valsartan C Perform genetic sequencing of the TTR gene D Perform endomyocardial biopsy Answer #29 Explanation The correct answer is C – perform genetic sequencing of the TTR gene. This patient has findings which raise suspicion for cardiac amyloidosis. There are both cardiac (low voltages on EKG and echocardiogram showing marked LVH with biatrial enlargement and small pericardial effusion as well as a characteristic strain pattern) and extra-cardiac (bilateral carpal tunnel syndrome and low back pain) features to suggest amyloidosis. The diagnosis of cardiac amyloidosis requires a high index of suspicion and most commonly occurs due to a deposition of monoclonal immunoglobulin light chains (AL-CM) or transthyretin (ATTR-CM). ATTR may cause cardiac amyloidosis as either a pathogenic variant (ATTRv) or as a wild-type protein (ATTRwt). Patients for whom there is a clinical suspicion for cardiac amyloidosis should have screening for serum and urine monoclonal light chains with serum and urine immunofixation electrophoresis and serum free light chains (Class 1, LOE B-NR). Immunofixation electrophoresis (IFE) is preferred because serum or urine plasma electrophoresis (SPEP or UPEP) are less sensitive. Together, measurement of serum IFE, urine IFE, and serum FLC is >99% sensitive for AL amyloidosis. Negative studies as in our patient essentially exclude AL amyloidosis from consideration. In patients with high clinical suspicion for cardiac amyloidosis, without evidence of serum or urine monoclonal light chains, bone scintigraphy should be performed to confirm the presence of transthyretin cardiac amyloidosis (Class 1, LOE B-NR). As in this patient’s case, the 99mTc-Pyrophosphate scan with a grade 2/3 cardiac uptake in the absence of a serum or urinary monoclonal protein has a very high specificity and positive predictive value for ATTR-CM. This allows for a noninvasive diagnosis of ATTR-CM, obviating the need for an endomyocardial biopsy and so option D is inaccurate. In patients for whom a diagnosis of transthyretin cardiac amyloidosis is made, genetic testing with TTR gene sequencing is recommended to differentiate hereditary variant from wild-type transthyretin cardiac amyloidosis (Class 1, LOE B-NR). Differentiating ATTRv from ATTRwt is important because confirmation of ATTRv would trigger genetic counseling and potential cascade screening of family members and TTR silencer therapies, such as inotersen and patisiran (currently only approved for the treatment of polyneuropathy caused by ATTRv amyloidosis). Routine guideline-directed medical treatment (GDMT) for neurohormonal blockade may be poorly tolerated in patients with ATTR-CM and EF ≤40%. Due to restrictive physiology, they may be predisposed to more hypotension with ARNi, ACEi, and ARB. Similarly, patients with ATTR-CM rely on their heart rate response to preserve the cardiac output, thus BB may worsen HF symptoms. In this case, our patient already has a borderline blood pressure without these medications. Both options A and B are false. Main Takeaway In patients for whom a diagnosis of transthyretin cardiac amyloidosis is made, TTR gene sequencing is recommended to differentiate pathologic variant (ATTRv) from wild-type transthyretin cardiac amyloidosis (ATTRwt). This has implications in terms of screening for family members and management options for ATTRv. For patients with ATTR-CM and EF ≤40%, GDMT may be poorly tolerated. Guideline Loc. Section 7.8, Figure 13 Decipher the Guidelines: 2022 Heart Failure Guidelines PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron!

Sep 27, 2023

The following question refers to Section 7.3 of the 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure. The question is asked by Palisades Medical Center medicine resident & CardioNerds Academy Fellow Dr. Maryam Barkhordarian, answered first by Hopkins Bayview medicine resident & CardioNerds Academy Faculty Dr. Ty Sweeny, and then by expert faculty Dr. Gregg Fonarow. Dr. Fonarow is the Professor of Medicine and Interim Chief of UCLA's Division of Cardiology, Director of the Ahmanson-UCLA Cardiomyopathy Center, and Co-director of UCLA's Preventative Cardiology Program. The Decipher the Guidelines: 2022 AHA / ACC / HFSA Guideline for The Management of Heart Failure series was developed by the CardioNerds and created in collaboration with the American Heart Association and the Heart Failure Society of America. It was created by 30 trainees spanning college through advanced fellowship under the leadership of CardioNerds Cofounders Dr. Amit Goyal and Dr. Dan Ambinder, with mentorship from Dr. Anu Lala, Dr. Robert Mentz, and Dr. Nancy Sweitzer. We thank Dr. Judy Bezanson and Dr. Elliott Antman for tremendous guidance. Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. Question #28 Mr. Gene D’aMeTi, a 53-year-old African American man with ischemic cardiomyopathy and heart failure with reduced ejection fraction (LVEF 30-35%), is recently admitted with acutely decompensated heart failure and acute kidney injury on chronic kidney disease stage III. His outpatient regiment includes sacubitril-valsartan 97-103mg BID, carvedilol 25mg BID, and hydralazine 50mg TID. Sacubitril-valsartan was held because of worsening renal function. Despite symptomatic improvement with diuresis, his renal function continues to decline. He is otherwise well perfused & with preservation of other end organ function. Throughout this hospitalization, he has steadily become more hypertensive with blood pressures persisting in the 170s/90s mmHg. What would be an appropriate adjustment to his medication regimen at this time? A Resume Losartan only B Start Amlodipine C Increase current Hydralazine dose D Start Isosorbide dinitrate therapy E Both C & D Answer #28 ExplanationThe correct answer is E – both increasing the current hydralazine dose (C) and starting isosorbide dinitrate therapy (D). Although ACEI/ARB therapy (choice A) has shown a mortality and morbidity benefit in HFrEF, caution should be used in patients with renal insufficiency. In this patient with ongoing decline in renal function, RAAS-inhibiting therapies (ACEi, ARB, ARNI, MRA) should be avoided. In this case, as his RAAS-I has been stopped, it would be reasonable to increase current therapies to target doses (or nearest dose tolerated), as these demonstrated both safety and efficacy in trials (Class 1, LOE A). Considering that his high dose ARNI was stopped, it is unlikely that either hydralazine or isosorbide dinitrate alone, even at maximal doses, would be sufficient to control his blood pressure (Options C and D, respectively). Interestingly, in the original study by Massie et. Al (1977), the decision was made to combine these therapies as the result was thought to be superior to either medication alone. ISDN would provide preload reduction, while Hydralazine would decrease afterload. Consequently, we do not have data looking at the individual benefit of either medication in isolation. In self-identified African Americans with NYHA class III or IV HFrEF already on optimal GDMT, the addition of hydralazine & isosorbide dinitrate is recommended to improve symptoms and reduce mortality and morbidity (Class 1, LOE A). In this case, as the patient has evidence of progressive renal disfunction, we are limited in using traditional RAAS-I, such as ACEI, ARB, or ARNI. In patients with current or previously symptomatic HFrEF who cannot be given first-line agents (like ARNi, ACEi, ARB) due to intolerance or renal insufficiency, combination therapy of hydralazine & isosorbide dinitrate might be considered to reduce morbidity and mortality (Class 2b, LOE C-LD). Dihydropyridine calcium channel blockers such as Amlodipine (choice B) are not recommended for treatment of HFrEF (COR 3, LOE A), though may be considered for treating elevated blood pressure despite optimization of GDMT.Main TakeawayIn self-identified African Americans, the addition of hydralazine & isosorbide dinitrate to GDMT has additional mortality & morbidity benefits. Should a patient have drug intolerances or renal dysfunction that precludes the use of ACEi/ARB/ARNi, hydralazine & isosorbide dinitrate is a reasonable alternative.Guideline Loc.· Section 7.3.5-8· Table 14, Table 15 Decipher the Guidelines: 2022 Heart Failure Guidelines PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron!

Sep 26, 2023

In this episode, CardioNerds Dr. Daniel Ambinder, Dr. Giselle Suero Abreu, and Dr. Saahil Jumkhawala discuss thromboembolic disease in cardio-oncology with faculty expert Dr. Joshua Levenson, the Associate Program Director of the cardiology fellowship and an Assistant Professor of Medicine at the University of Pittsburg School of Medicine. Venous (VTE) and arterial thromboembolic (ATE) events are precipitants of morbidity and mortality in patients with cancer. Here, we discuss the pathophysiology of thromboembolism, risk factors and epidemiology for ATE and VTE, the role of risk prediction and patient stratification, and the approach to treatment for and prophylaxis of thromboembolic events with anticoagulation. Show notes were drafted by Dr. Saahil Jumkhawala and episode audio was edited by CardioNerds Intern Dr. Tina Reddy. This episode is supported by a grant from Pfizer Inc. This CardioNerds Cardio-Oncology series is a multi-institutional collaboration made possible by contributions of stellar fellow leads and expert faculty from several programs, led by series co-chairs, Dr. Giselle Suero Abreu, Dr. Dinu Balanescu, and Dr. Teodora Donisan. CardioNerds Cardio-Oncology PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls and Quotes - Thromboembolic Disease in Cardio-oncology Patients with cancer are at higher risk of developing both arterial and venous thromboembolic events compared to the general population. Certain cancer subtypes are associated with a relatively higher risk of developing thromboembolic complications. Anticoagulation type and duration should be dependent on patient characteristics and risk factors, with shared decision-making between the patient and their providers. Subgroups of patients may benefit from more aggressive management of their atherosclerotic cardiovascular risk factors while being treated for cancer to reduce the risk of thromboembolic complications. Show notes - Thromboembolic Disease in Cardio-oncology What are the incidence and main manifestations of thromboembolic events (venous and arterial) in patients with active malignancy? Approximately 10% of outpatients with active cancer have venous thromboembolic events, many of which are asymptomatic. Clinically relevant VTEs are predominantly deep venous thrombosis (DVTs) with pain and/or swelling of the involved extremities or pulmonary emboli (PEs) resulting in chest pain and/or shortness of breath. VTE is the number one preventable cause of death for all hospitalized patients, and the ability to prevent and treat these events is crucial, particularly in high-risk populations such as patients with cancer. Are there any high-risk associations with specific cancer subtypes? Patients with metastatic disease and those receiving chemotherapy are more likely to develop arterial or venous thromboembolic events. Patients with acute myelogenous leukemia (AML) and thrombocytopenic patients are at the lowest risk for thromboembolic events. Multiple myeloma patients on medication such as proteasome inhibitors or lenalidomide appear at particular risk. Patients with localized, early-stage cancers such as breast, prostate, and melanoma are also at lower risk. What are the main risk factors to identify patients at a higher risk of developing thrombotic complications? Patients with a sedentary lifestyle, deconditioning, and undergoing active treatment with chemotherapy are at the highest risk of developing DVT or PE. How should we approach choosing the optimal type and duration of anticoagulation for acute pulmonary embolism (PE) in the setting of malignancy? This remains an area of active research. Historically, patients would receive systemic anticoagulation with heparin followed by warfarin. Low molecular weight heparin (LMWH) has been found to be superior to warfarin in this patient population. In the recent trials comparing LMWH to direct oral anticoagulants (DOACs), particularly apixaban, edoxaban, and rivaroxaban, a similar incidence of VTEs and relatively equivalent bleeding events have been found. This has transitioned the field towards the higher use of DOACs, except for gastric cancers, in which DOACs have been found to have higher bleeding risk. Dabigatran has been found to be associated with a higher incidence of bleeding and gastrointestinal side effects compared to other DOACs. Important considerations for the use of DOACs are the patient's renal function and the ability to take oral medications or issues with gastrointestinal absorption. For acute PE, three months of treatment is the minimum for the standard of care. For patients with ongoing treatment with systemic chemotherapy or radiation, treatment for at least six months may be considered, or even indefinitely, if risk factors for recurrence persist. Shared decision-making with patients regarding the relevant risks and benefits of ongoing anticoagulation remains critical. What are some risk assessment models to help identify patients at high risk for developing recurrent thrombotic events? The Khorana score, which includes prechemotherapy platelet count ≥350 x109/L, elevated WBC >11 x109/L, low hemoglobin 3 points have about 7% risk of PE or DVT in the following 2.5 months. How does one manage recurrent thrombotic events, particularly while patients are already on an oral anticoagulant? One major consideration in patients with recurrent thrombotic events is ensuring adherence, as there may be concerns with patient education, access, or cost which need to be addressed. Once compliance is confirmed, a patient can be switched from one DOAC to another DOAC or from one DOAC to LWMH, with the twice-daily dose having the strongest evidence for efficacy. Rarely, concurrent treatment with antiplatelet therapy and LWMH may be considered in patients at very high risk for recurrent thrombotic events, particularly in patients with widely disseminated cancers with vascular complications. Notably, workup for underlying hypercoagulability should be considered in patients with localized malignancies with recurrent thromboembolic events. What are considerations for scenarios with high bleeding risk when there is a strong indication for anticoagulation? For patients with chemotherapy-induced thrombocytopenia, thromboelastography (“TEG” scan) may be valuable in guiding whether patients are hyper- or hypo-coagulable. Patients with platelet count <20K should generally not be on anticoagulation. For patients anticipated to have thrombocytopenia sustained through treatment, discussion with the treating oncology team may guide towards withholding ongoing anticoagulation. Mobility and sequential compression devices (SCDs) should be advised for patients to avoid the development of DVTs while patients are in the hospital. As platelet counts rise, consideration of subtherapeutic doses of heparin may be considered. Any lesion with metastasis to the brain is at risk for bleeding. Discussion with oncology, neuro-oncology, and neurosurgery is crucial in identifying the risk of hemorrhage of these lesions. Primary brain tumors, such as glioblastoma, are associated with an elevated risk of DVT, likely attributable in part to reduced mobility and VEGF-targeted treatment. Management of malignant pericardial effusions varies by etiology. Patients with local malignant pericardial effusion may be managed with pericardiocentesis with catheter drainage versus pericardial window, depending on clinician availability and expertise. What is the role of inferior vena cava (IVC) filters in the management of patients at high risk for developing thromboembolic events? For patients with active DVT and PE burden with active or very high risk for bleeding, it may be considered to place a retrievable IVC filter with the goal of removal within 4-6 weeks, and anticoagulation restarted as soon as possible. Of note, IVC filters that remain in place for longer periods of time place the risk of the development of thrombi and distal embolization. How does the management of arterial thrombotic events for patients with active malignancy differ from the treatment of venous thromboembolic disease? Arterial thrombotic events may be sequelae of atherosclerotic cardiovascular disease, dysfunction of the coagulation cascade, or both. Patients with atherosclerotic cardiovascular disease are at higher risk for developing cardiovascular events when treated for cancer. Certain patients, such as men with prostate cancer, appear to be at higher risk related to hormonal derangements during treatment. Proactive management of atherosclerotic risk factors in these patients is imperative with modalities such as coronary computed tomography (CT) scans to identify the burden of atherosclerotic coronary disease with coronary calcium scoring. These patients may benefit from more aggressive treatment with statin therapy and antiplatelet therapy. Patients with preexisting coronary disease being treated with endocrine therapies or VEGF tyrosine kinase inhibitors (TKIs) may be at higher risk for atherosclerotic cardiovascular events during treatment and, therefore indicated for more aggressive lifestyle and risk factor modification. References - Thromboembolic Disease in Cardio-oncology Lyon, A.

Sep 19, 2023

Join CardioNerds Co-Founder Dr. Dan Ambinder, Dr. Nino Isakadze (EP Fellow at Johns Hopkins Hospital), Dr. Karan Desai (Cardiology Faculty at Johns Hopkins Hospital and Johns Hopkins Bayview) join Digital Health Expert, Dr. La Princess Brewer (Associate Professor of Medicine Mayo Clinic Rochester) for another installment of the Digital Health Series. In this specific episode, we discuss how digital health can both reduce and amplify health disparities. This series is supported by an ACC Chapter Grant in collaboration with Corrie Health. Notes were drafted by Dr. Karan Desai. Audio editing was performed by student Dr. Shivani Reddy. In this series, supported by an ACC Chapter Grant and in collaboration with Corrie Health, we hope to provide all CardioNerds out there a primer on the role of digital heath in cardiovascular medicine. Use of versatile hardware and software devices is skyrocketing in everyday life. This provides unique platforms to support healthcare management outside the walls of the hospital for patients with or at risk for cardiovascular disease. In addition, evolution of artificial intelligence, machine learning, and telemedicine is augmenting clinical decision making at a new level fueling a revolution in cardiovascular disease care delivery. Digital health has the potential to bridge the gap in healthcare access, lower costs of healthcare and promote equitable delivery of evidence-based care to patients. This CardioNerds Digital Health series is made possible by contributions of stellar fellow leads and expert faculty from several programs, led by series co-chairs, Dr. Nino Isakadze and Dr. Karan Desai. Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. CardioNerds Digital Health Series PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls and Quotes Digital redlining occurs when a particular group has limited access to key services based on race and ethnicity, perpetuating inequities. Throughout this podcast episode, Dr. Brewer emphasizes how community engagement early in the creation of digital health technologies can mitigate structural inequities. Dr. Brewer spoke about methods to develop innovative digital health tools that are culturally sensitive and inclusive, specifically community-based participatory research (CBPR). In CBPR, community members are partners with researchers in each step of the intervention. While certain individuals and communities may have physical access to digital health tools, they still may remain inaccessible for several reasons. Notes In this episode, we focus on achieving digital health equity and how the very technologies meant to reduce health disparities can widen them. We started by discussing a paper from Dr. Brewer and colleagues that crystallized how digital health disparities can occur with the example of Pokémon Go. As described in this paper, this mobile application was one of the most used applications worldwide. It incentivized users to collect virtual goods at various physical locations termed PokéStops. For public health professionals, this mobile app represented an engaging way to promote physical activity amongst users. However, some racial and ethnic minority groups in low-income, urban areas quickly took notice of the lack of PokéStops within their neighborhoods. As researchers noted, this could be considered examples of digital redlining, or limiting a particular group from key services based on race and ethnicity. As Dr. Brewer notes in the paper, the Pokémon Go developers relied on maps that were crowdsourced from a majority white male demographic. While it may not have been deliberate, the development process created a structural digital inequity placing certain communities at a home-court disadvantage. Throughout this podcast episode, Dr. Brewer emphasizes how community engagement early in the creation of digital health technologies can mitigate structural inequities. Dr. Brewer spoke about methods to develop innovative digital health tools that are culturally sensitive and inclusive, specifically community-based participatory research (CBPR). In CBPR, community members are equal partners with researchers and included at every phase of the project (or development of a digital health tool. Learn more about CBPR from Dr. Brewer and her FAITH! application by listening to our Narratives in Cardiology Series with Episode #131. As demonstrated by in Dr. Brewer’s own research and digital health tool creation, early and consistent community involvement led to high recruitment and retention rates of study participants (100% and 98%, respectively). We also discussed that one of the misunderstood aspects of the discussion around digital health equity is the concept of access. Access can mean many different things including broadband internet infrastructure or internet-enabled devices. But even if the infrastructure is available – as Dr. Brewer has noted in her research for instance, African Americans have similar smartphone ownership to the general populations – digital health tools may be inaccessible because digital health interventions are not tailored to specific populations References Brewer LC, Fortuna KL, Jones C, Walker R, Hayes SN, Patten CA, Cooper LA. Back to the Future: Achieving Health Equity Through Health Informatics and Digital Health. JMIR Mhealth Uhealth. 2020 Jan 14;8(1):e14512. Brewer LC, Hayes SN, Jenkins SM, Lackore KA, Breitkopf CR, Cooper LA, Patten CA. Improving cardiovascular health among African-Americans through mobile health: the FAITH! app pilot study. J Gen Intern Med. 2019 Aug;34(8):1376–8. Brewer LC, Jenkins S, Lackore K, Johnson J, Jones C, Cooper LA, Breitkopf CR, Hayes SN, Patten C. mHealth intervention promoting cardiovascular health among African-Americans: recruitment and baseline characteristics of a pilot study. JMIR Res Protoc. 2018 Jan 31;7(1):e31. Israel BA, Schulz AJ, Parker EA, Becker AB. Review of community-based research: Assessing partnership approaches to improve public health. Annu Rev Public Health. 1998;19:173–202. Weinstein JN, Geller A, Negussie Y, Baciu A. Communities in Action: Pathways to Health Equity. Washington, DC: National Academies Press; 2017.

Sep 12, 2023

CardioNerds co-founder Dr. Dan Ambinder joins CardioNerds join Dr. Pooja Prasad, Dr. Khoa Nguyen and expert Dr. Abigail Khan (Assistant Professor of Medicine, Division of Cardiovascular Medicine, School of Medicine) from Oregon Health & Science University and discuss a case of mechanical valve thrombosis. Audio editing by CardioNerds Academy Intern, student doctor Adriana Mares. A 23-year-old pregnant woman with a mechanical aortic valve presented to the maternal cardiac clinic for a follow-up visit. On physical exam, a loud grade three crescendo-decrescendo murmur was audible and transthoracic echocardiography revealed severely elevated gradients across the aortic valve. Fluoroscopy confirmed an immobile leaflet disk. Thrombolysis was successfully performed using a low dose ultra-slow infusion of thrombolytic therapy, leading to normal valve function eight days later. Treatment options for mechanical aortic valve thrombosis include slow-infusion, low-dose thrombolytic therapy or emergency surgery. In addition to discussing diagnosis and management of mechanical valve thrombosis, we highlight the importance of preventing valve thrombosis during the hypercoagulable state of pregnancy with careful pre-conception counseling and a detailed anticoagulation plan. See this case published in European Heart Journal - Case Reports. US Cardiology Review is now the official journal of CardioNerds! Submit your manuscript here. CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls - mechanical valve thrombosis The hypercoagulable state of pregnancy presents a risk for women with mechanical heart valves with contemporary data estimating the rate of valve thrombosis during pregnancy at around 5%. Thrombolytic therapy is a (relatively) safe alternative to surgery and should be considered first line for treatment of prosthetic valve thrombosis in all patients, especially in pregnant women. Pre-conception counselling and meticulous anticoagulation management for patients with mechanical heart valves are key aspects of their care. The evaluation for prosthetic valve thrombosis in pregnant persons requires a review of anti-coagulation history and careful choice of diagnostic testing to confirm the diagnosis and minimize risks to the parent and the baby. Multi-disciplinary care with close collaboration between cardiology and obstetrics is critical when caring for pregnant persons with cardiac disease. Show Notes - mechanical valve thrombosis How can we counsel and inform women with heart disease who are contemplating pregnancy? Use the Modified World Health Organization classification of maternal cardiovascular risk to counsel patients on their maternal cardiac event rate and recommended follow-up visits and location of delivery (local or expert care) if pregnancy is pursued. To learn about normal pregnancy cardiovascular physiology and pregnancy risk stratification in persons with cardiovascular disease, enjoy CardioNerds Episode #111. Cardio-Obstetrics: Normal Pregnancy Physiology with Dr. Garima Sharma. Adapted from the 2018 ESC Guidelines for the management of cardiovascular diseases during pregnancy What is the differential diagnosis for a new murmur in a pregnant person who has undergone heart valve replacement? Normal physiology - elevated flow from hyperdynamic state and/or expansion of blood volume in pregnancy. Pathologic - increased left ventricular outflow tract flow from turbulence of flow due to pannus ingrowth, new paravalvular leak, or obstructive mechanical disk motion from vegetation or thrombus. What are diagnostic modalities for the evaluation of suspected prosthetic valve thrombosis? The 2020 ACC/AHA guidelines gave a class I recommendation for evaluation of suspected mechanical prosthetic valve thrombosis using transthoracic echocardiogram, transesophageal echocardiogram (TEE), fluoroscopy, and/or multidetector computer tomography. The goals multi-modality imaging are to assess valve function, leaflet motion, and presence and extent of thrombus while weighing the risks, benefits, and limitations of each modality. The hemodynamic effects with sedation required for TEE and radiation involved with each modality should be carefully assessed when choosing what modalities to pursue, particularly with regards to both parent and baby health. What are the treatment options for prosthetic valve thrombosis in pregnant patients? The 2020 ACC/AHA guidelines gave a class I recommendation for treatment options using slow-infusion, low-dose fibrinolytic therapy or undergoing emergency surgery. Cardiac surgeries during pregnancy are associated with high rates of maternal and fetal adverse outcomes; therefore, a slow-infusion, low-dose fibrinolytic therapy is an attractive alternative option in hemodynamically stable patients. What are the anticoagulation and antiplatelet strategies for pregnant patients with mechanical heart valves? All patients should be on aspirin 81mg daily unless they have active bleeding contraindications. No anticoagulation strategy has been proven to be superior for both the parent and the fetus. If low molecular weight heparin is used, strict monitoring of anti-Xa levels is recommended to optimize anticoagulation and prevent complications. Warfarin can be used throughout pregnancy if the therapeutic doses is ≤5 mg/day to reduce the risk of fetal toxicity. Warfarin teratogenicity is highest during the first trimester. However, after the 36th week patients require admission for transition to heparin to minimize risk of fetal intracranial hemorrhage and maternal bleeding during delivery. To learn more about anticoagulation during pregnancy, enjoy CardioNerds Episode #163. Cardio-Obstetrics: Pregnancy and Anticoagulation with Dr. Katie Berlacher. References Van HI, Roos-Hesselink JW, Ruys TPE, Merz WM, Goland S, Gabriel H, et al. Pregnancy in women with a mechanical heart valve. Circulation 2015;132:132–142. Özkan M, Gündüz S, Gürsoy OM, Karakoyun S, Astarcioʇlu MA, Kalçik M, et al. Ultraslow thrombolytic therapy: a novel strategy in the management of PROsthetic MEchanical valve Thrombosis and the prEdictors of outcomE: the ultra-slow PROMETEE trial. Am Heart J 2015;170:409–418.e1. 5. Otto CM, Nishimura RA, Bonow RO, Carabello BA, Erwin JP, Gentile F, et al. 2020 ACC/AHA guideline for the management of patients with valvular heart disease: a report of the American College of Cardiology/American Heart Association Joint Committee on clinical practice guidelines. Circulation 2021;143:e35–e71. Vahanian A, Beyersdorf F, Praz F, Milojevic M, Baldus S, Bauersachs J, et al. 2021 ESC/ EACTS guidelines for the management of valvular heart disease: developed by the task force for the management of valvular heart disease of the European Society of Cardiology (ESC) and the European Association for Cardio-Thoracic Surgery (EACTS). Eur Heart J. 2022;43:561–632. Özkan M, Gündüz S, Biteker M, Astarcioglu MA, Çevik C, Kaynak E, et al. Comparison of different TEE-guided thrombolytic regimens for prosthetic valve thrombosis: the TROIA trial. JACC Cardiovasc Imaging 2013;6:206–216. Özkan M, Çakal B, Karakoyun S, Gürsoy OM, Çevik C, Kalçik M, et al. Thrombolytic therapy for the treatment of prosthetic heart valve thrombosis in pregnancy with lowdose, slow infusion of tissue-type plasminogen activator. Circulation 2013;128:532–540. Regitz-Zagrosek V, Roos-Hesselink JW, Bauersachs J, Blomström-Lundqvist C, Cífková R, De BM, et al. 2018 ESC guidelines for the management of cardiovascular diseases during pregnancy. Eur Heart J 2018;39:3165–3241. D’Souza R, Ostro J, Shah PS, Silversides CK, Malinowski A, Murphy KE, et al. Anticoagulation for pregnant women with mechanical heart valves: a systematic review and meta-analysis. Eur Heart J 2017;38:1509–1516.

Sep 5, 2023

The following question refers to Section 4.5 of the 2021 ESC CV Prevention Guidelines. The question is asked by Dr. Maryam Barkhordarian, answered first by pharmacy resident Dr. Anushka Tandon, and then by expert faculty Dr. Noreen Nazir. Dr. Nazir is Assistant Professor of Clinical Medicine at the University of Illinois at Chicago, where she is the director of cardiac MRI and the preventive cardiology program. The CardioNerds Decipher The Guidelines Series for the 2021 ESC CV Prevention Guidelines represents a collaboration with the ACC Prevention of CVD Section, the National Lipid Association, and Preventive Cardiovascular Nurses Association. Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. Question #33 Mr. V is a 37-year-old man who presents to clinic after a recent admission for anterior STEMI and is status-post emergent percutaneous intervention to the proximal LAD. He has mixed hyperlipidemia and a 10 pack-year history of (current) tobacco smoking. Which of the following points related to tobacco use is LEAST appropriate for today’s visit? A Providing assessment and encouragement for smoking cessation, even if for only a 30-second “very brief advice” intervention. B Reviewing and offering pharmacotherapy support options for smoking cessation if Mr. V expresses readiness to quit today. C Recommending a switch from traditional cigarettes to e-cigarettes as a first step towards cessation, as e-cigarettes are safer for use. D Discussing that smoking cessation is strongly recommended for all patients, regardless of potential weight gain. Answer #33 Explanation Answer C is LEAST appropriate and therefore is the correct answer. Answer C is not appropriate. Although e-cigarettes may be more effective than nicotine replacement therapy (NRT) for smoking cessation, the long-term effects of e-cigarettes on cardiovascular and pulmonary health are unknown. According to the 2019 ACC/AHA prevention guidelines, e-cigarettes may increase the risk of CV and pulmonary diseases; their use has been reportedly associated with arrhythmias and hypertension. Therefore, neither the ESC nor ACC/AHA suggest clinicians recommend e-cigarettes over traditional cigarettes to patients. Answer A: Smoking cessation is one of the most effective CVD risk-lowering preventive measures, with significant reductions in (repeat) myocardial infarctions or death. ESC guidelines emphasize the importance of encouraging smoking cessation even in settings where time is limited. “Very brief advice” on smoking is a proven 30-second clinical intervention, developed in the UK, which identifies smokers, advises them on the best method of quitting, and supports subsequent quit attempts. While ESC does not explicitly suggest a frequency of assessment, the 2019 ACC/AHA guidelines specifically recommend that “all adults should be assessed at every healthcare visit for tobacco use and their tobacco use status recorded as a vital sign to facilitate tobacco cessation.” Answer B: The ESC suggests (class 2) that offering follow-up support, nicotine replacement therapy, varenicline, and bupropion individually or in combination should be considered in smokers. A meta-analysis of RCTs in patients with ASCVD reflects that varenicline (RR 2.6), bupropion (RR 1.4), telephone therapy (RR 1.5), and individual counselling (RR 1.6) all increased quit rates versus placebo; NRT therapies were well-tolerated but had inconclusive effects on quit rates (RR 1.22 with 95% CI 0.72-2.06). The 2019 ACC/AHA recommendation to combine behavioral and pharmacotherapy interventions to maximize quit rates is a class 1 recommendation. Answer D: The ESC gives a class 1 recommendation to recommending smoking cessation regardless of weight grain. Smokers who quit may expect an average weight gain of 5 kg, but the health benefits of tobacco cessation (both CVD and non-CVD related) consistently outweigh risks from weight gain. Weight gain does not lessen the ASCVD benefits of cessation. The 2019 ACC/AHA guidelines do not specifically comment on weight considerations with smoking cessation. Main Takeaway Stopping smoking is potentially the most effective of all preventive measures. All smoking of tobacco should be stopped, as tobacco use is strongly and independently causal of ASCVD (Class 1). Smoking cessation should be regularly assessed for and encouraged, and pharmacotherapy and follow-up support for cessation should be considered for patients who are ready for a quit attempt. Guideline Loc. Section 4.5, Table 9 CardioNerds Decipher the Guidelines - 2021 ESC Prevention Series CardioNerds Episode Page CardioNerds Academy Cardionerds Healy Honor Roll CardioNerds Journal Club Subscribe to The Heartbeat Newsletter! Check out CardioNerds SWAG! Become a CardioNerds Patron!

Aug 30, 2023

The following question refers to Section 7.2 of the 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure. The question is asked by Cleveland Clinic internal medicine resident and CardioNerds Intern Akiva Rosenzveig, answered first by UPMC Harrisburg cardiology fellow and CardioNerds Academy House Faculty Leader Dr. Ahmed Ghoneem, and then by expert faculty Dr. Randall Starling. Dr. Starling is Professor of Medicine and an advanced heart failure and transplant cardiologist at the Cleveland Clinic where he was formerly the Section Head of Heart Failure, Vice Chairman of Cardiovascular Medicine, and member of the Cleveland Clinic Board of Governors. Dr. Starling is also Past President of the Heart Failure Society of America in 2018-2019. Dr. Staring was among the earliest CardioNerds faculty guests and has since been a valuable source of mentorship and inspiration. Dr. Starling’s sponsorship and support was instrumental in the origins of the CardioNerds Clinical Trials Program. The Decipher the Guidelines: 2022 AHA / ACC / HFSA Guideline for The Management of Heart Failure series was developed by the CardioNerds and created in collaboration with the American Heart Association and the Heart Failure Society of America. It was created by 30 trainees spanning college through advanced fellowship under the leadership of CardioNerds Cofounders Dr. Amit Goyal and Dr. Dan Ambinder, with mentorship from Dr. Anu Lala, Dr. Robert Mentz, and Dr. Nancy Sweitzer. We thank Dr. Judy Bezanson and Dr. Elliott Antman for tremendous guidance. Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. Question #27 Which of the following sentences regarding diuretics in the management of heart failure is correct? A In HF patients with minimal congestive symptoms, medical management with diuretics alone is sufficient to improve outcomes. B Prescribing a loop diuretic on discharge after a HF hospitalization may improve short term mortality and HF rehospitalization rates. C The combination of thiazide (or thiazide-like) diuretics with loop diuretics is preferred to higher doses of loop diuretics in patients with HF and congestive symptoms. D The maximum daily dose of furosemide is 300 mg. Answer #27 Explanation Choice B in correct. The guidelines give a Class 1 recommendation for diuretics in HF patients who have fluid retention to relieve congestion, improve symptoms, and prevent worsening heart failure. Recent data from the non-randomized OPTIMIZE-HF (Organized Program to Initiate Lifesaving Treatment in Hospitalized Patients with Heart Failure) registry revealed reduced 30-day all-cause mortality and hospitalizations for HF with diuretic use compared with no diuretic use after hospital discharge for HF. Choice A is incorrect. With the exception of mineralocorticoid receptor antagonists (MRAs), the effects of diuretics on morbidity and mortality are uncertain. As such, diuretics should not be used in isolation, but always combined with other GDMT for HF that reduce hospitalizations and prolong survival. Choice C is incorrect. The use of a thiazide or thiazide-like diuretic (e.g., metolazone) in combination with a loop diuretic inhibits compensatory distal tubular sodium reabsorption, leading to enhanced natriuresis. In a propensity-score matched analysis in patients with hospitalized HF, the addition of metolazone to loop diuretics was found to increase the risk for hypokalemia, hyponatremia, worsening renal function, and mortality, whereas use of higher doses of loop diuretics was not found to adversely affect survival. The guidelines recommend that the addition of a thiazide (e.g., metolazone) to treatment with a loop diuretic should be reserved for patients who do not respond to moderate- or high-dose loop diuretics to minimize electrolyte abnormalities (Class I, LOE B-NR). Choice D is incorrect. The guidelines recommend a maximum total daily dose of 600mg of furosemide or 10mg of bumetanide or 200mg of torsemide. Main Takeaway In summary, diuretics are recommended in heart failure patients who have fluid retention to relieve congestion, improve symptoms, and prevent worsening heart failure. Maintenance diuretics on HF hospitalization discharge may help prevent recurrent HF hospitalizations. They should be used in combination with other GDMT to improve HF outcomes. Combining loop and thiazide diuretics may cause serious electrolyte abnormalities and should be reserved for patients who do not respond to moderate- or high-dose loop diuretics. Guideline Loc. Section 7.2, Table 12 Decipher the Guidelines: 2022 Heart Failure Guidelines PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron!

Aug 24, 2023

Eisenmenger syndrome is an end-stage complication of congenital heart disease that occurs when a left to right shunt causes pulmonary over-circulation, leading to vascular remodeling, increased vascular resistance, and ultimately even shunt reversal. Aside from cardiac complications, this pathology has unique complications secondary to chronic cyanosis. In this episode of CardioNerds co-founder Dr. Amit Goyal, ACHD series co-chair Dr. Josh Saef, and Dr. Khaled Tuwairqi (ACHD cardiologist at King Faisal / Elite Hospitals) join Dr. Alexander (Sasha) Optowsky (Director of the Adult Congenital Heart Disease Program at Cincinnati Childrens) to discuss diagnosis and management of Eisenmenger syndrome. Show notes were drafted by Dr. Anna Scandinaro and episode audio was edited by CardioNerds Academy Intern Dr. Akiva Rosenzveig. The CardioNerds Adult Congenital Heart Disease (ACHD) series provides a comprehensive curriculum to dive deep into the labyrinthine world of congenital heart disease with the aim of empowering every CardioNerd to help improve the lives of people living with congenital heart disease. This series is multi-institutional collaborative project made possible by contributions of stellar fellow leads and expert faculty from several programs, led by series co-chairs, Dr. Josh Saef, Dr. Agnes Koczo, and Dr. Dan Clark. The CardioNerds Adult Congenital Heart Disease Series is developed in collaboration with the Adult Congenital Heart Association, The CHiP Network, and Heart University. See more CardioNerds Adult Congenital Heart Disease PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls - Eisenmenger Syndrome First described in 1897 by Victor Eisenmenger, Eisenmenger syndrome is a long-term complication of unrepaired left to right shunts, resulting from pulmonary vascular remodeling and pulmonary hypertension. This eventually leads to reversal of the shunt, with right to left flow causing cyanosis. Evaluation for Eisenmenger syndrome should include a comprehensive history, physical exam, ECG, echocardiogram, cardiac catheterization, and laboratory work to identify multi-system complications of cyanosis and secondary erythrocytosis. The most definitive means to diagnose Eisenmenger syndrome in a patient with a prior left-to-right shunt lesion is with a right heart cardiac catheterization showing right to left shunting (Qp:Qs L shunt causing cyanosis), may mimic Eisenmenger syndrome. Their management and natural history differ from Eisenmenger syndrome and can be reversed with treatment. 3. How should one initiate a workup for Eisenmenger syndrome? History - ask about symptoms of dyspnea, decreased exercise tolerance, and cyanosis. It is important to establish a detailed surgical history. Physical exam - specifically assess for the presence (or absence) of a murmur, loud P2 suggestive of pulmonary hypertension, and differential cyanosis (suggestive of PDA – hint see Episode 263 for more information on PDAs and Eisenmenger syndrome). Additional Pearl: take blood pressure on opposite side of a BTT shunt, as a BTT can affect the BP! EKG - look for evidence of right ventricular hypertrophy: RAD, RVH. CXR - may show prominent pulmonary trunk. Laboratory evaluation - should include CBC, iron panel, uric acid, CMP, and BNP to evaluate for signs of secondary erythrocytosis. Echocardiogram - define the anatomy, calculate right ventricular systolic pressure, pulmonary artery diastolic pressure from pulmonary regurgitation jet, and flow across RVOT and LVOT for estimate of Qp/Qs. Cardiac cath - measure pressures and saturations, calculate Qp/Qs, assess response to vasodilator challenge, calculate CO by Fick (not thermodilution assumptions for thermodilution are not met with shunts), and rule out mimics. Remember: You must have had a right heart cardiac catheterization to diagnose someone with Eisenmenger syndrome. When reviewing external data, it is always important to interpret the primary data yourself to ensure the right diagnosis and management. 4. What are some multi-organ complications that can be seen in Eisenmenger syndrome secondary to cyanosis and secondary erythrocytosis (kidney's response to cyanosis)? Gout due to over production and decreased excretion of uric acid Bilirubin gallstones due to high RBC turnover Stroke due to paradoxical emboli Paraglioma/pheochromocytoma due to mutations in the hypoxia pathway – VHL, succinate dehyrdrogenase, hypoxia inducible factor- curable cause of deterioration, should be investigated for in a patient with Eisenmenger syndrome and hypertension Thrombophilia Retinal changes Hypertrophic osteoarthropathy Kyphoscolisosis. 5. What is a life-threatening emergency that should be considered if a patient with Eisenmenger syndrome presents with neurologic symptoms? How about hemoptysis? In a patient with Eisenmenger syndrome presenting with neurologic symptoms there should be a high index of suspicion for cerebral abscess. Chronic hypoxemia leads to secondary erythrocytosis leading to hyperviscosity in the central venous blood, this causes a favorable environment for bacterial growth. Hemoptysis is not uncommon in this population and is a life threatening complication of Eisenmenger syndrome which requires a broad but direct differential to treat emergent cases quickly. The differential diagnosis includes pulmonary infections (Eisenmenger syndrome can cause decreased immune function), pulmonary vasoocclusive disease, aorto-pulmonary collaterals, as well as pulmonary artery in-situ thrombosis. Obtaining a Chest CTA is a high yield clinical tool to help establish this diagnosis. Interventional colleagues will be instrumental in treatment of many of these complications. Hemoptysis and iatrogenic surgical death used to be a high cause of mortality; this has decreased in recent years. 6. What steps can be taken to minimize operative risk in patients with Eisenmenger syndrome? Do we use routine phlebotomy in this population? Surgery should be performed with an experienced cardiac anesthesiologist. Operative risk in Eisenmenger syndrome is lower than in pulmonary arterial hypertension as patients with Eisenmenger syndrome are able to increase their cardiac output by increasing right to left shunting at the expense of their oxygenation. Bubble filters should be used as available to minimize risk of air and paradoxical embolism. For non-urgent operations, exchange transfusions before surgery can improve clotting function. Coagulations labs are affected by high hematocrit (less plasma = fewer clotting factors); you will need to adjust citrate in the tube for an accurate PT/PTT. Routine phlebotomy is no longer used in this population in the absence of moderate to severe hyperviscosity symptoms. Instead, the focus has shifted to iron deficiency. Repleting iron can improves symptoms of hyperviscosity, increases exercise capacity, and reduces stroke risk. 7. What is “Treat to Close” and should it be used in Eisenmenger syndrome? The new area of “Treat to Close” is an evolving area without much data to support its practice. There is a need for randomized clinical trials and further investigation to clarify its use. Indications for shunt closure can be found in the 2018 AHA/ACC and the 2020 ESC Guidelines for the Management of Adults with Congenital Heart Disease. It is contraindicated to close a shunt when Eisenmenger syndrome has developed. 8.

Aug 18, 2023

CardioNerds CardioOncology Series Co-Chairs, Dr. Teodora Donisan and Dr. Dinu Balanescu, and FIT Lead Dr. Bala Pushparaji discuss Interventional CardioOncology with Prof. Cezar Iliescu. In this episode, we discuss the spectrum of cardiovascular diseases encountered by the interventional onco-cardiologist, with a focus on nuances in endovascular therapies tailored to cancer patients and their unique comorbidities and complications. We also discuss certain special scenarios seen in the critically ill cancer patient, such as chronic thrombocytopenia, and how they alter standard of care compared to non-cancer patients. Show notes were drafted by Dr. Bala Pushparaji and episode audio editing was performed by Dr. Akiva Rosenzveig. This episode is supported by a grant from Pfizer Inc. This CardioNerds Cardio-Oncology series is a multi-institutional collaboration made possible by contributions of stellar fellow leads and expert faculty from several programs, led by series co-chairs, Dr. Giselle Suero Abreu, Dr. Dinu Balanescu, and Dr. Teodora Donisan. CardioNerds Cardio-Oncology PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls and Quotes - Interventional CardioOncology Cancer should be treated as a chronic illness akin to hypertension or diabetes and should not deprive patients from receiving appropriate cardiovascular treatment if otherwise indicated (e.g., PCI for acute coronary syndromes, etc.). In cancer patients with stable angina, along with maximizing medical therapy, multimodality imaging (CTA/PET), intravascular imaging (IVUS/OCT), and physiologic testing (iFR/FFR) should be used routinely to prevent unnecessary stenting. Caution is required in the cath lab for the cancer patient with thrombocytopenia. Techniques include utilizing micropuncture access, transfusing appropriate blood products based on thromboelastogram (TEG), and adjusting antiplatelet therapy regimens and duration. Transcatheter aortic valve replacement (TAVR) is now the recommended treatment for most cancer patients with symptomatic/severe aortic stenosis and, if otherwise indicated, should preferably be pursued prior to cancer treatment to optimize the patient’s cardiovascular fitness and tolerance of anti-cancer therapy. Pericardiocentesis in the cancer patient should be performed preferably under fluoroscopy with echocardiography and vascular ultrasound guidance (“triple guidance”). Show notes - Interventional CardioOncology What is the general approach to cardiovascular illness in the cancer patient? Cancer and cardiovascular diseases share numerous risk factors. In addition, cancer and cancer therapies can be atherogenic, by means of inducing pro-inflammatory and hyprecoagulable states, increasing the risk of ischemic heart disease, stroke, and peripheral arterial disease.1 In the outpatient setting, emphasis should be placed on optimizing cardiovascular risk factors and improving overall cardiovascular fitness by exercising, having a healthy diet, and having regular sleep hours as these favor survivorship after cancer treatment. Questions to be answered in the clinic are - Is the patient cardiovascularly fit? Will the patient’s heart withstand cancer treatment? Is there concern for coronary artery disease, valvular disease, pericardial disease, or pulmonary hypertension? Risk assessment and treatment for cancer patients with suspected or known cardiovascular disease should generally follow established ACC/AHA guidelines, with special considerations as outlined by the Society of Cardiovacular Angiography and Interventions (SCAI).2 Pre-chemotherapy cardioprotection for patients without coronary artery disease (CAD) with prophylactic beta-blockers, ACEi/ARB, and statins should be considered when appropriate. For high-risk patients with CAD, blood pressure control, frequent screening via echocardiography, and measurement of serum cardiac biomarkers is encouraged. What is the approach to stable angina in cancer patients? Start the evaluation by identifying cardiovascular risk factors and cardiovascular co-morbidities such as hypertension and diabetes. Review prior or active cancer treatments that might increase the risk for CAD (e.g., chest radiotherapy). Utilize prior imaging that the patient may have had for cancer staging, to look for coronary artery calcification. Depending on the patient’s risk profile for ischemic heart disease, stress testing/multi-modality imaging techniques ranging from coronary CTA to cardiac PET can be pursued to delineate coronary anatomy and identify the myocardium at risk. The final step is invasive coronary imaging – with the intent of fixing main vessel, proximal, and ostial lesions. A wait and watch approach with optimized medical management is preferred for stable lesions in small branches subtending smaller portions of the myocardium. Intravascular imaging (optical coherence tomography - OCT, intravascular ultrasound - IVUS) and physiologic techniques (iFR and FFR) add value to guide decision-making about revascularization. Maximally optimize medical therapy before resorting to an invasive strategy. Sometimes, in anticipation of progressing CAD following cancer treatment/cancer evolution, it may be pertinent to have an aggressive approach during the initial presentation of the patient in the clinic. Patients with advanced cancer may have anemia, thrombocytopenia, or pancytopenia which could make downstream coronary interventions more complicated. What is the approach to acute coronary syndromes (ACS) in cancer patients? Cancer patients with ACS typically present with dyspnea, followed inconsistently by chest pain thereby creating a layer of challenge in the diagnosis. A high index of suspicion is necessary in order to not miss this diagnosis. A subset of patients with ACS-type presentation could have stress induced cardiomyopathy or chemotherapy induced vasospasm/endothelial dysfunction (5-fluorouracil is the most common cause). After risk assessment, invasive approach with left heart catheterization/coronary angiogram with or without intervention can be the next best step in selected patients. Choosing the appropriate stent (bare metal stent, BMS, vs. drug eluting stent, DES) and antiplatelet regimen is key, especially in the setting of chronic thrombocytopenia.3 Although BMS were once commonly used in cancer patients due to their brief antiplatelet drug requirement, they are associated with increased risks for in-stent restenosis and are not preferred in the current era. Modern DES have safer profiles and evidence shows that abbreviated dual antiplatelet thearpy (DAPT) regimens can be implemented with DES as well, if needed. In cancer patients, due to various factors such as thrombocytopenia or need for cancer treatment resumption, DAPT duration may be abbreviated to 10,000/mL. DAPT with clopidogrel may be used when platelet counts 30,000–50,

Aug 16, 2023

The following question refers to Section 3.4 of the 2021 ESC CV Prevention Guidelines. The question is asked by student Dr. Adriana Mares, answered first by early career preventive cardiologist Dr. Dipika Gopal, and then by expert faculty Dr. Michael Wesley Milks.Dr. Milks is a staff cardiologist and assistant professor of clinical medicine at the Ohio State University Wexner Medical Center, where he serves as the Director of Cardiac Rehabilitation and an associate program director of the cardiovascular fellowship. He specializes in preventive cardiology and is a member of the American College of Cardiology's Cardiovascular Disease Prevention Leadership Council.The CardioNerds Decipher The Guidelines Series for the 2021 ESC CV Prevention Guidelines represents a collaboration with the ACC Prevention of CVD Section, the National Lipid Association, and Preventive Cardiovascular Nurses Association.Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. Question #32 Mr. Daniel Collins is a 58-year-old man with hypertension, chronic kidney disease (CKD), and obesity who presents to your clinic for a routine physical examination. Vitals are as follows: BP 143/79 mmHg, HR 89 bpm, O2 99% on room air, weight 106 kg, BMI 34.5 kg/m2. Recent laboratory testing revealed: creatinine 1.24 mg/dL, total cholesterol 203 mg/dL, HDL 39 mg/dL, LDL 112 mg/dL, TG 262 mg/dL. His current medications include lisinopril and rosuvastatin. You recommend increasing the dose of lisinopril to treat uncontrolled hypertension. What additional step(s) are indicated at this visit? A Order urine albumin-to-creatinine ratio B Ask the patient how often they have been bothered by trouble falling or staying asleep, or sleeping too much C Perform depression screening D All of the above Answer #32 Explanation The correct answer is D – all of the above.Answer A is correct. The ESC gives a Class I (LOE C) indication that all CKD patients, with or without diabetes, should undergo appropriate screening for ASCVD and kidney disease progression, including monitoring for changes in albuminuria. Cardiovascular disease is the leading cause of morbidity and death among patients with CKD. Even after adjusting for risk factors, including diabetes and hypertension, there is a linear increase in CV mortality with decreasing GFR below ~60-75 mm/min/1.73m2. Specific CKD-related risk factors include uremia-mediated inflammation, oxidative stress, and vascular calcification.Answer choice B is also correct. In patients with ASCVD, obesity, and hypertension, the ESC gives a Class I (LOE C) indication to regularly screen for non-restorative sleep by asking the question related to sleep quality as follows: “‘How often have you been bothered by trouble falling or staying asleep or sleeping too much?”. Additionally, if there are significant sleep problems that are not responding within four weeks to improving sleep hygiene, referral to a specialist is recommended (Class I, LOE C). However, despite the strong association of OSA with CVD, including hypertension, stroke, heart failure, CAD, and atrial fibrillation, treatment of OSA with CPAP has failed to improve hard CVD outcomes in patients with established CVD. Interventions that focus on risk factor modification, including reduction of obesity, alcohol intake, stress, and improvement of sleep hygiene, are important.Answer choice C is also correct. The ESC gives a Class I (LOE C) recommendation that mental health disorders with either significant functional impairment or decreased use of healthcare systems be considered as influencing total CVD risk. All mental disorders are associated with the development of CVD and reduced life expectancy. Additionally, the onset of CVD is associated with an approximately 2-3x increased risk of mental health disorders compared to a healthy population. As such, screening for mental health disorders should be performed at every consultation (2-4x/year).Main TakeawayIn addition to traditional ASCVD risk factors, other clinical conditions, including sleep apnea, CKD, and mental health conditions, are important to screen for and treat if present.Guideline Loc.Sections 3.4.1, 3.4.9, 3.4.10 CardioNerds Decipher the Guidelines - 2021 ESC Prevention SeriesCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor RollCardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron!

Aug 14, 2023

The following question refers to Section 4.3 of the 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure.The question is asked by Texas Tech University medical student and CardioNerds Academy Intern Dr. Adriana Mares, answered first by Rochester General Hospital cardiology fellow and Director of CardioNerds Journal Club Dr. Devesh Rai, and then by expert faculty Dr. Eldrin Lewis.Dr. Lewis is an Advanced Heart Failure and Transplant Cardiologist, Professor of Medicine and Chief of the Division of Cardiovascular Medicine at Stanford University. The Decipher the Guidelines: 2022 AHA / ACC / HFSA Guideline for The Management of Heart Failure series was developed by the CardioNerds and created in collaboration with the American Heart Association and the Heart Failure Society of America. It was created by 30 trainees spanning college through advanced fellowship under the leadership of CardioNerds Cofounders Dr. Amit Goyal and Dr. Dan Ambinder, with mentorship from Dr. Anu Lala, Dr. Robert Mentz, and Dr. Nancy Sweitzer. We thank Dr. Judy Bezanson and Dr. Elliott Antman for tremendous guidance.Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. Question #26 A 45-year-old man presents to cardiology clinic to establish care. He has had several months of progressive dyspnea on exertion while playing basketball. He also reports intermittent palpitations for the last month. Two weeks ago, he passed out while playing and attributed this to exertion and dehydration. He denies smoking and alcohol intake. Family history is significant for sudden cardiac death in his father at the age of 50 years. Autopsy has shown a thick heart, but he is unaware of the exact diagnosis. He has two children, ages 12 and 15 years old, who are healthy. Vitals signs are blood pressure of 124/84 mmHg, heart rate of 70 bpm, and normal respiratory rate. On auscultation, a systolic murmur is present at the left lower sternal border. A 12-lead ECG showed normal sinus rhythm with signs of LVH and associated repolarization abnormalities. Echocardiography reveals normal LV chamber volume, preserved LVEF, asymmetric septal hypertrophy with wall thickness up to 16mm, systolic anterior motion of the anterior mitral valve leaflet with 2+ eccentric posteriorly directed MR, and resting LVOT gradient of 30mmHg which increases to 60mmHg on Valsalva. You discuss your concern for an inherited cardiomyopathy, namely hypertrophic cardiomyopathy. In addition to medical management of his symptoms and referral to electrophysiology for ICD evaluation, which of the following is appropriate at this time? A Order blood work for genetic testing B Referral for genetic counseling C Cardiac MRI D Coronary angiogram E All of the above Answer #26 Explanation The correct answer is B – referral for genetic counseling. Several factors on clinical evaluation may indicate a possible underlying genetic cardiomyopathy. Clues may be found in: · Cardiac morphology – marked LV hypertrophy, LV noncompaction, RV thinning or fatty replacement on imaging or biopsy · 12-lead ECG – abnormal high or low voltage or conduction, and repolarization, altered RV forces · Presence of arrhythmias – frequent NSVT or very frequent PVCs, sustained VT or VF, early onset AF, early onset conduction disease · Extracardiac features – skeletal myopathy, neuropathy, cutaneous stigmata, and other possible manifestations of specific syndromes In select patients with nonischemic cardiomyopathy, referral for genetic counseling and testing is reasonable to identify conditions that could guide treatment for patients and family members (Class 2a, LOE B-NR). In first-degree relatives of selected patients with genetic or inherited cardiomyopathies, genetic screening and counseling are recommended to detect cardiac disease and prompt consideration of treatments to decrease HF progression and sudden death (Class 1, LOE B-NR). No controlled studies have shown clinical benefits of genetic testing for cardiomyopathy, but genetic testing contributes to risk stratification and has implications for treatment, currently most often for decisions regarding defibrillators for primary prevention of sudden death and regarding exercise limitation for hypertrophic cardiomyopathy and the desmosomal variants. Consultation with a trained counselor before and after genetic testing helps patients to understand and weigh the implications of possible results for their own lives and those of family members, including possible discrimination on the basis of genetic information. Unless shown to be free of the genetic variant(s) implicated in the proband, first-degree relatives of affected probands should undergo periodic screening with echocardiography and electrocardiography. In this patient with likely hypertrophic cardiomyopathy, a family history of sudden cardiac death, recent unexplained syncope, and two children, a referral for genetic counseling is appropriate at this time. However, option A is incorrect because ordering genetic testing without meeting a trained counselor is not advised. Main Takeaway Patients with the possibility of genetic cardiomyopathies should be referred to trained genetic counselors before and after genetic testing to understand the implications of the testing and results. Guideline Loc. Section 4.3, Table 7 Decipher the Guidelines: 2022 Heart Failure Guidelines PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron!

Aug 10, 2023

CardioNerds co-founder Dr. Dan Ambinder joins Dr. Abdelrhman Abumoawad, Dr. Leili Behrooz from the Boston University Vascular Medicine over hot chocolate in Boston. They discuss two interesting cases of lower extremity edema caused by May-Thurner syndrome. Dr. Naomi Hamburg (Professor of Vascular Medicine and Cards at BU/BMC) provides the ECPR for this episode. Audio editing by CardioNerds Academy Intern, Dr. Akiva Rosenzveig. US Cardiology Review is now the official journal of CardioNerds! Submit your manuscript here. CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Case Synopses - May-Thurner syndrome Case 1: A 34-year-old woman with HIV on HAART presenting with left leg swelling and non-healing new foot ulcer for 3 months. She works as a cashier. On exam, her BMI is 35 kg/m2 and there are intact pulses bilaterally. Her left leg has varicose veins in the territory of the great saphenous vein, hyperpigmentation, edema, and a foot ulcer. Her right leg appears normal. Venous Duplex ultrasonography showed chronic partially occlusive thrombus in the left common femoral and profunda femoral veins and decreased doppler respiratory variation on the left side. She was treated with debridement and compression therapy for ulcer healing. She was referred to vascular surgery and underwent contrast venography that demonstrated collateral circulation from the left lower extremity (LE) to the right lower extremity, and stenotic lesion at the left common iliac vein (LCIV). She was diagnosed with May-Thurner syndrome, and a venous stent was placed, and the patient was started on aspirin 81 mg daily for 6 months. Case 2: A 71-year-old man presented with left lower extremity pain and edema. He underwent a left lower extremity venous Duplex ultrasound that showed chronic thrombus in the left proximal to distal femoral vein and acute thrombus in the left popliteal vein and was started on anticoagulation (AC). The patient was also having palpitations and was found to have paroxysmal atrial fibrillation. He underwent pulmonary vein isolation during which it was noted that his LCIV was subtotally occluded. He underwent CT venogram which showed lumbosacral osteophytic compression of the LCIV known as bony May-Thurner syndrome. Given minimal symptoms, the decision was made not to pursue interventional options and to manage conservatively with AC which the patient needs regardless. Case Media - May-Thurner syndrome Pearls - May-Thurner syndrome An often under-recognized, but treatable cause of DVT is left common iliac vein compression known as May-Thurner syndrome. Most patients who have May-Thurner anatomy are asymptomatic. Only a minority of patients with the May-Thurner anatomy present with symptoms such as left leg edema/pain and DVT. Young women are at a higher risk of developing May-Thurner syndrome compared to men. A high degree of suspicion is needed to investigate patients with unilateral left-sided leg symptoms and venous duplex features of May-Thurner syndrome. The diagnosis is made with non-invasive imaging including venous duplex, CT/MR venography, intravascular Ultrasound (IVUS), and catheter-based venography. Although IVUS is the gold standard for diagnosis, due to its invasive nature, it has been replaced by CT/MR imaging. Treatment includes anticoagulation if a thrombus is present. Most patients receive venous stenting at the obstructed site to prevent compression of the left common iliac vein. Some patients need catheter-directed thrombolysis prior to stent placement. Show Notes -May-Thurner syndrome What is May-Thurner syndrome? Classic May-Thurner syndrome is venous outflow obstruction due to external compression of the left common iliac vein by the right common iliac artery causing venous stasis which can lead to DVT. It is more common in women of reproductive age. Osteophytic/bony variant of May-Thurner Syndrome is when a prominent vertebral osteophyte compresses the iliac vein which is more common in older patients. For another fascinating case of May-Thurner Syndrome, presenting with CTEPH, enjoy CardioNerds episode 53. Case Report: CTEPH & May Thurner Syndrome – Temple University. What is the presentation of May-Thurner Syndrome and what are the risk factors? May-Thurner syndrome is often asymptomatic but may present with pain and swelling of the left leg with or without the presence of DVT. Some patients will develop signs of venous insufficiency such as varicose veins, pigmentations, and venous ulcers. Risk factors include scoliosis, female sex, use of oral contraceptives, and pregnancy. As demonstrated in CardioNerds episode #53, chronic thrombo-embolic pulmonary hypertension may be a long-term sequela. How do we diagnose May-Thurner Syndrome? Features suggestive of proximal obstruction in the venous Duplex for the initial assessment of DVT or venous insufficiency raise suspicion for May-Thurner syndrome. These features include loss of respiratory variation of the venous blood flow. IVUS is the gold standard to diagnose May-Thurner Syndrome and can also provide information regarding the chronicity of the thrombus, which could help decide management (for example, whether to perform thrombolysis of acute clot burden). CT/MR venography may have high sensitivity and specificity to detect iliac vein compression nearing 95%. It is also useful in ruling out other causes of iliac vein compression such as osteophyte compression of the iliac vein. How do you treat May-Thurner Syndrome? Management mainly focuses on addressing the patient’s symptoms. For patients with moderate to severe symptoms and significant venous stenosis, endovenous stenting is used rather than conservative management. There are a paucity of data to clarify the optimal antithrombotic regimen following venous stent placement. Practrice patterns varry significantly in terms of antiplatelet/anticoagulant choice and the duration of treatment. The presenct of complications such as DVT, venous stasis ulcer, etc should be managed as usual. References Mangla A, Hamad H. May-Thurner Syndrome. In: StatPearls. Treasure Island (FL): StatPearls Publishing; November 30, 2022. https://www.ncbi.nlm.nih.gov/books/NBK554377/ Kaltenmeier CT, Erben Y, Indes J, et al. Systematic review of May-Thurner syndrome with emphasis on gender differences. J Vasc Surg Venous Lymphat Disord. 2018;6(3):399-407.e4. doi:10.1016/j.jvsv.2017.11.006 https://pubmed.ncbi.nlm.nih.gov/29290600/ Poyyamoli S, Mehta P, Cherian M, et al. May-Thurner syndrome. Cardiovasc Diagn Ther. 2021;11(5):1104-1111. doi:10.21037/cdt.2020.03.07 https://pubmed.ncbi.nlm.nih.gov/34815961/ Knuttinen MG, Naidu S, Oklu R, et al. May-Thurner: diagnosis and endovascular management. Cardiovasc Diagn Ther. 2017;7(Suppl 3):S159-S164. doi:10.21037/CDT.2017.10.14 https://cdt.amegroups.com/article/view/17529/18075

Aug 8, 2023

CardioNerds co-founder Dr. Amit Goyal and episode leads Dr. Jaya Kanduri (FIT Ambassador from Cornell University) and Dr. Jenna Skowronski (FIT Ambassador from UPMC) discuss Complications of acute myocardial infarction with expert faculty Dr. Jeffrey Geske. They discuss various complications of acute MI such as cardiogenic shock, bradyarrythmias, left ventricular outflow tract obstruction, ruptures (papillary muscle rupture, VSD, free wall rupture), and more. Show notes were drafted by Dr. Jaya Kanduri. Audio editing by CardioNerds Academy Intern, student doctor Tina Reddy. The CardioNerds Beyond the Boards Series was inspired by the Mayo Clinic Cardiovascular Board Review Course and designed in collaboration with the course directors Dr. Amy Pollak, Dr. Jeffrey Geske, and Dr. Michael Cullen. CardioNerds Beyond the Boards SeriesCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls and Quotes - Complications of Acute Myocardial Infarction Sinus tachycardia is a “harbinger of doom”! The triad for RV infarction includes hypotension, elevated JVP, and clear lungs. These patients are preload dependent and may need fluid resuscitation despite having an elevated JVP. Bradyarrythmias in inferior MIs are frequently vagally mediated. The focus should be on medical management before committing to a temporary transvenous pacemaker, such as reperfusion, maintaining RV preload and inotropy, avoiding hypoxia, and considering RV-specific mechanical circulator support (MCS). Worsening hypotension with inotropic agents (e.g., dobutamine, epinephrine, dopamine, norepinephrine) after a large anterior-apical MI should raise suspicion for dynamic left ventricular outflow tract obstruction due to compensatory hyperdynamic basal segments. The myocardium after a late presentation MI is as “mushy as mashed potatoes”! Need to look out for papillary muscle rupture, VSD, and free wall rupture as potential complications. Papillary muscle rupture can occur with non-transmural infarcts, and often presents with flash pulmonary edema. VSDs will have a harsh systolic murmur and are less likely to present with pulmonary congestion. Free wall rupture can present as a PEA arrest. All of these complications require urgent confirmation on imaging and early involvement of surgical teams. Notes - Complications of Acute Myocardial Infarction How should we approach cardiogenic shock (CS) in acute myocardial infarction (AMI)? Only 10% of AMI patients present with CS, but CS accounts for up to 70-80% of mortality associated with AMI, usually due to extensive LV infarction with ensuing pump failure. Physical examSinus tachycardia is considered a “harbinger of doom”, when the body compensates for low cardiac output by ramping up the heart rateThe presence of sinus tachycardia and low pulse and/or blood pressure in a patient with a large anterior MI should raise suspicion for cardiogenic shockBe wary of giving IV beta blockers in this situation as negative inotropes can precipitate cardiogenic shock (Commit Trial) When interpreting a patient’s blood pressure in the acute setting, it is helpful to know their baseline blood pressure and if they have a significant history of hypertension. Patients <75 years of age with CS have improved survival at 6 months and at 1 year with early revascularization (SHOCK trial) Mechanical circulatory supportIntra-aortic balloon pump (IABP)No mortality benefit with IABP use in CS at 30 days and at 1 year (IABP-SHOCK II trial)ACC/AHA guidelines give IABP a class IIa recommendation for medically refractory AMI-CS in the USA, whereas the ESC guidelines give it a class III recommendation.Percutaneous left ventricular assist device (Impella)No difference in mortality between IABP or Impella use after 30 days or 6 months (IMPRESS trial)However, observational data like the Detroit & VAD registries show improvement in survival with Impella use in AMI-CS with the cost of excess complications (vascular injury, bleeding, etc)Upcoming trials (DanGer Shock and Recover IV) will hopefully have more promising data supporting the use of Impella in AMI-CS In the setting of discrepant guidelines, the decision for MCS should be multidisciplinary and based on clinical expertise. For more on AMI-CS, enjoy CardioNerds #223. CCC: Approach to Acute Myocardial Infarction Cardiogenic Shock with Dr. Venu Menon How does RV infarction present? Physical examRV infarct triad: hypotension, elevated JVP, clear lungsHypotension precipitated by nitroglycerin administration highlights the preload dependent state of an infarcted RVGI symptoms (nausea and emesis) are common Patients may actually need fluids despite an elevated JVP because of an underfilled left ventricle EKG Consider a right sided leads (ST elevation in V1 and V4R are the most sensitive EKG markers of RV injury), but this should not delay emergent coronary angiography +/- PCI if suspicion for AMI is high RhythmAV synchrony plays an important role in RV infarct given the dependence on preloadIf a patient loses AV synchrony due to heart block or atrial fibrillation, they can become more unstable due to a further drop in RV preload and overall cardiac outputHowever, bradyarrythmias in inferior MIs are frequently vagally mediated, and therefore temporary Strategy for management of an inferior MI with RV infarct should be to optimize all other aspects hemodynamically before placing a temporary transvenous pacemaker (risk of RV perforation)Prompt reperfusionMaintain RV preloadInotropesAvoid hypoxia (potent pulmonary vasoconstriction, can increase RV afterload) MCS providing RV support (Protek-Duo, RP Impella, VA-ECMO) For more on RV-predominant cardiogenic shock, enjoy CardioNerds #239. CCC: Approach to RV Predominant Cardiogenic Shock with Dr. Ryan Tedford How does LVOT obstruction in a large anterior MI present? Hypotension with dobutamine or norepinephrine in a patient with an anterior MI and apical infarct, should raise suspicion for dynamic left ventricular outflow tract obstruction due to compensatory hyperdynamic basal walls Echocardiography is invaluable for diagnosis! ManagementPrompt reperfusionIV fluids (preload dependent)Beta blockers (eg: esmolol quick on, quick off)Phenylephrine (can improve BP by increasing afterload)Avoid positive inotropes (e.g., norepinephrine, epinephrine, dopamine, dobutamine, milrinone) Avoid IABP What are the different types of ruptures which may complicate a late-presentating MI? Papillary muscle rupturePosteromedial papillary more likely to be affected due to single coronary blood supplyPapillary muscles are subendocardial so rupture can occur with non-transmural infarctsPresents with acute dyspnea from flash pulmonary edema and hypotension from drop in cardiac outputExam with new systolic murmur which may not be audible due to rapid equalization of pressures. For the same reason, Doppler may also underestimate the degree of MR. V wave from mitral regurgitation Ventricular septal ruptureRisk factors: advanced age, female sex, first MI with lack of coronary collateralsPresents with hypotension, chest discomfort, dyspneaExam with harsh systolic murmur with palpable thrill; pulmonary congestion is unusual unusualV wave from increased flow through the pulmonary circuit (but not high enough to cause flash pulmonary edema)Step up in RV saturation during right heart catheterizationInferobasal VSD with RCA infarcts (near the valves and conduction tissue and with more serpentine lesions, leading to worse outcomes) Apical VSD with LAD infarcts (can miss on TTE) Free wall ruptureRisk factors: advanced age, female sex, first MI with lack of coronary collateralsPartial rupture may present as a vagal event that heralds the initial tear; TTE with new pericardial effusion should raise suspicion of an incomplete ruptureFull rupture can present as PEA arrest with abysmally low survival May partially heal as a pseudo-aneurysm How do we manage rupture complications? For any of the three rupture scenarios (VSR, papillary muscle rupture, or free wall rupture), time is of the essence to confirm the site of rupture and to get the surgical team involved Can have abrupt, unexpected, unpredictable progression so need to bring in surgical expertise early Papillary muscle rupture will need mitral valve replacement For VSR closure, can pursue surgical versus percutaneous options depending on anatomical features of the lesion and patient characteristicsIntervention is more challenging in inferobasal VSRs with higher operative mortality, but also less amenable to percutaneous closure (less likely to have appropriate rims for closure)If poor operative candidacy, more likely to opt for percutaneous options If size of defect large, would more likely lean towards surgery Can consider bridging with MCS if patient in CS (eg: IABP, Impella) as long as this will not delay the surgical intervention References Early intravenous then oral metoprolol in 45 852 patients with acute myocardial infarction: Randomised placebo-controlled trial. The Lancet. 2005;366(9497):1622-1632. doi:10.1016/s0140-6736(05)67661-1. https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(05)67661-1/fulltext Dzavik V. Early revascularization is associated with improved survival in elderly patients with acute myocardial infarction complicated by cardiogenic shock: A report from the Shock Trial Registry. European Heart Journal. 2003;24(9):828-837. doi:10.1016/s0195-668x(02)00844-8. https://www.nejm.org/doi/full/10.1056/nejm199908263410901 Thiele H, Zeymer U, Neumann F-J, et al. Intraaortic balloon support for myocardial infarction with Cardiogenic shock. New England Journal of Medicine.

Aug 6, 2023

The following question refers to Figures 6-8 from Sections 3.2 of the 2021 ESC CV Prevention Guidelines. The question is asked by student Dr. Hirsh Elhence, answered first by Ohio State University Cardiology Fellow Dr. Alli Bigeh, and then by expert faculty Dr. Eugene Yang.Dr. Yang is Professor of Medicine at the University of Washington where he is also the Medical Director of the Eastside Specialty Center and the co-Director of the Cardiovascular Wellness and Prevention Program. Dr. Yang is former Governor of the ACC Washington Chapter and as well as former Chair of the ACC Prevention of CVD Section. The CardioNerds Decipher The Guidelines Series for the 2021 ESC CV Prevention Guidelines represents a collaboration with the ACC Prevention of CVD Section, the National Lipid Association, and Preventive Cardiovascular Nurses Association.Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. Question #31 The 2021 ESC CV Prevention guidelines recommend a stepwise approach to risk stratification and treatment options. What is the first step in risk factor treatment regardless of past medical history, risk factors, or established ASCVD?AInitiate statin for goal LDL <100 mg/dlBAssess family history of premature CVDCCounsel on ketogenic dietDStop smoking and lifestyle recommendations Answer #31 ExplanationThe correct answer is D – stop smoking and lifestyle recommendations. Smoking cessation and lifestyle modifications are recommended for everyone across the spectrum of ASCVD risk including for both primary and secondary prevention (Class 1). It is worth noting that many patients can move themselves towards a lower risk category without taking drugs just by stopping smoking.Option A is incorrect. While initiating statin therapy for goal LDL <100 mg/dL may be an appropriate treatment option for some patients, it is not the first step per the “stepwise approach” recommended in the ESC guidelines. Whether or not to initiate a statin depends on a multitude of factors including estimated 10-year CVD risk, age, comorbidities, established ASCVD, and patient preference. The first step for patients with established ASCVD includes LDL-C reduction to goal <70 mg/dL (class I) with intensification to a goal LDL-C <55mg/dL based on residual 10-year CVD risk, lifetime CVD risk and treatment benefit, comorbidities, frailty, and patient preference. Primary prevention of ASCVD first targets LDL-C goal <100 (class IIa) in appropriately selected patients.Option B is incorrect. While assessing family history of premature CVD should be part of an initial evaluation and certainly considered a risk enhancing factor, it is not a modifiable risk factor with regards to treatment.Option C is incorrect. A ketogenic diet is not endorsed nor recommended by ACC/AHA or ESC.Studies have shown the benefit of a stepwise approach to treatment intensification. Attainment of treatment goals is similar, side effects are fewer, and patient satisfaction is significantly greater with such an approach. It is not recommended to stop assessment of treatment goals after the first step.Main TakeawayA stepwise approach to treatment intensification is recommended. The first steps for all patients are to stop smoking and institute lifestyle recommendations.Guideline Loc.· 3.2.3 Figures 6-8 CardioNerds Decipher the Guidelines - 2021 ESC Prevention SeriesCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor RollCardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron!

Aug 6, 2023

The following question refers to Sections 6.1 and 7.3 of the 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure. The question is asked by Keck School of Medicine USC medical student & former CardioNerds Intern Hirsh Elhence, answered first by Greater Baltimore Medical Center medicine resident and CardioNerds Academy Fellow Dr. Alaa Diab, and then by expert faculty Dr. Mark Drazner. Dr. Drazner is an advanced heart failure and transplant cardiologist, Professor of Medicine, and Clinical Chief of Cardiology at UT Southwestern. He is the past President of the Heart Failure Society of America. The Decipher the Guidelines: 2022 AHA / ACC / HFSA Guideline for The Management of Heart Failure series was developed by the CardioNerds and created in collaboration with the American Heart Association and the Heart Failure Society of America. It was created by 30 trainees spanning college through advanced fellowship under the leadership of CardioNerds Cofounders Dr. Amit Goyal and Dr. Dan Ambinder, with mentorship from Dr. Anu Lala, Dr. Robert Mentz, and Dr. Nancy Sweitzer. We thank Dr. Judy Bezanson and Dr. Elliott Antman for tremendous guidance. Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. Question #25 A 50-year-old man with a history of type 2 diabetes mellitus, persistent atrial fibrillation, coronary artery disease with prior remote percutaneous coronary intervention, and ischemic cardiomyopathy with HFrEF (LVEF 38%) presents to your outpatient clinic. He denies dyspnea on exertion, orthopnea, bendopnea, paroxysmal nocturnal dyspnea, or peripheral edema. His heart rate is irregularly irregular at 112 beats per minute and blood pressure is 112/67 mmHg. Routine laboratory studies reveal a hemoglobin A1c of 7.7%. Which of the following medications should not be used to control this patient’s comorbidities? A Metoprolol succinate B Verapamil C Dapagliflozin D Pioglitizone E Both B and D Answer #25 Explanation The correct answer is E – both verapamil and pioglitazone should be avoided here. Both verapamil and pioglitizone are associated with harm in patients with LVEF < 50% (Class 3: Harm). Verapamil and diltiazem are non-dihydropyridine calcium channel blockers. These medications can cause negative inotropic effects through inhibition of calcium influx and may be harmful in this patient population. Pioglitizone belongs to a class of diabetic medications known as the thiazolidinediones. This class of medications may increase the risk of fluid retention, heart failure, and hospitalization in patients with LVEF of less than 50%. Metoprolol succinate, and other evidence-based beta blockers, have a Class 1 recommendation for patients with reduced ejection fraction ≤ 40% to prevent symptomatic heart failure and reduce mortality. It may additionally help with rate control in this patient with atrial fibrillation and rapid ventricular response. SGLT2 inhibitors including dapagliflozin have a Class I recommendation for patients with symptomatic chronic HFrEF to reduce hospitalization for HF and cardiovascular mortality, irrespective of the presence of type 2 diabetes (Class 1, LOE A). They also have a Class I recommendation in patients with type 2 diabetes and either established CVD or at high cardiovascular risk to prevent hospitalization for HF (Class 1, LOE A). Our patient has asymptomatic, or pre-HF (Stage B) heart failure with poorly controlled diabetes, and so use of an SGLT2 inhibitor would be appropriate. Main Takeaway Non-dihydropyridine calcium channel blockers and thiozolidinediones both have Class 3 recommendations for harm in patients with reduced LV systolic dysfunction. Guideline Loc. Section 6.1 and 7.3 Decipher the Guidelines: 2022 Heart Failure Guidelines PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron!

Aug 4, 2023

Stroke is a potentially devastating TAVR complication. In this episode, CardioNerds (Drs. Amit Goyal, Nikolaos Spilias, Ahmed Ghoneem, and Chelsea Amo-Tweneboah) discuss TAVR and stroke risk, stroke prevention strategies, and future directions with Dr. Samir Kapadia, Department chair and chief, Cardiovascular Medicine at Cleveland Clinic. They also discuss device innovation and randomized controlled trial implementation for testing device safety and efficacy. Audio editing by CardioNerds Academy Intern, Dr. Chelsea Amo Tweneboah. As an adjunct to this episode and for a deeper review of cerebral embolic protection devices, read “Cerebral Embolic Protection Devices: Current State of the Art” by Agrawal, Kapadia et al., in US Cardiology Review. CardioNerds Aortic Stenosis SeriesCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! References - TAVR and Stroke Leon MB, Smith CR, Mack M, et al. Transcatheter Aortic-Valve Implantation for Aortic Stenosis in Patients Who Cannot Undergo Surgery. New England Journal of Medicine. 2010;363(17):1597-1607. Kapadia SR, Makkar R, Leon M, et al. Cerebral Embolic Protection during Transcatheter Aortic-Valve Replacement. New England Journal of Medicine. 2022;387(14):1253-1263. Kapadia SR, Kodali S, Makkar R, et al. Protection Against Cerebral Embolism During Transcatheter Aortic Valve Replacement. Journal of the American College of Cardiology. 2017;69(4):367-377. Khan MZ, Zahid S, Khan MU, et al. Use and outcomes of cerebral embolic protection for transcatheter aortic valve replacement: A US nationwide study. Catheter Cardiovasc Interv. 2021;98(5):959-968.

Jul 28, 2023

CardioNerds cofounders Dr. Amit Goyal and Dr. Daniel Ambinder join Dr. Isabel Balachandran, Dr. Diego Celli from the Texas Heart Institute. They discuss the nuances of risk stratification management of intermediate risk pulmonary embolism. The ECPR for this episode was provided by Dr. Alam Mahboob (Associate Professor of Medicine at Baylor College of Medicine and the Department of Medicine and Associate Program Director for the Cardiovascular Disease Fellowship Program at Baylor). Audio editing by CardioNerds Academy Intern, Dr. Chelsea Amo Tweneboah. US Cardiology Review is now the official journal of CardioNerds! Submit your manuscript here. CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Case Media - Caring for the Middle Child of Pulmonary Embolism – Texas Heart Institute Pearls - Caring for the Middle Child of Pulmonary Embolism – Texas Heart Institute Submassive pulmonary embolism is defined as an intermediate risk group of acute pulmonary embolism, which presents with signs of RV dysfunction and myocardial injury without hemodynamic instability. The AHA, ACCP, and ESC have variable definitions of submassive PE. Non-invasive tools such as EKG, TTE, and CT are critical to defining RV dysfunction. The Pulmonary Embolism Severity Index (PESI) score is a validated tool to help risk stratify patients with PE. Advanced therapies for submassive PE include systemic thrombolysis, catheter-based intervention, surgical embolectomy, and mechanical circulatory support. The decision between these therapies is based on individual patient risk profiles, local expertise, and the risk of major bleeding. There is a spectrum of long-term complications after an acute PE, ranging from post PE syndrome to CTEPH (chronic thromboembolic pulmonary hypertension) caused by a maladaptive vascular remodeling from residual thrombus or arteriopathy. Thrombolytic therapies are still controversial in reducing the risk of post PE complications. PERT is a multidisciplinary group of clinicians who can rapidly assess and triage patients with acute PE, coordinate access to medical and advanced therapies, and provide the necessary follow up care. Show Notes - Caring for the Middle Child of Pulmonary Embolism – Texas Heart Institute How do you define “submassive” pulmonary embolism? Venous thromboembolism, which includes deep vein thrombosis and acute pulmonary emboli (PE) are the third most common cardiovascular disorder in the United States with approximately 900,000 cases occurring each year (1). The morbidity and mortality associated with pulmonary emboli are also great, with approximately 33% of PE cases being fatal (1).Until recently, PE was previously classified into massive or non-massive. Massive PE was defined as those with cardiogenic shock. A newer group, “submassive PE”, was defined as an “intermediate” risk group. According to the American Heart Association (AHA) Scientific Statement on the management of massive and submassive PE, patients in this group presented with signs of RV dysfunction and myocardial necrosis without hemodynamic instability (2). Intermediate-risk PE covers a broad range of risk and management decisions remain challenging. Intermediate-risk PE convers increased risk for mortality and complications compared with low-risk PE. How do you risk-stratify intermediate-risk pulmonary emboli? The AHA, American College of Chest Physicians (ACCP), and European Society of Cardiology (ESC) have variable definitions of submassive PE and which biomarkers should be used (1,3). The contents are summarized as below (Table 1) Each major guideline highlights the importance of the evaluation of RV dysfunction (RVD) and elevated biomarkers. To summarize, the AHA defines submassive PE with either RVD or elevated biomarkers, specifically troponin levels (2). The ACCP similarly defines an intermediate risk PE with either RVD or elevated biomarkers, though with both elevated BNP/NT-proBNP or troponin levels (4). Finally, the ESC subdivides intermediate risk into intermediate-high and intermediate-low risk groups based on the PESI score and if there are elevated troponin levels (3). As of 2019, the AHA published a consensus statement revising the nomenclature of PE. The terminology is now high risk, intermediate risk, and low risk (4). The AHA 2011 guidelines define RVD based on the following non-invasive tools (EKG, CT and transthoracic echocardiography) (2).By EKG, concerning changes include a new or incomplete right bundle branch block, anteroseptal ST elevation or depression, or anteroseptal T wave inversions. Other pertinent findings include sinus tachycardia (the most common abnormality), atrial arrhythmias, low voltages, right axis deviation, S1Q3T3, or Qr pattern in V1 (2).By CT, RV enlargement is defined as an RV to LV diameter ratio > 0.90 (2).By TTE, RV enlargement (RV to LV diameter ratio > 0.9), systolic dysfunction (TAPSE 2.7 m /sec. Finally, there can also be direct visualization of thrombus within the right sided chambers (5). The PESI or Pulmonary Embolism Severity Index is a validated tool using markers such as age, sex, vital signs, presence of hypoxemia, altered mental status, and comorbidities (such as cancer, heart failure, and chronic lung disease) to risk stratify patients with PE. A high PESI score is suggestive of an elevated 30-day mortality (6). What is the general approach to therapeutic interventions and treatment for submassive PE? With confirmed PE and no contraindications to systemic anticoagulation prompt use of low molecular weight heparin (LMWH), unfractionated heparin, or fondaparinux should be used. For those confirmed with heparin induced thrombocytopenia, a non-heparin based anticoagulant (such as argatroban or bivalirudin) should be used (2). In regards to direct oral anticoagulation (DOAC), in large studies (including the EINSTEIN and AMPLIFY trials), patients with submassive PE predominantly received LMWH prior to DOAC initiation. It is uncertain whether direct initiation of DOAC is comparable in outcomes (1). Treatment with systemic anticoagulation alone in normotensive patients with RV dysfunction, is controversial and the use of more aggressive therapies has been studied extensively. Advanced therapies for submassive PE include systemic thrombolysis, catheter-based interventions, surgical embolectomy, and mechanical circulatory support. The decision between these therapies is based on individual patient risk as well as the risk of major bleeding, best guided by pulmonary embolism response teams (PERT) (7). Finally, surgical embolectomy is considered in those with submassive and massive PE in whom fibrinolytic therapy has failed or is contraindicated. Other indications include paradoxical emboli, clot in transit, or hemodynamic collapse. In large, high-volume centers, this has been found to be a safe and effective approach (1). Hemodynamic support is important to consider for management of RV failure. If a limited intravenous fluid trial fails, early vasopressor and inotropic support should be initiated. ECMO is indicated for hemodynamic and ventilatory support in patients with severe RV failure and refractory cardiogenic shock (7). When do you consider systemic thrombolysis or catheter directed therapies for patients with intermediate-risk PE? Systemic thrombolysis works by rapidly acting on acute thrombus, thereby reducing pulmonary pressures and RV dysfunction, along with improving hemodynamics. This has been shown to be superior to anticoagulation alone in massive PE with reductions in mortality at the cost of increased major bleeding (1,2). The PEITHO trial was the largest randomized control trial of systemic thrombolysis in PE. Thrombolytic treatment with Tenecteplase reduced a composite outcome of all-cause mortality at 7 days and hemodynamic decompensation versus anticoagulation with heparin alone. This, however, came at the expense of an increased risk of major bleeding (including intracranial hemorrhage) (8). Given this concern, the MOPPET-3 trial in 2013 evaluated the effect of low dose thrombolysis on outcomes in patients with submassive PE. It was found that low dose tPA reduced the incidence of pulmonary hypertension. However, tPA did not reduce the rates of a combined outcome of recurrent PE or all-cause mortality (9). Catheter-based therapy, including pharmacomechanical therapy, catheter-directed thrombolysis, and mechanical embolectomy, is a widely studied approach for treating pulmonary embolism (PE) (10). In 2013, the ULTIMA trial compared CDT plus anticoagulation versus anticoagulation alone in intermediate-high risk PE and found that CDT resulted in a statistically significant improvement in the right ventricular/left ventricular (RV/LV) ratio at 24 hours. At 90 days, there was no difference in mortality or major bleeding events between the two groups (11). A recent meta-analysis compared CDT to systemic anticoagulation (sAC) alone and showed lower rates of in-hospital, 30-day, and 90-day mortality, with no differences in major or minor bleeding or blood transfusions (10). The most widely studied technique is ultrasound-facilitated catheter-directed fibrinolysis (EKOS), which combines local fibrinolysis with mechanical thrombectomy. The SEATTLE II trial found a reduction in mean RV/LV ratio and mean pulmonary artery systolic pressure at 48 hours post-thrombolysis.

Jul 17, 2023

CardioNerds cofounder Dr. Daniel Ambinder, series co-chair Dr. Dinu Balanescu (FIT, Mayo Clinic), and episode lead Dr. Anjali Rao (FIT, UTSW) discuss training in cardio-oncology with Dr. Stephanie Feldman from Rutgers University. In this episode, the group discusses some of the most burning questions about educating the next wave of cardio-oncologists. As Dr. Feldman mentions, the projected number of cancer survivors is predicted to be around 24 million by 2024, underscoring the growing importance of cardio-oncology in our practice. We highlight some of the challenges facing trainees and training programs alike, including how to integrate cardio-oncology education into general cardiology training, the optimal structure for an advanced cardio-oncology fellowship, and the role of cardio-oncology in the inpatient setting. We also talk about the takeaways from the ACC Cardio-Oncology Leadership Council document. Dr. Feldman reflects on the importance of flexibility in education in the current landscape, drawing on her personal experience as a cardio-oncologist during the COVID-19 era. Notes were drafted by Dr. Anjali Rao. Audio editing was performed by student doctor, Shivani Reddy. This episode is supported by a grant from Pfizer Inc. This CardioNerds Cardio-Oncology series is a multi-institutional collaboration made possible by contributions of stellar fellow leads and expert faculty from several programs, led by series co-chairs, Dr. Giselle Suero Abreu, Dr. Dinu Balanescu, and Dr. Teodora Donisan. Pearls • Notes • References • Production Team CardioNerds Cardio-Oncology PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls and Quotes - Cardio-Oncology: Training and Future Directions It may be possible to achieve “COCATS level 2” cardio-oncology training during general cardiology fellowship. A dedicated cardio-oncology year may appeal to trainees who want to achieve “COCATS level 3”, i.e., dedicate their practice to caring for patients with complex cardio-oncology needs, become involved in clinical trials, and lead cardio-oncology clinical and training programs. Supplemental learning opportunities for general fellows can include: Rotating in a cardio-oncology clinic, ideally attached to a National Cancer Institute-designated cancer center Multi-modality cardiac imaging Participating in cardio-oncology research Some currently available educational opportunities include:The International Cardio-Oncology Society (ICOS) weekly webinarsThe American Society of Echocardiography (ASE) webinars on global longitudinal strainThe American Society of Nuclear Cardiology lecture series on cardiac amyloidosis Cardio-oncology focused conferences, such as the American College of Cardiology’s (ACC) Advancing the Cardiovascular Care of the Oncology Patient and Memorial Sloan Kettering’s Cardio-Oncology Symposium. Each institution may have different inpatient cardio-oncology needs depending on whether there is a stand-alone cancer hospital or another format. Examples of inpatient consults that may benefit from having a cardio-oncologist involved include:Cardiovascular risk assessment prior to bone marrow transplant or cancer related surgery in a patient with known coronary artery diseaseImmune checkpoint inhibitor myocarditisChemotherapy-related cardiac dysfunction Management of systemic anticoagulation in a patient with high CHA2DS2-VASc and chemotherapy related thrombocytopenia. Show notes - Cardio-Oncology: Training and Future Directions The need for cardio-oncology experience is undeniable given the growing population of patients with cancer and cardiovascular disease, particularly given the number of anti-neoplastic therapies with potential cardiovascular side effects. There are several strategies for incorporating cardio-oncology experiences into general cardiology training. These may include rotating through a cardio-oncology clinic, enhanced exposure to multimodality cardiac imaging including global longitudinal strain and participating in cardio-oncology research. The need for dedicated formal training in cardio-oncology is more nuanced. If the goals of a formal fellowship align with a trainee’s career goals, an additional year of training can provide advanced exposure to complex medical decision-making, cardio-oncology specific imaging training (i.e., global longitudinal strain, MRI, PET), and even inpatient cardio-oncology experience at several centers. Prospective cardio-oncology trainees should gain clinical exposure during general cardiology fellowship and research exposure where available, and these experiences can factor into their decision to pursue a cardio-oncology fellowship. Additional resources from national societies (e.g., ICOS, ACC, ASE) for cardio-oncology education can be made available to general cardiology trainees to expand their knowledge base. In some institutions, inpatient cardio-oncology consults may be appropriate. As a general rule, consultations regarding chemo- or immunotherapy-related cardiotoxicities or pre-stem cell transplant risk stratification may benefit from involvement of cardio-oncology in some form. The future of cardio-oncology is bright, especially with the development of programs to train the next generation of cardio-oncologists! References - Cardio-Oncology: Training and Future Directions Tuzovic M, Brown SA, Yang EH, et al. Implementation of Cardio-Oncology Training for Cardiology Fellows. JACC CardioOncol. 2020;2(5):795-799. Published 2020 Dec 15. · CardioOncology Education and Training. Alvarez-Cardona JA, Ray J, Carver J, et al. Cardio-Oncology Education and Training: JACC Council Perspectives. J Am Coll Cardiol. 2020;76(19):2267-2281. Cardio-oncology Training in the COVID-19 Era. Feldman S, Liu J, Steingart R, Gupta D. Cardio-oncology Training in the COVID-19 Era. Curr Treat Options Oncol. 2021;22(7):58. Published 2021 Jun 7.

Jul 14, 2023

The following question refers to Section 6.1 of the 2021 ESC CV Prevention Guidelines. The question is asked by MGH internal medicine resident Dr. Christian Faaborg-Andersen, answered first by UCSD early career preventive cardiologist Dr. Harpreet Bhatia, and then by expert faculty Dr. Eugenia Gianos. Dr. Gianos specializes in preventive cardiology, lipidology, cardiovascular imaging, and women’s heart disease; she is the Director of Women’s Heart Health at Lenox Hill Hospital and Director of Cardiovascular Prevention for Northwell Health. The CardioNerds Decipher The Guidelines Series for the 2021 ESC CV Prevention Guidelines represents a collaboration with the ACC Prevention of CVD Section, the National Lipid Association, and Preventive Cardiovascular Nurses Association. Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. Question #30 A 65-year-old woman with a history of hypertension, type 2 diabetes mellitus, and coronary artery disease with remote PCI to the RCA presents for follow-up. She has stable angina symptoms that are well controlled with metoprolol tartrate 25 mg BID and are not lifestyle limiting. She takes aspirin 81 mg daily and atorvastatin 40 mg daily. Her LDL-C is 70 mg/dL, hemoglobin A1c is 7.0%, and eGFR is >60. In clinic, her BP is 118/80 mmHg. What is the next step in management?AIncrease atorvastatin for goal LDL-C < 55 mg/dLBNo change in managementCAdd isosorbide mononitrate 30 mg dailyDStop aspirinEStart a sulfonylurea Answer #30 Explanation The correct answer is A – increase atorvastatin for goal LDL-C < 55 mg/dL.In patients with established ASCVD, the ESC guidelines advocate for an LDL goal of < 55 mg/dL with at least a 50% reduction from baseline levels (Class I, LOE A). This patient has stable angina which is not lifestyle limiting; as such, further anti-anginal therapy is not necessary. She has known CAD with prior PCI, so aspirin therapy is appropriate for secondary prevention (Class I, LOE A). There is no indication for a sulfonylurea as her diabetes is well controlled. Notably, in persons with type 2 DM and ASCVD, the use of a GLP-1RA or SGLT2 inhibitor with proven outcome benefits is recommended to reduce CV and/or cardiorenal outcomes (Class I, LOE A).Main TakeawayFor people with established ASCVD, the ESC-recommended LDL-C goal is < 55 mg/dL with a goal reduction of at least 50%.Guideline Loc.Section 6.1 CardioNerds Decipher the Guidelines - 2021 ESC Prevention SeriesCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor RollCardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron!

Jul 13, 2023

The following question refers to Sections 10.2 of the 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure. The question is asked by Western Michigan University medical student and CardioNerds Intern Shivani Reddy, answered first by Mayo Clinic Cardiology Fellow and CardioNerds Academy House Faculty Leader Dr. Dinu Balanescu, and then by expert faculty Dr. Ileana Pina. Dr. Pina is Professor of Medicine and Quality Officer for the Cardiovascular Line at Thomas Jefferson University, Clinical Professor at Central Michigan University, and Adjunct Professor of Biostats and Epidemiology at Case Western University. She serves as Senior Fellow and Medical Officer at the Food and Drug Administration’s Center for Devices and Radiological Health. The Decipher the Guidelines: 2022 AHA / ACC / HFSA Guideline for The Management of Heart Failure series was developed by the CardioNerds and created in collaboration with the American Heart Association and the Heart Failure Society of America. It was created by 30 trainees spanning college through advanced fellowship under the leadership of CardioNerds Cofounders Dr. Amit Goyal and Dr. Dan Ambinder, with mentorship from Dr. Anu Lala, Dr. Robert Mentz, and Dr. Nancy Sweitzer. We thank Dr. Judy Bezanson and Dr. Elliott Antman for tremendous guidance. Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. Question #24 Mr. E. Regular is a 61-year-old man with a history of HFrEF due to non-ischemic cardiomyopathy (latest LVEF 40% after >3 months of optimized GDMT) and persistent atrial fibrillation. He has no other medical history. He has been on metoprolol and apixaban and has also undergone multiple electrical cardioversions and catheter ablations for atrial fibrillation but remains symptomatic with poorly controlled rates. His blood pressure is 105/65 mm Hg. HbA1c is 5.4%. Which of the following is a reasonable next step in the management of his atrial fibrillation? A Anti-arrhythmic drug therapy with amiodarone. Stop apixaban. B Repeat catheter ablation for atrial fibrillation. Stop apixaban. C AV nodal ablation and RV pacing. Shared decision-making regarding anticoagulation. D AV nodal ablation and CRT device. Shared decision-making regarding anticoagulation. Answer #24 Explanation The correct answer is D – AV nodal ablation and CRT device along with shared decision-making regarding anticoagulation.” Maintaining sinus rhythm and atrial-ventricular synchrony is helpful in patients with heart failure given the hemodynamic benefits of atrial systole for diastolic filling and having a regularized rhythm. Recent randomized controlled trials suggest that catheter-based rhythm control strategies are superior to rate control and chemical rhythm control strategies with regards to outcomes in atrial fibrillation. For patients with heart failure and symptoms caused by atrial fibrillation, ablation is reasonable to improve symptoms and quality of life (Class 2a, LOE B-R). However, Mr. Regular has already had multiple failed attempts at ablations (option B). For patients with AF and LVEF ≤50%, if a rhythm control strategy fails or is not desired, and ventricular rates remain rapid despite medical therapy, atrioventricular nodal ablation with implantation of a CRT device is reasonable (Class 2a, LOE B-R). The PAVE and BLOCK-HF trials suggested improved outcomes with CRT devices in these patients. RV pacing following AV nodal ablation has also been shown to improve outcomes in patients with atrial fibrillation refractory to other rhythm control strategies. In patients with EF >50%, there is no evidence to suggest that CRT is more beneficial compared to RV-only pacing. However, RV pacing may produce ventricular dyssynchrony and when compared to CRT in those with reduced EF (≤ 50%), CRT produced more benefit (Option C). Although adjustments in antiarrhythmic medications and repeat ablation may be considered, these are unlikely to provide long-term benefit to Mr. E. Regular, who already failed antiarrhythmic regimens and multiple attempts at cardioversion and ablation (Options A, B). In patients with chronic heart failure and atrial fibrillation, the decision to use anticoagulation for the prevention of cerebrovascular events is generally based on the CHA2DS2-VASc score. Mr. Regular’s CHA2DS2-VASc score is 1 (+1 for HF, no points for: hypertension, age 65-74 or ≥75, diabetes, stroke/TIA/TE, vascular disease, female gender). Chronic anticoagulation therapy is recommended for patients with CHA2DS2-VASc scores ≥2 for men and ≥3 for women (Class 1, LOE A). Therefore, based on the CHA2DS2-VASc score alone, Mr. Regular would not necessarily warrant anticoagulation. However, HF is a hypercoagulable state and serves as an independent risk factor for stroke, systemic embolism, and mortality in the setting of AF. In patients with HF and a CHA2DS2-VASc score of 1, those with AF had a 3-fold higher risk compared with individuals without concomitant AF. Because HF is a risk factor, additional risk factors may not be required to support the use of anticoagulation in patients with HF, and the decision to anticoagulate can be individualized according to risk versus benefit. The guidelines give a Class 2a recommendation for chronic anticoagulation in men and women with chronic HF and permanent-persistent-paroxysmal AF who have no additional risk factors (LOE B-NR). Therefore, decisions regarding anticoagulation in this context should incorporate patient values, comorbidities, and informed shared decision making. Main Takeaway In summary, the “ablate and pace” strategy of AV nodal ablation and CRT device implantation improve outcomes in patients with heart failure with reduced LVEF and atrial fibrillation refractory to chemical and catheter-based rhythm control strategies and failure of rate control options. Guideline Loc. Section 10.2 Decipher the Guidelines: 2022 Heart Failure Guidelines PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron!

Jul 12, 2023

In this episode, CardioNerds co-founder Amit Goyal joins Dr. Iva Minga, Dr. Kevin Lee, and Dr. Juan Pablo Salazar Adum from the University of Chicago - Northshore in Evanston, IL to discuss a case of primary cardiac diffuse large B-cell lymphoma. The ECPR for this episode is provided by Dr. Amit Pursnani (Advanced Cardiac Imaging, Fellowship program director, NorthShore University HealthSystem). Audio editing by CardioNerds Academy Intern, Dr. Akiva Rosenzveig. Case synopsis: A 77-year-old man with no significant medical history presents to the emergency department with progressive shortness of breath for 1 week. He reports an unintentional 15-pound weight loss in the prior month as well as constipation and abdominal/flank pain. On examination he was found to be tachycardic with a regular rhythm and further evaluation with a chest X-ray and chest CT scan demonstrated a large pericardial effusion. This was further investigated with an urgent echocardiogram that revealed a large pericardial effusion with a large mass attached to the pericardial side of the RV free wall, as well as signs of early cardiac tamponade. A pericardiocentesis was performed and 550mL of bloody fluid was withdrawn. The fluid was sent for laboratory analysis and cytology. A cardiac MRI demonstrated a large invasive mass in the pericardium and RV wall consistent with cardiac lymphoma. Cytology confirmed diffuse large B-cell lymphoma. Subsequent CT and PET scans did not find any other site of malignancy, giving the patient a diagnosis of primary cardiac diffuse large B-cell lymphoma. The patient underwent R-CHOP chemotherapy and was followed closely with repeat cardiac MRI and PET scans which demonstrated resolution of the cardiac mass at his one-year surveillance follow-up. This case was published in US Cardiology Review, the official journal of CardioNerds. To learn more, access the case report article here. CardioNerds is collaborating with Radcliffe Cardiology and US Cardiology Review journal (USC) for a ‘call for cases’, with the intention to co-publish high impact cardiovascular case reports, subject to double-blind peer review. Case Reports that are accepted in USC journal and published as the version of record (VOR), will also be indexed in Scopus and the Directory of Open Access Journals (DOAJ). CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls - A Mystery Mass in the Heart - Cardiac Lymphoma The most common cause of malignant cardiac masses is metastasis. Primary cardiac tumors are rare. Cardiac tumors are separated into 2 categories: benign and malignant. They are often differentiated based on their location and their degree of tissue invasion. Multimodality imaging is essential in the diagnosis, management, and surveillance of cardiac masses. A multidisciplinary team approach is invaluable for management of patients with cardiac tumors. Show Notes - A Mystery Mass in the Heart - Cardiac Lymphoma 1. What is the clinical presentation of cardiac masses? Cardiac masses can have a variable presentation. They can present with arrhythmias, angina, heart failure symptoms, or pericardial effusion. Patients can also be asymptomatic; the masses can be found incidentally on cardiac or chest imagining. 2. What is the differential diagnosis for cardiac masses? Cardiac masses are separated into benign and malignant. The most common malignant cardiac masses are metastases from a distant source. The location of the mass is important in narrowing the differential. 3. What imaging modalities are used to diagnose cardiac masses? Multimodality imaging is needed to describe the mass in detail and guide diagnosis. An echocardiogram is usually the first imaging modality. Cardiac MRI is a great modality that allows for the detailed visualization as well as tissue characterization of the mass. Cardiac CT, chest CT, and PET scans are also imagining modalities that can be used in the management of the mass. 4. How do you manage cardiac masses? Management of cardiac masses depends on etiology (benign or malignant) and the associated hemodynamic changes associated with it. For example, if a benign cardiac mass is associated with significant valvular regurgitation, cardiac surgery needs to be considered for management. A multidisciplinary team including cardiology, heart failure, critical care cardiology, cardio-oncology, oncology, cardiac surgery, and other specialties may be involved in the management of cardiac masses and their manifestations. References - A Mystery Mass in the Heart - Cardiac Lymphoma 1. Alerhand, S., & Carter, J. (2019). What echocardiographic findings suggest a pericardial effusion is causing tamponade? American Journal of Emergency Medicine, 37(2), 321-326. 2. McAllister, H. A., & Fenoglio, J. J. (1978). Tumors of the Cardiovascular System. Atlas of Tumor Pathology, Series 2. Armed Forces Institute of Pathology, Washington DC, 2, 20. 3. Tyebally, S., Chen, D., Bhattacharyya, S., Mughrabi, A., Hussain, Z., Manisty, C., Westwood, M., Ghosh, A. K., & Guha, A. (2020). Cardiac Tumors: JACC CardioOncology State-of-the-Art Review. JACC. CardioOncology, 2(2), 293-311. 4. Motwani, M., Kidambi, A., Herzog, B. A., Uddin, A., Greenwood, J. P., & Plein, S. (2013). MR imaging of cardiac tumors and masses: a review of methods and clinical applications. Radiology, 268(1), 26-43. 5. Spodick, D. H. (2003). Acute cardiac tamponade. New England Journal of Medicine, 349(7), 684-690.

Jul 11, 2023

In this episode, Dr. Gurleen Kaur (medicine resident at Brigham and Women’s Hospital and Director of CardioNerds Internship) and CardioNerds Academy interns Dr. Akiva Rosenzveig (medicine intern at Cleveland Clinic), Dr. Chelsea Tweneboah (medicine intern at Stonybrook University), student doctor Shivani Reddy (medical student at Western Michigan University), student doctor Diane Masket (medical student at Rowan School of Osteopathic Medicine), and student doctor Tina Reddy (medical student at Tulane University School of Medicine) discuss with Dr. Michelle Kittleson (Director of Education in Heart Failure and Transplantation, Director of HF Research, and Professor of Medicine at Cedars Sinai) about Mastering the Art of Patient Care. Dr. Kittleson shares pearls of wisdom from her book on topics including career transitions, mentorship, dealing with uncertainty, learning from mistakes, delivering difficult news, and being a woman and parent in medicine. This episode was planned by Dr. Gurleen Kaur and episode audio was edited by student doctor Tina Reddy. Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. CardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron!

Jul 9, 2023

Dr. Amit Goyal (CardioNerds co-founder), Dr. Jessie Holtzman (House Faculty in CardioNerds Academy and cardiology fellow at UCSF), and Dr. Megan McLaughlin (CardioNerds Scholar and cardiology fellow at UCSF) discuss stimulant-associated cardiomyopathy with Dr. Jonathan Davis (Associate Professor at UCSF the Director of the Heart Failure Program at Zuckerberg San Francisco General Hospital) and Dr. Soraya Azari (Associate Clinical professor at UCSF, with specialty in hospital medicine, primary care, HIV medicine, and addiction medicine). Methamphetamine-associated heart failure admissions have steadily increased in the United States over the past decade. Substance use disorders more broadly are thought to complicate at least 15% of all heart failure hospitalizations and amphetamine use has been shown to be an independent predictor of heart failure readmission across the country. At safety net and public hospitals, these numbers may rise even higher. This episode reviews the pathophysiology of stimulant associated cardiomyopathy, highlights treatment options for stimulant use disorder, and discusses novel models of co-management of heart failure and substance use disorder. Notes were drafted by Dr. Jessie Holtzman. Audio editing by CardioNerds academy intern, Pace Wetstein. Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. CardioNerds Heart Success Series PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls - Stimulant-Associated Cardiomyopathy Though there are no pathognomonic traits of stimulant-associated cardiomyopathy, common echocardiographic features include biventricular dilated cardiomyopathy and/or pulmonary hypertension with a dilated, hypokinetic right ventricle and underfilled left ventricle. Enjoy CardioNerds Episode 312. Case Report: Life in the Fast Lane Leads to a Cardiac Conundrum to learn from a case of stimulant associated pulmonary arterial hypertension. Not all cardiomyopathy in patients who use stimulants is due to stimulant use. Do your due diligence. Patients who use stimulants should undergo a broad work-up to diagnose the etiology of cardiomyopathy. Tips for taking a substance use history: Ask permission to discuss the topic. Normalize the behavior. Use specific drug names (also, learn the local drug nicknames!). Ask about any history of prior treatment and periods of abstinence. Screen for risk of harm or overdose Try using a phrase like “I’m asking you this because I want to know if the way you are using drugs can impact your health and keep you safe.” There are no FDA-approved medications to treat stimulant use disorder. Common off-label therapies include mirtazapine and bupropion/naltrexone. Contingency management programs work off the principle of operant conditioning; they reward patients for maintaining abstinence from substance use. For clinicians to seek assistance in providing treatment for stimulant use disorder, important resources include: SAMSA (national help line 1-800-662-HELP or online resource locator) HarmReduction.Org Never Use Alone hotline (800-484-3731) Show notes - Stimulant-Associated Cardiomyopathy 1. What are common clinical presentations of stimulant-associated cardiomyopathy? Stimulants have multifactorial physiologic impacts, due both to pharmacologic properties (adrenergic stimulation and vasoconstriction) and direct toxic effects. Clinical manifestations may include hypertension, tachyarrhythmias, acute myocardial infarction, cardiomyopathy, pulmonary hypertension, aortic dissection, and sudden cardiac death. On echocardiogram, stimulant-associated cardiomyopathy may manifest as biventricular dilated cardiomyopathy, compensatory tachycardia, LV thrombus, and/or pulmonary hypertension (WHO Group I) 2. What is the pathophysiology of stimulant associated cardiomyopathy? Though the exact mechanisms driving stimulant-associated cardiomyopathy are unknown, myocardial injury is thought to be related to excess catecholamines and the generation of reactive oxygen species, mitochondrial dysfunction, and the downstream effects of microvascular dysfunction and vasospasm. Some authors have proposed a two-hit phenomenon whereby stimulant use and vulnerable genetics result in more severe clinical presentations. 3. What are common treatment options for stimulant-associated cardiomyopathy and stimulant use disorder in the presence of cardiovascular disease? As with heart failure in general, start by ensuring that patients receive appropriate goal-directed medical therapy (GDMT) with an ACEI/ARB/ARNI, beta-blocker, MRA, and SGLTi. If patients struggle with medication adherence, be sure to address the social determinants of health to allow for improved adherence. For instance, consider using bubble packs to help mitigate polypharmacy. 4. What is the Heart Plus Clinic and how can cardiologists work in an interdisciplinary fashion to address both cardiovascular disease and substance use disorders? The Heart Plus clinic is a multidisciplinary team that links addiction medicine providers and the cardiovascular teams together. The clinic uses contingency management to incentivize abstinence from substance use and works to address barriers to getting medications, taking medications, and navigating polypharmacy. Results are promising so far, with a pilot study demonstrating less stimulant use, more GDMT use, less urgent care use, and more primary care use, along with greater engagement, continuity, and rapport. 5. How do you take a substance use history? Ask permission: “Is it ok if I ask you about ***” Normalize the behavior: “Substance use is common” or “I have a lot of patients struggling with ***” Use specific names when obtaining a drug use history (not just alcohol, tobacco, “drugs”). Learn the names of drugs in your region. Try using phrases like “I’m asking you this because I want to know if the way you are using drugs can impact your health and keep you safe.” Ask about their history of past treatment and periods of abstinence. Screen for patients at risk of harm and/or overdose due to patterns of use and be sure to prescribe naloxone. 6. What are some useful resources for treating patients with active substance use disorders? Though there currently no FDA-approved medications to treat stimulant use disorder, common off-label therapies include mirtazapine and bupropion/naltrexone. Contingency management programs work off the principle of operant conditioning and reward patients for maintaining abstinence from substance use. In contingency management programs, a behavior is chosen that you want to see more frequently, and a reward is given. The reward must be given close to the time of behavior and be of sufficient magnitude to demonstrate the desired effect. There are many resources to help both clinicians and patients treat substance sue disorders. Resources include the SAMSA national help line (1-800-662-HELP) or online resource locator for clinicians. Patients may also access HarmReduction.Org and the NeverUseAlone hotline (800-484-3731) for harm reduction resources. References - Stimulant-Associated Cardiomyopathy 1. DesJardin J, Leyde S, Davis J. Weathering the perfect storm: management of heart failure in patients with substance use disorders. Heart. 2021;107(16):1353-4. doi: 10.1136/heartjnl-2021-319103. 2. Kevil CG, Goeders NE, Woolard MD, Bhuiyan MS, Dominic P, Kolluru GK, et al. Methamphetamine Use and Cardiovascular Disease. Arterioscler Thromb Vasc Biol. 2019;39(9):1739-46. doi: 10.1161/ATVBAHA.119.312461. 3. Kolaitis NA, Saggar R, De Marco T. Methamphetamine-associated pulmonary arterial hypertension. Curr Opin Pulm Med. 2022;28(5):352-60. 4. Leyde S, Abbs E, Suen LW, Martin M, Mitchell A, Davis J, et al. A Mixed-methods Evaluation of an Addiction/Cardiology Pilot Clinic With Contingency Management for Patients With Stimulant-associated Cardiomyopathy. J Addict Med. 2023;17(3):312-8. doi: 10.1097/ADM.0000000000001110. 5. Manja V, Nrusimha A, Gao Y, Sheikh A, McGovern M, Heidenreich PA, et al. Methamphetamine-associated heart failure: a systematic review of observational studies. Heart. 2023;109(3):168-77. doi: 10.1136/heartjnl-2022-321610. 6. Reddy PKV, Ng TMH, Oh EE, Moady G, Elkayam U. Clinical Characteristics and Management of Methamphetamine-Associated Cardiomyopathy: State-of-the-Art Review. J Am Heart Assoc. 2020;9(11):e016704. doi: 10.1161/JAHA.120.016704. https://www.ahajournals.org/doi/epub/10.1161/JAHA.120.016704

Jun 23, 2023

CardioNerds (Drs. Amit Goyal and Dan Ambinder) join Dr. Emily Lee (LAC+USC Internal medicine resident) and Dr. Charlie Lin (LAC+USC Cardiology fellow) as the discuss an important case of stimulant-related (methamphetamine) cardiovascular toxicity that manifested in right ventricular dysfunction due to severe pulmonary hypertension. Dr. Jonathan Davis (Director, Heart Failure Program at Zuckerberg San Francisco General Hospital and Trauma Center) provides the ECPR for this episide. Audio editing by CardioNerds Academy Intern, student doctor Akiva Rosenzveig. With the ongoing methamphetamine epidemic, the incidence of stimulant-related cardiovascular toxicity continues to grow. We discuss the following case: A 36-year-old man was hospitalized for evaluation of dyspnea and volume overload in the setting of previously untreated, provoked deep venous thrombosis. Transthoracic echocardiogram revealed severe right ventricular dysfunction as well as signs of pressure and volume overload. Computed tomography demonstrated a prominent main pulmonary artery and ruled out pulmonary embolism. Right heart catheterization confirmed the presence of pre-capillary pulmonary arterial hypertension without demonstrable vasoreactivity. He was prescribed sildenafil to begin management of methamphetamine-associated cardiomyopathy and right ventricular dysfunction manifesting as severe pre-capillary pulmonary hypertension. CardioNerds is collaborating with Radcliffe Cardiology and US Cardiology Review journal (USC) for a ‘call for cases’, with the intention to co-publish high impact cardiovascular case reports, subject to double-blind peer review. Case Reports that are accepted in USC journal and published as the version of record (VOR), will also be indexed in Scopus and the Directory of Open Access Journals (DOAJ). CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Case Media - stimulant-related (methamphetamine) cardiovascular toxicity Pearls - stimulant-related (methamphetamine) cardiovascular toxicity 1. Methamphetamine, and stimulants in general, can have a multitude of effects on the cardiovascular and pulmonary systems. Effects of methamphetamine are thought to be due to catecholamine toxicity with direct effects on cardiac and vascular tissues. Acutely, methamphetamine can cause vascular constriction and vasospasm, while chronic exposure is associated with endothelial damage. Over time, methamphetamine can cause pulmonary hypertension, atherosclerosis, cardiac arrhythmias, and dilated cardiomyopathy. 2. Methamphetamines are the second most commonly misused substances worldwide after opiates. Patients with methamphetamine-associated pulmonary arterial hypertension (PAH) have more severe pulmonary vascular disease, more dilated and dysfunctional right ventricles, and worse prognoses when compared to patients with idiopathic PAH. Additionally, patients with methamphetamine-associated cardiomyopathy and PAH have significantly worse outcomes and prognoses when compared to those with structurally normal hearts without evidence of PAH. Management includes multidisciplinary support, complete cessation of methamphetamine use, and guideline-directed treatment of PAH. 3. The diagnosis of pulmonary hypertension (PH) begins with the history and physical, followed by confirmatory testing using echocardiography and invasive hemodynamics (right heart catheterization). Initial serological evaluation may include routine biochemical, hematologic, endocrine, hepatic, and infectious testing. Though PH is traditionally diagnosed and confirmed in a two-step, echocardiogram-followed-by-catheterization model, other diagnostics often include electrocardiography, blood gas analysis, spirometry, ventilation/perfusion assessment, CT scans, MRIs, and/or genetic testing to evaluate for the myriad of etiologies that may contribute to the development of PH. 4. PH is characterized by remodeling of the pulmonary vasculature and a progressive increase of pulmonary vascular load, often resulting in right ventricular hypertrophy, remodeling, and dysfunction. PH is defined hemodynamically by a mean pulmonary arterial pressure ≥ 20 mmHg at rest when measured by right heart catheterization (RHC). Pre-capillary pulmonary hypertension due to pulmonary vascular disease is further defined by an elevation in pulmonary vascular resistance (PVR) of at least 3 wood units (WU). 5. Medications used to treat pulmonary arterial hypertension fall into four general mechanistic classes: calcium channel blockers, endothelin receptor antagonists, phosphodiesterase-5 inhibitors, and prostacyclin receptor agonists. Show Notes - stimulant-related (methamphetamine) cardiovascular toxicity How is pulmonary hypertension diagnosed with right heart catheterization (RHC)? Pulmonary hypertension is defined by mean pulmonary arterial pressure (mPAP) ≥ 20 mmHg at rest. Pulmonary hypertension has three hemodynamic phenotypes – pre-capillary PH, post-capillary PH, and combined pre-/post-capillary PH. Isolated pre-capillary PH is defined by pulmonary vascular resistance (PVR) ≥ 3 woods units and pulmonary artery wedge pressure (PAWP) ≤ 15 mmHg. Isolated post-capillary PH is defined by PVR 15 mmHg. PVR is calculated by dividing the mean trans-pulmonary gradient (= PAWP - mPAP) by the cardiac output. CharacteristicsClinical groupsIsolated pre-capillary PHmPAP >20 mmHgPAWP ≤ 15 mmHgPVR ≥ 3 WUWHO 1,3,4, and 5Isolated post-capillary PHmPAP >20 mmHgPAWP > 15 mmHgPVR 20 mmHgPAWP > 15 mmHgPVR ≥ 3 WUWHO 2 and 5 Classification of PAH by WHO Groups: WHO Group 1Pulmonary Arterial HypertensionWHO Group 2Pulmonary hypertension due to left sided heart diseaseWHO Group 3Pulmonary hypertension due to lung disease or hypoxiaWHO Group 4Chronic thromboembolic pulmonary hypertension and other pulmonary artery obstructionsWHO Group 5Pulmonary hypertension with multifactorial mechanismsIdiopathicLeft ventricular systolic and/or diastolic dysfunctionChronic obstructive pulmonary diseaseChronic thromboembolic pulmonary hypertensionHematological Disease (Sickle cell disease)HereditaryLeft-sided valvular heart diseaseInterstitial lung diseaseObstruction of the pulmonary circulation by tumor or inflammationSystemic disorders (Sarcoidosis, Langerhans cell granulomatosis)Drug and toxin inducedOther mixed restrictive or obstructive lung diseaseMetabolic disorders (Gaucher's disease)Associated with connective tissue diseaseSleep-disordered breathingAssociated with HIV infectionAlveolar hypoventilation disordersAssociated with portal hypertensionChronic exposure to high altitudeCongenital heart diseaseSchistosomiasis What is vasoreactivity testing? Pulmonary vasoreactivity testing is used to identify patients who may respond favorably to calcium channel blocker (CCB) treatment. Typically, this includes patients with idiopathic pulmonary arterial hypertension, heritable pulmonary arterial hypertension, or substance-related pulmonary arterial hypertension. It is usually performed at the time of RHC. Inhaled nitric oxide (NO) at 10–20 parts per million (ppm) is the standard of care for vasoreactivity testing with alternatives including intravenous adenosine and epoprostenol. A significant response to vasodilator therapy is defined by a reduction of the mean PAP by at least 10 mmHg and concurrent decrement of the absolute value to less than 40 mmHg, without a decrease in cardiac output. Vasoreactive PH should be treated with CCB therapies such as nifedipine, diltiazem, and amlodipine. Vasoreactivity is relatively rare, occurring in 10% or fewer individuals with PH who undergo testing. PH without vasoreactivity of significant response to CCB therapy should be managed with alternative class of medications (see below). What is the medical treatment for PAH? Medication treatment of pulmonary arterial hypertension comes in 4 general categories with the general mechanism is listed: Calcium channel blockers (nifedipine, diltiazem and amlodipine used in high doses) – used in patients with positive vasoreactivity testing. Endothelin receptor antagonists (ambrisentan, bosentan, macitentan) – inhibit binding of endothelin, a vasoconstrictive peptide, to its receptors on smooth muscle cells, which is enriched in pulmonary vasculature, resulting in vasodilation and subsequent decrease in pulmonary arterial pressure. Phosphodiesterase 5 inhibitors and guanylate cyclase stimulators (sildenafil, tadalafil, riociguat) – ihibition of the cyclic guanosine monophosphate (cGMP) degrading enzyme phosphodiesterase type 5 results in vasodilation through the NO/cGMP pathway in the pulmonary vasculature, which contains substantial amounts of this enzyme. Prostacyclin analogues and prostacyclin receptor agonists (epoprostenol, iloprost, treprostinil, beraprost) – prostacyclin is produced predominantly by endothelial cells and induces potent vasodilation of all vascular beds and patients with PAH have been shown to have a reduction of prostacyclin synthase expression in the pulmonary arteries. References - Ben-Yehuda O, Siecke N. Crystal Methamphetamine: A Drug and Cardiovascular Epidemic. JACC Heart Fail. Mar 2018;6(3):219-221. doi:10.1016/j.jchf.2018.01.004 Benza RL, Gomberg-Maitland M, Miller DP, et al. The REVEAL Registry risk score calculator in patients newly diagnosed with pulmonary arterial hypertension. Chest. Feb 2012;141(2):354-362. doi:10.1378/chest.11-0676 Benza RL, Gomberg-Maitland M, Elliott CG, et al. Predicting Survival in Patients With Pulmonary Arterial Hypertension: The REVEAL Risk Score Calculator 2.

Jun 22, 2023

The following question refers to Section 5.2 of the 2021 ESC CV Prevention Guidelines. The question is asked by MGH medicine resident Dr. Christian Faaborg-Andersen, answered first by Dr. Jessie Holtzman, and then by expert faculty Dr. Laurence Sperling.Dr. Laurence Sperling is the Katz Professor in Preventive Cardiology at the Emory University School of Medicine and Founder of Preventive Cardiology at the Emory Clinic. Dr. Sperling was a member of the writing group for the 2018 Cholesterol Guidelines, serves as Co-Chair for the ACC's Cardiometabolic and Diabetes working group, and is Co-Chair of the WHF Roadmap for Cardiovascular Prevention in Diabetes.The CardioNerds Decipher The Guidelines Series for the 2021 ESC CV Prevention Guidelines represents a collaboration with the ACC Prevention of CVD Section, the National Lipid Association, and Preventive Cardiovascular Nurses Association.Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. Question #29 What percentage of the European population currently meets the recommended physical activity guidelines (150 minutes moderate-intensity activity weekly or 75 minutes vigorous-intensity activity weekly)?A 75% Answer #29 ExplanationThe correct answer is A: <10% of the European population currently meets the recommended physical activity guidelines.The American Heart Association, European Society of Cardiology, and World Health Organization all share the recommendation that adults should engage in 150 minutes per week of moderate-intensity physical activity or 75 minutes per week of vigorous-intensity activity. They recognize that additional health benefits may be garnered from incremental increases to 300 minutes per week of moderate intensity activity or 150 minutes per week of vigorous intensity activity, with a recommendation to include both aerobic and muscular strength training activities.According to the WHO, physical inactivity is the 4th leading cause of death in the world. The statistics regarding physical inactivity are staggering. Recent studies have shown that <10% of the European population meets the minimum recommended levels of physical activity. Similarly, ¼ adults and ¾ adolescents (aged 11-17) do not currently meet the global recommendations for physical activity. The World Health Organization has created a Global Action Plan on Physical Activity 2018-2030 with the goal to achieve a 15% relative reduction in the global prevalence of physical inactivity by 2030.Society level interventions to increase physical activity have been proposed including school-based activity programs, improved accessibility of exercise facilities across the socioeconomic spectrum, and governmental consideration of physical activity when designing cities (i.e. including pedestrian and cycling lanes). Other policy suggestions with varying levels of evidence include focused media campaigns, economic incentives, targeting labeling of physical activity opportunities, and work-place wellness programs.Main TakeawayDespite growing awareness of the health consequences of sedentary behavior, fewer than 10% of adults currently meet the minimum recommended quantity of physical activity. Public health leaders may continue to consider novel legislative initiatives to augment physical activity on a societal level with architectural design and financial incentives.Guideline Loc.Section 5.2 CardioNerds Decipher the Guidelines - 2021 ESC Prevention SeriesCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor RollCardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron!

Jun 19, 2023

The following question refers to Section 9.3 of the 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure.The question is asked by Keck School of Medicine USC medical student & CardioNerds Intern Hirsh Elhence, answered first by Cedars Sinai medicine resident, soon to be Vanderbilt Cardiology Fellow, and CardioNerds Academy Faculty Dr. Breanna Hansen, and then by expert faculty Dr. Anu Lala.Dr. Lala is an advanced heart failure and transplant cardiologist, associate professor of medicine and population health science and policy, Director of Heart Failure Research, and Program Director for the Advanced Heart Failure and Transplant fellowship training program at Mount Sinai. Dr. Lala is Deputy Editor for the Journal of Cardiac Failure. Dr. Lala has been a champion and role model for CardioNerds. She has been a PI mentor for the CardioNerds Clinical Trials Network and continues to serve in the program’s leadership. She is also a faculty mentor for this very 2022 heart failure decipher the guidelines series.The Decipher the Guidelines: 2022 AHA / ACC / HFSA Guideline for The Management of Heart Failure series was developed by the CardioNerds and created in collaboration with the American Heart Association and the Heart Failure Society of America. It was created by 30 trainees spanning college through advanced fellowship under the leadership of CardioNerds Cofounders Dr. Amit Goyal and Dr. Dan Ambinder, with mentorship from Dr. Anu Lala, Dr. Robert Mentz, and Dr. Nancy Sweitzer. We thank Dr. Judy Bezanson and Dr. Elliott Antman for tremendous guidance.Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. Question #23 Mrs. Hart is a 63-year-old woman with a history of non-ischemic cardiomyopathy and heart failure with reduced ejection fraction (LVEF 20-25%) presenting with 5 days of worsening dyspnea and orthopnea. At home, she takes carvedilol 12.5mg BID, sacubitril-valsartan 24-46mg BID, empagliflozin 10mg daily, and furosemide 40mg daily. On admission, her exam revealed a blood pressure of 111/79 mmHg, HR 80 bpm, and SpO2 94%. Her cardiovascular exam was significant for a regular rate and rhythm with an audible S3, JVD to 13 cm H2O, bilateral lower extremity pitting edema with warm extremities and 2+ pulses throughout. What initial dose of diuretics would you give her? A Continue home Furosemide 40 mg PO B Start Metolazone 5 mg PO C Start Lasix 100 mg IV D Start Spironolactone Answer #23 Explanation The correct answer is C – start Furosemide 100 mg IV. This is the most appropriate choice because patients with HF admitted with evidence of significant fluid overload should be promptly treated with intravenous loop diuretics to improve symptoms and reduce morbidity (Class 1, LOE B-NR). Intravenous loop diuretic therapy provides the most rapid and effective treatment for signs and symptoms of congestion. Titration of diuretics has been described in multiple recent trials of patients hospitalized with HF, often initiated with at least 2 times the daily home diuretic dose (mg to mg) administered intravenously. Titration to achieve effective diuresis may require doubling of initial doses, adding a thiazide diuretic, or adding an MRA that has diuretic effects in addition to its cardiovascular benefits. Choice A is incorrect as continuing oral loop diuretics is not recommended for acute decongestion. Moreover, Ms. Hart has become congested despite her home, oral diuretic regimen. Choice B and D are incorrect as starting a thiazide diuretic or a mineralocorticoid receptor antagonist are not first-line therapy for acute HF. Rather, in patients hospitalized with HF when diuresis is inadequate to relieve symptoms and signs of congestion, it is reasonable to intensify the diuretic regimen using either: a. higher doses of intravenous loop diuretics; or b. addition of a second diuretic (Class 2a, LOE B-NR). After instituting intravenous loop diuretic therapy, escalating attempts to achieve net diuresis include serial doubling of intravenous loop diuretic doses, which can be done by bolus or infusion, and sequential nephron blockade with addition of a thiazide diuretic, as detailed specifically in the protocol for the diuretic arms of the CARRESS and ROSE trials. MRAs have mild diuretics properties and the addition of MRAs can help with diuresis in addition to significant cardiovascular benefits in patients with HF. For patients hospitalized with HF, therapy with diuretics and other guideline-directed medications should be titrated with a goal to resolve clinical evidence of congestion to reduce symptoms and rehospitalizations (Class 1, LOE B-NR). For patients requiring diuretic treatment during hospitalization for HF, the discharge regimen should include a plan for adjustment of diuretics to decrease rehospitalizations (Class 1, LOE B-NR). Main Takeaway Patients admitted with acute HF should be promptly treated with intravenous loop diuretics. If current level of diuresis becomes inadequate to relieve symptoms and signs of congestion, it is reasonable to intensify the diuretic regimen using either: higher doses of intravenous loop diuretics or addition of a second diuretic (e.g., thiazide or MRA). All patients should have their diuretic regimen updated on discharge. Guideline Loc. Section 9.3 Decipher the Guidelines: 2022 Heart Failure Guidelines PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron!

Jun 18, 2023

Dr. Daniel Ambinder (CardioNerds Co-Founder), Dr. Kelly Arps (Series Co-Chair and EP fellow at Duke University), Dr. Stephanie Fuentes Rojas (FIT Lead and EP fellow at Houston Methodist), and Dr. Ingrid Hsiung (Cardiology Fellow at Baylor Scott & White Health) discuss situational assessment of stroke and bleeding risk with expert faculty Dr. Hafiza Khan (Electrophysiologist at Baylor Scott & White Health). In this episode, we discuss stroke and bleeding risk in specific situations such as prior to cardioversion, triggered episodes, and perioperatively. These are scenarios that are commonly encountered and pose specific challenges. Episode notes were drafted by Dr. Stephanie Fuentes. Audio editing by CardioNerds Academy Intern, Dr. Maryam Barkhordarian. This CardioNerds Atrial Fibrillation series is a multi-institutional collaboration made possible by contributions of stellar fellow leads and expert faculty from several programs, led by series co-chairs, Dr. Kelly Arps and Dr. Colin Blumenthal. This series is supported by an educational grant from the Bristol Myers Squibb and Pfizer Alliance. All CardioNerds content is planned, produced, and reviewed solely by CardioNerds. We have collaborated with VCU Health to provide CME. Claim free CME here! Disclosures: Dr. Ellis discloses grant or research support from Boston Scientific, Abbott-St Jude, advisor for Atricure and Medtronic. CardioNerds Atrial Fibrillation PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls and Quotes - Atrial Fibrillation: Situational Assessment of Stroke and Bleeding Risk In patients with persistent atrial fibrillation with tachycardia induced cardiomyopathy, timely restoration of normal rhythm is important. In patients not on established oral anticoagulation one option is to wait 3 weeks on oral anticoagulation prior to considering cardioversion. Another option is to pursue TEE prior to cardioversion as TEE is currently the gold standard imaging modality to exclude a LAA thrombus. Following cardioversion (chemical or electrical), anticoagulation must not be interrupted for 4 weeks due to atrial stunning. This is especially true for patients who have been in atrial fibrillation for an extended period of time. Individualizing assessment of stroke and bleeding risk is imperative when determining perioperative anticoagulation (AC) management. ACC has a helpful app (ManageAnticoag App) to make this easier. When considering AC in triggered atrial fibrillation (e.g., pneumonia, sepsis), it is important to consider the substrate that made the patient susceptible to developing atrial fibrillation. AC is favored in patients with high CHA2DS2-VAsC score and many traditional risk factors for atrial fibrillation as they are at high risk for future development of atrial fibrillation. Atrial fibrillation is a marker of poor outcomes in patients who have undergone coronary artery bypass graft (CABG) surgery. It is unclear if patients should be started on long-term AC for new onset atrial fibrillation after CABG regardless of risk factors. This is currently being investigated in the PACES trial. Notes - Atrial Fibrillation: Situational Assessment of Stroke and Bleeding Risk How do we choose an imaging modality for excluding LAA thrombus exclusion prior to cardioversion? TEE is the gold standard. It also provides other information that is important for management of atrial fibrillation (e.g. LA size/volume, presence/degree of mitral regurgitation/stenosis, ejection fraction). Gated cardiac CTA may have a growing role for evaluation of LAA thrombus. What is the data behind the recommendation for uninterrupted AC following cardioversion and what is atrial stunning? All patients should be anticoagulated for four weeks after cardioversion, regardless of the mechanism of cardioversion or CHA2DS2-VAsC score. As discussed in prior episodes, those who meet long term criteria for AC should be anticoagulated indefinitely. The term “atrial stunning” refers to the electro-mechanical dissociation of the LAA following cardioversion. The longer one is in atrial fibrillation, the longer it takes for the LAA contraction/LAA flow velocities to recover after restoration of normal rhythm. During the period of atrial stunning, there is increased risk of LAA thrombus formation, hence AC should not be interrupted. The first 72 hours post cardioversion are the highest risk for LAA thrombus formation followed by the subsequent 4 weeks. What is the approach of perioperative AC management in patients with atrial fibrillation? ACC has a helpful app (ManageAnticoag App), to individualize the decision of when/how to stop and resume AC peri-procedurally. One needs to ascertain three factors: 1) surgical bleeding risk, 2) stroke risk, and 3) the patient’s individual bleeding risk (e.g., medications, supplements, renal function, etc.). The BRDIGE trial investigated the need to bridge patients on and off anticoagulation perioperatively. The trial was small and patient characteristics of the study (mostly male, low percentage of patients with high CHADS score) do not allow for generalizability of study findings to all patients. Many patients do not require perioperative bridging, but individual patient factors should be used to make this decision. High risk features that warrant heparin bridging include recent stroke, mechanical valve, or mitral stenosis. Should consider bridging in patients with high CHA2DS2-VAsC score as these patients only made up a small portion of the BRIDGE trial. What is the approach to AC in patients with triggered atrial fibrillation? Similar to a fire, atrial fibrillation requires a substrate (i.e., combustible material) and a trigger (i.e., a match) to initiate. Though you can treat and therefore remove the trigger (e.g., pneumonia), patients with a substrate conducive to atrial fibrillation remain at high risk of atrial fibrillation in the future. If they were to convert to atrial fibrillation without clear symptoms in the future, they would be at risk for stroke and might not be started on AC. As such, long-term AC should be evaluated in a similar manner to those with paroxysmal or persistent atrial fibrillation without a clear trigger. The patient population with true “triggered” atrial fibrillation may be limited to those with thyrotoxicosis as hyperthyroidism can trigger atrial fibrillation even in patients with structurally normal hearts and background risk for future atrial fibrillation. Atrial fibrillation after cardiac surgery (e.g., CABG, mitral valve repair/replacement) should be managed with a coordinated heart team approach. Anticoagulation should likely be favored if bleeding risk is acceptable and patient has known risk factors, especially in valve surgeries where patients often have had longstanding LA pressure or volume overload. Atrial fibrillation following CABG has been associated with poor outcomes, though it is currently unclear if patients without traditional risk factors require long-term AC. This is currently being studied in the PACES trial. References January, C.T, Wann, L.S, Alpert, J.S., Calkins, H, Cigarroa, J.E., Cleveland, J.C., Conti, J.B., Ellinor P.T et al 2014 AHA/ACC/HRS guideline for the management of patients with atrial fibrillation: a report of the American college of Cardiology/American heart Asocciation Task Force on Practice Guidelines and the Heart Rhythm Society. Journal of the American College of Cardiology, 6421, e1-76. Dagres N, Kornej J, Hindricks G, et al. Prevention of Thromboembolism After Cardioversion of Recent-Onset Atrial Fibrillation. J Am Coll Cardiol. 2013 Sep, 62 (13) 1193–1194.https://doi.org/10.1016/j.jacc.2013.06.019

Jun 12, 2023

The following question refers to Section 4.7 and Table 18 of the 2021 ESC CV Prevention Guidelines. The question is asked by CardioNerds Academy Intern Student Dr. Shivani Reddy, answered first by Fellow at Johns Hopkins Dr. Rick Ferraro, and then by expert faculty Dr. Roger Blumenthal.Dr. Roger Blumenthal is professor of medicine at Johns Hopkins where he is Director of the Ciccarone Center for the Prevention of Cardiovascular Disease. He was instrumental in developing the 2018 ACC/AHA CV Prevention Guidelines. Dr. Blumenthal has also been an incredible mentor to CardioNerds from our earliest days.The CardioNerds Decipher The Guidelines Series for the 2021 ESC CV Prevention Guidelines represents a collaboration with the ACC Prevention of CVD Section, the National Lipid Association, and Preventive Cardiovascular Nurses Association.Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. Question #28 Mr. A. C. is a 78-year-old gentleman with a long-standing history of HTN receiving antihypertensive medications & dietary management for blood pressure control. What is the target diastolic blood pressure recommendation for all treated patients such as Mr. A.C.?A 80 years) and those who are frail. Also, in these older and especially frail patients, it may be difficult to achieve the recommended target BP range due to poor tolerability or adverse effects, and high-quality measurement and monitoring for tolerability and adverse effects is especially important in these groups. Main Takeaway The first step in HTN management in all groups is a reduction to SBP < 140 mmHg and DBP < 80 mmHg, with further targets depending on age and comorbidities as specified by Table 18 of the 2021 ESC Prevention Guidelines. Guideline Loc. 1. 4.7.5.3 page 3285 2. Table 18 page 3287 CardioNerds Decipher the Guidelines - 2021 ESC Prevention SeriesCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor RollCardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron!

Jun 9, 2023

The following question refers to Section 8.3 of the 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure. The question is asked by Western Michigan University medical student & CardioNerds Intern Shivani Reddy, answered first by University of Southern California cardiology fellow and CardioNerds FIT Trialist Dr. Michael Francke, and then by expert faculty Dr. Prateeti Khazanie. Dr. Khazanie is an associate professor and advanced heart failure and transplant Cardiologist at the University of Colorado. Dr. Khazanie is an author on the 2022 ACC/AHA/HFSA HF Guidelines, the 2021 HFSA Universal Definition of Heart Failure, and multiple scientific statements. The Decipher the Guidelines: 2022 AHA / ACC / HFSA Guideline for The Management of Heart Failure series was developed by the CardioNerds and created in collaboration with the American Heart Association and the Heart Failure Society of America. It was created by 30 trainees spanning college through advanced fellowship under the leadership of CardioNerds Cofounders Dr. Amit Goyal and Dr. Dan Ambinder, with mentorship from Dr. Anu Lala, Dr. Robert Mentz, and Dr. Nancy Sweitzer. We thank Dr. Judy Bezanson and Dr. Elliott Antman for tremendous guidance. Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. Clinical Trials Talks Question #22 You are taking care of a 34-year-old man with chronic systolic heart failure from NICM with LVEF 20% s/p CRT-D. The patient was admitted 1 week prior with acute decompensated heart failure. Despite intravenous diuretics the patient developed acute kidney injury, and ultimately placed on intravenous inotropes on which he now seems dependent. He has been following up with an advanced heart failure specialist as an outpatient and has been undergoing evaluation for heart transplantation, which was subsequently completed in the hospital. His exam is notable for an elevated JVP, a III/VI holosystolic murmur, and warm extremities with bilateral 1+ edema. His most recent TTE shows LVEF 20%, moderate MR, moderate-severe TR and estimated RVSP 34 mmHg. His most recent laboratory data shows Na 131 mmol/L, Cr 1.2 mg/dL, and lactate 1.6 mmol/L. Pulmonary artery catheter shows RA 7 mmHg, PA 36/15 mmHg, PCWP 12 mmHg, CI 2.4 L/min/m2 and SVR 1150 dynes*sec/cm5. The patient was presented at transplant selection committee and approved for listing for orthotopic heart transplant. What is the most appropriate next step in the management of this patient? A Refer patient for transcatheter edge-to-edge repair for MR B Continue IV inotropes as a bridge-to-transplant C Refer patient for tricuspid valve replacement D Initiate 1.5L fluid restriction Answer #22 Explanation The correct answer is B – continue IV inotropes as a bridge-to-transplant. Positive inotropic agents may improve hemodynamic status, but have not been shown to improve survival in patients with HF. These agents may help HF patients who are refractory to other therapies and are suffering consequences from end-organ-hypoperfusion. Our patient is admitted with worsening advanced heart failure requiring intravenous inotropic support. He has been appropriately evaluated and approved for heart transplant. He has demonstrated the requirement of continuous inotropic support to maintain perfusion. In patients such as this with advanced (stage D) HF refractory to GDMT and device therapy who are eligible for and awaiting MCS or cardiac transplantation, continuous intravenous inotropic support is reasonable as “bridge therapy” (Class 2a, LOE B-NR). Continuous IV inotropes also have a Class 2b indication (LOE B-NR) in select patients with stage D HF despite optimal GDMT and device therapy who are ineligible for either MCS or cardiac transplantation, as palliative therapy for symptom control and improvement in functional status. Conversely, long-term use of either continuous or intermittent intravenous inotropic agents, for reasons other than palliative care or as a bridge to advanced therapies, is potentially harmful (Class 3: Harm, LOE B-R). As of yet there is lack of clear evidence suggesting the benefit of one inotrope over another. To minimize adverse effects, the lowest possible dose of inotropes should be used, although the potential for development of tachyphylaxis should be acknowledged and the choice/dose of agent may need to be changed over time for longer periods of use. In addition, the ongoing need for inotropic support and the possibility of discontinuation should be regularly assessed. Although guidelines give a Class 2a recommendation for transcatheter edge-to-edge MV repair in patients with reduced EF and severe MR with persistent symptoms despite GDMT, this patient’s MR was graded as moderate on his most recent TTE and as such, he would not be an appropriate candidate for TEER. Although guidelines give a Class 1 recommendation for multidisciplinary management of patients with HF and VHD, as well as referral for consideration of intervention in patients with refractory TR, there are currently no guideline recommendations supporting surgical TVR in advanced HF patients with TR. Although fluid restriction has been associated with modest improvements in hyponatremia in patients with advanced HF, the clinical benefits of this therapy remain uncertain and as such was given a Class 2b recommendation in the clinical guidelines. Main Takeaway Continuous intravenous inotropic support can be considered in patients with advanced heart failure refractory to GDMT who are awaiting durable MCS or heart transplant as “bridge therapy” (Class 2a) or for palliative therapy in patients with advanced HF who are ineligible for MCS/transplant (Class 2b), but is potentially harmful for long-term use for reasons beyond palliation or bridge to advanced therapies (class 3 recommendation). Guideline Loc. Section 8.3 Table 20 Decipher the Guidelines: 2022 Heart Failure Guidelines PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron!

Jun 8, 2023

The CardioNerds and Pulm PEEPs have joined forces to co-produce this important episode, delving into the management of decompensated right ventricular failure in pulmonary arterial hypertension. Joining us for this informative discussion are Pulm PEEPs co-founders, Dr. David Furfaro and Dr. Kristina Montemayor, along with Dr. Leonid Mirson (Internal Medicine Resident at Johns Hopkins Osler Medical Residency and Associate Editor of Pulm PEEPs), Dr. Bavya Varma (Internal Medicine Resident at Johns Hopkins, rising Cardiology Fellow at NYU, and CardioNerds Academy graduate), Dr. Mardi Gomberg-Maitland (Medical Director of the Pulmonary Hypertension Program at George Washington Hospital), and Dr. Rachel Damico (Pulmonologist and Associate Professor of Medicine at Johns Hopkins Hospital). Audio editing by CardioNerds Academy Intern, student doctor Adriana Mares. Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. CardioNerds Heart Success Series PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Show notes - Decompensated Right Ventricular Failure in Pulmonary Arterial Hypertension A 21-year-old woman with a past medical history notable for congenital heart disease (primum ASD and sinus venosus with multiple surgeries) complicated by severe PAH on home oxygen, sildenafil, ambrisentan, and subcutaneous treprostinil is presenting with palpitations, chest pain, and syncope. She presented as a transfer from an outside ED where she arrived in an unknown tachyarrhythmia and had undergone DCCV due to tachycardia into the 200s and hypotension. On arrival at our hospital, she denied SOB but did endorse nausea, leg swelling, and poor medication adherence. Her initial vitals were notable for a BP of 80/50, HR 110, RR 25, and saturating 91% on 5L O2. On exam, she was uncomfortable appearing but mentating well. She had cool extremities with 1-2+ LE edema. Her JVP was 15cm H2O. She has an RV Heave and 2/6 systolic murmur. Her lungs were clear bilaterally. Her labs were notable for Cr 2.0, an anion gap metabolic acidosis (HCO3 = 11), elevated lactate (4.1), elevated troponin to 14, and a pro-BNP of ~5000. Her CBC was unremarkable. Her EKG demonstrated 2:1 atrial flutter at a rate of 130. Diagnosing RV failure in patients with PH: RV dysfunction and RV failure are two separate entities. RV dysfunction can be measured on echocardiography, but RV failure can be thought of as a clinical syndrome where there is evidence of RV dysfunction and elevated right sided filling pressures. RV failure is a spectrum and can present with a range of manifestations from evidence of R sided volume overload and markers of organ dysfunction, all the way to frank cardiogenic shock. Most patients with RV failure are not in overt shock. One of the first signs of impending shock in patients with RV failure is the development of new or worsening hypoxemia. Patients with decompensated RV failure approaching shock often do not present with symptoms classic for LV low flow state. Instead, hypoxia 2/2 VQ mismatching may be the first sign and they can be otherwise well appearing. Particularly because patients with PH tend to be younger, they can often appear compensated until they rapidly decompensate. Causes of decompensation for patients with RV dysfunction and PH: Iatrogenesis (inadvertent cessation of pulmonary vasodilators by providers, surgery if providers are not familiar with risks of anesthesia), non-adherence to pulmonary vasodilators (either due to affordability issues or other reasons), infections, arrhythmias (particularly atrial arrhythmias), and progression of underlying disease. Patients with atrial arrhythmias (atrial flutter or atrial fibrillation) and pulmonary hypertension do not tolerate the loss of the atrial kick well as it contributes a significant amount to their RV filling and impacts their cardiac output. It is often difficult to determine if the atrial arrhythmia is a cause or effect of decompensated RV failure, but its presence is associated with a worse prognosis. Efforts should be made to re-establish normal sinus rhythm in patients with decompensated RV failure and atrial arrhythmias. A patient’s home PH medications should never be stopped for any reason upon admission unless on the basis of recommendations by a pulmonary hypertension provider as this is often a cause of decompensation inpatient Interpreting findings on echocardiogram: Echo is a useful screening tool. When interpreting evidence of RV dysfunction, it is important to look at the global picture and not just one measurement. RVSP, though commonly reported, may be of limited value when evaluating for decompensation. It’s a function of blood pressure, heart rate, and cardiac output. RVSP may even decline as shock worsens. TAPSE is useful as a marker of RV dysfunction if it is reduced, but it is difficult to follow over time and only gives information about cardiac function around the annulus; it may be normal even when apical RV function is depressed. RV fractional area of change may be more useful for global RV function. It is important to pay attention to the RV size overall, the degree of TR, and the presence of effusion all of which are associated with RV dysfunction. ­Tips regarding the interpretation of invasive hemodynamics: Cardiac output by thermodilution is the standard way to calculate PVR. Despite the degree of TR that is typically present, it is thought to be a better representation of cardiac output than the estimated Fick calculation. Our experts agree that routine monitoring of invasive hemodynamics for acute decompensated RV failure is likely not helpful and has significant risks. A good external volume exam or CVP off a central venous catheter + central venous saturation will likely be all you need to navigate a patient with shock secondary to RV failure. A right heart catheterization (should be only done under fluoroscopy for patients with large RVs) may be helpful if the etiology of shock is unclear. Management of decompensated RV failure in patients with pulmonary hypertension Managing preload is of utmost importance, perhaps the most important tenant of management of decompensated RV failure. The overwhelming majority of patients with PH and decompensation are volume overloaded, it is exceptionally rare that someone would be dry. Furthermore, the myth that the RV is “preload responsive” is only true in the setting of acute RV injury (eg. RV infarction) and not so in patients with acute on chronic RV dysfunction. It is important to optimize preload in someone in decompensated RV failure and it is safe to do this more rapidly than traditionally taught. Exact goals varied between our experts, but anywhere from 2-4L net negative per day is reasonable especially if the patient is hemodynamically tolerating the fluid removal. If the patient is not responding to diuretics, hemodialysis with ultrafiltration may be necessary to optimize the patient. Afterload is the next tenant of management. Optimizing the following parameters will reduce the patient’s pulmonary vascular resistance and reduce afterload to the right ventricle. — Avoiding hypoxic pulmonary vasoconstriction, liberalize the patient’s O2 goal — Avoid permissive hypercapnia and academia in this patient population — Do not withhold a patient’s pulmonary vasodilator until discussion with the PH team. If stopped inadvertently, restart this medication immediately. For patients with malfunctioning pumps, there is a phone number on the back that you can call for rapid troubleshooting. Sildanefil can be given IV if a patient is NPO. — Inhaled nitric oxide can improve oxygenation and reduce afterload — Intubation and mechanical ventilation greatly increase PVR and are poorly tolerated. Exacting care must be taken to titrate PEEP and tidal volume, and avoid intubation when possible. — Starting a new systemic pulmonary vasodilator in decompensated RV failure may be considered under close guidance from the pulmonary hypertension team Management of atrial arrhythmias: As above, patients with severe pulmonary hypertension do not tolerate loss of sinus rhythm well. If they are decompensated, every effort should be made to re-establish normal sinus rhythm. Management of RV perfusion: Unlike the LV, the RV is perfused during BOTH systole and diastole. Maintaining effective coronary perfusion to the RV is essential in RV failure. For this reason, the systemic systolic pressure (as well as the mean arterial pressure) should be kept high enough to ensure that the RV is able to perfuse. There is no great body of evidence as to which pressor works best. Norepinephrine, vasopressin, and even phenylephrine are all reasonable choices to maintain appropriate perfusing blood pressure. Inotropy: Patients in shock and RV failure do not always require inotropes, but if they do it’s often a sign of a grim prognosis. Either dobutamine or milrinone is reasonable, but the negative effects of these drugs (arrhythmias, tachycardia, and systemic hypotension) may limit their uses. Mechanical circulatory support: Limited options are available. Balloon pumps and Impella devices have limited roles except in expert centers, and ECMO remains the standard of care. ECMO (either V-V or V-A) may have utility as a bridge to recovery if a reversible cause is identified, or a bridge to transplant if the patient is on the transplant list. Goals of care: The prognosis of a patient admitted to the ICU with acute on chronic decompensated RV failure is guarded, with very high mortality rates even if not in shock

Jun 6, 2023

The following question refers to Section 4.3 of the 2021 ESC CV Prevention Guidelines. The question is asked by CardioNerds Academy Intern Dr. Maryam Barkhordarian, answered first by medicine resident CardioNerds Academy House Chief Dr. Ahmed Ghoneem, and then by expert faculty Dr. Kim Williams.Dr. Williams is Chief of the Division of Cardiology and is Professor of Medicine and Cardiology at Rush University Medical Center. He has served as President of ASNC, Chairman of the Board of the Association of Black Cardiologists (ABC, 2008-2010), and President of the American College of Cardiology (ACC, 2015-2016). The CardioNerds Decipher The Guidelines Series for the 2021 ESC CV Prevention Guidelines represents a collaboration with the ACC Prevention of CVD Section, the National Lipid Association, and Preventive Cardiovascular Nurses Association. Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. Question #27 Mr. O is a 48-year-old man with a past medical history significant for obesity (BMI is 42kg/m2), hypertension, type 2 diabetes mellitus, and hypercholesterolemia. His calculated ASCVD risk score today is 18.8%. You counsel him on the importance of weight loss in the context of CVD risk reduction. Which of the following weight loss recommendations is appropriate?AMaintaining a weight loss of at least 25% from baseline is required to influence blood pressure, cholesterol, and glycemic control. BHypocaloric diets lead to short term weight loss, but a healthy diet should be maintained over time to reduce CVD risk.CLiraglutide can be used to induce weight loss, as an alternative to diet and exercise.DBariatric surgery is effective for weight loss but has no ASCVD risk reduction benefit. Answer #27 Explanation The correct answer is B. Energy restriction is the cornerstone of management of obesity. All the different types of hypocaloric diets achieve similar short-term weight loss, but these effects tend to diminish by 12 months. It is a class I recommendation to maintain a healthy diet over time to achieve CVD risk reduction. The Mediterranean diet is an example of a diet that can have persistent CV benefit beyond the 12 months. Choice A is incorrect because maintaining even a moderate weight loss of 5 – 10% from baseline has favorable effects on risk factors including blood pressure, cholesterol, and glycemic control, as well as on premature all-cause mortality. Choice C is incorrect because medications approved as aids to weight loss (such as liraglutide, orlistat and naltrexone/bupropion) may be used in addition to lifestyle measures to achieve weight loss and maintenance; they are not alternatives to a healthy lifestyle. Meta-analysis of medication-assisted weight loss found favorable effects on BP, glycemic control, and ASCVD mortality. Choice D is incorrect because patients undergoing bariatric surgery had over 50% lower risks of total ASCVD and cancer mortality compared with people of similar weight who did not have surgery. Bariatric surgery should be considered for obese high-risk individuals when lifestyle change does not result in maintained weight loss (Class IIa). The ACC/AHA guidelines focused primarily on lifestyle interventions for obesity and had no specific recommendations for bariatric surgery or medication-assisted weight loss. Main Takeaway Weight reduction (even as low as 5-10% from baseline) and long-term maintenance of a healthy diet are recommended to improve the CVD risk profile of overweight and obese people. Medication and/or bariatric surgery may have a useful adjunctive role in some patients. Guideline Loc. Section 4.3.3 CardioNerds Decipher the Guidelines - 2021 ESC Prevention SeriesCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor RollCardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron!

May 31, 2023

The following question refers to Section 7.6 of the 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure.The question is asked by premedical student and CardioNerds Intern Pacey Wetstein, answered first by Mayo Clinic Cardiology Fellow and CardioNerds Academy Chief Dr. Teodora Donisan, and then by expert faculty Dr. Nancy Sweitzer.Dr. Sweitzer is Professor of Medicine, Vice Chair of Clinical Research for the Department of Medicine, and Director of Clinical Research for the Division of Cardiology at Washington University School of Medicine. She is the editor-in-chief of Circulation: Heart Failure. Dr. Sweitzer is a faculty mentor for this Decipher the HF Guidelines series.The Decipher the Guidelines: 2022 AHA / ACC / HFSA Guideline for The Management of Heart Failure series was developed by the CardioNerds and created in collaboration with the American Heart Association and the Heart Failure Society of America. It was created by 30 trainees spanning college through advanced fellowship under the leadership of CardioNerds Cofounders Dr. Amit Goyal and Dr. Dan Ambinder, with mentorship from Dr. Anu Lala, Dr. Robert Mentz, and Dr. Nancy Sweitzer. We thank Dr. Judy Bezanson and Dr. Elliott Antman for tremendous guidance.Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. Clinical Trials Talks Question #21 Ms. Smith is a 56-year-old woman following up in the cardiology clinic for a history of heart failure with reduced ejection fraction. Two years ago, she was diagnosed with non-ischemic cardiomyopathy with a left ventricular ejection fraction (LVEF) of 30%. Over time, she was initiated and optimized on guideline directed medical therapy. She is currently on Carvedilol 12.5 mg BID, Sacubitril/Valsartan 49/51 mg BID, Spironolactone 25 mg daily, Empagliflozin 10 mg daily, and Furosemide PRN for weight gain. On today’s visit, her BP is 110/80 mmHg, and her HR is 67 bpm. Labs show a creatinine of 0.9 mg/dL, potassium of 5.1 mEq/L, NT-proBNP of 150 ng/L, and a HbA1c of 5.8%. Follow up transthoracic echocardiogram showed an improvement in LVEF to 55%. What are the most appropriate therapy recommendations for Ms. Smith? A Discontinue spironolactone B Discontinue empagliflozin C Decrease the dose of carvedilol D Continue current therapy Answer #21 The correct answer is D – continue current therapy. The patient described above was initially diagnosed with HFrEF and experienced significant symptomatic improvement with GDMT, so she now has heart failure with improved ejection fraction (HFimpEF). In patients with HFimpEF after treatment, GDMT should be continued to prevent relapse of HF and LV dysfunction, even in patients who may become asymptomatic (Class 1, LOE B-R). Although symptoms, functional capacity, LVEF and reverse remodeling can improve with GDMT, structural abnormalities of the LV and its function do not fully normalize, causing symptoms and biomarker changes to persist or recur if treatment is deescalated. Improvements in EF do not always reflect sustained recovery; rather, they signify remission. Of note, HF relapse can be defined by at least 1 of the following: o A drop in the EF by >10% and to 10% and to higher than the normal range o A 2-fold rise in NT-proBNP concentration and to > 400 ng/L o Clinical evidence of HF on examination Choice A is incorrect as it would be incorrect to discontinue spironolactone. A potassium of 5.1 is still within the acceptable limit in a patient who has been on Spironolactone for two years, and this medication is an important part of GDMT for HFrEF. Despite the improvement in Hb A1c, empagliflozin should be continued for heart failure with improved ejection fraction, as it is part of routine GDMT of HFrEF even in the absence of diabetes. Choice B is thus incorrect. Similarly, carvedilol should be continued at the same dose as the patient’s heart rate is within the desired range. Furthermore, all GDMT should be continued in patients with HFimpEF, as emphasized above. Choice C is therefore also incorrect. In patients with HFimpEF after treatment, GDMT should be continued to prevent relapse of HF and LV dysfunction, even in patients who may become asymptomatic. (Class 1, LOE B-R). Section 7.6.2 Decipher the Guidelines: 2022 Heart Failure Guidelines PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron!

May 29, 2023

CardioNerds Co-Founder, Dr. Amit Goyal, along with Series Co-Chairs, Dr. Yoav Karpenshif and Dr. Eunice Dugan, and episode Lead, Dr. Sean Dikdan, had the opportunity to expand their knowledge on the topic of ventricular tachycardia and electrical storm from esteemed faculty expert, Dr. Janice Chyou. Audio editing by CardioNerds Academy Intern, Dr. Maryam Barkhordarian. Electrical storm (ES) is a life-threatening arrhythmia syndrome. It is characterized by frequently occurring bouts of unstable cardiac arrythmias. It typically occurs in patients with susceptible substrate, either myocardial scar or a genetic predisposition. The adrenergic input of the sympathetic nervous system can perpetuate arrythmia. In the acute setting, identifying reversible triggers, such as ischemia, electrolyte imbalances, and heart failure, is important. Treatment is complex and varies based on previous treatments received and the presence of intra-cardiac devices. Many options are available to treat ES, including medications, intubation and sedation, procedures and surgeries targeting the autonomic nervous system, and catheter ablation to modulate the myocardial substrate. A multidisciplinary team of cardiologists, intensivists, electrophysiologists, surgeons, and more are necessary to manage this complex disease. The CardioNerds Cardiac Critical Care Series is a multi-institutional collaboration made possible by contributions of stellar fellow leads and expert faculty from several programs, led by series co-chairs, Dr. Mark Belkin, Dr. Eunice Dugan, Dr. Karan Desai, and Dr. Yoav Karpenshif. Pearls • Notes • References • Production Team CardioNerds Cardiac Critical Care PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls and Quotes - Management of Ventricular Tachycardia and Electrical Storm Electrical storm is defined as 3 or more episodes of VF, sustained VT, or appropriate ICD shocks within 24 hours. It occurs more commonly in ischemic compared to non-ischemic cardiomyopathy, and it is associated with a poor prognosis and high cardiovascular mortality. The classic triad of electrical storm is a trigger, a myocardial susceptible substrate, and autonomic input perpetuating the storm. Triggers for electrical storm include ischemia, heart failure, electrolyte abnormalities, hypoxia, drug-related arrhythmogenicity, and thyrotoxicosis. A thorough evaluation of possible triggers is necessary for each patient, but it is uncommonly found. The evaluation may include laboratory studies, genetic testing, advanced imaging, or invasive testing. Acute treatment options involve acute resuscitation, pharmacotherapy with antiarrhythmics and beta-blockers, device interrogation and possible reprogramming, and sedation. Subacute treatment involves autonomic modulation and catheter ablation. Surgical treatments include sympathectomies and, ultimately, heart transplant. Catheter ablation is safe and effective for the treatment of electrical storm. In select patients, hemodynamic peri-procedural hemodynamic support should be considered. Show notes - Management of Ventricular Tachycardia and Electrical Storm Simple diagram of the classic “triad” of ES (see reference 10). Treatment algorithm provided by the 2017 AHA/ACC/HRS guidelines (see reference 1). 1. Define electrical storm. Electrical storm (ES), also called “arrhythmic storm” or “VT storm” refers to a state of cardiac instability associated with 3 or more episodes of VF, sustained VT, or appropriate ICD shocks within 24 hours. Sustained VT refers to 30 seconds of VT or hemodynamically unstable VT requiring termination in < 30 seconds. Incessant VT refers to continued, sustained hemodynamically stable VT that lasts longer than one hour. VT is incessant or recurrent when it recurs promptly despite repeated intervention for termination.1,2 In patients with ICDs for secondary prevention, ES is estimated to occur in 10-28% of patients.3–5 This incidence is much lower in patients who have ICDs implanted for primary prevention in whom the incidence has been estimated as low as 4% at 20 months of follow up.6 ES occurs at similar rates in patients with ischemic or non-ischemic cardiomyopathy.7 ES is associated with a poor prognosis and high cardiovascular mortality. The three-month mortality in patients with an episode of ES has been estimated at up to 18 times higher than in patients without any VT.6 Risk factors for the development of ES include male sex, advanced age, low left ventricular ejection fraction, use of class 1A antiarrhythmic drugs, and the presence of cardiovascular comorbidities.8,9 2. Evaluate the cause of VT storm (e.g., evaluation for ischemia, sarcoidosis , etc) The classic triad of ES is a trigger, a substrate susceptible to ES, and autonomic input perpetuating the storm.10 Potential triggers are varied and typically include myocardial ischemia, decompensated heart failure, electrolyte abnormalities, hypoxia, drug-related arrhythmogenicity, and thyrotoxicosis.4,11 A clear trigger is often not found (only 13% of the time by some estimates).12 Searching for a trigger should not delay management decisions in the acute setting. Structural heart disease unrelated to ischemia such as congenital heart disease and infiltrative cardiomyopathies can serve as the substrate for ES. Conditions related to genetic causes such as long QT syndrome or catecholaminergic polymorphic VT may be a rare etiology. These conditions represent an electrophysiologic substrate as opposed to a structural substrate.13 3. Choose an initial management strategy for patients with electrical storm in the CCU. Treatment of ES is complex. The initial steps in management involve resuscitation, pharmacotherapy, device interrogation and reprogramming, and sedation. ACLS should be used in patients with pulseless VT or VF. Patients with and without cardioverter-defibrillators may be treated differently. Defibrillations from an implanted device accentuate sympathetic tone and may perpetuate further arrhythmia. Once a patient is stabilized, more advanced therapies involving autonomic modulation or catheter ablation (CA) can be utilized. In the patient with ischemia, emergent revascularization should be pursued. The need for mechanical circulatory support (MCS) should be determined. Inotropes and many vasopressors are sympathetic agonists and may worsen the arrhythmia by accentuating adrenergic tone, and so the benefits of improved hemodynamics need to be weighed against the risk of worsening electrical instability. Initial pharmacotherapy in ES includes an antiarrhythmic drug and a beta blocker. Typically loading the patient with IV amiodarone and administering a non-selective beta blocker like propranolol is done. This combination has been shown in ES patients to have superior freedom of arrhythmia compared to using metoprolol.14 Propranolol’s superiority may also be due to its ability to cross the blood-brain barrier. Lidocaine has improved efficacy in ischemic VT.15,16 Procainamide has been shown to be useful in patients with hemodynamically stable VT.17 4. Identify predisposing conditions that should be managed to help treat electrical storm such as ischemia and AHF. Identifying and managing specific triggers is an important initial step in the management of ES. Hypoxia on vital signs or evidence of decompensated HF on exam (with JVD, edema, crackles on auscultation) can implicate volume overload; this can be managed with diuresis. Ischemic ECG changes on the 12-lead ECG when the patient’s ventricular arrhythmia is broken, can suggest myocardial ischemia. If ischemia is believed to be the trigger, urgent revascularization should be pursued while resuscitation is underway. Blood work should include screening for electrolyte abnormalities and thyroid disease. Carefully screening the patient’s medication list and checking a digoxin level (when appropriate) can help detect drug-induced arrhythmia. Once out of the acute setting, genetic testing may be important in patients without structural disease for determining an etiology. Idiopathic VT, Brugada syndrome, long QT syndrome, short QT syndrome, early repolarization syndrome, catecholaminergic polymorphic VT, arrhythmogenic right ventricular cardiomyopathy, and cardiac sarcoidosis are potential etiologies that may be related to ES.10 5. Recognize when to use general anesthesia to aid in the stabilization of electrical storm and incessant VT. Intubation and deep sedation are immediate next steps to minimize the sympathetic drive contributing to the arrhythmia. This treatment is very effective at terminating arrythmia and preventing immediate recurrence.18,19 This step is used in the acute setting for ES that persists despite pharmacotherapy. Note that propofol is a negative inotrope with the potential to worsen heart failure in decompensated patients and precipitate shock. In addition to breaking the sympathetic cycle that drives this pathophysiology, sedation mitigates some of the psychological stress that repeated ICD shocks can cause in patients.20 6. Describe considerations specific to patients with implanted ICDs. If a patient with an ICD presents with ES, the device should be interrogated. It is important to confirm the shocks are appropriate. Inappropriate shocks can occur in up to 40% of patients with an ICD; causes may include atrial arrythmia, oversensing, and lead fracture.21,22 Inappropriate ICD shocks are associated with a worse outcome. Overdrive pacing is a possible therapy to prevent ES. If the ES is hemodynamically stable, then the ICD therapies may be disabled manually or with the use of a magnet. If anti-tachycardia pacing (ATP) treats the ventricular arrythmia effectively,

May 28, 2023

The following question refers to Sections 3.3 and 3.4 of the 2021 ESC CV Prevention Guidelines. The question is asked by CardioNerds Academy Intern student Dr. Adriana Mares, answered first by Brigham & Women’s medicine resident & Director of CardioNerds Internship Dr. Gurleen Kaur, and then by expert faculty Dr. Allison Bailey. Dr. Bailey is an advanced heart failure and transplant cardiologist at Centennial Heart. She is the editor-in-chief of the American College of Cardiology’s Extended Learning (ACCEL) editorial board and was a member of the writing group for the 2018 American Lipid Guidelines. The CardioNerds Decipher The Guidelines Series for the 2021 ESC CV Prevention Guidelines represents a collaboration with the ACC Prevention of CVD Section, the National Lipid Association, and Preventive Cardiovascular Nurses Association. Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. Question #26 Ms. Priya Clampsia is a 58-year-old never-smoker with a history of hypertension. Her BMI is 29 kg/m2. She also mentions having pre-eclampsia during her pregnancy many years ago. She describes a predominately sedentary lifestyle and works as a receptionist. You see her in the clinic to discuss routine preventive care. Her most recent lipid panel results were LDL of 101 mg/dL, HDL of 45 mg/dL, and triglycerides of 190 mg/dL. What additional step will provide valuable information regarding her CVD risk profile? A Send additional lab workup including C-reactive protein and lipoprotein (a) B Measure her waist circumference C Assess her work stress D Ask her about history of preterm birth E B, C, and D Answer #26 Explanation The correct answer is E – measuring her waist circumference, assessing her occupational stress, and obtaining history about adverse pregnancy outcomes including preterm birth all add valuable information for CVD risk stratification. BMI is easily measured and can be used to define categories of body weight. However, body fat stores in visceral tissue carry higher risk than subcutaneous fat and therefore, waist circumference can be a simple way to measure global and abdominal fat. When waist circumference is ≥102 cm in men and ≥88 cm in women, weight reduction is advised. While these WHO thresholds are widely accepted in Europe, it is important to note that different cut-offs may be appropriate in different ethnic groups. Work stress is important to ascertain as well because there is preliminary evidence of the detrimental impact of worse stress on ASCVD health, independent of conventional risk factors and their treatment. Work stress is determined by job strain (i.e., the combination of high demands and low control at work) and effort-reward imbalance. Pre-eclampsia is associated with increase in CVD risk by factor of 1.5-2.7 compared with all women. Both preterm (RR 1.6) and still birth (RR 1.5) are also associated with a moderate increase in CVD risk. Taking a thorough pregnancy history is important in determining future cardiovascular risk in women. The ESC guidelines give a Class IIb (LOE B) recommendation that in women with history of premature or stillbirth, periodic screening for hypertension and DM may be considered. Of note, the 2018 ACC/AHA guidelines include preeclampsia and premature menopause (occurring at age 50mg/dL or >125nmol/L) and elevated apoB (≥130 mg/dL) as risk-enhancing factors. Specific indications for measuring Lp(a) include family history of premature ASCVD and specific indications for measuring apoB include triglyceride ≥200mg/dL. Main Takeaway The ESC guidelines do not recommend routine measurement of additional circulating and urine biomarkers as further data and research is still needed in this area; however, there are specific situations in which these biomarkers may be warranted. Guideline Loc. Section 3.3.7, 3.3.9, 3.3.10, 3.4.12 CardioNerds Decipher the Guidelines - 2021 ESC Prevention Series CardioNerds Episode Page CardioNerds Academy Cardionerds Healy Honor Roll CardioNerds Journal Club Subscribe to The Heartbeat Newsletter! Check out CardioNerds SWAG! Become a CardioNerds Patron!

May 25, 2023

The following question refers to Sections 7.3.2, 7.3.8, and 7.6.2 of the 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure. The question is asked by Palisades Medical Center medicine resident & CardioNerds Intern Dr. Maryam Barkhordarian, answered first by Hopkins Bayview medicine resident & CardioNerds Academy Fellow Dr. Ty Sweeny, and then by expert faculty Dr. Robert Mentz. Dr. Mentz is associate professor of medicine and section chief for Heart Failure at Duke University, a clinical researcher at the Duke Clinical Research Institute, and editor-in-chief of the Journal of Cardiac Failure. Dr. Mentz is a mentor for the CardioNerds Clinical Trials Network as lead principal investigator for PARAGLIDE-HF and is a series mentor for this very Decipher the Guidelines Series. For these reasons and many more, he was awarded the Master CardioNerd Award during ACC22. The Decipher the Guidelines: 2022 AHA / ACC / HFSA Guideline for The Management of Heart Failure series was developed by the CardioNerds and created in collaboration with the American Heart Association and the Heart Failure Society of America. It was created by 30 trainees spanning college through advanced fellowship under the leadership of CardioNerds Cofounders Dr. Amit Goyal and Dr. Dan Ambinder, with mentorship from Dr. Anu Lala, Dr. Robert Mentz, and Dr. Nancy Sweitzer. We thank Dr. Judy Bezanson and Dr. Elliott Antman for tremendous guidance. Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. Question #20 Ms. Betty Blocker is a 60-year-old woman with a history of alcohol-related dilated cardiomyopathy who presents for follow up. She has been working hard to improve her health and is glad to report that she has just reached her 5-year sobriety milestone. Her current medications include metoprolol succinate 100mg daily, sacubitril-valsartan 97-103mg BID, spironolactone 25mg daily, and empagliflozin 10mg daily. She is asymptomatic at rest and up to moderate exercise, including chasing her grandchildren around the yard. A recent transthoracic echocardiogram shows recovered LVEF from previously 35% now to 60%. Ms. Blocker does not love taking so many medications and asks about discontinuing her metoprolol. Which of the following is the most appropriate response to Ms. Blocker’s request? A Since the patient is asymptomatic, metoprolol can be stopped without risk B Stopping metoprolol increases this patient’s risk of worsening cardiomyopathy regardless of current LVEF or symptoms C Because the LVEF is now >50%, the patient is now classified as having HFpEF and beta-blockade is no longer indicated; metoprolol can be safely discontinued D Metoprolol should be continued, but it is safe to discontinue either ARNi or spironolactone Answer #20 Explanation The correct answer is B – stopping metoprolol would increase her risk of worsening cardiomyopathy. Heart failure tends to be a chronically sympathetic state. The use of beta-blockers (specifically bisoprolol, metoprolol succinate, and carvedilol) targets this excess adrenergic output and has been shown to reduce the risk of death in patients with HFrEF. Beyond their mortality benefit, beta-blockers can improve LVEF, lessen the symptoms of HF, and improve clinical status. Therefore, in patients with HFrEF, with current or previous symptoms, use of 1 of the 3 beta blockers proven to reduce mortality (e.g., bisoprolol, carvedilol, sustained-release metoprolol succinate) is recommended to reduce mortality and hospitalizations (Class 1, LOE A). Beta-blockers in this setting provide a high economic value. Table 14 of the guidelines provides recommendations for target doses for GDMT medications. Specifically for beta blockers, those targets are 25-50mg twice daily for carvedilol (or 80mg once daily for the continuous release formulation), 200mg once daily for metoprolol succinate, and 10mg once daily for bisoprolol. While we should be cognizant of pill-burden and other barriers to our patients’ quality of life, we must counsel them about the risks of discontinuing any element of guideline directed medical therapy (GDMT). The 2022 heart failure guidelines recommend the long-term use of beta blockers for patients diagnosed with HFrEF, even if symptoms improve (Option A). Conversely, long-term treatment should also be maintained even if symptoms do not improve to reduce the risk of major cardiovascular events. Importantly, the abrupt withdrawal of beta blockers can lead to clinical deterioration. Our patient here has heart failure with improved ejection fraction (HFimpEF) defined as having a previous LVEF ≤ 40% and a ≥ 10-point increase from baseline with a follow-up measurement of LVEF > 40%. HFimpEF is distinct from HFpEF and was proposed in the “Universal Definition and Classification of Heart Failure” by Bozkurt et al published in JCF 2021 in order to distinguish those who benefit from continued GDMT. Accordingly, in patients with HFimpEF after treatment, GDMT should be continued to prevent relapse of HF and LV dysfunction, even in patients who may become asymptomatic (Class 1, LOE B-R). While GDMT may improve symptoms, functional capacity, LVEF, and reverse remodeling in patients with HFrEF, these favorable changes do not reflect full and sustained recovery but rather remission with susceptibility to worsening with GDMT withdrawal. Therefore, stopping any element of her GDMT (BB, ARNi, or MRA) would be incorrect (Options A, C, D). Main Takeaway In patients with HFrEF who experience improvement in heart failure symptoms and cardiac function on GDMT (develop HFimpEF), it is important to continue optimizing GDMT to prevent relapse, even if asymptomatic. Guideline Loc. Section 7.3.2 Section 7.3.8, Table 14 Section 7.6.2 Decipher the Guidelines: 2022 Heart Failure Guidelines Page CardioNerds Episode Page CardioNerds Academy Cardionerds Healy Honor Roll CardioNerds Journal Club Subscribe to The Heartbeat Newsletter! Check out CardioNerds SWAG! Become a CardioNerds Patron!

May 23, 2023

CardioNerds (Drs. Amit Goyal and Dan Ambinder) join Dr. Mina Fares, Dr. Johannes Bergehr, and Dr. Christina Peter from Cambridge University Hospitals in the UK. They discuss a case involving a man man in his 40’s presented with progressive heart failure symptoms. He has extensive background cardiac history including prior episodes of myocarditis and complete heart block status post permanent pacemaker implantation. Ultimately a diagnosis of Danon disease is made. Dr. Sharon Wilson provides the E-CPR for this episode. Audio editing by CardioNerds Academy Intern, Hirsh Elhence. CardioNerds is collaborating with Radcliffe Cardiology and US Cardiology Review journal (USC) for a ‘call for cases’, with the intention to co-publish high impact cardiovascular case reports, subject to double-blind peer review. Case Reports that are accepted in USC journal and published as the version of record (VOR), will also be indexed in Scopus and the Directory of Open Access Journals (DOAJ). CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Case Summary - A Presentation of Heart Failure and Heart Block with Elusive Genetic Origins - Cambridge University A man in his 40s with a history of cardiac issues, including prior myocarditis and complete heart block, presented with progressive heart failure symptoms. Extensive cardiac investigations were conducted, revealing dilated left ventricle, mild to moderate left ventricular systolic dysfunction, normal coronaries, infero-lateral late gadolinium enhancement on cardiac MRI, and low-level uptake on PET-CT. Differential diagnosis included worsening underlying cardiomyopathy, recurrent myocarditis, tachycardia-related cardiomyopathy, pacemaker-induced LV dysfunction, and sarcoidosis. The patient's condition improved with heart failure medications, and cardiac MRI showed a mildly dilated left ventricle with moderate systolic dysfunction and active inflammation in the anterior wall. Further evaluation indicated a family history of hereditary cardiomyopathy, and the patient exhibited phenotypic features such as early-onset heart disease, arrhythmias, family history of cardiomyopathy, learning problems, intellectual disability, and mild proximal myopathy. Genetic testing confirmed a LAMP2 mutation, leading to the diagnosis of Danon disease. Case Media - A Presentation of Heart Failure and Heart Block with Elusive Genetic Origins - Cambridge University Show Notes -A Presentation of Heart Failure and Heart Block with Elusive Genetic Origins - Cambridge University References - Danon, M. J., Oh, S. J., DiMauro, S., Miranda, A., De Vivo, D. C., & Rowland, L. P. (1981). Lysosomal glycogen storage disease with normal acid maltase. Neurology, 31(1), 51-7. Nishino, I., Fu, J., Tanji, K., Nonaka, I., & Ozawa, T. (2000). Mutations in the gene encoding LAMP2 cause Danon disease. Nature, 406(6798), 906-10. Tanaka, K., Nishino, I., Nonaka, I., Fu, J., & Ozawa, T. (2000). Danon disease is caused by mutations in the gene encoding LAMP2, a lysosomal membrane protein. Nature, 406(6798), 902-6. Maron, B. J., Haas, T. S., Ackerman, M. J., Ahluwalia, A., Spirito, P., Nishino, I., ... & Seidman, C. E. (2009). Hypertrophic cardiomyopathy and sudden death in a family with Danon disease. JAMA, 301(12), 1253-9. Hashem, S., Zhang, J., Zhang, Y., Wang, H., Zhang, H., Liu, L., ... & Wang, J. (2015). AAV-mediated gene transfer of LAMP2 improves cardiac function in Danon disease mice. Stem cells, 33(11), 2343-2350. Chi, L., Wang, H., Zhang, J., Zhang, Y., Liu, L., Wang, J., ... & Hashem, S. (2019). CRISPR/Cas9-mediated gene editing of LAMP2 in patient-derived iPSCs ameliorates Danon disease phenotypes. Proceedings of the National Academy of Sciences, 116(4), 556-565.

May 15, 2023

The following question refers to Section 3.2 of the 2021 ESC CV Prevention Guidelines. The question is asked by student Dr. Hirsh Elhence, answered first by Mayo Clinic Fellow Dr. Teodora Donisan, and then by expert faculty Dr. Eugene Yang.Dr. Yang is professor of medicine of the University of Washington where he is medical director of the Eastside Specialty Center and the co-Director of the Cardiovascular Wellness and Prevention Program. Dr. Yang is former Governor of the ACC Washington Chapter and chair of the ACC Prevention of CVD Section.The CardioNerds Decipher The Guidelines Series for the 2021 ESC CV Prevention Guidelines represents a collaboration with the ACC Prevention of CVD Section, the National Lipid Association, and Preventive Cardiovascular Nurses Association.Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. Question #25 Please choose the CORRECT statement from the ones below.ACAC scoring can be considered to improve ASCVD risk classification around treatment decision thresholds.BPatients with type 1 or type 2 diabetes are considered very high CV risk, regardless of comorbidities and other risk factors.CCKD does not increase the cardiovascular risk in the absence of other risk factors.DMen and women older than 65 years old are at high cardiovascular risk. Answer #25 ExplanationOption A is correct. Coronary artery calcium (CAC) scoring can reclassify CVD risk upwards and downwards in addition to conventional risk factors and may thus be considered in men and women with calculated risks around decision thresholds (Class IIb, Level B). If CAC is detected, its extent should be compared with what would be expected for a patient of the same sex and age. CAC scoring does not provide direct information on total plaque burden or stenosis severity and can be low or even zero in middle-aged patients with soft non-calcified plaque.Option B is false. Not all patients with diabetes are very high risk by default.· Moderate risk: well controlled diabetes, 300 mg/g)· Presence of microvascular disease in at least 3 different sites (e.g., microalbuminuria + retinopathy + neuropathyOption C is false. CKD carries at least a high CVD risk even in the absence of diabetes or ASCVD.· Moderate CKD carries a high CVD risk: o eGFR 30−44 mL/min/1.73 m2 and ACR 300· Severe CKD carries a very high CVD risk:o eGFR 30 Option D is false. There is an age difference between men and women with regards to cardiovascular risk. Age is a major CVD risk driver, but age cutoffs should be used with flexibility.· Women 75 years-old and men > 65 years-old are usually at high 10-year CVD risk.· Only between the ages of 55 – 75 years in women and 40 – 65 years in men does the 10-year CVD risk vary around commonly used thresholds for intervention. Of note:· In younger, apparently healthy patients, we also discuss lifetime CVD risk estimates since 10-year risk assessments often underestimate risk.· In an aging population, treatment decisions should take competing non-CVD risk into account.· In patients with established ASCVD we can discuss about residual CVD – defined as the risk estimated after initial lifestyle changes and risk factor treatment.Main TakeawayEstimating CVD risk is not only important in apparently healthy patients, but also in patients with diabetes, renal disease, established ASCVD, or older patients. This can provide information to allow shared decision making and personalized approach for our patients.Guideline Loc.Table 3, page 3237; Section 3.2.3., page 3243; Table 4, page 3244 CardioNerds Decipher the Guidelines - 2021 ESC Prevention SeriesCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor RollCardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron!

May 12, 2023

The following question refers to Section 7.1 of the 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure. The question is asked by New York Medical College medical student and CardioNerds Intern Akiva Rosenzveig, answered first by Lahey Hospital and Medical Center internal medicine resident and CardioNerds Academy House Faculty Leader Dr. Ahmed Ghoneem, and then by expert faculty Dr. Clyde Yancy. Dr. Yancy is Professor of Medicine and Medical Social Sciences, Chief of Cardiology, and Vice Dean for Diversity and Inclusion at Northwestern University, and a member of the ACC/AHA Joint Committee on Clinical Practice Guidelines. The Decipher the Guidelines: 2022 AHA / ACC / HFSA Guideline for The Management of Heart Failure series was developed by the CardioNerds and created in collaboration with the American Heart Association and the Heart Failure Society of America. It was created by 30 trainees spanning college through advanced fellowship under the leadership of CardioNerds Cofounders Dr. Amit Goyal and Dr. Dan Ambinder, with mentorship from Dr. Anu Lala, Dr. Robert Mentz, and Dr. Nancy Sweitzer. We thank Dr. Judy Bezanson and Dr. Elliott Antman for tremendous guidance. Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. Question #19 Ms. M is a 36-year-old G1P1 woman 6 months postpartum who was diagnosed with peripartum cardiomyopathy at the end of her pregnancy. She is presenting for a follow up visit today and notes that while her leg edema has resolved, she continues to have dyspnea when carrying her child up the stairs. She also describes significant difficulty sleeping, though denies orthopnea, and notes she is not participating in hobbies she had previously enjoyed. She is currently prescribed a regimen of sacubitril-valsartan, metoprolol succinate, spironolactone, and empagliflozin. What are the next best steps? A Screen for depression B Counsel her to follow a strict low sodium diet with goal of < 1.5g Na daily C Recommend exercise therapy and refer to cardiac rehabilitation D A & C Answer #19 Explanation The correct answer is D – both A (screening for depression) and C (referring to cardiac rehabilitation) are appropriate at this time. Choice A is correct. Depression is a risk factor for poor self-care, rehospitalization, and all-cause mortality among patients with HF. Interventions that focus on improving HF self-care have been reported to be effective among patients with moderate/severe depression with reductions in hospitalization and mortality risk. Social isolation, frailty, and marginal health literacy have similarly been associated with poor HF self-care and worse outcomes in patients with HF. Therefore, in adults with HF, screening for depression, social isolation, frailty, and low health literacy as risk factors for poor self-care is reasonable to improve management (Class 2a, LOE B-NR). Choice C is correct. In patients with HF, cardiac rehabilitation has a Class 2a recommendation (LOE B-NR) to improve functional capacity, exercise tolerance, and health-related QOL; exercise training (or regular physical activity) for those able to participate has a Class 1 recommendation (LOE A) to improve functional status, exercise performance, and QOL. Choice B is incorrect. For patients with stage C HF, avoiding excessive sodium intake is reasonable to reduce congestive symptoms (Class 2a, LOE C-LD). However, strict sodium restriction does not have strong supportive data and is not recommended. There are ongoing studies to better understand the impact of sodium restriction on clinical outcomes and quality of life. The AHA currently recommends a reduction of sodium intake to <2300 mg/d for general cardiovascular health promotion; however, there are no trials to support this level of restriction in patients with HF. Main Takeaway Depression is a risk factor for poor HF self-care and worse outcomes in patients with heart failure and so it is reasonable to screen for depression in these patients. Exercise therapy and cardiac rehabilitation have been shown to improve outcomes in HF patients. While avoiding excess sodium intake is reasonable in HF patients to reduce congestive symptoms, there is no specific strict sodium level recommended. Guideline Loc. Section 7.1 Decipher the Guidelines: 2022 Heart Failure Guidelines Page CardioNerds Episode Page CardioNerds Academy Cardionerds Healy Honor Roll CardioNerds Journal Club Subscribe to The Heartbeat Newsletter! Check out CardioNerds SWAG! Become a CardioNerds Patron!

May 10, 2023

CardioNerds (Daniel Ambinder) join Dr. Tomio Tran, Dr. Vid Yogeswaran, and Dr. Amanda Cai from the University of Washington for a break from the rain at the waterfront near Pike Place Market. They discuss the following case: A 46-year-old woman presents with cardiac arrest and was found to have cor triatriatum sinistrum (CTS). CTS is a rare congenital cardiac malformation in which the left atrium is divided by a fenestrated membrane, which can restrict blood flow and cause symptoms of congestive heart failure. Rarely, the condition can present in adulthood. To date, there have been no cases of sudden cardiac death attributed to CTS. Dr. Jill Steiner provides the E-CPR for this episode. Audio editing by CardioNerds Academy Intern, student doctor Akiva Rosenzveig. CardioNerds is collaborating with Radcliffe Cardiology and US Cardiology Review journal (USC) for a ‘call for cases’, with the intention to co-publish high impact cardiovascular case reports, subject to double-blind peer review. Case Reports that are accepted in USC journal and published as the version of record (VOR), will also be indexed in Scopus and the Directory of Open Access Journals (DOAJ). CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Case Media - A Sinister Cause of Sudden Cardiac Death – University of Washington A 40-year-old woman with a history of recurrent exertional syncope had sudden loss of consciousness while kissing her partner. The patient received bystander CPR while 911 was called. EMS arrived within 10 minutes of the call and found the patient apneic and unresponsive. Initial rhythm check showed narrow complex tachycardia at a rate of 136 BPM. ROSC was eventually achieved. A 12-lead ECG showed that the patient was in atrial fibrillation with rapid ventricular rate. The patient was intubated and brought to the emergency department. The patient spontaneously converted to sinus rhythm en route to the hospital. In the emergency department, vital signs were remarkable for hypotension (76/64 mmHg) and sinus tachycardia (110 BPM). The physical exam was remarkable for an inability to follow commands. Laboratory data was remarkable for hypokalemia (2.5 mmol/L), transaminitis (AST 138 units/L, ALT 98 units/L), acidemia (pH 7.12), and hyperlactatemia (11.2 mmol/L). CT scan of the chest revealed a thin membrane within the left atrium. Transthoracic echocardiogram showed normal biventricular size and function, severe tricuspid regurgitation, pulmonary artery systolic pressure of 93 mmHg, and the presence of a membrane within the left atrium with a mean gradient of 25 mmHg between the proximal and distal left atrial chambers. Vasopressors and targeted temperature management were initiated. The patient was able to be re-warmed with eventual discontinuation of vasopressors, however she had ongoing encephalopathy and seizures concerning for hypoxic brain injury. There was discussion with the adult congenital heart disease team about next steps in management, however the patient was too sick to undergo any definitive treatment for the intracardiac membrane within the left atrium. The patient developed ventilator associated pneumonia and antibiotics were initiated. The patient ultimately developed bradycardia and pulseless electrical activity; ROSC was unable to be achieved, resulting in death. Autopsy was remarkable for the presence of a fenestrated intracardiac membrane within the left atrium and lack of other apparent congenital heart defects. There was right ventricular hypertrophy and pulmonary artery intimal thickening with interstitial fibrosis suggestive of pulmonary hypertension. There were bilateral acute subsegmental pulmonary emboli present. The cause of death was declared to be arrhythmia in the setting of pulmonary hypertension and right sided heart failure caused by cor triatriatum sinistrum with a significant contribution from acute subsegmental pulmonary emboli. Case Media - A Sinister Cause of Sudden Cardiac Death – University of Washington Pearls - A Sinister Cause of Sudden Cardiac Death – University of Washington In a patient presenting with syncope, the following feature may indicate an underlying cardiac etiology: exertional syncope, sudden syncope without a prodrome, structural heart disease, advanced age, and family history of sudden cardiac or unexplained death. Cor triatriatum sinistrum is diagnosed by CT, echocardiography, or MRI and is often found incidentally in adults. Acute management of CTS is similar to mitral stenosis and consists of 1) careful volume management to avoid both hypovolemia and hypervolemia, and 2) avoidance of tachycardia to allow for adequate LV filling during diastole. Surgical resection of the membrane is definitive. A mean gradient of ≥ 8 mmHg across a CTS membrane is hemodynamically significant and should prompt surgical evaluation for membrane resection. Show Notes -A Sinister Cause of Sudden Cardiac Death – University of Washington SyncopeLoss of consciousness due to transient decrease in cerebral blood flowDifferentialOrthostaticNeurally mediatedCardiogenicMimickers of syncope: seizures, head trauma causing loss of consciousness, hypoglycemiaRed flag symptoms of cardiogenic syncopeAdvanced ageExertional or while lying downPalpitations prior to eventStructural heart diseaseFamily history of unexplained or sudden cardiac deathStructural heart disease etiologiesGenerally left sided and causes obstruction to blood flowValvular stenosesHypertrophic cardiomyopathyCardiac tumors Arrhythmia etiologiesCan be caused by any brady- or tachyarrhythmia, especially in the setting of structural heart disease Most commonlySinus node diseaseHigh degree heart block Ventricular arrhythmia Pulse pressureDifference between systolic and diastolic pressureNormal ~ 40 mmHgNarrow - 100 mmHgWide pulse pressure etiologiesPhysical conditioning (normal variant)Aortic regurgitationSevere iron deficiency anemiaHyperthyroidismArteriosclerosisShunting from arteriovenous fistulas Narrow pulse pressure etiologies – indicates low stroke volume/cardiac outputHeart failureHypovolemiaBlood lossValvular stenosisCardiac tamponade Pulmonary embolism Cor triatriatum sinisterPresence of a membrane within the left atrium that divides the left atrium into 2 chambersPathophysiologyTheorized to be caused by misincorporation of the pulmonary veins within the left atrium causing a membrane within the left atriumIf restrictive, sequelae include congestive heart failure, pulmonary hypertension, and right ventricular dysfunctionOften associated with other congenital heart disease (ASD, pulmonary venous return, mitral regurgitation)EpidemiologyAmong the rarest of all congenital heart disease (up to 0.4% of all congenital heart disease, but true incidence is unknown as many can be asymptomatic)Found more often in infancy/childhood; often found incidentally in adultsSigns/symptomsMany are asymptomaticOver time, membrane may become fibrotic or calcified and cause significant obstructionInfants/children – pulmonary congestion, respiratory infections, cyanosis, growth restrictionAdults – dyspnea, chest pain, palpitations, syncopeThrombotic events are common likely from vascular injury and congestion/stasisAtrial arrhythmia is associated with CTS, possibly from scarring of the membrane vs chronic elevation of left atrial pressureDiagnosisMade by imaging (CT chest/cardiac, echocardiography, MRI)Primary competing differential diagnosis is supravalvular mitral ringIf intra-atrial membrane contains the left atrial appendage and pulmonary veins -> supravalvular mitral ringAssociated with Schone complex (supravalvular mitral ring, parachute mitral valve, subaortic stenosis, aortic coarctationCTS rarely associated with Shone complexIf intra-atrial membrane contains only the pulmonary veins -> CTSCan be found incidentally and cause technical issues in cardiac procedures that require transeptal atrial puncturesQuantify degree of restriction with echocardiography; gradients ≥ 8 mmHg are significant per AHA guidelines TreatmentAcute:Diuretics to treat congestionFluids to avoid hypovolemia due to preload dependence for cardiac outputTreat underlying causes of tachycardia to optimize diastolic fillingTreat tachyarrhythmia with anti-arrhythmis and AV nodal blockers Chronic/definitive: Surgical resection of the membrane offers a good and durable outcome Low recurrence rate, residual gradients likely due to incomplete resection Pulmonary hypertension WHO classificationGroup 1 – Pulmonary arterial hypertension (idiopathic, toxin induced, HIV, connective tissue disease, congenital heart diseaseCongenital heart disease comprises a small portion of group 1, typically from shunt lesionsGroup 2 – Left sided heart diseaseGroup 3 – Pulmonary diseaseGroup 4 – CTEPH Group 5 – Unclear mechanisms (sickle cell, sarcoid, metabolic disease) References - Albassam OT, Redelmeier RJ, Shadowitz S, Husain AM, Simel D, Etchells EE. Did This Patient Have Cardiac Syncope?: The Rational Clinical Examination Systematic Review. JAMA. 2019;321(24):2448-2457. doi:10.1001/jama.2019.8001 Jegier W, Gibbons JE, Wigglesworth FW. Cortriatriatum: clinical, hemodynamic and pathological studies surgical correction in early life. Pediatrics. 1963;31:255-267. Jha AK, Makhija N. Cor Triatriatum: A Review. Semin Cardiothorac Vasc Anesth. 2017;21(2):178-185. doi:10.1177/1089253216680495 Rudienė V, Hjortshøj CMS, Glaveckaitė S, et al. Cor triatriatum sinistrum diagnosed in the adulthood: a systematic review. Heart. 2019;105(15):1197-1202. doi:10.1136/heartjnl-2019-314714 Saxena P, Burkhart HM,

May 5, 2023

The following question refers to Section 6.3 of the 2021 ESC CV Prevention Guidelines. The question is asked by Dr. Christian Faaborg-Andersen, answered first by UCSD cardiology fellow Dr. Harpreet Bhatia, and then by expert faculty Dr. Jaideep Patel.Dr. Patel recently graduated from Virginia Commonwealth University cardiology fellowship and is now a preventive cardiologist at the Johns Hopkins Hospital.The CardioNerds Decipher The Guidelines Series for the 2021 ESC CV Prevention Guidelines represents a collaboration with the ACC Prevention of CVD Section, the National Lipid Association, and Preventive Cardiovascular Nurses Association.Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. Question #24 A 65-year-old man with a history of ischemic stroke 6 months ago presents to cardiology clinic to establish care. An event monitor was negative for atrial fibrillation and TTE with agitated saline study was negative for a patent foramen ovale. Therefore, his ischemic stroke was presumed to be non-cardioembolic in origin. He is currently taking lisinopril 5 mg daily for hypertension (BP in clinic is 115/70) and atorvastatin 40 mg daily. He has no history of significant gastrointestinal or other bleeding. What do you recommend next?AStart apixaban 5 mg BIDBIncrease lisinopril to 10 mg dailyCStart aspirin 81 mg dailyDStart aspirin 81 mg daily and clopidogrel 75 mg dailyEStart aspirin 81 mg daily and ticagrelor 90 mg BID Answer #24 ExplanationThe correct answer is C – start aspirin 81mg daily.For the secondary prevention of non-cardioembolic ischemic stroke or TIA, anti-platelet therapy is recommended with aspirin only (75-150 mg/day), dipyridamole + aspirin (slightly superior to aspirin), or clopidogrel alone (slightly superior to aspirin) (Class I, LOE A).DAPT with aspirin and clopidogrel or aspirin and ticagrelor should be considered in the immediate period after a minor ischemic stroke or TIA (3 weeks after event, Class IIa), but not 6 months after an ischemic stroke. Dual antiplatelet therapy with aspirin and clopidogrel increases bleeding risk without a significant benefit over either agent alone. Dual antiplatelet therapy with aspirin and ticagrelor increases bleeding risk, but does not improve disability incidence.Oral anticoagulation would be recommended for a cardioembolic stroke, which does not fit the clinical picture.His BP is well controlled so increasing lisinopril is not necessary.Main TakeawayFor the secondary prevention of an ischemic stroke or TIA, anti-platelet therapy with aspirin, aspirin + dipyridamole, or clopidogrel alone is recommended.Guideline Loc.6.3, page 3296-3297 CardioNerds Decipher the Guidelines - 2021 ESC Prevention SeriesCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor RollCardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron!

May 4, 2023

The following question refers to Sections 3.2, 4.1, 4.3, and 4.4 of the 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure. The question is asked by Texas Tech University medical student and CardioNerds Academy Intern Dr. Adriana Mares, answered first by Baylor University cardiology fellow and CardioNerds FIT Trialist Dr. Shiva Patlolla, and then by expert faculty Dr. Shelley Zieroth. Dr. Zieroth is an advanced heart failure and transplant cardiologist, Head of the Medical Heart Failure Program, the Winnipeg Regional Health Authority Cardiac Sciences Program, and an Associate Professor in the Section of Cardiology at the University of Manitoba. Dr. Zieroth is a past president of the Canadian Heart Failure Society. She is a steering committee member for PARAGLIE-HF and a PI Mentor for the CardioNerds Clinical Trials Program. The Decipher the Guidelines: 2022 AHA / ACC / HFSA Guideline for The Management of Heart Failure series was developed by the CardioNerds and created in collaboration with the American Heart Association and the Heart Failure Society of America. It was created by 30 trainees spanning college through advanced fellowship under the leadership of CardioNerds Cofounders Dr. Amit Goyal and Dr. Dan Ambinder, with mentorship from Dr. Anu Lala, Dr. Robert Mentz, and Dr. Nancy Sweitzer. We thank Dr. Judy Bezanson and Dr. Elliott Antman for tremendous guidance. Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. Question #18 Ms. AH is a 48-year-old woman who presents with a 3-month history of progressively worsening exertional dyspnea and symmetric bilateral lower extremity edema. She has no history of recent upper respiratory symptoms or chest pain. She denies any tobacco, alcohol, or recreational drug use. There is no family history of premature CAD or HF. On exam, her blood pressure is 110/66 mmHg, heart rate is 112 bpm, and respiration rate is 18 breaths/min with oxygen saturation of 98% on ambient room air. She has jugular venous distention of about 12cm H2O, bibasilar crackles, an S3 heart sound, and bilateral lower extremity edema. Complete blood count, serum electrolytes, kidney function tests, liver chemistry tests, glucose level, iron studies, and lipid levels are unremarkable. An electrocardiogram shows sinus tachycardia with normal intervals and no conduction delays. A transthoracic echocardiogram demonstrates a left ventricular ejection fraction of 25%, normal right ventricular size and function, and no valvular abnormalities. Which of the following diagnostic tests has a Class I indication for further evaluation? A Cardiac catheterization B Referral for genetic counseling C Thyroid function studies D Cardiac MRI Answer #18 Explanation The correct answer is C – thyroid function studies have a Class 1 indication for the evaluation of HF. The common causes of HF include coronary artery disease, hypertension, and valvular heart disease. Other causes may include arrhythmia-associated, toxic, inflammatory, metabolic including both endocrinopathies and nutritional, infiltrative, genetic, stress induced, peripartum, and more. It is important to evaluate for the etiology of a given patient’s heart failure as diagnosis may have implications for treatment, counseling, and family members. For patients who are diagnosed with HF, laboratory evaluation should include complete blood count, urinalysis, serum electrolytes, blood urea nitrogen, serum creatinine, glucose, lipid profile, liver function tests, iron studies, and thyroid-stimulating hormone to optimize management (Class 1, LOR C-EO). These studies provide important information regarding comorbidities, suitability for and adverse effects of treatments, potential causes or confounders of HF, and severity and prognosis of HF. HF is often caused by coronary atherosclerosis, and evaluation for ischemic heart disease can help in determining the presence of significant coronary artery disease (CAD). Noninvasive stress imaging with echocardiography or nuclear scintigraphy can be helpful in identifying patients likely to have obstructive CAD. Invasive or computed tomography coronary angiography can detect and characterize the extent of CAD. Therefore, in patients with HF, an evaluation for possible ischemic heart disease can be useful to identify the cause and guide management (Class 2a, LOE B-NR). Familial cardiomyopathy is increasingly recognized and may be the underlying etiology of patients previously classified as having idiopathic dilated cardiomyopathy. A detailed family history may provide the first clue to a genetic basis. A 3-generation family pedigree obtained by genetic health care professionals improved the rate of detection of a familial process as compared with routine care. Furthermore, a family history of cardiomyopathy, as determined by a 3-generation pedigree analysis, was associated with findings of gadolinium enhancement on cardiac magnetic resonance imaging (MRI) and increased major adverse cardiac events. The possibility of an inherited cardiomyopathy provides the impetus for cascade screening of undiagnosed family members, thereby potentially avoiding preventable adverse events in affected relatives by implementation of GDMT and other management that otherwise would not be initiated. Therefore, in patients with cardiomyopathy, a 3-generation family history should be obtained or updated when assessing the cause of the cardiomyopathy to identify possible inherited disease (Class 1, LOE B-NR). In selecting patients with nonischemic cardiomyopathy, referral for genetic counseling and testing is reasonable to identify conditions that could guide treatment for patients and family members (Class 2a, LOE B-NR). CMR provides noninvasive characterization of the myocardium that may provide insights into HF cause. Registry data show that CMR findings commonly impact patient care management and provide diagnostic information in patients with suspected myocarditis or cardiomyopathy. However, routine screening with CMR is not recommended. The OUTSMART HF trial recently demonstrated routine cardiac MRI use did not yield more specific HF causes than a selective strategy based on echocardiographic and clinical findings. The guidelines give a Class 2a recommendation for the use of CMR in diagnosis or management in patients with HF or cardiomyopathy (LOE B-NR). Main Takeaway The common causes of HF include ischemic heart disease, hypertension, and valvular heart disease. When a patient presents with new-onset heart failure, a complete initial evaluation including laboratory testing for potentially reversible causes such as thyroid disease, or other endocrine, metabolic, and nutritional causes should be performed. Guideline Loc. Section 3.2, 4.1, 4.3, and 4.4 Table 5 Decipher the Guidelines: 2022 Heart Failure Guidelines PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron!

May 2, 2023

CardioNerds (Amit Goyal and Daniel Ambinder), ACHD series co-chairs Dr. Dan Clark and Dr. Josh Saef, and ACHD FIT lead Dr. J.D. Serfas (Duke University) and Cardiology Fellow Dr. Victoria Thomas (Vanderbilt University) join ACHD experts Dr. Jamil Aboulhosn (Professor of Medicine at UCLA and the director of the Ahmanson/UCLA Adult Congenital Heart Disease Center) and Dr. Joanna Ghobrial, Medical and Interventional Director of the Adult Congenital Heart Disease Center at Cleveland Clinic. They discuss common ACHD pathologies that benefit from interventional cardiology procedures such as transcatheter pulmonic valve replacement (TPVR) and share new advancements in transcatheter approaches to correct sinus venosus defects. They end with a brief discussion on how to become an adult cardiology interventionalist that performs ACHD interventions. Episode notes were drafted by Dr. Victoria Thomas. Audio editing by CardioNerds Academy Intern, student doctor Akiva Rosenzveig. The CardioNerds Adult Congenital Heart Disease (ACHD) series provides a comprehensive curriculum to dive deep into the labyrinthine world of congenital heart disease with the aim of empowering every CardioNerd to help improve the lives of people living with congenital heart disease. This series is multi-institutional collaborative project made possible by contributions of stellar fellow leads and expert faculty from several programs, led by series co-chairs, Dr. Josh Saef, Dr. Agnes Koczo, and Dr. Dan Clark. The CardioNerds Adult Congenital Heart Disease Series is developed in collaboration with the Adult Congenital Heart Association, The CHiP Network, and Heart University. See more Disclosures: None CardioNerds Adult Congenital Heart Disease PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls - ACHD: Interventional Cardiology The ductus arteriosus, which is formed from the distal portion of the left sixth arch, is key to fetal circulation because it allows blood to bypass Transcatheter pulmonic valve replacement (TPVR) is a treatment for many ACHD patients that can spare them repeat sternotomies. This is important as many ACHD patients hava already undergone multiple surgeries in their childhood. Before any ACHD cardiology intervention, appropriate imaging (TEE, TTE, Cardiac MRI, Cardiac CTA, and/or 3D printing) is imperative to understanding the relevant anatomy and hemodynamics to guide procedural indication and planning. As with other structural interventions, consider a SENTINEL device (cerebral embolic protection system) to provide embolic protection in procedures that could lead to debris/embolic dislodgement when appropriate. Sinus venosus defects can be repaired via a transcatheter approach with a covered stent in the superior vena cava (SVC). Consider using 3D printing or 3D digital imaging when preparing for complex ACHD interventions. Notes- ACHD: Interventional Cardiology 1. When considering a patient for TPVR there are 3 types of landing zones for pulmonic valves in ACHD patients: Pulmonary conduits or homografts. These are typically seen in patients with TOF or prior Ross or Rastelli procedure. These may be calcified and stenotic and so pre-dilatation is often needed before valve replacement. Bioprosthetic Valves. (Valve in Valve TPVR) Native outflow tract 2. What are some of the more severe complications to consider when talking to an ACHD patient about a TPVR? Coronary artery compression Conduit rupture Vessel injury (including the pulmonary bed) Valve embolization Endocarditis 3. What are some of the hemodynamic measurements one would want to pay attention to in a patient with a Fontan heart? You will see higher CVPs in patients with a Fontan palliation. The CVP will typically be higher than your wedge pressure, as the circuit relies on passive transpulmonary blood flow. Evaluating the wedge pressure is crucial. Elevation may indicate arrythmias and or ventricular dysfunction. 4. When considering closing a fenestration of a Fontan circuit, what are the measurements that one would want to consider? You would want to temporarily occlude the fenestration with a balloon on a wedge catheter for 10-15 minutes roughly to observe the patient’s Fontan pressure/CVP, wedge pressure, arterial saturation, PA saturation, and systemic blood pressure. You may want to reconsider occlusion if there is a significant drop in systemic pressures or cardiac output; or significantly increased Fontan pressure/CVP. 5. What are the technical considerations to consider when occluding a fenestration in a Fontan circuit? You want to make sure there is no thrombus in the fenestration or Fontan circuit. Consider using the SENTINEL cerebral protection system/device (a device that can provide embolic protection from dislodged debris or emboli). However, this device is typically unable to be used in ACHD who have undergone a BTT shunt due to stenosis. 6. How does a transcatheter intervention help a sinus venosus defect? Placement of the covered stent in the SVC with a dilated portion into the right atrium creates the closure of the sinus venosus defect. The covered stent also helps with rerouting the anomalous pulmonary vein(s) posteriorly to drain into the left atrium. To learn more about PAPVR, enjoy Episode #106. Case Report: A Hole in the HFpEF Diagnosis. 7. What are some of the concerns to consider when closing a sinus venosus defect via a transcatheter approach? Plan for increased left atrial pressures and pulmonary venous pressures in older patients. This is due to your left heart using the sinus venosus defect as a pop-off mechanism before closure, especially in elderly patients with a small left ventricle or diastolic dysfunction. Once the sinus venosus defect is closed/fixed, the blood is no longer able to shunt over to the right atrium and so more blood returns to the (potentially low compliance) left system. You also must watch for pulmonary vein compression when placing your covered stent in the SVC. You also need to consider the length of your covered stent, as the superior portion of the stent needs to be well-anchored above the entry point of the anomalous pulmonary vein to prevent embolization. To counteract this, Dr. Aboulhosn suggests that before placing a covered stent in the SVC to fix the sinus venosus defect consider placing a catheter in the left atrium via the transeptal approach. This will then allow a wire to be placed from the left atrium into the most superior pulmonary veins for protection if there is any stenosis/compression after placing the covered stent in the SVC. The transeptal puncture will then serve as a small defect to allow for some mild left-to-right shunting and decompress the left atrium. The transeptal puncture typically endothelializes over time. References - ACHD Interventional Cardiology Stout KK, Daniels CJ, Aboulhosn JA, et al. 2018 AHA/ACC Guideline for the Management of Adults With Congenital Heart Disease: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines. Circulation. Apr 2 2019;139(14):e698-e800. https://www.ahajournals.org/doi/10.1161/CIR.0000000000000603 European Society of G, Association for European Paediatric C, German Society for Gender M, et al. ESC Guidelines on the management of cardiovascular diseases during pregnancy: the Task Force on the Management of Cardiovascular Diseases during Pregnancy of the European Society of Cardiology (ESC). European heart journal. Dec 2011;32(24):3147-3197. https://academic.oup.com/eurheartj/article/39/34/3165/5078465 Hansen, J. H., Duong, P., Jivanji, S. G., Jones, M., Kabir, S., Butera, G., ... & Rosenthal, E. (2020). Transcatheter correction of superior sinus venosus atrial septal defects as an alternative to surgical treatment. Journal of the American College of Cardiology, 75(11), 1266-1278. https://doi.org/10.1016/j.jacc.2019.12.070 Aboulhosn, J. A., Hijazi, Z. M., Kavinsky, C. J., McElhinney, D. B., Asgar, A. W., Benson, L. N., ... & Levi, D. S. (2020). SCAI position statement on adult congenital cardiac interventional training, competencies and organizational recommendations. Catheterization and cardiovascular interventions: official journal of the Society for Cardiac Angiography & Interventions, 96(3), 643-650. https://doi.org/10.1002/ccd.28885 Meet Our Collaborators! Adult Congenital Heart AssociationFounded in 1998, the Adult Congenital Heart Association is an organization begun by and dedicated to supporting individuals and families living with congenital heart disease and advancing the care and treatment available to our community. Our mission is to empower the congenital heart disease community by advancing access to resources and specialized care that improve patient-centered outcomes. Visit their website (https://www.achaheart.org/) for information on their patient advocacy efforts, educational material, and membership for patients and providers CHiP Network The CHiP network is a non-profit organization aiming to connect congenital heart professionals around the world. Visit their website (thechipnetwork.org) and become a member to access free high-quality educational material, upcoming news and events, and the fantastic monthly Journal Watch, keeping you up to date with congenital scientific releases. Visit their website (https://thechipnetwork.org/) for more information. Heart UniversityHeart University aims to be “the go-to online resource” for e-learning in CHD and paediatric-acquired heart disease.

May 1, 2023

CardioNerds (Amit Goyal and Daniel Ambinder), ACHD series co-chairs Dr. Dan Clark and Dr. Josh Saef, and ACHD FIT lead Dr. J.D. Serfas (Duke University) and Cardiology Fellow Dr. Victoria Thomas (Vanderbilt University) join ACHD experts Dr. Jamil Aboulhosn (Professor of Medicine at UCLA and the director of the Ahmanson/UCLA Adult Congenital Heart Disease Center) and Dr. Joanna Ghobrial, Medical and Interventional Director of the Adult Congenital Heart Disease Center at Cleveland Clinic. They discuss common ACHD pathologies that benefit from interventional procedures such as transcatheter pulmonic valve replacement (TPVR) and share new advancements in transcatheter approaches to correct sinus venosus defects. They end with a brief discussion on how to become an adult cardiology interventionalist that performs ACHD interventions. Episode notes were drafted by Dr. Victoria Thomas. Audio editing by CardioNerds Academy Intern, student doctor Akiva Rosenzveig. The CardioNerds Adult Congenital Heart Disease (ACHD) series provides a comprehensive curriculum to dive deep into the labyrinthine world of congenital heart disease with the aim of empowering every CardioNerd to help improve the lives of people living with congenital heart disease. This series is multi-institutional collaborative project made possible by contributions of stellar fellow leads and expert faculty from several programs, led by series co-chairs, Dr. Josh Saef, Dr. Agnes Koczo, and Dr. Dan Clark. The CardioNerds Adult Congenital Heart Disease Series is developed in collaboration with the Adult Congenital Heart Association, The CHiP Network, and Heart University. See more Disclosures: None CardioNerds Adult Congenital Heart Disease PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls - ACHD: Interventional Cardiology The ductus arteriosus, which is formed from the distal portion of the left sixth arch, is key to fetal circulation because it allows blood to bypass Transcatheter pulmonic valve replacement (TPVR) is a treatment for many ACHD patients that can spare them repeat sternotomies. This is important as many ACHD patients hava already undergone multiple surgeries in their childhood. Before any ACHD cardiology intervention, appropriate imaging (TEE, TTE, Cardiac MRI, Cardiac CTA, and/or 3D printing) is imperative to understanding the relevant anatomy and hemodynamics to guide procedural indication and planning. As with other structural interventions, consider a SENTINEL device (cerebral embolic protection system) to provide embolic protection in procedures that could lead to debris/embolic dislodgement when appropriate. Sinus venosus defects can be repaired via a transcatheter approach with a covered stent in the superior vena cava (SVC). Consider using 3D printing or 3D digital imaging when preparing for complex ACHD interventions. Notes- ACHD: Interventional Cardiology 1. When considering a patient for TPVR there are 3 types of landing zones for pulmonic valves in ACHD patients: Pulmonary conduits or homografts. These are typically seen in patients with TOF or prior Ross or Rastelli procedure. These may be calcified and stenotic and so pre-dilatation is often needed before valve replacement. Bioprosthetic Valves. (Valve in Valve TPVR) Native outflow tract 2. What are some of the more severe complications to consider when talking to an ACHD patient about a TPVR? Coronary artery compression Conduit rupture Vessel injury (including the pulmonary bed) Valve embolization Endocarditis 3. What are some of the hemodynamic measurements one would want to pay attention to in a patient with a Fontan heart? You will see higher CVPs in patients with a Fontan palliation. The CVP will typically be higher than your wedge pressure, as the circuit relies on passive transpulmonary blood flow. Evaluating the wedge pressure is crucial. Elevation may indicate arrythmias and or ventricular dysfunction. 4. When considering closing a fenestration of a Fontan circuit, what are the measurements that one would want to consider? You would want to temporarily occlude the fenestration with a balloon on a wedge catheter for 10-15 minutes roughly to observe the patient’s Fontan pressure/CVP, wedge pressure, arterial saturation, PA saturation, and systemic blood pressure. You may want to reconsider occlusion if there is a significant drop in systemic pressures or cardiac output; or significantly increased Fontan pressure/CVP. 5. What are the technical considerations to consider when occluding a fenestration in a Fontan circuit? You want to make sure there is no thrombus in the fenestration or Fontan circuit. Consider using the SENTINEL cerebral protection system/device (a device that can provide embolic protection from dislodged debris or emboli). However, this device is typically unable to be used in ACHD who have undergone a BTT shunt due to stenosis. 6. How does a transcatheter intervention help a sinus venosus defect? Placement of the covered stent in the SVC with a dilated portion into the right atrium creates the closure of the sinus venosus defect. The covered stent also helps with rerouting the anomalous pulmonary vein(s) posteriorly to drain into the left atrium. To learn more about PAPVR, enjoy Episode #106. Case Report: A Hole in the HFpEF Diagnosis. 7. What are some of the concerns to consider when closing a sinus venosus defect via a transcatheter approach? Plan for increased left atrial pressures and pulmonary venous pressures in older patients. This is due to your left heart using the sinus venosus defect as a pop-off mechanism before closure, especially in elderly patients with a small left ventricle or diastolic dysfunction. Once the sinus venosus defect is closed/fixed, the blood is no longer able to shunt over to the right atrium and so more blood returns to the (potentially low compliance) left system. You also must watch for pulmonary vein compression when placing your covered stent in the SVC. You also need to consider the length of your covered stent, as the superior portion of the stent needs to be well-anchored above the entry point of the anomalous pulmonary vein to prevent embolization. To counteract this, Dr. Aboulhosn suggests that before placing a covered stent in the SVC to fix the sinus venosus defect consider placing a catheter in the left atrium via the transeptal approach. This will then allow a wire to be placed from the left atrium into the most superior pulmonary veins for protection if there is any stenosis/compression after placing the covered stent in the SVC. The transeptal puncture will then serve as a small defect to allow for some mild left-to-right shunting and decompress the left atrium. The transeptal puncture typically endothelializes over time. References Stout KK, Daniels CJ, Aboulhosn JA, et al. 2018 AHA/ACC Guideline for the Management of Adults With Congenital Heart Disease: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines. Circulation. Apr 2 2019;139(14):e698-e800. https://www.ahajournals.org/doi/10.1161/CIR.0000000000000603 European Society of G, Association for European Paediatric C, German Society for Gender M, et al. ESC Guidelines on the management of cardiovascular diseases during pregnancy: the Task Force on the Management of Cardiovascular Diseases during Pregnancy of the European Society of Cardiology (ESC). European heart journal. Dec 2011;32(24):3147-3197. https://academic.oup.com/eurheartj/article/39/34/3165/5078465 Hansen, J. H., Duong, P., Jivanji, S. G., Jones, M., Kabir, S., Butera, G., ... & Rosenthal, E. (2020). Transcatheter correction of superior sinus venosus atrial septal defects as an alternative to surgical treatment. Journal of the American College of Cardiology, 75(11), 1266-1278. https://doi.org/10.1016/j.jacc.2019.12.070 Aboulhosn, J. A., Hijazi, Z. M., Kavinsky, C. J., McElhinney, D. B., Asgar, A. W., Benson, L. N., ... & Levi, D. S. (2020). SCAI position statement on adult congenital cardiac interventional training, competencies and organizational recommendations. Catheterization and cardiovascular interventions: official journal of the Society for Cardiac Angiography & Interventions, 96(3), 643-650. https://doi.org/10.1002/ccd.28885 Meet Our Collaborators! Adult Congenital Heart AssociationFounded in 1998, the Adult Congenital Heart Association is an organization begun by and dedicated to supporting individuals and families living with congenital heart disease and advancing the care and treatment available to our community. Our mission is to empower the congenital heart disease community by advancing access to resources and specialized care that improve patient-centered outcomes. Visit their website (https://www.achaheart.org/) for information on their patient advocacy efforts, educational material, and membership for patients and providers CHiP Network The CHiP network is a non-profit organization aiming to connect congenital heart professionals around the world. Visit their website (thechipnetwork.org) and become a member to access free high-quality educational material, upcoming news and events, and the fantastic monthly Journal Watch, keeping you up to date with congenital scientific releases. Visit their website (https://thechipnetwork.org/) for more information. Heart UniversityHeart University aims to be “the go-to online resource” for e-learning in CHD and paediatric-acquired heart disease.

Apr 30, 2023

The following question refers to Section 6.1 of the 2021 ESC CV Prevention Guidelines. The question is asked by Dr. Christian Faaborg-Andersen, answered first by Houston Methodist medicine resident Dr. Najah Khan, and then by expert faculty Dr. Eugenia Gianos.Dr. Gianos specializes in preventive cardiology, lipidology, cardiovascular imaging, and women’s heart disease; she is the director of Women s Heart Health at Lenox Hill Hospital and director of Cardiovascular Prevention for Northwell Health.The CardioNerds Decipher The Guidelines Series for the 2021 ESC CV Prevention Guidelines represents a collaboration with the ACC Prevention of CVD Section, the National Lipid Association, and Preventive Cardiovascular Nurses Association.Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. Question #23 An asymptomatic 55-year-old man with no past medical history presents to clinic after having a cardiac CT as part of an executive physical. His coronary artery calcium (CAC) score was 200 and the coronary CTA demonstrated isolated 70% stenosis of the left circumflex coronary artery. He is asymptomatic and able to jog 2 miles daily without limitation. He was recently started on aspirin 81 mg daily and atorvastatin 40 mg daily by his primary care provider. His LDL is 50 mg/dL, HbA1c is 6.0%. His BP is 108/70. What would you recommend?AStop aspirin 81 mg daily as he has not had an ASCVD event or revascularizationBCardiac catheterization and stent placement in the left circumflexCIncrease atorvastatin to 80 mg dailyDStress testENo change in management Answer #23 Answer choicesAStop aspirin 81 mg daily as he has not had an ASCVD event or revascularizationBCardiac catheterization and stent placement in the left circumflexCIncrease atorvastatin to 80 mg dailyDStress testENo change in managementExplanationThe correct answer is E – no change in management.Though the patient has not had an ASCVD event or revascularization, low-dose aspirin may be considered with definite evidence of CAD on imaging (Class IIb, LOE C).He is asymptomatic and does not have high risk anatomy on CT (i.e., proximal LAD, left main disease, multivessel disease), so percutaneous coronary intervention or stress testing are not indicated.His LDL is well controlled, so increasing atorvastatin would not be appropriate at this time.Main TakeawayAspirin 75-100 md daily may be considered in the absence of MI or revascularization when there is definitive evidence of CAD on imaging (Class IIb, LOE C).Guideline Loc.Section 6.1 CardioNerds Decipher the Guidelines - 2021 ESC Prevention SeriesCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor RollCardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron!

Apr 28, 2023

The following question refers to Section 5.1 of the 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure. The question is asked by Keck School of Medicine USC medical student & CardioNerds Intern Hirsh Elhence, answered first by Greater Baltimore Medical Center medicine resident / Johns Hopkins MPH student and CardioNerds Academy House Chief Dr. Alaa Diab, and then by expert faculty Dr. Biykem Bozkurt. Dr. Bozkurt is the Mary and Gordon Cain Chair, Professor of Medicine, Director of the Winters Center for Heart Failure Research, and an advanced heart failure and transplant cardiologist at Baylor College of Medicine in Houston, TX. She is former President of HFSA, former senior associate editor for Circulation, and current Editor-In-Chief of JACC Heart Failure. Dr. Bozkurt was the Vice Chair of the writing committee for the 2022 Heart Failure Guidelines. The Decipher the Guidelines: 2022 AHA / ACC / HFSA Guideline for The Management of Heart Failure series was developed by the CardioNerds and created in collaboration with the American Heart Association and the Heart Failure Society of America. It was created by 30 trainees spanning college through advanced fellowship under the leadership of CardioNerds Cofounders Dr. Amit Goyal and Dr. Dan Ambinder, with mentorship from Dr. Anu Lala, Dr. Robert Mentz, and Dr. Nancy Sweitzer. We thank Dr. Judy Bezanson and Dr. Elliott Antman for tremendous guidance. Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. Question #17 A 63-year-old man with CAD s/p CABG 3 years prior, type 2 diabetes mellitus, hypertension, obesity, and tobacco use disorder presents for routine follow-up. His heart rate is 65 bpm and blood pressure is 125/70 mmHg. On physical exam, he is breathing comfortably with clear lungs, with normal jugular venous pulsations, a regular rate and rhythm without murmurs or gallops, and no peripheral edema. Medications include aspirin 81mg daily, atorvastatin 80mg daily, lisinopril 20mg daily, and metformin 1000mg BID. His latest hemoglobin A1C is 7.5% and recent NT-proBNP was normal. His latest transthoracic echocardiogram showed normal biventricular size and function. Which of the following would be a good addition to optimize his medical therapy? A DPP-4 inhibitor B Dihydropyridine calcium channel blocker C SGLT2 inhibitor D Furosemide Answer #17 Explanation The correct answer is C: SGLT2 inhibitor. This patient is at risk for HF (Stage A) given absence of signs or symptoms of heart failure but presence of coronary artery disease and several risk factors including diabetes, hypertension, obesity, and tobacco smoking. At this stage, the focus should be on risk factor modification and prevention of disease onset. Healthy lifestyle habits such as maintaining regular physical activity; normal weight, blood pressure, and blood glucose levels; healthy dietary patterns, and not smoking have been associated with a lower lifetime risk of developing HF. Multiple RCTs in patients with type 2 diabetes who have established CVD or are at high risk for CVD, have shown that SGLT2i prevent HF hospitalizations compared with placebo. The benefit for reducing HF hospitalizations in these trials predominantly reflects primary prevention of symptomatic HF, because only approximately 10% to 14% of participants in these trials had HF at baseline. As such, in patients with type 2 diabetes and either established CVD or at high cardiovascular risk, SGLT2i should be used to prevent hospitalizations for HF (Class 1, LOE A). The mechanisms for the improvement in HF events from SGLT2i have not been clearly elucidated but seem to be independent of glucose lowering. Proposed mechanisms include reductions in plasma volume, cardiac preload and afterload, alterations in cardiac metabolism, reduced arterial stiffness, and interaction with the Na+/H+ exchanger. SGLT2i are generally well tolerated, but these agents have not been evaluated in those with severe renal impairment (estimated glomerular filtration rate [eGFR] <25 mL/min/1.73 m2). Main Takeaway It is important to identify patients who are at risk for HF (Stage A) and focus on risk factor optimization to prevent disease onset and progression. Guideline Loc. Section 5.1 Decipher the Guidelines: 2022 Heart Failure Guidelines Page CardioNerds Episode Page CardioNerds Academy Cardionerds Healy Honor Roll CardioNerds Journal Club Subscribe to The Heartbeat Newsletter! Check out CardioNerds SWAG! Become a CardioNerds Patron!

Apr 23, 2023

The following question refers to Section 4.6 of the 2021 ESC CV Prevention Guidelines. The question is asked by Student Dr. Shivani Reddy, answered first by Johns Hopkins Cardiology Fellow Dr. Rick Ferraro, and then by expert faculty Dr. Eileen Handberg. Dr. Handberg is an Adult Nurse Practitioner, Professor of Medicine, and Director of the Cardiovascular Clinical Trials Program in the Division of Cardiovascular Medicine at the University of Florida. She has served as Chair of the Cardiovascular Team Section and the Board of Trustees with the ACC and is the President for the PCNA. The CardioNerds Decipher The Guidelines Series for the 2021 ESC CV Prevention Guidelines represents a collaboration with the ACC Prevention of CVD Section, the National Lipid Association, and Preventive Cardiovascular Nurses Association. Question #22 Mr. HC is a 50-year-old man presenting for a routine clinic visit. He is not sure the last time he had a lipid panel drawn, and would like one today, but ate lunch just prior to your appointment – a delicious plate of 50% fruits and vegetables, 25% lean meats, and 25% whole grains as you had previously recommended. True or False: Mr. HC should return another day to obtain a fasting lipid panel. TRUE FALSE Answer #22 Answer choices TRUE FALSE Explanation This statement is False. A non-fasting lipid panel is appropriate for risk stratification and lipid evaluation in most patients per the ESC guidelines. While no level of evidence in provided in the ESC guidelines, this recommendation is consistent with AHA/ACC cholesterol guidelines, which have also largely moved away from fasting lipid panels for most patients and give a Class 1 (LOE B) recommendation to obtaining a fasting or nonfasting plasma lipid profile for ASCVD estimation and baseline LDL-C in adults 20 years of age or older. The ESC recommendation is based upon large trials showing that results of fasting and non-fasting panels are largely similar. This is similar to the AHA/ACC guidelines, which note non-fasting and fasting LDL-C change minimal over time following a normal meal, while HDL-C and tryiglycerides appear to have similar prognostic significance with cardiovascular outcomes in fasting or nonfasting states. A fasting lipid panel should be considered in those with hypertriglyceridemia, metabolic syndrome, and diabetes mellitus, as consumption of food or drink can have direct and immediate effects on TG and blood glucose values. Main Takeaway A non-fasting lipid panel is appropriate for the majority of patients undergoing lipid evaluation and cardiovascular risk stratification. Guideline Loc. Section 4.6.1 CardioNerds Decipher the Guidelines - 2021 ESC Prevention Series CardioNerds Episode Page CardioNerds Academy Cardionerds Healy Honor Roll CardioNerds Journal Club Subscribe to The Heartbeat Newsletter! Check out CardioNerds SWAG! Become a CardioNerds Patron!

Apr 19, 2023

The following question refers to Sections 11.3 of the 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure. The question is asked by Western Michigan University medical student and CardioNerds Intern Shivani Reddy, answered first by Johns Hopkins Osler internal medicine resident and CardioNerds Academy Fellow Dr. Justin Brilliant, and then by expert faculty Dr. Harriette Van Spall. Dr. Van Spall is Associate Professor of Medicine, cardiologist, and Director of E-Health at McMaster University. Dr Van Spall is a Canadian Institutes of Health Research-funded clinical trialist and researcher with a focus on heart failure, health services, and health disparities. The Decipher the Guidelines: 2022 AHA / ACC / HFSA Guideline for The Management of Heart Failure series was developed by the CardioNerds and created in collaboration with the American Heart Association and the Heart Failure Society of America. It was created by 30 trainees spanning college through advanced fellowship under the leadership of CardioNerds Cofounders Dr. Amit Goyal and Dr. Dan Ambinder, with mentorship from Dr. Anu Lala, Dr. Robert Mentz, and Dr. Nancy Sweitzer. We thank Dr. Judy Bezanson and Dr. Elliott Antman for tremendous guidance. Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. Question #16 Ms. Augustin is a 33 y/o G1P1 woman from Haiti who seeks counseling regarding family planning as she and her husband dream of a second child. Her 1st pregnancy 12 months ago was complicated by pre-eclampsia and peripartum cardiomyopathy (LVEF 35%). Thankfully she delivered a healthy baby via C-section. She has no other past medical history and is currently on losartan 25 mg daily and metoprolol succinate 200 mg daily. She has been asymptomatic. Which of the following statements is recommended to medically optimize Ms. Augustin prior to her 2nd pregnancy? A No medical optimization or preconception planning is needed as her 1st pregnancy resulted in a healthy infant. B Discontinue losartan and metoprolol with no other needed pregnancy planning C Change her medication regimen, consider repeat TTE, and provide patient-centered counseling regarding risk of a future pregnancy D Continue losartan and metoprolol and advise against repeat pregnancy Answer #16 Explanation The correct answer is C – change her medication regimen, consider repeat TTE, and provide patient-centered counseling regarding risk of a future pregnancy. Heart failure may complicate pregnancy either secondary to an existing pre-pregnancy cardiomyopathy or as a result of peripartum cardiomyopathy. In women with history of heart failure or cardiomyopathy, including previous peripartum cardiomyopathy, patient-centered counseling regarding contraception and the risks of cardiovascular deterioration during pregnancy should be provided (Class I, LOE C-LD) Peripartum cardiomyopathy (PPCM) is defined as systolic dysfunction, typically LVEF 30 years, African ancestry, multiparity, multigestation, preeclampsia/eclampsia, anemia, diabetes, obesity, and prolonged tocolysis. The pathogenesis of peripartum cardiomyopathy is complex and it is likely a multifactorial process. The combination of hemodynamic changes of pregnancy, inflammation of the myocardium, hormonal changes, genetic factors, and an autoimmune response have all been proposed as possible mechanisms and these may certainly be interrelated. While pregnancy is generally well-tolerated in women with cardiomyopathy and NYHA class I status pre-pregnancy, clinical deterioration can occur and so counseling and shared decision-making are important. In fact, the ROPAC study of pregnancy outcomes for women with structural heart disease showed that women with pre-pregnancy or previous peripartum CM had the highest mortality rate at 2.4%. Subsequent pregnancies for women with previous peripartum cardiomyopathy have been associated with further decreases in LV function, maternal death, and adverse fetal outcomes. LVEF < 50% prior to a subsequent pregnancy is the strongest prognostic determinant. Different strategies are needed to optimize the cardiovascular health of women with a prior history of PPCM before embarking on a subsequent pregnancy including pre-conception counseling regarding risk of subsequent pregnancies, pharmacologic strategies, and a multi-disciplinary approach to expectant management. Pre-conception counseling: can utilize cardiovascular risk tools including ZAHARA I and CARPREG II scores (which predict outcomes during pregnancy in women with prior heart disease) and obtain a baseline TTE prior to conception to inform shared decision making. Pharmacologic strategies: in women with HF or cardiomyopathy who are pregnant or currently planning for pregnancy, ACEi, ARB, ARNi, MRA, SGLT2i, ivabradine, and vericiguat should not be administered because of significant risks of fetal harm (Class 3: Harm, LOE C-LD). Beta blockers (preferably metoprolol), hydralazine, and nitrates are considered acceptable during pregnancy, when guided by multidisciplinary shared decision-making regarding benefits and potential risks. Diuretic dosing should be discussed (if applicable) to minimize the risk of placental hypoperfusion. A repeat TTE should be performed 3 months following changes in heart failure medicine regimen. Of note, postpartum women who breastfeed can start an ACEi (enalapril or captopril are preferred), and metoprolol remains the preferred beta blocker. Multidisciplinary care may include consultations with genetics, gynecology, and maternal-fetal medicine teams, as appropriate to the outcome of shared decision making. During pregnancy, for women with decompensated HF or evidence of hemodynamic instability antepartum, delivery planning will include obstetrics and maternal-fetal medicine, cardiac anesthesia, cardiology, and neonatology teams. Therefore, answer choice C is correct because pre-conception counseling is essential to guide pertinent discussions on risk stratification prior to subsequent pregnancies. Additionally, her medications need to be modified by discontinuing her ARB prior to conception. Choice A is incorrect because she is high risk for worsening cardiomyopathy and repeat preeclampsia in her next pregnancy. Choice B is incorrect because shared decision making and risk stratification prior to 2nd pregnancy are essential. Choice D is incorrect because, although she is at high risk for complications including worsening cardiomyopathy, preeclampsia/eclampsia, and neonatal demise, repeat pregnancy is not absolutely contraindicated and should be an informed decision after appropriate education within the construct of a multidisciplinary team. See Heart Failure and Pregnancy Infographic created by Dr. Alaa Diab, CardioNerds Academy Chief. Main Takeaway In summary, when a patient with history of peripartum cardiomyopathy is planning on a repeat pregnancy, patient-centered counseling regarding risks and management strategies should be provided with guidance from a multidisciplinary team and medications should be adjusted to balance GDMT for heart failure against risks to fetal development. Guideline Loc. Section 11.3, Table 30 Decipher the Guidelines: 2022 Heart Failure Guidelines PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron!

Apr 18, 2023

The CardioNerds Academy welcomes Dr. Melanie Sulistio to give the 2nd Annual Sanjay V. Desai Lecture in Medical Education to mark the graduation of the 2022 CardioNerds Academy Class. Join us as Dr. Sulistio and CardioNerds Academy Program Director Dr. Tommy Das discuss the humanity deficiency in medicine, and how the practice of compassionate assumption can lead us to be better physicians for our patients, our colleagues, our learners, and ourselves. Credit to rising CardioNerds Academy chiefs Dr. Rawan Amir, Dr. Kate Wilcox, Dr. Alaa Diab, and Dr. Gurleen Kaur for their terrific acting in this episode. Audio editing by CardioNerds academy intern, Pace Wetstein. Dr. Sanjay V Desai serves as the Chief Academic Officer, The American Medical Association and is the former Program Director of the Osler Medical Residency at The Johns Hopkins Hospital. Dr. Melanie Sulistio is an Associate Professor of Medicine in the Division of Cardiology at the University of Texas Southwestern. Additionally, she is an Associate Dean for Student Affairs and Distinguished Teaching Professor at the University of Texas Southwestern Medical School and co-chairs the ACC Internal Medicine Residency Program. She has a passion for medical education and promoting humanity in medicine, and is actively involved in the work of teaching communication skills that encompass meaningful care, discussions with patients, and difficult conversations with colleagues. Relevant disclosures: None CardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron!

Apr 14, 2023

CardioNerds join Dr. Samid Muhammad Farooqui, Dr. Hiba Hammad, and Dr. Syed Talal Hussain, from the University of Oklahoma Pulmonary and Critical Care Medicine Fellowship Program, in Oklahoma City. The fellows will take us in a fascinating discussion of a case of rapidly progressing dyspnea and pulmonary hypertension in a patient with metastatic breast cancer. They will then reveal an interesting etiology of pulmonary hypertension, where the secret was on the wedge! University of Oklahoma faculty and expert in pulmonary hypertension and right ventricular physiology, Dr. Roberto J. Bernardo provides the E-CPR for this episode. Audio editing by CardioNerds Academy Intern, Dr. Christian Faaborg-Andersen. A septuagenarian female, with a past medical history of metastatic breast adenocarcinoma, presented to the hospital with worsening dyspnea over a period of 3 weeks. She was found to be in rapidly progressive hypoxic respiratory failure with unremarkable chest x-ray, CTA chest, and V/Q scan. Transthoracic echocardiogram revealed elevated RVSP and a subsequent right heart catheterization showed pre-capillary pulmonary hypertension with a low cardiac index. She was treated for rapidly progressive RV dysfunction with inotropic support and inhaled pulmonary vasodilators until she decided to pursue comfort measures. Wedge cytology came back positive for malignant cells, confirming a diagnosis of Pulmonary Tumoral Thrombotic Microangiopathy (PTTM). CardioNerds is collaborating with Radcliffe Cardiology and US Cardiology Review journal (USC) for a ‘call for cases’, with the intention to co-publish high impact cardiovascular case reports, subject to double-blind peer review. Case Reports that are accepted in USC journal and published as the version of record (VOR), will also be indexed in Scopus and the Directory of Open Access Journals (DOAJ). CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Case Media - When Tumors Take Your Breath Away - University of Oklahoma College of Medicine Pearls - When Tumors Take Your Breath Away - University of Oklahoma College of Medicine Pulmonary arterial hypertension (PAH) is a progressive disorder of the pulmonary vasculature, characterized by progressive obliteration and remodeling of the pulmonary circulation, resulting in increased pulmonary vascular resistance and increased right ventricular (RV) wall stress, abnormal right ventricular mechanics, and eventually RV dysfunction and death. Pulmonary hypertension (PH) is divided into pre-capillary and post-capillary profiles, where pre-capillary PH is hemodynamically characterized by a mean pulmonary artery pressure (mPAP) > 20 mmHg, pulmonary artery wedge pressure (PAWP) ≤ 15 mmHg and a pulmonary vascular resistance (PVR) ≥ 3 Woods Units (WU), and post-capillary PH is defined as mPAP > 20 mmHg, PAWP ≥ 15 mmHg, and PVR can be either < 3 WU (isolated post-capillary PH) or ≥ 3 WU (combined pre- and post-capillary PH). Pulmonary arterial hypertension (PAH) falls under the pre-capillary PH profile. Dyspnea on exertion is the most common manifestation of PH, and the most common initial complain. Other symptoms and physical findings such as venous congestion, peripheral edema, signs of RV dysfunction or syncope present later in the disease course. As such, PH has to be considered in the differential diagnosis of dyspnea, especially in cases of undifferentiated or unexplained dyspnea. PAH is a chronic but progressive condition, where symptoms progress over the course of months to years. Subacute or rapidly progressive forms of PH (symptoms rapidly worsening over the course of weeks) should warrant consideration for alternative etiologies (i.e., pulmonary embolism or a different cardiopulmonary disorder as the main driver of symptoms), or unique rapidly progressive phenotypes of PAH such as pulmonary tumor thrombotic microangiopathy (PTTM). PH in the setting of malignancy warrants special consideration, where the pulmonary vascular disorder could be related to venous thromboembolic disease, external compression of the pulmonary vasculature (if the tumor directly compresses mediastinal structures), related to chemotherapeutic agents (such as tyrosine kinase inhibitors) or thoracic radiotherapy (ie. fibrosing mediastinitis), or related to tumor emboli per se, such as in PTTM. PTTM is a unique manifestation of PH in the setting of malignancy, known to be rapidly progressive, associated with poor RV adaptation, and almost universally fatal. The confirmatory testing of PTTM is by pathology (autopsy), although as in our case, sometimes tumor cells can be identified during cytology of pulmonary artery wedge samples. Show Notes - When Tumors Take Your Breath Away - University of Oklahoma College of Medicine 1. How do you approach dyspnea? Dyspnea is a subjective sensation of uncomfortable breathing. It can be caused by pathologies in cardiac, pulmonary, neuromuscular systems as well as in systemic illnesses. Dyspnea is also a manifestation of psychogenic disorders. Presentation of dyspnea can be divided into acute and chronic forms and the etiology can be identified by a thorough evaluation. A detailed history and physical exam can help identify the organ system involved. Certain physical signs can be suggestive of the culprit organ system e.g., lower extremity edema in congestive heart failure, increased antero-posterior diameter of the chest in obstructive lung disease, etc. Imaging modalities can be very helpful in determining the cause of dyspnea. Chest radiographs, CT scans of the chest, and echocardiograms can help identify the etiology of dyspnea. Additionally, other testing like pulmonary functions tests can be used too. 2. What are the different Pulmonary Hypertension groups? Pulmonary Hypertension (PH) is divided into 5 main groups in the WHO classification, as follows: Group IPulmonary Arterial Hypertension (PAH) Idiopathic, heritable, drugs, congenital heart disease, liver disease, connective tissue disease, toxins, anorexigens among other causesGroup IIPH due to Left Heart DiseaseLeft sided heart failure, valvular pathologyGroup IIIPH due to Lung DiseaseCOPD, Interstitial Lung Disease, Sleep ApneaGroup IVPH due to Chronic Thromboembolic DiseasePulmonary emboliGroup VPH due to Other CausesSarcoidosis, ESRD, Sickle Cell Anemia, Chronic Hemolytic Anemia, Certain Metabolic Disorders 3. How do you approach a patient with Pulmonary Hypertension? The goal is to discover an identifiable etiology for proper classification of pulmonary hypertension according to the WHO groups, in order to guide prognostication and management. A thorough history and physical exam is the first step in the diagnosis of pulmonary hypertension. Exertional dyspnea is the most common presenting symptom. Due to the nonspecific symptoms, there is often a delay in the diagnosis. Other symptoms include chest pain, fatigue, edema. In severe cases, patients may have syncopal episodes. Physical Exam findings concerning for pulmonary hypertension include signs of volume overload (i.e., edema, elevated JVP). Cardiac auscultation may reveal a loud P2 component. Laboratory workup includes basic assessment of hematology along with testing for HIV and serological markers of connective tissue diseases. Biomarkers of cardiovascular system like BNP are important in identification and prognostication of pulmonary hypertension. Radiological studies like chest radiographs, CT scans of the chest and ventilation/perfusion scans of the lung are used to identify pulmonary pathologies and the presence of thromboembolic disease respectively. Echocardiographic assessments are important for diagnosis and assessment of pulmonary hypertension. It allows for the assessment of the left side as well as a detailed analysis of the right side which has diagnostic and prognostic value. Finally, the gold standard for diagnosis is a right heart catheterization, which allows for accurate measurements of the pressure in the different chambers of the heart and allows for the phenotyping of pulmonary hypertension. 4. What are the considerations for Pulmonary Hypertension etiologies in patient with malignancy? How is Pulmonary Tumoral Thrombotic Microangiopathy diagnosed? Pulmonary hypertension in a patient with malignancy requires special attention. Apart from the common reasons for pulmonary hypertension, use of chemotherapeutic agents has been associated with the development of pulmonary arterial hypertension, particularly with Tyrosine Kinase Inhibitors. Pulmonary Veno-Occlusive Disease (PVOD) can be precipitated by the use of many chemotherapeutic agents especially alkylating agents. Detrimental effects of chemotherapeutic agents on myocytes can cause Group II pulmonary hypertension. Chemotherapy and radiation therapy induced lung damage can also cause Group III pulmonary hypertension. Large tumors may directly compress mediastinal structures causing elevated pulmonary pressures due to external compression. In patients with adenocarcinoma, tumoral thrombotic microangiopathy can result in sub-acute pulmonary hypertension known as Pulmonary Tumoral Thrombotic Microangiopathy (PTTM). PTTM results in rapid clinical deterioration and hence requires a high suspicion of index. It is mostly diagnosed postmortem, but can be diagnosed by performing wedge cytology. 5. What is the prognosis of PTTM and how is it treated? PTTM carries a grave prognosis. It causes accelerated occlusion of pulmonary arteries resulting in acute to subacute pulmonary hypertension and ensuing RV dysfunction and failure.

Apr 11, 2023

The following question refers to Section 4.4 of the 2021 ESC CV Prevention Guidelines. The question is asked by Dr. Maryam Barkhordarian, answered first by medicine resident Dr. Ahmed Ghoneem, and then by expert faculty Dr. Noreen Nazir. Dr. Nazir is Assistant Professor of Clinical Medicine at the University of Illinois at Chicago, where she is the director of cardiac MRI and the preventive cardiology program. The CardioNerds Decipher The Guidelines Series for the 2021 ESC CV Prevention Guidelines represents a collaboration with the ACC Prevention of CVD Section, the National Lipid Association, and Preventive Cardiovascular Nurses Association. Question #21 Ms. J is a 57-year-old woman with a past medical history of myocardial infarction resulting in ischemic cardiomyopathy, heart failure with reduced ejection fraction, and major depressive disorder who presents today for follow-up. She reports feeling extremely overwhelmed lately due to multiple life stressors. She is on appropriate cardiovascular GDMT agents and is not prescribed any medications for her mood disorder. True or false: in addition to psychotherapy for stress management, it is appropriate to consider Ms. J for anti-depressant SSRI pharmacotherapy at this time to improve cardiovascular outcomes. A True B False Answer #21 Explanation The correct answer is FALSE. An ESC class 3 recommendation states that SSRIs, SNRIs, and tricyclic antidepressants are not recommended in patients with heart failure and major depression; this is based on data suggesting potential lack of SSRI efficacy for reducing depression or cardiovascular events, as well as safety data indicating an association between SSRI use and increased risk of CV events and all-cause as well as cardiovascular mortality among HF patients. Mental health disorders are associated with worse outcomes in patients with ASCVD and appropriate treatment effectively reduces stress symptoms and improves quality of life. Nonpharmacologic modalities of treatment (exercise therapy, psychotherapy, collaborative care) should be considered before pharmacotherapy to improve cardiovascular outcomes in patients with heart failure. Of note, the ESC suggests SSRI treatment be considered for patients with coronary heart disease (without HF) and moderate-to-severe major depression based on data that SSRI treatment is associated with lower rates of CHD readmission (RR 0.63), all-cause mortality (RR 0.56), and the composite endpoint of all-cause mortality/MI/PCI (HR 0.69) vs. no treatment. This is a class 2a recommendation. ESC also gives a class 2a recommendation to consider referral to psychotherapeutic stress management for individuals with stress and ASCVD to improve CV outcomes and reduce stress symptoms. The ACC/AHA guidelines do not provide focused recommendations regarding mental health considerations in patients with elevated cardiovascular risk. Main Takeaway It is important to consider mental health treatment in patients with ASCVD as mental disorders are associated with increased CVD risk and poor patient prognosis, and data support that mental health interventions can improve overall and CVD outcomes, as well as improve quality of life. Guideline Loc. Section 4.4 CardioNerds Decipher the Guidelines - 2021 ESC Prevention Series CardioNerds Episode Page CardioNerds Academy Cardionerds Healy Honor Roll CardioNerds Journal Club Subscribe to The Heartbeat Newsletter! Check out CardioNerds SWAG! Become a CardioNerds Patron!

Apr 11, 2023

The following question refers to Section 10.1 of the 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure. The question is asked by Western Michigan University medical student and CardioNerds Intern Shivani Reddy, answered first by Boston University cardiology fellow and CardioNerds Ambassador Dr. Alex Pipilas, and then by expert faculty Dr. Ileana Pina.Dr. Pina is Professor of Medicine and Quality Officer for the Cardiovascular Line at Thomas Jefferson University, Clinical Professor at Central Michigan University, and Adjunct Professor of Biostats and Epidemiology at Case Western University. She serves as Senior Fellow and Medical Officer at the Food and Drug Administration’s Center for Devices and Radiological Health.The Decipher the Guidelines: 2022 AHA / ACC / HFSA Guideline for The Management of Heart Failure series was developed by the CardioNerds and created in collaboration with the American Heart Association and the Heart Failure Society of America. It was created by 30 trainees spanning college through advanced fellowship under the leadership of CardioNerds Cofounders Dr. Amit Goyal and Dr. Dan Ambinder, with mentorship from Dr. Anu Lala, Dr. Robert Mentz, and Dr. Nancy Sweitzer. We thank Dr. Judy Bezanson and Dr. Elliott Antman for tremendous guidance.Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. Question #15 Mrs. Framingham is a 65-year-old woman who presents to her cardiologist’s office for stable angina and worsening dyspnea on minimal exertion. She has a history of non-insulin dependent type 2 diabetes mellitus and hypertension. She is taking metformin, linagliptin, lisinopril, and amlodipine. Blood pressure is 119/70 mmHg. Labs are notable for a hemoglobin of 14.2 mg/dL, iron of 18 mcg/dL, ferritin 150 ug/L, transferrin saturation 15%, and normal creatine kinase. An echocardiogram shows reduced left ventricular ejection fraction of 25%. Coronary angiography shows obstructive lesions involving the proximal left anterior descending, left circumflex, and right coronary arteries. In addition to optimizing GDMT, which of the following are recommendations for changes in management? A Anticoagulation, percutaneous revascularization, and IV iron B A change in her diabetic regimen, percutaneous revascularization, and PO iron C A change in her diabetic regimen, surgical revascularization, and IV iron D A change in her diabetic regimen, medical treatment alone for CAD, and PO iron E Anticoagulation and surgical revascularization Answer #15 Explanation The correct answer is C – a change in her diabetic regimen, surgical treatment and IV iron. Multimorbidity is common in patients with heart failure. More than 85% of patients with HF also have at least 2 additional chronic conditions, of which the most common are hypertension, ischemic heart disease, diabetes, anemia, chronic kidney disease, morbid obesity, frailty, and malnutrition. These conditions can markedly impact patients’ tolerance to GDMT and can inform prognosis. Not only was Mrs. F found with HFrEF (most likely due to ischemic cardiomyopathy), but she also suffers from severe multi-vessel coronary artery disease, hypertension, and non-insulin dependent type 2 diabetes mellitus. In addition to starting optimized GDMT for HF, specific comorbidities in the heart failure patient warrant specific treatment strategies. Mrs. Framingham would benefit from a change in her diabetic regimen, namely switching from linagliptin to an SGLT2 inhibitor (e.g., empagliflozin, dapagliflozin). In patients with HF and type 2 diabetes, the use of SGLT2i is recommended for the management of hyperglycemia and to reduce HF related morbidity and mortality (Class 1, LOE A). Furthermore, as she has diabetes, symptomatic severe multi-vessel CAD, and LVEF≤35%, surgical revascularization with coronary artery bypass grafting is warranted to improve symptoms, cardiovascular hospitalizations, and long-term all-cause mortality (Class 1, LOE B-R). Given the severity of her coronary disease, presence of diabetes mellitus, and coronary anatomy suitable for bypass, percutaneous (i.e., PCI) or medical treatment alone are inappropriate (options B, D). Although she does not have anemia, she may benefit from IV iron. IV iron supplementation has been shown in the FAIR-HF, IRONOUT HF, and AFFIRM-AHF trials to significantly improve NYHA functional class, 6-minute walk test, quality of life, and decrease hospitalizations for HF, independently of anemia. These effects were not seen with iron given orally (options B, D). Iron deficiency is usually defined as ferritin level <100 μg /L or 100 to 300 μg/L, if the transferrin saturation is <20%. Therefore, in patients with HFrEF and iron deficiency with or without anemia, intravenous iron replacement is reasonable to improve functional status and QOL (Class 2a, LOE B-R). Although HF is a pro-thrombotic state, anticoagulation is not warranted empirically in Mrs. F, who has no evidence of thrombus or high-risk features suggesting impending thrombus (options A, E). Main Takeaway In summary, multimorbidity is frequent in heart failure patients and treatment targeted to specific morbidities is warranted. In patients with heart failure and diabetes, an SGLT2 inhibitor should be part of the medication regimen. Intravenous iron supplementation should be considered in iron-deficient patients independent of anemia. In patients with heart failure with LVEF≤35% and severe coronary artery disease with suitable anatomy, coronary artery bypass grafting is recommended. Guideline Loc. Section 10.1, Figure 14 Decipher the Guidelines: 2022 Heart Failure Guidelines PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron!

Apr 10, 2023

CardioNerds Amit Goyal, Dr. Colin Blumenthal, Dr. Kelly Arps and Dr. Justice Oranefo discuss mechanical stroke prevention in atrial fibrillation with Dr. Christopher Ellis, cardiac electrophysiology lab director and director of the left atrial appendage closure program at Vanderbilt University. There has been a significant increase in the number of patients undergoing left atrial appendage occlusion (LAAO). This trend is expected to continue with current and upcoming clinical data on this topic. In this episode we dive into the rationale behind LAAO and explore several historical facts. We then proceed to the current state of practice including currently available options, appropriate indications, post op care, and potential complications. Notes were drafted by Dr. Justice Oranefo. Audio editing by CardioNerds Academy Intern, student doctor Chelsea Amo Tweneboah. This CardioNerds Atrial Fibrillation series is a multi-institutional collaboration made possible by contributions of stellar fellow leads and expert faculty from several programs, led by series co-chairs, Dr. Kelly Arps and Dr. Colin Blumenthal. This series is supported by an educational grant from the Bristol Myers Squibb and Pfizer Alliance. All CardioNerds content is planned, produced, and reviewed solely by CardioNerds. We have collaborated with VCU Health to provide CME. Claim free CME here! Disclosures: Dr. Ellis discloses grant or research support from Boston Scientific, Abbott-St Jude, advisor for Atricure and Medtronic. CardioNerds Atrial Fibrillation PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls and Quotes - Atrial Fibrillation: Mechanical Stroke Prevention in Atrial fibrillation Surgical or catheter based left atrial appendage occlusion results in mechanical exclusion of the left atrial appendage, which is the most common source of thrombus leading to embolic events in patients with non-rheumatic atrial fibrillation. Surgical LAAO should be considered in patients with atrial fibrillation and CHA2DS2VASC score ≥ 2 undergoing cardiac surgery for other indications. Endocardial LAAO devices such as WATCHMAN FLX and AMULET are approved for stroke prevention in patients with atrial fibrillation with a CHA2DS2VASC score ≥ 2 and have an appropriate reason to seek a non-drug alternative to anticoagulation therapy. Appropriate patient selection and post-operative anticoagulation and imaging strategy are crucial for prevention and management of complications related to LAAO. Notes - Atrial Fibrillation: Mechanical Stroke Prevention in Atrial fibrillation What are the types of LAAO device? Left atrial appendage occlusion devices can be divided into epicardial closure and endocardial closure. Epicardial techniques/devices include surgical ligation, Atriclip, and Lariat. These techniques require pericardial access (either by open thoracotomy or thoracoscopic access). The goals are complete exclusion and ischemic necrosis of the LAA. LARIAT device Atriclip device Endocardial techniques include WATCHMAN FLX and AMULET devices. These techniques require the use of nitinol-based devices which are delivered into the LAA via a transeptal approach. These devices become endothelialized over time resulting in occlusion of the LAA. AMULET device WATCHMAN FLX Who is the ideal candidate for surgical LAAO? Several studies have evaluated the efficacy of surgical LAA occlusion. The most prominent being the LAOS III trial which randomized 4770 patients with atrial fibrillation and CHA2DS2VASC ≥ 2 undergoing cardiac surgery for other reasons to surgical LAAO vs no LAAO (3,4). The primary outcome of ischemic stroke or systemic embolization occurred in 4.8% of patients in the LAAO group vs 7% of patients in control group over an average follow-up of 3.8 years. Though patients were randomized to LAAO, there was no requirement to stop anticoagulation and this difference was seen despite 75% of patients continuing anticoagulation. Additionally, there was no significant difference in operation time and bleeding complications. Based on these findings, LAAO should be considered in patients with atrial fibrillation undergoing cardiac surgery for other reasons regardless of the anticipated anticoagulation strategy. This ability to perform surgical LAAO requires safe access to the pericardial space. For this reason, conditions that create pericardial adhesions (e.g., prior cardiac surgery, chest radiation or trauma, multiple prior ablations) can limit the ability to perform surgical LAAO. Who is the ideal candidate for endocardial LAAO? Several randomized controlled trials and cohort studies have evaluated the utility of both the AMULET and WATCHMAN devices in stroke prevention with the most notable being the PREVAIL, PROTECT AF, and AMULET IDE trials (5,6,7,8,9,10). Based on the available data, these devices are indicated for stroke prevention in patients with non-valvular atrial fibrillation, a CHA2DS2VASC score ≥ 2 and an appropriate reason to seek a non-drug alternative to anticoagulation therapy. A classic example is a patient with recurrent GI bleeding despite multiple attempts to tolerate anticoagulation. These devices can also be considered in patients with high-risk professions suck as police officers or fire fighters. Several individual factors also affect the feasibly of endocardial LAAO. A suitable LAA anatomy is necessary for safe device implant (13). Other important considerations are nickel allergy (consider formal allergy testing in patients with suspected nickel allergy), surgical repair of the atrial septum, and severe kyphoscolisis (making adequate transeptal access difficult). There is no strong data comparing LAAO to DOAC in patients without high bleeding risk, however this question is being studied in 2 ongoing trials, CHAMPION AF (WATCHMAN FLX) and CATALYST (AMULET). What are the complications of LAAO? Surgical LAAO is safe and effective when there is complete occlusion of the LAA, however, historically ~ 20-30% are unsuccessful due to incomplete occlusion. More modern surgical techniques including confirmation with intra-operative transesophageal echocardiogram and the Atriclip have demonstrates a higher rate of success. Though the addition of a LAAO has not been shown to add significant time or risk to an already planned cardiac surgery, this requires a patient to already have an indication for surgery and carries the associated risks of that procedure. Endocardial LAAO has the advantage of being minimally invasive, but procedural complications such as cardiac tamponade, bleeding, and stroke can occur. More recent data has shown a < 1% procedural risk with the WATCHMAN FLX device. Other post procedural complications of endocardial LAAO devices include peridevice leak (~ 10% incidence; leaks ≥ 3mm are associated with an increased risk of stroke) and device related thrombus (DRT; 2-3% incidence). Device embolism is rare but carries potentially devastating consequences (12). What is the anticipated post operative care following LAAO? Post operative care with surgical LAAO is predominently dictated by the primary indication for surgery. Due to the high incidence incomplete exclusion, an intra or post-operative TEE is necessary to document complete LAA occlusion. As for anticoagulation, there is no current randomized control trial data that supports using surgical LAAO as an alternative to AC. As previously discussed, a lower incidence of stroke was seen in the LAOS III trial, but this trial specifically studied using surgical LAAO as an adjunct to OAC, not as a replacement. With endocardial LAAO, appropriate patient and device selection as well as adequate post-operative care is crucial to maximize safety and efficacy. Patients must be able to tolerate some degree of short-term anticoagulation with the goal to safely transition to single anti-platelet therapy while minimizing the risk of stroke and bleeding. This involves OAC for at least 45 days followed by aspirin monotherapy if no DRT or peridevice leak is seen on post-op imaging. DAPT (aspirin and clopidogrel) can be used instead of OAC in the early phase however there is not strong data for this strategy (11). Post-op imaging (TEE or CTA) is required approximately ~45 days, 6 months, and 1 year after the procedure. In patients who have undergone LAAO, LAA imaging is recommended prior to cardioversion, however, in the absence of DRT or device leaks anticoagulation is not necessary post cardioversion (14,15). References Belcher, J.R. & Somerville, W., 1955. Systemic Embolism and Left Auricular Thrombosis in Relation to Mitral Valvotomy. British Medical Journal, 2(4946), pp.1000–1003. Blackshear, J.L. & Odell, J.A., 1996. Appendage obliteration to reduce stroke in cardiac surgical patients with atrial fibrillation. The Annals of thoracic surgery, 61(2), pp.755–759. Friedman, D.J. et al., 2018. Association Between Left Atrial Appendage Occlusion and Readmission for Thromboembolism Among Patients With Atrial Fibrillation Undergoing Concomitant Cardiac Surgery. JAMA : the journal of the American Medical Association, 319(4), pp.365–374. Whitlock, R.P. et al., 2021. Left Atrial Appendage Occlusion during Cardiac Surgery to Prevent Stroke. The New England journal of medicine, 384(22), pp.2081–2091. Reddy, V.Y. et al., 2014. Percutaneous Left Atrial Appendage Closure vs Warfarin for Atrial Fibrillation: A Randomized Clinical Trial. JAMA : the journal of the American Medical Association, 312(19), pp.1988–1998. Belgaid, D.R. et al., 2016.

Apr 5, 2023

It’s another session of CardioNerds Rounds! In these rounds, Dr. Jenna Skowronski (Chief FIT at University of Pittsburgh) and Dr. Natalie Stokes (Formerly FIT at University of Pittsburgh and now General Cardiology Faculty at University of Pittsburgh) join transformational leader, educator and researcher, Dr. Mary Norine Walsh (Director of Heart Failure and Transplantation at Ascension St. Vincent Heart Center and Program Director of AHFT at St. Vincent) to discuss cardio-obstetrics and heart failure cases. Amongst her many accomplishments, Dr. Walsh is past president of the American College of Cardiology, Deputy Editor of JACC Case Reports, and a preeminent voice and thought leader in women’s cardiovascular health. Audio editing by CardioNerds academy intern, Pace Wetstein. This episode is supported with unrestricted funding from Zoll LifeVest. A special thank you to Mitzy Applegate and Ivan Chevere for their production skills that help make CardioNerds Rounds such an amazing success. All CardioNerds content is planned, produced, and reviewed solely by CardioNerds. Case details are altered to protect patient health information. CardioNerds Rounds is co-chaired by Dr. Karan Desai and Dr. Natalie Stokes. CardioNerds Rounds PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Show notes - Cardio-Obstetrics and Heart Failure Case 1 Synopsis: A woman in her earlier 30s, G1P1, with a history significant for peripartum cardiomyopathy presents to clinic for pre-conception counseling. Her prior pregnancy was in her late 20s with an uneventful pre-natal course and a spontaneous vaginal delivery at 37w2d. Two weeks after delivery, she experienced symptoms of heart failure and was found to have a new diagnosis of HFrEF. At that time TTE showed LVEF 30-35%, LVIDd 5.1cm (top normal size), diffuse hypokinesis. At that time, she was diuresed and discharged on metoprolol succinate 25mg po daily and furosemide 20mg po daily. She had one follow up visit 6 months postpartum and the furosemide was discontinued. Today in your office, she has NYHA Class I symptoms with no signs of symptoms of congestion. She walks daily and does vigorous exercise 1-2 times per week, while remaining on metoprolol. Repeat TTE with LVEF 45-50% and similar LV size. She would like to have another child and was referred to you for counseling. Case 1 Rounding Pearls: Dr. Walsh discussed extensively the importance of full GDMT in this patient who was initially undertreated with only a beta blocker. If patients are breastfeeding, clinicians should consider the addition of ACE-Inhibitor and Spironolactone. Otherwise, if not breastfeeding, they should receive maximally tolerated doses of full GDMT. For more details on medical therapy for Heart Failure during pregnancy and after, refer to this previous CardioNerds Episode with Dr. Julie Damp. Patients with peripartum cardiomyopathy are at highest risk of worsening LV systolic function when they have persistent LV systolic dysfunction from their initial diagnosis. In this circumstance, shared decision making is paramount. These patients should receive counseling on contraception and risk of pregnancy on worsening LV function, death, & fetal demise. In addition, counseling includes discussing with patients limited options in some states for complete, comprehensive reproductive care, including pregnancy termination. If patients with prior peripartum cardiomyopathy do become pregnant, a team-based approach including cardiologists, maternal fetal medicine, and obstetrics (amongst other team members) is essential to determine care & delivery timing/method. These patients should also be examined for signs of decompensation throughout the pregnancy, including rales, S3 or a reported history of PND. For more about pregnancy physiology and signs of Heart Failure in pregnancy, refer to this previous episode with Dr. Garima Sharma. Case 2 Synopsis: A woman in her early 30s, G4P2022, with a history significant for polysubstance use disorder is transferred to your hospital POD #0 from an emergent C-section at 37w in cardiogenic shock. She presented to the local hospital with cough, dyspnea, and abdominal pain and urine toxicology was positive for methamphetamines. During evaluation she went into an SVT that was treated with metoprolol and was complicated by fetal decelerations. TTE showed LVEF 15%, LV dilation, and RV dysfunction. Given the fetal decelerations she had an emergent C-Section. We discussed her management as she progressed into SCAI Stage E Cardiogenic Shock. Case 2 Rounding Pearls: The etiology of cardiomyopathy in this patient could be tachycardia induced, peripartum, toxic, or familial. A full evaluation is essential to determine if anything is reversible. SVT ablation could be considered if this was felt to be a driver. Approaches to durable mechanical circulatory support (MCS) such as a durable LVAD in patients with polysubstance use disorders are institution specific. Multidisciplinary input should be sought, including cardiology, cardiothoracic surgery, social work, nursing, nutrition, palliative care, and pharmacy. Consideration of temporary MCS as a bridge to transplant vs durable MCS should be considered again on a case-by-case basis, keeping in mind the current transplant allocation system that has made those patients with durable LVAD less likely to receive a transplant. We have previously discussed cases on the CardioNerds podcast that reflect this nuance. Consider listening again to these episodes from the CardioNerds team at Medical College Wisconsin and the University of Pennsylvania. Infographic by CardioNerds Academy Chief of House Jones (2023) Dr. Alaa Diab References - Cardio-Obstetrics and Heart Failure Bauersachs J, Arrigo M, Hilfiker-Kleiner D, et al. Current management of patients with severe acute peripartum cardiomyopathy: practical guidance from the Heart Failure Association of the European Society of Cardiology Study Group on peripartum cardiomyopathy. Eur J Heart Fail. 2016;18(9):1096-1105. doi:10.1002/ejhf.586 Bauersachs J, König T, van der Meer P, et al. Pathophysiology, diagnosis and management of peripartum cardiomyopathy: a position statement from the Heart Failure Association of the European Society of Cardiology Study Group on peripartum cardiomyopathy. Eur J Heart Fail. 2019;21(7):827-843. doi:10.1002/ejhf.1493 Davis MB, Arany Z, McNamara DM, Goland S, Elkayam U. Peripartum Cardiomyopathy: JACC State-of-the-Art Review. J Am Coll Cardiol. 2020;75(2):207-221. doi:10.1016/j.jacc.2019.11.014 Writing Committee Members; ACC/AHA Joint Committee Members. 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure. J Card Fail. 2022;28(5):e1-e167. doi:10.1016/j.cardfail.2022.02.010 Production Team Karan Desai, MD Natalie Stokes, MD Amit Goyal, MD Daniel Ambinder, MD

Apr 5, 2023

The following question refers to Section 3.4 of the 2021 ESC CV Prevention Guidelines. The question is asked by student Dr. Adriana Mares, answered first by Brigham & Women’s medicine intern & Director of CardioNerds Internship Dr. Gurleen Kaur, and then by expert faculty Dr. Michael Wesley Milks. Dr. Milks is a staff cardiologist and assistant professor of clinical medicine at the Ohio State University Wexner Medical Center where he serves as the Director of Cardiac Rehabilitation and an associate program director of the cardiovascular fellowship. He specializes in preventive cardiology and is a member of the American College of Cardiology's Cardiovascular Disease Prevention Leadership Council. The CardioNerds Decipher The Guidelines Series for the 2021 ESC CV Prevention Guidelines represents a collaboration with the ACC Prevention of CVD Section, the National Lipid Association, and Preventive Cardiovascular Nurses Association. Question #20 Ms. Ruma Toid is a 65-year-old African American woman who presents to your clinic in Ohio for routine follow up. She has a history of rheumatoid arthritis, hypertension, obesity, and sleep apnea. Her medications include methotrexate and atenolol. Her blood pressure in the office is 120/80 mmHg, heart rate 68 bpm, and oxygen saturation 99% on room air. Recent lipid testing revealed total cholesterol 165 mg/dL, HDL 42 mg/dL, and LDL 118 mg/dL. She was recently advised to talk to her doctor about taking a statin due to her risk factors but in the past has heard negative things about those medications and would like your advice on next steps. Her calculated ASCVD risk score based on the Pooled Cohort Equation is 7%. Which of the following choices would be the next step?AShe is at borderline risk for ASCVD events. A statin is not indicated at this time.BDue to her history of rheumatoid arthritis, her calculated ASCVD risk should be multiplied by 1.5, yielding an ASCVD risk of 10.5% placing her in the intermediate risk category. Moderate intensity statin would be indicated.CWhen other risk factors are present, rheumatoid arthritis is no longer an enhancing risk factor.DStatins are contraindicated when taking methotrexate. Answer #20 ExplanationThe correct answer is B. Due to her history of rheumatoid arthritis, her calculated ASCVD risk should be multiplied by 1.5, yielding an ASCVD risk of 10.5% placing her in the intermediate risk category. Moderate intensity statin would be indicated. Due to her history of rheumatoid arthritis, her calculated ASCVD risk should be multiplied by 1.5, yielding an ASCVD risk of 10.5% placing her in the intermediate risk category. Moderate intensity statin would be indicated. The ESC gives a Class IIa (LOE B) indication to multiply the calculated total CVD risk by a factor of 1.5 in adults with rheumatoid arthritis due to the observed 50% increased CVD risk in patients with rheumatoid arthritis. This 50% increase in CVD risk attributed to RA is present beyond traditional risk factors, making answer choice C wrong. Answer A is incorrect because when borderline risk is calculated, one should still look for risk enhancers that could potentially increase ASCVD risk before final determination of statin indication. Answer choice D is false as there is no contraindication to take both methotrexate and statins together. Note that it is appropriate to use the pool cohort equations and American risk thresholds for this patient since she is in America where the PCE was validated (versus using SCORE2 risk model which would be more appropriate for European populations).Main TakeawayInflammatory conditions including rheumatoid arthritis and inflammatory bowel disease increase a person’s risk for ASCVD events. Specifically for rheumatoid arthritis, there is a Class IIa indication to multiply the calculated risk score by 1.5 to account for rheumatoid arthritis as a risk enhancer.Guideline Loc.Section 3.4.6 CardioNerds Decipher the Guidelines - 2021 ESC Prevention SeriesCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor RollCardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron!

Apr 4, 2023

The following question refers to Section 9.5 of the 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure. The question is asked by Keck School of Medicine USC medical student & CardioNerds Intern Hirsh Elhence, answered first by Duke University cardiology fellow and CardioNerds FIT Ambassador Dr. Aman Kansal, and then by expert faculty Dr. Javed Butler. Dr. Butler is an advanced heart failure and transplant cardiologist, President of the Baylor Scott and White Research Institute, Senior Vice President for the Baylor Scott and White Health, and Distinguished Professor of Medicine at the University of Mississippi. The Decipher the Guidelines: 2022 AHA / ACC / HFSA Guideline for The Management of Heart Failure series was developed by the CardioNerds and created in collaboration with the American Heart Association and the Heart Failure Society of America. It was created by 30 trainees spanning college through advanced fellowship under the leadership of CardioNerds Cofounders Dr. Amit Goyal and Dr. Dan Ambinder, with mentorship from Dr. Anu Lala, Dr. Robert Mentz, and Dr. Nancy Sweitzer. We thank Dr. Judy Bezanson and Dr. Elliott Antman for tremendous guidance. Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. Question #14 Mrs. Hart is a 70-year-old woman hospitalized for a 2-week course of progressive exertional dyspnea, increasing peripheral edema, and mental status changes. She has a history of coronary artery disease, hypertension, and heart failure for which she takes aspirin, furosemide, carvedilol, lisinopril, and spironolactone. On physical exam, the patient is afebrile, BP is 80/60 mmHg, heart rate is 120 bpm, and respiratory rate is 28 breaths/min with O2 saturation of 92% breathing room air. She is sitting upright and is confused. Jugular venous pulsations are elevated. Cardiac exam reveals an S3 gallop. There is ascites and significant flank edema on abdominal exam. Her lower extremities have 2+ pitting edema to her knees and are cool to touch. Her labs are significant for an elevated serum Creatinine of 3.0 from a baseline of 1.0 mg/dL, lactate of 3.0 mmol/L, and liver enzyme elevation in the 300s U/L. Which of the following is the most appropriate initial treatment? A Increase carvedilol B Start dobutamine C Increase lisinopril D Start nitroprusside Answer #14 Explanation The Correct answer is B – start dobutamine. This patient with progressive congestive symptoms, mental status changes, and signs of hypoperfusion and end-organ dysfunction meets the clinical criteria of cardiogenic shock. The Class 1 recommendation is that in patients with cardiogenic shock, intravenous inotropic support should be used to maintain systemic perfusion and maintain end-organ performance (LOE B-NR). Their broad availability, ease of administration, and clinician familiarity favor such agents as first line when signs of hypoperfusion persist. Interestingly, despite their ubiquitous use for management of cardiogenic shock, there is a lack of robust evidence to suggest the clear benefit of one agent over another. Therefore, the choice of a specific agent is guided by additional factors including vital signs, concurrent arrhythmias, and availability. For this patient, dobutamine is the only inotrope listed. Although she is tachycardic, her lack of arrhythmia makes dobutamine relatively lower risk and does not outweigh the potential benefits. Choice A – Increase carvedilol – is not correct. Beta-blockers should be continued in HF hospitalization whenever possible; however, in a patient with low cardiac output and signs of shock, beta-blockers should be discontinued due to their negative inotropic effects. Choice C – Increase lisinopril – is not correct. Afterload reduction is reasonable to decrease myocardial oxygen demand. However, given the hypotension and renal dysfunction, increasing lisinopril could be potentially dangerous by further exacerbating hypotension and renal dysfunction. Furthermore, given her tenuous hemodynamic status, it would be more beneficial to start an IV medication that is easier to monitor and rapidly titrate. Choice D – Start nitroprusside – is not correct. Intravenous Vasodilators are helpful for improving cardiac output in high SVR states when the patient is normotensive or even hypertensive. However, this patient is HYPOtensive and so vasodilators should be held. Main Takeaway In patients with cardiogenic shock, intravenous inotropic support should be used to maintain systemic perfusion and preserve end-organ performance. Guideline Loc. Section 9.5 Decipher the Guidelines: 2022 Heart Failure Guidelines Page CardioNerds Episode Page CardioNerds Academy Cardionerds Healy Honor Roll CardioNerds Journal Club Subscribe to The Heartbeat Newsletter! Check out CardioNerds SWAG! Become a CardioNerds Patron!

Apr 2, 2023

The practice of critical care cardiology relies on the use of invasive hemodynamics, mechanical ventilation, mechanical circulatory support, and other advanced techniques to help our patients recover from critical cardiac illnesses. To facilitate these interventions, it is essential to have a broad understanding of how sedation and analgesia keep our patients comfortable and safe throughout their time in the CICU. In this episode, series co-chair, Dr. Yoav Karpenshif, and CardioNerds co-founder, Dr. Daniel Ambinder, are joined by Dr. Natalie Tapaskar, cardiology fellow and CardioNerds FIT Ambassador from Stanford, and faculty expert, Dr. Chris Domenico, to discuss sedation in the cardiac ICU. Notes were drafted by Dr. Natalie Tapaskar. Audio editing by CardioNerds academy intern, Anusha Gandhi. We discuss the use of analgesics and sedative medications in the cardiac ICU. We dissect three cases of VT storm, heart failure associated cardiogenic shock, and cardiac arrest. We assess the hemodynamic, arrhythmic, and metabolic effects of opioids and sedatives and delve into the altered pharmacokinetics of these drugs during targeted temperature management. Most importantly, we highlight the use of structured pain and sedation scoring systems and discuss the recognition and management of ICU delirium both from a pharmacologic and non-pharmacologic standpoint. The CardioNerds Cardiac Critical Care Series is a multi-institutional collaboration made possible by contributions of stellar fellow leads and expert faculty from several programs, led by series co-chairs, Dr. Mark Belkin, Dr. Eunice Dugan, Dr. Karan Desai, and Dr. Yoav Karpenshif. Pearls • Notes • References • Production Team CardioNerds Cardiac Critical Care PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls and Quotes - Sedation in the Cardiac ICU with Dr. Christopher Domenico Think about analgesia and sedation as separate entities with management of analgesia first and sedation second. Frequent re-assessment of needs should be performed to reduce ICU delirium and improve long-term outcomes. Fentanyl is generally a good starting point for analgesia in the ICU since it is fast on/fast off, but can stick around for a long time the longer it is used. The choice of bolus or continuous infusion opioids depends on the clinical scenario and personal/institutional preference. Remember to administer bolus doses that are 50-100% of the hourly continuous infusion dose to reach steady state faster. When managing refractory VT storm with sedative agents (propofol, benzodiazepines and/or dexmedetomidine), you should target the deepest level of sedation necessary to suppress sympathetic drive. For cardiogenic shock patients, the choice of sedative agent is a nuanced decision. Think about etomidate first for intubation as it has the least cardiovascular and hemodynamic impact. And remember the propofol trifecta: negative inotropy, direct vasodilation, and bradycardia! Pharmacokinetics are disrupted during targeted temperature management, thus be weary of overly sedating patients due to reduced drug clearance. Show notes - Sedation in the Cardiac ICU with Dr. Christopher Domenico How do we initiate analgesics and sedatives? Analgesia first and sedation second! Analgesia: think about how to reduce a patient’s painEveryone has a different pain tolerance and critically ill patients can have moderate to severe pain at baseline. Metrics to assess pain include self-reported scales, behavioral scales, facial expressions, extremity movement, compliance with the ventilator, tachycardia, tachypnea, and hypertension. Sedation: think about how to reduce a patient’s agitation or anxietyThe target depth of sedation depends on the clinical scenario.For example, a patient with a femoral balloon pump may need more sedation if agitation is causing excessive lower extremity movement and thus a higher risk of device dislodgement. Use the Richmond Agitation and Sedation Scale (RASS) for titrating sedation leve.-5 – Unarousable. No response to voice or physical stimuli-4 – Deep sedation. No response to voice, but movement or eye opening to physical stimulation-3 – Moderate sedation. Movement or eye-opening to voice-2 – Light sedation. Briefly awakens to voice-1 – Drowsy. Not fully alert, but has sustained awakening to voice0 – Alert and calm+1 – Restless. Anxious, apprehensive, but not aggressive+2 – Agitated. Frequent non-purposeful movement, fights vent+3 – Very agitated. Pulls or removes tubes/catheters +4 – Combative. Violent, immediate danger to staff What are the different opioid options and when should we use them? Break down opioids into 3 groups (as per Dr. Domenico):Group 1 (morphine, hydromorphone, fentanyl) for pain management in the ICU.Onset of action: Fentanyl is the quickest on/off (30 seconds-2 minutes), but is highly lipophilic, redistributing in fatty tissues after ~30 minutes. The longer you use fentanyl, the longer it will stick around – i.e. “context-sensitive half-time.” Morphine and Hydromorphone have an onset from 5-15 minutes.Half-life: All 3 are similar at 2-4 hours. (Fentanyl can be even higher the longer it is used).Metabolism: Morphine is metabolized by the liver, but has active metabolites that are renally cleared; thus, be cautious with high doses in renal impairment. Fentanyl is metabolized by the CYP system thus it accumulates in hepatic dysfunction.Group 2 (remifentanil and sufentanil) generally for use in the operating room.Onset of action: Both are very quick on/off ranging from 1-3 minutes.Half-life: Remifentanil’s is 3-10 minutes, whereas sufentanil’s is 2-3 hours.Metabolism: Remifentanil demonstrates no accumulation in hepatic or renal impairment, thus is a good choice in these scenarios. Beware of the rare possibility of serotonin syndrome with both these agents. Group 3 (methadone) as a bridge to wean off from long term infusions of other opioids.Onset of action: 1-20 minutes when given intravenously, but 3-5 days when given orally.Half-life: Ranges from 8-60 hours. Metabolism: Hepatic, exercise caution with dysfunction. Also monitor for QT prolongation. Should we administer opioids as boluses or continuous infusions? There is no strong data to guide bolus versus continuous infusion dosing of opioids and the choice is often left up to personal/institutional preference. Small studies in emergency department patients suggest there is less ICU delirium post-intubation with bolus dosing over continuous infusions of opioids. Generally, think about starting with bolus dosing to assess a patient’s true needs, but patients may require continuous infusions if they are receiving frequent boluses. When increasing the rate of a continuous infusion, one can reach steady state faster by administering bolus doses at 50-100% of the hourly dose of the infusion. How should we use analgesics and sedatives for management of arrhythmias, specifically VT storm? The main goal in refractory VT storm is to sedate the patient as deeply as necessary to suppress their sympathetic drive. Generally, the choice of sedative agent is less important than the level of sedation achieved.Propofol, benzodiazepines, and dexmedetomidine can all decrease sympathetic drive.Propofol has some anti-arrhythmic effects via autonomic nervous system modulation.Dexmedetomidine may increase the arrhythmogenic threshold. Benzodiazepines have no direct effect on the conduction system. Opioids have GABA agonist properties and thus have some anti-arrhythmic properties. However, opioids alone are rarely effective in managing malignant arrhythmias unless pain is the main trigger for the arrhythmia. In some animal studies, fentanyl and morphine are thought to increase the ventricular fibrillation threshold, but this is not validated with hard outcomes in clinical trials. What sedatives are safe to use for intubation in cardiogenic shock? Induction: Etomidate, ketamine, and propofol are common agents used for induction of sedation peri-intubation.Etomidate - has minimal cardiovascular/hemodynamic effects and should be considered first for induction in cardiogenic shock. Can lead to adrenal insufficiency. Ketamine - is a direct vasoconstrictor (including coronary arteries) and results in hypertension and tachycardia. It should be avoided in patients with ACS. It may have a direct myocardial depressant effect, so its use is avoided in prolonged shock states. Propofol - has a plethora of properties-sedative, hypnotic, amnestic, antiemetic, and anticonvulsant, but importantly has NO ANALGESIC properties. Remember its hemodynamic trifecta: negative inotropy, direct vasodilation, and bradycardia. It is also highly lipophilic, with a long half-life with extended infusions- i.e. “context-sensitive half-time”. Don’t forget to check triglyceride levels at baseline and at regular intervals while on a continuous infusion. Maintenance: Propofol, benzodiazepines, and dexmedetomidine can be used for maintenance of sedation post-intubation.BenzodiazepinesAlso have a plethora of properties- sedative, amnestic, anticonvulsant, anxiolytic, and hypnotic but NO ANALGESIC properties.Midazolam is quicker on/off (2-5 minutes) compared to lorazepam. Midazolam can accumulate in renal dysfunction. Think about polyethylene toxicity when patients on lorazepam at high doses for extended periods of time develop metabolic acidosis.In general, benzodiazepines use is associated with increased ventilator time, ICU delirium, and ICU length of stay. Dexmedetomidine Is an alpha 2 agonist and thus monitor for hypotension and bradycardia with ongoing use. It does not cause respiratory depression.

Mar 29, 2023

The following question refers to Section 3.2 of the 2021 ESC CV Prevention Guidelines. The question is asked by CardioNerds Academy Intern, student Dr. Hirsh Elhence, answered first by Ohio State University Cardiology Fellow Dr. Alli Bigeh, and then by expert faculty Dr. Eugene Yang. Dr. Yang is professor of medicine of the University of Washington where he is medical director of the Eastside Specialty Center and the co-Director of the Cardiovascular Wellness and Prevention Program. Dr. Yang is former Governor of the ACC Washington Chapter and current chair of the ACC Prevention of CVD Section. The CardioNerds Decipher The Guidelines Series for the 2021 ESC CV Prevention Guidelines represents a collaboration with the ACC Prevention of CVD Section, the National Lipid Association, and Preventive Cardiovascular Nurses Association. Question #19 True or False: A 70-year-old male has an estimated 10-year ASCVD risk (using SCORE2-OP) of 7.5% which confers a very high CVD risk and necessitates treatment with a statin. TRUE FALSE Answer #19 Explanation FALSE – CVD risk thresholds for risk factor treatment are higher in apparently healthy people 70 years and older in order to prevent overtreatment in the elderly. A 10-year CVD risk ≥15% is considered “very high risk” for individuals ≥70 years of age (compared to a ≥7.5% cut-off for “very high risk” in younger patients 70 years of age, a 10-year CVD risk of 7.5 to 70 years of age, a 10-year CVD risk of <7.5 is considered “low-to-moderate risk” and would generally not qualify for risk factor treatment unless one or several risk modifiers are present. Smoking cessation, lifestyle recommendations and a SBP <160 mmHg are recommended for all. Main Takeaway CVD risk assessment for patients 70-years and older is estimated using the SCORE2-OP algorithm. A predicted 10-year CVD risk score of ≥15% confers a very high CVD risk, however, this it is a class IIb indication to initiate/intensify lipid lowering therapies in these patients. Decision should be individualized and based on benefits vs risk assessment. Guideline Loc. 3.2.3.5 CardioNerds Decipher the Guidelines - 2021 ESC Prevention Series CardioNerds Episode Page CardioNerds Academy Cardionerds Healy Honor Roll CardioNerds Journal Club Subscribe to The Heartbeat Newsletter! Check out CardioNerds SWAG! Become a CardioNerds Patron!

Mar 29, 2023

The following question refers to Section 9.1 of the 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure. The question is asked by Keck School of Medicine USC medical student & CardioNerds Intern Hirsh Elhence, answered first by Duke University cardiology fellow and CardioNerds FIT Ambassador Dr. Aman Kansal, and then by expert faculty Dr. Anu Lala. Dr. Lala is an advanced heart failure and transplant cardiologist, associate professor of medicine and population health science and policy, Director of Heart Failure Research, and Program Director for the Advanced Heart Failure and Transplant fellowship training program at Mount Sinai. Dr. Lala is deputy editor for the Journal of Cardiac Failure. Dr. Lala has been a champion and role model for CardioNerds. She has been a PI mentor for the CardioNerds Clinical Trials Network and continues to serve in the program’s leadership. She is also a faculty mentor for this very 2022 heart failure decipher the guidelines series. The Decipher the Guidelines: 2022 AHA / ACC / HFSA Guideline for The Management of Heart Failure series was developed by the CardioNerds and created in collaboration with the American Heart Association and the Heart Failure Society of America. It was created by 30 trainees spanning college through advanced fellowship under the leadership of CardioNerds Cofounders Dr. Amit Goyal and Dr. Dan Ambinder, with mentorship from Dr. Anu Lala, Dr. Robert Mentz, and Dr. Nancy Sweitzer. We thank Dr. Judy Bezanson and Dr. Elliott Antman for tremendous guidance. Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. Question #13 Mrs. Hart is a 63-year-old woman with a history of non-ischemic cardiomyopathy and heart failure with reduced ejection fraction (LVEF 20-25%) presenting with 5 days of worsening dyspnea and orthopnea. She takes carvedilol 12.5mg BID, sacubitril-valsartan 24-46mg BID, empagliflozin 10mg daily, and furosemide 40mg daily and reports that she has been able to take all her medications. What is the initial management for Mrs. H? A Assess her degree of congestion and hypoperfusion B Search for precipitating factors C Evaluate her overall trajectory D All of the above E None of the above Answer #13 Explanation The correct answer is D – all of the above. Choice A is correct because in patients hospitalized with heart failure, the severity of congestion and adequacy of perfusion should be assessed to guide triage and initial therapy (Class 1, LOE C-LD). Congestion can be assessed by using the clinical exam to gauge right and left-sided filling pressures (e.g., elevated JVP, S3, edema) which are usually proportional in decompensation of chronic HF with low EF; however, up to 1 in 4 patients have a mismatch between right- and left-sided filling pressures. Hypoperfusion can be suspected from narrow pulse pressure and cool extremities, intolerance to neurohormonal antagonists, worsening renal function, altered mental status, and/or an elevated serum lactate. For more on the bedside evaluation of heart failure, enjoy Episode #142 – The Role of the Clinical Examination in Patients With Heart Failure – with Dr. Mark Drazner. Choice B, searching for precipitating factors is also correct. In patients hospitalized with HF, the common precipitating factors and the overall patient trajectory should be assessed to guide appropriate therapy (Class 1, LOE C-LD). Common precipitating factors include ischemic and nonischemic causes, such as acute coronary syndromes, atrial fibrillation and other arrhythmias, uncontrolled HTN, other cardiac disease (e.g., endocarditis), acute infections, anemia, thyroid dysfunction, non-adherence to medications or new medications. When initial clinical assessment does not suggest congestion or hypoperfusion, symptoms of HF may be a result of transient ischemia, arrhythmias, or noncardiac disease such as chronic pulmonary disease or pneumonia, and more focused assessments may be warranted. Lastly, Choice C, evaluation of a patient’s trajectory is correct as hospitalization for HF is a sentinel event that signals worse prognosis and provides key opportunities to redirect the disease trajectory – including establishment of optimal volume status before and after discharge. During the HF hospitalization, the approach to management should include and address precipitating factors, comorbidities, and previous limitations to ongoing disease management related to social determinants of health. The disease trajectory for patients hospitalized with reduced EF is markedly improved by optimization of recommended medical therapies, which should be initiated or increased toward target doses once the efficacy of diuresis has been shown. Main Takeaway In summary, when a patient is admitted for acute decompensated heart failure, initial management involves assessing the patient’s degree of congestion and hypoperfusion, identifying and addressing precipitating factors, and evaluating overall patient trajectory to guide appropriate triage and therapy. Guideline Loc. Section 9.1, Table 21 Decipher the Guidelines: 2022 Heart Failure Guidelines Page CardioNerds Episode Page CardioNerds Academy Cardionerds Healy Honor Roll CardioNerds Journal Club Subscribe to The Heartbeat Newsletter! Check out CardioNerds SWAG! Become a CardioNerds Patron!

Mar 28, 2023

CardioNerds (Amit and Dan) join Dr. Maria Pabon (cardiology fellow), Dr. Kevin Bersell (cardiology fellow), Dr. Saad Sultan Ghumman (interventional cardiology fellow), and Dr. Rhanderson Cardoso (cardiovascular imaging fellow) from Brigham and Women’s Hospital. Together, they explore a complex case of STEMI that was further complicated by ventricular free wall rupture. Additionally, Dr. Ajar Kochar, Program Director for Interventional Cardiology at Brigham and Women's Hospital, provides an insightful "ECPR" segment, adding a unique perspective to the case. Audio editing by CardioNerds Academy Intern, student doctor Chelsea Amo Tweneboah. This is the case of a patient who presented with STEMI and was found to have a moderate pericardial effusion with echogenic material within the pericardial space concerning for thrombus. Urgent CTA/CT surgery was engaged due to concern for dissection, but no evidence of dissection, rupture or intramural hematoma was found. The patient underwent an urgent pericardiocentesis which yielded 350cc of hemorrhagic fluid, leading to an improvement in hemodynamic status. A coronary angiogram was performed which showed a 100% thrombotic occlusion of OM 1, the culprit lesion for the STEMI. Due to the possibility of a delayed STEMI and high suspicion for mechanical complication of MI, aspirin and IV cangrelor were chosen as the preferred antiplatelet strategy. However, cangrelor was held and cardiac surgery was consulted, as LV free wall rupture was suspected. The patient underwent urgent repair of the LV free wall rupture, with an uneventful post-op recovery and discharge on day 8 to cardiac rehab. CardioNerds is collaborating with Radcliffe Cardiology and US Cardiology Review journal (USC) for a ‘call for cases’, with the intention to co-publish high impact cardiovascular case reports, subject to double-blind peer review. Case Reports that are accepted in USC journal and published as the version of record (VOR), will also be indexed in Scopus and the Directory of Open Access Journals (DOAJ). CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Case Media Pearls - When Infarction Brings the Walls Down - Brigham and Women’s Hospital In the era of primary PCI, mechanical complications of MI are relatively rare. Timely recognition using multi-modality imaging and prompt surgical intervention can result in favorable outcomes. An approach that involves a Heart Team can be advantageous in optimizing outcomes in such complex cases. Show Notes - When Infarction Brings the Walls Down - Brigham and Women’s Hospital Incidence of post AMI LV free wall rupture: 0.1-1% Risk factors for LV Free wall Rupture: Older age Female sex Prior HTN 1st lateral or Anterior Wall MI Protective factors towards free wall rupture: LV hypertrophy CHF Hx of prior infarcts Chronic ischemic heart disease Early use of beta blockers post MI Timely intervention Incidence of Mortality associated with mechanical rupture related to AMI: 8-10% When to suspect a mechanical complication of AMI: AMI with shock/hypotension New murmur New pericardial effusion > 10mm on bedside echo Other etiologies that can cause free wall rupture: Trauma Cardiac infection Aortic dissection Cardiac tumors Infiltrative diseases Iatrogenic from PCI or surgical procedures References - When Infarction Brings the Walls Down - Brigham and Women’s Hospital Varghese S, Ohlow MA. Left ventricular free wall rupture in myocardial infarction: A retrospective analysis from a single tertiary center. JRSM Cardiovasc Dis. 2019 Jan-Dec;8:2048004019896692. doi: 10.1177/2048004019896692. PMID: 31970072. Pineda-De Paz, D.O., Hernández-del Rio, J.E., González-Padilla, C. et al. Left ventricular free-wall rupture, a potentially lethal mechanical complication of acute myocardial infarction: an unusual and illustrative case report. BMC Cardiovasc Disord 19, 80 (2019). https://doi.org/10.1186/s12872-019-1063-x Yip HK, Wu CJ, Chang HW, Wang CP, Cheng CI, Chua S, Chen MC. Cardiac rupture complicating acute myocardial infarction in the direct percutaneous coronary intervention reperfusion era. Chest 2003;124:565–71. doi: 10.1378/chest.124.2.565. PMID: 12907558. Sutherland FW, Guell FJ, Pathi VL, Naik SK. Postinfarction ventricular free wall rupture: strategies for diagnosis and treatment. Ann Thorac Surg 1996;61:1281–5. doi: 10.1016/0003-4975(95)00953-6. PMID: 8627055. Meta-analysis of corticosteroid treatment in acute myocardial infarction. Am J Cardiol 2003;91:1055–9. doi: 10.1016/S0002-9149(03)00216-4. PMID: 12745097.

Mar 22, 2023

CardioNerds (Dr. Amit Goyal), Dr. Sonu Abraham (CardioNerds Ambassador from Lahey Hospital and Medical Center, Burlington, MA) discuss left ventricular assist devices (LVAD) and the implications of renal dysfunction with Dr. Brian Houston and Dr. Nisha Bansal. This episode will focus on the intersection of left ventricular assist devices and renal dysfunction. Patients with a combination of heart failure and renal dysfunction overall have a guarded prognosis and their management poses unique challenges to the clinician. We initially discuss the basics of an LVAD and general approach to LVAD candidacy evaluation. We then discuss specific implications of acute kidney injury, presence of preexisting CKD, and end stage renal disease in patients with/being considered for an LVAD. Risk factor identification and prognostication allows for appropriate selection of the right candidates for an LVAD in the context of renal disease. Dr. Brian Houston is the Director of the Mechanical Circulatory Support program at Medical University of South Carolina. Dr. Nisha Bansal is an Associate Professor and the Arthur Stach Family Endowed Professor in the Division of Nephrology, an investigator at the Kidney Research Institute, the Director of Nephrology Clinical and Research Education, and the Director of the Kidney-Heart Service at the University of Washington. Notes were drafted by Dr. Sonu Abraham and episode audio was edited by student Dr. Chelsea Amo-Tweneboah. Check out the CardioNerds Failure Heart Success Series Page for more heart success episodes and content! CardioNerds Heart Success Series PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls - Left Ventricular Assist Devices and Renal Dysfunction End stage renal disease (CKD on dialysis) is considered an absolute contraindication for LVAD implantation. Select young patients who are being considered for heart-kidney transplantation in the near future may be candidates for an LVAD as a bridge to heart-kidney transplantation. LVAD implantation can improve kidney function in the short term in patients with AKI primarily caused by cardio-renal syndrome. Patients with pre-existing CKD (not dialysis dependent) have a greater risk of developing AKI after LVAD implantation. Several dialysis modalities including in-center hemodialysis, home hemodialysis, and peritoneal dialysis are available for LVAD patients. However, there are several challenges associated with each modality. An AV graft is a useful vascular access option in LVAD patients undergoing hemodialysis due to a lower risk of infection and ease of immediate use. Causes for anemia in patients with an LVAD and renal dysfunction include anemia of chronic disease, gastrointestinal bleeding, and pump thrombosis leading to hemolysis. Show notes - Left Ventricular Assist Devices and Renal Dysfunction Notes: (drafted by Dr. Sonu Abraham) What is a left ventricular assist device (LVAD) and what are its components? An LVAD supports circulation by unloading the left ventricle and providing increased cardiac output to help support organ perfusion. Use in properly selected patients is associated with improved quality of life and increased survival. The current iteration of LVADs offer continuous flow, as opposed to the older versions which employed pulsatile flow. Components of the LVAD: Inflow cannula (sucks blood from the LV) Pump Outflow cannula (dumps blood into the aorta) Percutaneous driveline Electrical controller How is a patient evaluated for LVAD candidacy? The 2 main questions to be answered during the evaluation of a patient for an LVAD are: 1. Are they sick enough? Do they have end stage heart failure? 2. Do we expect the benefits of an LVAD to outweigh the risks? Presence/absence of right ventricular failure Other life limiting organ failure: Kidney failure/lung disease/liver failure/vascular disease Anatomic concerns (ex. LV size) Surgical risk (ex. Prior sternotomies, calcified aorta, etc) Psychosocial aspects Shared decision making (Does the patient want the device?) What are the outcomes of patients with end stage renal disease (chronic kidney disease on dialysis) after LVAD implantation? Patients with ESRD have a high burden of comorbidities. 40% of dialysis patients have heart failure. The combination of heart failure and ESRD propounds a poor prognosis. Patients with ESRD without heart failure have a 40% survival in 5 years. Conversely, those with ESRD and heart failure have a 30% after LVAD implantation. In patients who have AKI after LVAD implantation, 30-day mortality is 18% and 1 year mortality is 40% with increased risk of infection, multisystem organ failure, and longer length of stay. Common causes of AKI after LVAD implantation include:Right ventricular failureBleeding requiring blood products and crystalloids, contributing to congestion.Longer cardio-pulmonary bypass Hemolysis Based on a 10-year case series from the Mayo clinic, 15% of patients with LVAD require renal replacement therapy. If GFR<45 and there is proteinuria, the risk increased to 40%. The 4 risk factors to predict AKI and RRT requirement after LVAD: Presence of a low GFR Proteinuria Increased RA pressure Longer cardio-pulmonary bypass time The HEARTMATE III Risk Score provides individual survival prediction at 1- and 2-years post LVAD implantation - includes BUN and sodium levels What are the options available to patients in terms of long-term dialysis once LVAD patients are dialysis dependent? There are 3 main options for long term RRT:In-center hemodialysisHome hemodialysis Peritoneal dialysis Considerations:In center Hemodialysis:Challenges: large ultrafiltration rates can lead to lower MAPs, anticoagulation considerations (bleeding complications), high risk of infection (central venous catheter), pragmatic challenges (technical expertise of the dialysis staff, comfort of the attending nephrologist, transportation issues). Peritoneal dialysis:Benefits: decreased risk of infection (however anatomical considerations with respect to proximity to the driveline should be taken into account), more physiological and less hemodynamic instability, no need for anticoagulation. Challenge: home based therapy (burden on the patient and family members) What are the options in terms of vascular access in patients with an LVAD who are started on hemodialysis? Central venous HD catheters – high risk of infection and therefore, not preferred. AV fistula – low rates of infection, however, it takes 2-3 months for fistula maturation. AV graft – preferred due to lower risk of infection, ability to use immediately. What are the causes for anemia in patients with an LVAD and renal dysfunction? Anemia of chronic disease Increased risk of gastrointestinal bleedAnticoagulation requirementAcquired Von Willebrand deficiency Higher burden of arterio-venous malformations Pump thrombosis can lead to hemolysis

Mar 20, 2023

CardioNerds (Amit and Dan) join Dr. Khaled Abdelrahman, Dr. Gurleen Kaur, and Dr. Danny Pipilas from the Brigham and Women’s Hospital Residency Program for Italian food and cannolis at the North End in Boston as they discuss the case of an elderly man with primary cardiac lymphoma. They review an approach to intracardiac masses, discuss advantages and disadvantages of various imaging modalities for the evaluation of intracardiac masses, and also delve into anthracycline toxicity. The E-CPR segment is provided by Dr. Ron Blankstein, Associate Director of the Cardiovascular Imaging Program and Director of Cardiac Computed Tomography at Brigham and Women’s Hospital. Audio editing by CardioNerds Academy Intern, student doctor Akiva Rosenzveig. A 76-year-old man with a history of hyperlipidemia presented with one month of progressively worsening fatigue, weight loss, and dyspnea on exertion. Physical exam was notable for a 3/6 systolic murmur at the left upper sternal border, a flopping sound along the sternum heard throughout the cardiac cycle, and JVP elevated to the level of the mandible. TTE revealed a large heterogeneous echodensity in the right ventricular (RV) free wall that extended into the pericardium and into the RV myocardium with mobile components in the RV cavity and obstruction of the RV outflow tract. Nongated CT chest showed a solid nodule in the periphery of the left lower lung lobe. Gated cardiac CTA revealed a large heterogenous mass in the right atrioventricular groove that encased the proximal thoracic aorta and pulmonary artery and invaded the RV myocardium and RV outflow tract along with a large pericardial effusion. On cardiac MRI, the mass was isointense to the myocardium on T1-weighted images, hyperintense on T2-weighted images, and had heterogenous enhancement on late gadolinium enhancement images. Overall, the imaging findings were highly suspicious for cardiac lymphoma which was confirmed with biopsy of the lung nodule; pathology showed a large B cell lymphoma. The patient was treated with R-CHOP therapy (rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone), and TTE after 6 cycles of chemotherapy demonstrated resolution of the RV mass. CardioNerds is collaborating with Radcliffe Cardiology and US Cardiology Review journal (USC) for a ‘call for cases’, with the intention to co-publish high impact cardiovascular case reports, subject to double-blind peer review. Case Reports that are accepted in USC journal and published as the version of record (VOR), will also be indexed in Scopus and the Directory of Open Access Journals (DOAJ). CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Case Media 1. There is a large homogeneous mass in the right atrioventricular groove that extends anterior to the right ventricular outflow tract, pulmonary artery, and ascending aorta, measuring up to 9.4 x 7.1 cm (axial) x 13 cm (craniocaudal). The mass encases the proximal thoracic aorta and pulmonary artery. The mass invades the right ventricular myocardium, the right ventricular outflow tract, the pulmonary artery, and proximal main pulmonary artery. There is severe stenosis of the right ventricular outflow tract due to obstruction by the mass. The mass encases the right coronary artery, without compression of the artery. There is enhancement of this mass on delayed contrast imaging. Collectively, these findings suggest cardiac lymphoma. 2. There is a large pericardial effusion, circumferential, measuring up to 2.2 cm adjacent to the right atrium and up to 2.3 cm anterior to the intraventricular septum. There is pericardial enhancement, indicative of pericardial inflammation. 3. This study was not optimized for the assessment of the coronary arteries. However, there are severe coronary artery calcifications. There is possible severe stenosis of the mid LAD. 4. Aneurysmal dilatation of the thoracic aorta, with measurements as reported in the narrative. 1. Normal left ventricular size and function. 2. There is a large homogenous, soft-tissue intensity mass in the right atrioventricular groove infiltrating the right ventricle free wall and cranially extending anterior to the aorta and main pulmonary artery. The mass encases the main pulmonary artery, the aortic root, the right coronary artery, and the left main coronary artery. The mass invades the right ventricular outflow tract and proximal main pulmonary artery, resulting in severe luminal narrowing at the level of the RVOT/pulmonary artery valve. For the dimensions of the mass, please refer to cardiac CT from 12/1/2021. The mass is isointense to myocardium on T1-weighted images and hyperintense on T2-weighted images. The mass avidly enhances on first-pass perfusion images. There is heterogeneous enhancement of the mass on late gadolinium enhancement images. 3. There is a large circumferential pericardial effusion, measuring up to 2.3 cm. The left ventricular cavity size and wall thickness are normal. Left ventricular systolic function is normal. There are no segmental left ventricular wall motion abnormalities noted. The estimated ejection fraction is 60%. The right ventricular size is normal. Right ventricular systolic function is mildly decreased. Mildly dilated ascending aorta. Mild AI. Mild MR. There is large heterogenous echodensity in the RV free wall that extends into the parietal pericardium and also into the RV myocardium with mobile components in the RV cavity apical to the tricuspid valve and immediately adjacent to the pulmonic valve. There is obstruction of flow out of the RVOT with a peak and mean gradient of 27 and 16 mmHg respectively. There appears to be some vascularity to this structure (seen best on clips 17 and 18) and overall findings are highly suspicious for tumor. There is a small to moderate pericardial effusion. Anterior to the RV there is a larger collection that is probably pleural in etiology. Recommend cross-sectional imaging for further evaluation. There is no RV chamber collapse to suggest tamponade physiology. 1. Intensely FDG avid infiltrative mediastinal most likely high-grade lymphoma..2. Additional discrete mediastinal and hilar nodes, and left lower lobe nodule, most likely additional areas of lymphomatous involvement. Moderate uptake along right adrenal nodule may represent additional site of lymphomatous involvement3. Small bilateral pleural effusions and small to moderate pericardial effusion. Pearls - A Rare Cause Of Fatigue, Dyspnea, And Weight Loss In An Elderly Man - Brigham and Women’s Hospital In the diagnostic approach for cardiac masses, consider: 1) age of patient at time of presentation, 2) epidemiologic likelihood and clinical probability, 3) location of tumor, and 4) tissue characterization of the mass on CMR. CMR allows for better characterization of soft tissues and can assess mass morphology, dimensions, homogeneity, and infiltration into surrounding tissues. On CMR, cardiac lymphoma typically shows isointensity on T1 imaging and hyperintensity on T2 images. Cardiac CT allows for high spatial and temporal resolution, and can be useful to define cardiac masses that involve the coronary arteries; compared to CMR, cardiac CT has a greater ability to assess calcifications within a mass itself. Cardiac lymphomas have a predilection of right heart chambers, especially right atrium and can affect the AV groove, encasing the right coronary artery. Global systolic longitudinal myocardial strain on TTE is an indicator of early anthracycline-induced cardiomyopathy before overt reduction in ejection fraction. Show Notes - A Rare Cause Of Fatigue, Dyspnea, And Weight Loss In An Elderly Man - Brigham and Women’s Hospital What is the approach to an enlarged cardiac silhouette noted on chest x-ray?Cardiothoracic ratio of greater than 50%.Two possible “buckets” of diagnoses to consider are enlargement of heart related to cardiomegaly as opposed to a pericardial process like a pericardial effusion.For cardiomegaly, it can be from dilated or hypertrophic cardiomyopathy with most common causes including coronary artery disease, hypertension, valvular heart disease, and arrythmia-induced cardiomyopathy. Other buckets to consider are inflammatory causes, either infectious or autoimmune, as well as infiltrative diseases like amyloid or sarcoid, toxins (alcohol, cocaine, medications), endocrine, and nutritional causes (like a B1 or selenium deficiency).The most sensitive sign of a pericardial effusion on chest x-ray is enlargement of cardiac silhouette with a sensitivity of around 71%, but low specificity (1). With pericardial effusion, symmetric expansion of the heart contour leads to a globular appearance which is commonly referred to as flask-shaped or the water bottle sign (1). What is the approach to intracardiac masses?First, consider the age of the patient at the time of presentation since certain clinical entities like rhabdomyomas and fibromas are more common in the pediatric population (2).Second, consider the epidemiologic likelihood and clinical probability. In a patient with a recent anterior wall MI and akinetic ventricular apex, a cardiac mass on echo would raise concern for an intracardiac thrombus (2).Third, consider the location of the tumor. If the mass is on the valves, consider thrombus or a vegetation. While masses in the chambers can still represent thrombus, would also consider myxomas, lymphomas, and metastases (2). Fourth, consider the tissue characterization of the mass on further diagnostic imaging such as CMR (2). What is the role of multimodality imaging in the evaluation of intracardiac masses? TTE is the first modality utilized in evaluation of a cardiac mass.

Mar 16, 2023

CardioNerds co-founder Amit Goyal, Dr. Dinu Balanescu, Dr. Teodora Donisan, and Dr. Anjali Agarwalla get the cardiologist perspective of Cancer Therapy-Related Cardiac Dysfunction (CTRCD) from Dr. Joerg Hermann. We previously learned from the oncologist perspective with Dr. Susan Dent in Episode #261! In this episode, we discuss the history of cancer therapies and our developing understanding of how these life-saving medications can cause cardiac toxicities. As we manage patients in the CardioNerds CardioOncology clinic, we ask Dr. Hermann how the general cardiologist should approach patients with a cancer diagnosis, when should a patient be referred to a cardiooncology specialist, and what are the common cardiotoxicities to look out for. We’ll also place a quick consult to our guest expert’s goldendoodle! Audio editing by CardioNerds Academy Intern, student doctor Chelsea Amo Tweneboah. This episode is supported by a grant from Pfizer Inc. This CardioNerds Cardio-Oncology series is a multi-institutional collaboration made possible by contributions of stellar fellow leads and expert faculty from several programs, led by series co-chairs, Dr. Giselle Suero Abreu, Dr. Dinu Balanescu, and Dr. Teodora Donisan. Pearls • Notes • References • Production Team CardioNerds Cardio-Oncology PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls and Quotes - Cancer Therapy-Related Cardiac Dysfunction (CTRCD) – The Cardiologist Perspective with Dr. Joerg Hermann Patients with malignancy will incur several “hits” in addition to their malignancy and its subsequent treatment — these include their genetics, environment, and comorbidities. The role of the cardiologist is to identify how the combination of these “hits” can bring cardiovascular disease to the forefront and where we can intervene upon it. The sooner we recognize cardiotoxicity, the better the outcome for our patients. Patients should receive baseline risk assessment with TTE and biomarkers with routine surveillance. You cannot assign a percentage to cardiac risk in cancer. Patients require a multidisciplinary approach with constant monitoring and surveillance. Consider exercise testing when conducting pre-treatment risk assessment and during monitoring. Peak VO2 abnormalities is often the first marker of cardiotoxicity — though note that it correlates well with global longitudinal strain (GLS). If someone develops a cardiovascular complication of chemotherapy, this should prompt referral to cardiooncology. Show notes - Cancer Therapy-Related Cardiac Dysfunction (CTRCD) – The Cardiologist Perspective with Dr. Joerg Hermann What types of cardiovascular pathology occur in the setting of cancer and its treatment? We conventionally thought of cardiotoxicities as being of two types: Type 1: irreversible cardiac injury that does not improve despite withdrawal of offending chemotherapeutic (protype = classic anthracycline cardiotoxicity) Type 2: reversible cardiac dysfunction that improves with discontinuation of chemotherapeutic (prototype = classic traztuzumab cardiotoxicity) However, we have begun moving away from this thought process as it has become more evident that injuries historically thought of as “type 1” may not be as relentless as previously understood, and that patients with type 2 dysfunction may not actually be returning to completely normal after the offending agent is withdrawn. As such, this episode proposes two other ways to frame our understanding of cardiotoxicities: a clinical/practical approach, based on symptoms (symptomatic vs asymptomatic — this is the approach used by the ESC guidelines), and a mechanistic approach: direct effect on cardiac myocytes, indirect effects (e.g., effect on coronaries), and inflammatory effects. The 2021 International Cardiooncology Society (ICOS) consensus statement defines five major forms of cancer therapy related cardiac dysfunction (CTRCD): Cardiac dysfunction/heart failure:Asymptomatic: defined by changes in ejection fraction. This may be mild (LVEF >50% AND either new decline in GLS by >15% from baseline or new rise in troponin or NTproBNP), moderate (new LVEF reduction by ≥10 percentage points to 40 - 49% AND either new decline in GLS by >15% from baseline or new rise in troponin or NTproBNP), or severe (new LVEF reduction to < 40%). Symptomatic: defined by severity of symptoms and intensity of treatment required. This may be mild (mild HF symptoms, no intensification of therapy required), moderate (need for outpatient intensification of diuretic and HF therapy), severe (HF hospitalization), or very severe (requiring inotropic or mechanical circulatory support, consideration for transplant). Vascular toxicity: namely, myocardial infarction or stroke. Three primary forms:VasospasmThrombosis Atherosclerosis Arrhythmia/QTc prolongation Hypertension Myocarditis: made especially prominent by immune checkpoint inhibitors Note that the definitions for these toxicities require a baseline assessment of LVEF, global longitudinal strain, and cardiac biomarkers. As such, these should be considered part of pre-treatment risk assessment for any patient planned to undergo therapy known to be cardiotoxic. Who are the “usual suspects” in CTRCD? The “five pillars” of cancer therapy can each cause a form of cardiotoxicity. These pillars are: Conventional chemotherapeutics: designed to stop highly proliferative cells from proliferating by inhibiting DNA synthesis.Anthracyclines, such as doxorubicin, etoposide. Mechanism: intercalates into DNA, disrupting topoisomerase-mediated DNA repair and replication. Primary form of cardiotoxicity: cardiomyopathy (can also cause arrhythmia).Alkylating agents, such as cyclophosphamide. Mechanism: cross-links DNA. Primary form of cardiotoxicity: high doses can cause hemorrhagic pericarditis; we also see arrhythmia, cardiomyopathy, and arterial vascular disease. Antimetabolites, such as 5-fluorouracil, gemcitabine. Mechanism: replaces base pairs, preventing synthesis. Primary form of cardiotoxicity: cardiomyopathy, arterial vascular disease. Targeted therapies: monoclonal antibodies that inhibit cell signaling pathways that are pivotal in tumor cells.HER2 inhibitorsTyrosine kinase inhibitors VEGF inhibitors, such as bevacizumab. Mechanism: inhibits angiogenesis via VEGF inhibition. Primary form of cardiotoxicity: hypertension, thrombosis, and occasionally cardiomyopathy. Immune therapies: immunologic therapies that are “targeted” at receptors identified on specific tumor receptorsCAR-T cell therapy Immune checkpoint inhibitors Radiation therapy Surgery The first three of these — conventional chemotherapeutics, targeted therapies, and immune therapies — are the three classes we think about as causing CTRCD. Pearls from the ESC 2022 guidelines Cardiovascular risk in patients with cancer is a dynamic variable that requires a multidisciplinary team approach. All patients with cancer who are scheduled to receive a potentially cardiotoxic anticancer therapy should receive a baseline cardiovascular risk assessment that includes transthoracic echocardiography with measurement of global longitudinal strain as well as baseline cardiac biomarkers. In patients who are at high risk or very high risk of CTRCD as based on the risk stratification provided in the guidelines, efforts should be made to minimize the use of cardiotoxic agents (including the consideration of dexrazoxane and liposomal anthracyclines) and to initiate cardioprotective agents (like ACE-i/ARB, beta blockers, and statins). In patients who develop asymptomatic, mild decreases in LVEF, especially in the setting of HER2 inhibitors, chemotherapy should be continued with the addition of cardioprotective therapy. After the completion of chemotherapeutics, cardioprotective medications should be de-escalated in patients at low risk of future cardiovascular events. Pearl from the ACC.23 meeting (March 4-6, 2023, New Orleans, LA) The STOP-CA trial is a multicenter, randomized, double-blind, placebo-controlled study presented at ACC.23. The study analyzed 286 patients with lymphoma undergoing treatment with anthracyclines. Baseline left ventricular ejection fraction (LVEF) was 63%. Patients were randomized into a group receiving atorvastatin 40 mg daily and a group receiving placebo. The primary endpoint of LVEF decline ≥10% at 12 months was seen in 9% of patients in the atorvastatin group and 22% of patients in the placebo group, with no difference in rates of adverse events. In conclusion, statins may have an important role in the prevention of anthracycline-associated cardiac dysfunction in lymphoma patients. For more on the STOP-CA trial, check out the ACC Fits-On-The-Go coverage by CardioNerds CardioOncology series co-chair Dr. Teodora Donisan, with lead authors Dr. Tomas Neilan and Dr. Marielle Scherrer-Crosbie. The STOP-CA trial was presented after the recording of this episode and is thus not addressed in the episode. References - Cancer Therapy-Related Cardiac Dysfunction (CTRCD) – The Cardiologist Perspective with Dr. Joerg Hermann Herrmann J, McCullough KB, Habermann TM. How I treat cardiovascular complications in patients with lymphoid malignancies. Blood. 2022;139(10):1501-1516. doi:10.1182/blood.2019003893 Herrmann J, Lenihan D, Armenian S, et al. Defining cardiovascular toxicities of cancer therapies: an International Cardio-Oncology Society (IC-OS) consensus statement. Eur Heart J. 2022;43(4):280-299. doi:10.1093/eurheartj/ehab674 Lyon AR, López-Fernández T, Couch LS, et al. 2022 ESC Guidelines on cardio-oncology developed in collaboration with the European Hematology Association (EHA),

Mar 14, 2023

Join CardioNerds Co-Founder Dr. Dan Ambinder, Dr. Nino Isakadze (EP Fellow at Johns Hopkins Hospital), Dr. Karan Desai (Cardiology Faculty at Johns Hopkins Hospital and Johns Hopkins Bayview) and student Dr. Shivani Reddy (Medical Student at Western Michigan University Homer Stryker SOM), as they discuss how digital health in changing the landscape of CV Disease Management with Dr. Dipti Itchhaporia (Past President of the ACC). The overall goal of this episode is to broadly describe the current landscape of digital health for cardiovascular disease, define “digital health tools” and describe their role in cardiovascular disease management. Episode audio was edited by student Dr. Shivani Reddy and show notes were developed by Dr. Nino Isakadze. In this series, supported by an ACC Chapter Grant and in collaboration with Corrie Health, we hope to provide all CardioNerds out there a primer on the role of digital heath in cardiovascular medicine. Use of versatile hardware and software devices is skyrocketing in everyday life. This provides unique platforms to support healthcare management outside the walls of the hospital for patients with or at risk for cardiovascular disease. In addition, evolution of artificial intelligence, machine learning, and telemedicine is augmenting clinical decision making at a new level fueling a revolution in cardiovascular disease care delivery. Digital health has the potential to bridge the gap in healthcare access, lower costs of healthcare and promote equitable delivery of evidence-based care to patients. This CardioNerds Digital Health series is made possible by contributions of stellar fellow leads and expert faculty from several programs, led by series co-chairs, Dr. Nino Isakadze and Dr. Karan Desai. Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. CardioNerds Digital Health Series PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls and Quotes COVID 19 pandemic accelerated the digital transformation of healthcare. Digital health tools exist for disease prediction, diagnosis and management. Digital health can increase access to care and lower overall cost expenditure. Clinicians, policy makers, and insurance providers should be involved to facilitate rapid and effective adoption of digital health interventions to better patient and population health. Notes 1. How did the COVID-19 pandemic accelerate the process of adopting digital health tools in healthcare including cardiovascular disease management? Although technological advances and technological transformation have been implemented in many aspects of our lives, their adoption in healthcare, including cardiovascular disease management has lagged behind. The COVID-19 pandemic was a force that led to the Tech-celeration as we adopted telemedicine and remote patient monitoring platforms in a short time to preserve access to healthcare. Technology became essential not to replace but to support face to face interactions. Reimbursement models were rapidly created that fit digital healthcare delivery; however it remains unclear whether these models will continue to be in effect in the post pandemic era. 2. Can you discuss broadly the current landscape of evidence-based digital health tools available for cardiovascular disease management? Three components of digital health landscape can be broken down as follows:Virtual care/telehealth platformsRemote patient monitoring systems including implanted devices, patches, wearables, smartphone applications and more Artificial intelligence to allow meaningful use of the big data obtained from remote patient monitoring systems in therapeutic and disease management pathways 3. How can we balance benefits and burden of digital health tools? The pure definition of digital transformation is using digital tools to make lives of patients and clinicians better. The data we derive from digital health technologies is only useful insofar that it can be used to affect change. We need analytical tools like AI to create actionable information and summary sheets to summarize data in meaningful ways. While developing digital health tools, companies should engage in co-designing processes with end users. In the case, clinicians should receive iterative feedback so that tools that are developed meet user needs. 4. What are the ways to ensure inclusiveness in design and delivery of digital health tools for disease management to every patient, including those from underrepresented racial and ethnic groups? We need to improve access to infrastructure needed to operate digital health tools. This requires engagement with institutions, organizations and legislators. Digital health tools need to be co-designed with a diverse set of users including those with low tech literacy as well as multiple stakeholders. We need to communicate with community members when translating science to make sure that the process is transparent to address any trust issues or skepticism. 5. How do we ensure data privacy, especially when health data is stored on different servers? There are gaps in federal legislation that need to be addressed. IT health standards for handling data collected outside hospital settings with digital health tools should be developed in an iterative manner. When health IT standards are developed, we need to enforce them and ensure that they are working well with feedback systems. Individuals need to control how their data is health systems and other entities use and store their data. Clinicians need to trust that data is stored in a secure manner when appropriate channels are utilized. Data management should be a transparent process. Confidentiality is going to be fundamental and all entities involved should be subject to HIPPA rules. 6. How can big organizations help advocate for updated reimbursement models and policy changes to allow for greater adoption of digital health tools? Big professional organizations have pivotal roles in promoting the digital transformation, and implementing digital re-design. Big professional organizations can act as conduits between different stakeholders, promote digital literacy in public as well as among professionals. They can create standards and guidelines on proper use of digital health technology, facilitate robust studies to test clinical impact, and advocate for reimbursement and policy changes. 7. What are the near future and long-term opportunities of digital health tools in cardiovascular disease management? Digital transformation is in progress, and we need clinicians to be at the center of innovation to drive development of care pathways and care delivery models. Digital solutions should promote health equity, add value to healthcare systems, and promote wellbeing of clinicians References Bayoumy K, Gaber M, Elshafeey A, et al. Smart wearable devices in cardiovascular care: where we are and how to move forward. Nat Rev Cardiol. 2021 Aug;18(8):581-599. doi: 10.1038/s41569-021-00522-7. Epub 2021 Mar 4. PMID: 33664502. Cowie MR, Lam CSP. Remote monitoring and digital health tools in CVD management. Nat Rev Cardiol. 2021 Jul;18(7):457-458. doi: 10.1038/s41569-021-00548-x. PMID: 33824486; PMCID: PMC8023506. Itchhaporia D. Navigating the Path to Digital Transformation. J Am Coll Cardiol. 2021 Jul 27;78(4):412-414. doi: 10.1016/j.jacc.2021.06.018. PMID: 34294274.

Mar 12, 2023

It’s another session of CardioNerds Rounds! In these rounds, Dr. Karan Desai (Formerly FIT at University of Maryland Medical Center and currently faculty at Johns Hopkins School of Medicine) joins Dr. Dan Burkhoff (Director of Heart Failure, Hemodynamics and MCS Research at the Cardiovascular Research Foundation) to discuss mechanical circulatory support options through the lens of pressure-volume loops! Dr. Burkhoff is the author of Harvi, an interactive simulation-based application for teaching and researching many aspects of ventricular hemodynamics. Don’t miss this wonderfully nerdy episode with a world-renowned expert in hemodynamics and MCS! Audio editing by CardioNerds Academy Intern, student doctor Chelsea Amo Tweneboah. This episode is supported with unrestricted funding from Zoll LifeVest. A special thank you to Mitzy Applegate and Ivan Chevere for their production skills that help make CardioNerds Rounds such an amazing success. All CardioNerds content is planned, produced, and reviewed solely by CardioNerds. Case details are altered to protect patient health information. CardioNerds Rounds is co-chaired by Dr. Karan Desai and Dr. Natalie Stokes. Challenging Cases - Atrial Fibrillation with Dr. Hugh Calkins CardioNerds Rounds PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Show notes - Hemodynamics and Mechanical Circulatory Support Case Synopsis: Case SynopsisWe focused on one case during these rounds. A man in his mid-50s presented to his local community hospital with 3 days of chest pain, nausea, and vomiting. He appeared ill in the emergency room with HR in the 150s, BP 90/70s and ECG demonstrating inferior ST elevations. He was taken emergently to the catheterization lab and received overlapping stents to his right coronary artery. Over the next 24 hours, he developed a new harsh systolic murmur heard throughout his precordium and progressed to cardiogenic shock. Echocardiogram demonstrated a large basal inferoseptum ventricular septal rupture. From this point, we discussed the hemodynamics of VSR and MCS options. Case Takeaways Dr. Burkhoff took us through the hemodynamics of VSR with pressure-volume loops to better understand the pathology and impact of various MCS options. Of note, there are no MCS devices specifically approved to treat acute ventricular septal rupture. In regards to the acute hemodynamic effects of a VSR (an abrupt left to right shunt), there are several aspects to note. First, the effective LV afterload is reduced; however, there is less “forward flow” as well and as a consequence, decreased left-sided cardiac output (“Qs”) and blood pressure. At the same time, flow through the pulmonary artery increases (the “Qp”). Additionally, due to the abrupt shunt flow, there is increased RV “loading” with increasing central venous pressure and pulmonary artery pressure. The hemodynamic priorities in treating patients with cardiogenic shock and VSR are to normalize blood pressure, cardiac output, and oxygen delivery, while attempting to minimize shunt flow to allow healing. However, medications and MCS are unlikely to completely normalize hemodynamics. For instance, if the patient was placed on peripheral VA ECMO, while total CO and BP may increase, flow across the VSR could also increase at high ECMO flows (e.g., by introducing more LV afterload). In patients with persistent cardiogenic shock and VSR, short-term MCS to divert flow away from the shunt can be an effective strategy. LV-to-aorta or LA-to-arterial MCS may provide the best single-device hemodynamic profiles by decreasing shunt flow, reducing pulmonary capillary wedge pressure, and improving blood pressure. Surgical and percutaneous VSD repair are the definitive treatment options. If able to stabilize patients and pursue delayed repair, it may lead to better outcomes by allowing for better tissue substrate for a more effective repair. Enjoy this ACC.org Expert Analysis by Goyal and Menon to learn more about post-myocardial infarction ventricular septal rupture. References Pahuja M, Schrage B, Westermann D et al. Hemodynamic Effects of Mechanical Circulatory Support Devices in Ventricular Septal Defect. Circ Heart Fail. 2019 Jul;12(7):e005981. doi: 10.1161/CIRCHEARTFAILURE.119.005981. TEACH Videos via Harvi.Org: https://harvi.org/book/data/00%20-%20TeachVideos/TeachVideos.html Production Team Karan Desai, MD Natalie Stokes, MD Amit Goyal, MD Daniel Ambinder, MD

Mar 8, 2023

The following question refers to Section 9.5 of the 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure. The question is asked by Western Michigan University medical student & CardioNerds Intern Shivani Reddy, answered first by Brigham & Women’s medicine resident and Director of CardioNerds Internship Dr. Gurleen Kaur, and then by expert faculty Dr. Shashank Sinha. Dr. Sinha is an Assistant Professor of Medical Education at the University of Virginia School of Medicine and an advanced heart failure, MCS, and transplant cardiologist at Inova Fairfax Medical Campus. He currently serves as both the Director of the Cardiac Intensive Care Unit and Cardiovascular Critical Care Research Program at Inova Fairfax. He is also a Steering Committee member for the multicenter Cardiogenic Shock Working Group and Critical Care Cardiology Trials Network and an Associate Editor for the Journal of Cardiac Failure, the official Journal of the Heart Failure Society of America. The Decipher the Guidelines: 2022 AHA / ACC / HFSA Guideline for The Management of Heart Failure series was developed by the CardioNerds and created in collaboration with the American Heart Association and the Heart Failure Society of America. It was created by 30 trainees spanning college through advanced fellowship under the leadership of CardioNerds Cofounders Dr. Amit Goyal and Dr. Dan Ambinder, with mentorship from Dr. Anu Lala, Dr. Robert Mentz, and Dr. Nancy Sweitzer. We thank Dr. Judy Bezanson and Dr. Elliott Antman for tremendous guidance. Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. Question #12 Mr. Shock is a 65-year-old man with a history of hypertension and non-ischemic cardiomyopathy (LVEF 25%) who is admitted with acute decompensated heart failure. He is currently being diuresed with a bumetanide drip, but is only making 20 cc/hour of urine. On exam, blood pressure is 85/68 mmHg and heart rate is 110 bpm. His JVP is at 12 cm and extremities are cool with thready pulses. Bloodwork is notable for a lactate of 3.5 mmol/L and creatinine of 2.5 mg/dL (baseline Cr 1.2 mg/dL). What is the most appropriate next step? A Augment diuresis with metolazone B Start sodium nitroprusside C Start dobutamine D Start oral metoprolol E None of the above Answer #12 Explanation The correct answer is C – start dobutamine. In this scenario, the patient is in cardiogenic shock given hypotension and evidence of end-organ hypoperfusion on exam and labs. The patient’s cool extremities, low urine output, elevated lactate, and elevated creatinine all point towards hypoperfusion. In patients with cardiogenic shock, intravenous inotropic support should be used to maintain systemic perfusion and preserve end-organ function (Class 1, LOE B-NR). Further, in patients with cardiogenic shock whose end-organ function cannot be maintained by pharmacologic means, temporary MCS is reasonable to support cardiac function (Class 2a, LOE B-NR). The SCAI Cardiogenic Shock Criteria can be used to divide patients into stages. Stage A is a patient at risk for cardiogenic shock but currently not with any signs or symptoms, for example, a patient presenting with a myocardial infarction without present evidence of shock. Stage B is “pre-shock” – this may be a patient who has volume overload, tachycardia, and hypotension but does not have hypoperfusion based on exam and lab evaluation. Stage C is classic cardiogenic shock – the cold and wet profile. Bedside findings for Stage C shock include cool extremities, weak pulses, altered mental status, decreased urine output, and/or respiratory distress. Lab findings include impaired renal function, increased lactate, increased hepatic enzymes, and/or acidosis. Stage D is deteriorating with worsening hypotension and hypoperfusion with escalating use of pressors or mechanical circulatory support. Finally, stage E is extremis with refractory hypotension and hypoperfusion, with circulatory collapse. Our patient in the question stem is in SCAI stage C, or classic cardiogenic shock. Choice A is incorrect. Augmenting diuresis with metolazone can be useful in a patient with diuretic resistance and decompensated heart failure. However, this patient is hypotensive and fits the wet and cool profile and will benefit from inotropic support to increase end organ perfusion. Choice B is incorrect. Sodium nitroprusside can be used to increase cardiac output in cardiogenic shock and is particularly useful in patients with high systemic vascular resistance. Indeed, intravenous nitroglycerin and nitroprusside have a Class 2a indication (LOE B-NR) in patients who are admitted with decompensated HF without systemic hypotension as an adjuvant to diuretic therapy for relief of dyspnea. However, our patient is hypotensive and so vasodilators would not be appropriate at this time. Choice C is incorrect. Metoprolol, a negative inotropic agent, should not be used in this patient with cardiogenic shock. Relevant to this question is the use of invasive hemodynamic monitoring to guide therapy. The use a PA line has a Class 2b indication (LOE B-NR) in patients presenting with cardiogenic shock to define hemodynamic subsets and appropriate management strategies. Obtaining hemodynamic data via a PA line can also be particularly useful when escalating to mechanical circulatory support, when there is diagnostic uncertainty, or when a patient in shock is not responding to empiric initial shock measures. While the use of PA catheters has been controversial since the ESCAPE trial which showed no benefit in decompensated HF, the trial did not actually enroll patients with cardiogenic shock. Several observational studies have shown association between PA catheter use and improved outcomes in cardiogenic shock, particularly in conjunction with short-term MCS. PA catheters are a diagnostic tool and are best utilized when hemodynamic information can be translated into appropriate interventions, such as determining response to medical and MCS therapy, weaning off of MCS support, or uncovering right ventricular failure to guide appropriate therapy. In the case of cardiogenic shock, studies have shown benefit with multidisciplinary teams of HF and critical care specialists, interventional cardiologists, and cardiac surgeons. Such teams should also be capable of providing appropriate palliative care. There is a Class 2a (LOE B-NR) recommendation for management of patients with cardiogenic shock by an experienced multidisciplinary team. Main Takeaway In summary, it is important to recognize cardiogenic shock early based on clinical criteria of hypotension and hypoperfusion and begin prompt initiation of IV inotropic agents such as dobutamine and/or MCS to optimize end-organ perfusion. When there is insufficient clinical improvement with initial measures, invasive hemodynamic assessment is recommended. Guideline Loc. Section 9.5 Tables 22-24 Decipher the Guidelines: 2022 Heart Failure Guidelines PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron!

Mar 7, 2023

The following question refers to Section 8.1 of the 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure. The question is asked by Western Michigan University medical student & CardioNerds Intern Shivani Reddy, answered first by Brigham & Women’s medicine resident and Director of CardioNerds Internship Dr. Gurleen Kaur, and then by expert faculty Dr. Prateeti Khazanie. Dr. Khazanie is an Associate Professor and Advanced Heart Failure and Transplant Cardiologist at the University of Colorado. She was an undergraduate at Duke University as a B.N. Duke Scholar. She spent two years at the NIH in the lab of Dr. Anthony Fauci and completed a dual MD-MPH program at Duke Medical School. When she started residency, she thought she was going to be an ID doctor, but she fell in love with cardiology at Stanford where she was an intern, resident, and then chief resident. She went back to Duke for her general cardiology and advanced heart failure/transplant fellowships as well as research training at the DCRI. Dr. Khazanie joined the University of Colorado in 2015 as a health services clinician researcher with a focus on improving health equity and bioethics in advanced heart failure care. She mentors medical students, residents, and fellows and is a faculty mentor for the University of Colorado Cardiology Fellows “House of Cards” mentoring group. She has research funding from the NIH/NHLBI K23, NIH Ethics Grant, and Ludeman Center for Women’s Health Research. Dr. Khazanie is an author on the 2022 ACC/AHA/HFSA HF Guidelines, the 2021 HFSA Universal Definition of Heart Failure, and multiple scientific statements. The Decipher the Guidelines: 2022 AHA / ACC / HFSA Guideline for The Management of Heart Failure series was developed by the CardioNerds and created in collaboration with the American Heart Association and the Heart Failure Society of America. It was created by 30 trainees spanning college through advanced fellowship under the leadership of CardioNerds Cofounders Dr. Amit Goyal and Dr. Dan Ambinder, with mentorship from Dr. Anu Lala, Dr. Robert Mentz, and Dr. Nancy Sweitzer. We thank Dr. Judy Bezanson and Dr. Elliott Antman for tremendous guidance. Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. Question #11 A 64-year-old woman with a history of chronic systolic heart failure secondary to NICM (LVEF 15-20%) s/p dual chamber ICD presents for routine follow-up. She reports several months of progressive fatigue, dyspnea, and peripheral edema. She has been hospitalized twice in the past year with acute decompensated heart failure. Efforts to optimize guideline directed medical therapy have been tempered by episodes of lightheadedness and hypotension. Her exam is notable for an elevated JVP, an S3 heart sound, and a III/VI holosystolic murmur best heard at the apex with radiation to the axilla. Labs show Na 130 mmol/L, Cr 1.8 mg/dL (from 1.1 mg/dL 6 months prior), and NT-proBNP 1,200 pg/mL. ECG in clinic shows sinus rhythm and a nonspecific IVCD with QRS 116 ms. Her most recent TTE shows biventricular dilation with LVEF 15-20%, moderate functional MR, moderate functional TR and estimated RVSP of 40mmHg. What is the most appropriate next step in management? A Refer to electrophysiology for upgrade to CRT-D B Increase sacubitril-valsartan dose C Refer for advanced therapies evaluation D Start treatment with milrinone infusion Answer #11 Explanation The correct answer is C – refer for advanced therapies evaluation. Our patient has multiple signs and symptoms of advanced heart failure including NYHA Class III-IV functional status, persistently elevated natriuretic peptides, severely reduced LVEF, evidence of end organ dysfunction, multiple hospitalizations for ADHF, edema despite escalating doses of diuretics, and progressive intolerance to GDMT. Importantly, the 2018 European Society of Cardiology revised definition of advanced HF focuses on refractory symptoms rather than cardiac function and more clearly acknowledges that advanced HF can occur in patients without severely reduced LVEF, such as in those with isolated RV dysfunction, uncorrectable valvular or congenital heart disease, and in patients with preserved and mildly reduced LVEF. In such patients with advanced heart failure, when consistent with the patient’s goals of care, timely referral for HF specialty care is recommended to review HF management and assess suitability for advanced HF therapies (eg, LVAD, cardiac transplantation, palliative care, and palliative inotropes) (Class I, LOE C-LD). Clinical indicators of advanced heart failure should prompt a possible referral to an advanced HF specialist and can be remembered by the INEEDHELP acronym: · I – IV inotropes · N – NYHA IIIb-VI or persistently elevated natriuretic peptides · E – End-organ dysfunction · E – EF ≤ 35% · D – Defibrillator shocks · H – Hospitalizations > 1 in past year · E – Edema despite escalating diuretics · L – Low systolic blood pressure (≤90) or high heart rate · P – Prognostic medication; progressive intolerance or down-titration of GDMT It would not be appropriate to refer to EP for CRT-D upgrade as this is a Class 3 recommendation (LOE B-R) in patients with QRS duration <120 ms for no benefit. Increasing the dose of sacubitril-valsartan would not be appropriate in this setting as the patient would be likely unable to tolerate a higher dose given her complaints of lightheadedness and episodes of hypotension. Initiating treatment with IV inotropes would not be appropriate in this setting. Although the use of IV inotropes is given a Class 1 recommendation (LOE B-NR) for the treatment of cardiogenic shock, the patient described in the question stem does not meet clinical criteria for cardiogenic shock. Main Takeaway Clinical indicators for advanced heart failure can be remembered by the I-Need-Help acronym, and there is a Class 1, LOE C recommendation for these patients to be referred to HF specialists for further management and assessment for advanced therapies, when consistent with the patient’s goals of care. Guideline Loc. Section 8.1 Tables 16-18 Decipher the Guidelines: 2022 Heart Failure Guidelines Page CardioNerds Episode Page CardioNerds Academy Cardionerds Healy Honor Roll CardioNerds Journal Club Subscribe to The Heartbeat Newsletter! Check out CardioNerds SWAG! Become a CardioNerds Patron!

Feb 28, 2023

The following question refers to Section 7.7 of the 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure. The question is asked by St. George's University medical student and CardioNerds Intern Chelsea Tweneboah, answered first by Baylor College of Medicine Cardiology Fellow and CardioNerds Ambassador Dr. Jamal Mahar, and then by expert faculty Dr. Michelle Kittleson.Dr. Kittleson is Director of Education in Heart Failure and Transplantation, Director of Heart Failure Research, and Professor of Medicine at the Smidt Heart Institute, Cedars-Sinai. She is Deputy Editor of the Journal of Heart and Lung Transplantation, on Guideline Writing Committees for the American College of Cardiology (ACC)/American Heart Association, is the Co Editor-in-Chief for the ACC Heart Failure Self-Assessment Program, and on the Board of Directors for the Heart Failure Society of America. Her Clinician’s Guide to the 2022 Heart Failure guidelines, published in the Journal of Cardiac Failure, are a must-read for everyone!The Decipher the Guidelines: 2022 AHA / ACC / HFSA Guideline for The Management of Heart Failure series was developed by the CardioNerds and created in collaboration with the American Heart Association and the Heart Failure Society of America. It was created by 30 trainees spanning college through advanced fellowship under the leadership of CardioNerds Cofounders Dr. Amit Goyal and Dr. Dan Ambinder, with mentorship from Dr. Anu Lala, Dr. Robert Mentz, and Dr. Nancy Sweitzer. We thank Dr. Judy Bezanson and Dr. Elliott Antman for tremendous guidance.Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. Question #10 Ms. Heffpefner is a 54-year-old woman who comes to your office for a routine visit. She does report increased fatigue and dyspnea on exertion without new orthopnea or extremity edema. She was previously diagnosed with type 2 diabetes, morbid obesity, obstructive sleep apnea, and TIA. She is currently prescribed metformin 1000mg twice daily, aspirin 81mg daily, rosuvastatin 40mg nightly, and furosemide 40mg daily. In clinic, her BP is 140/85 mmHg, HR is 110/min (rhythm irregularly irregular, found to be atrial fibrillation on ECG), and BMI is 43 kg/m2. Transthoracic echo shows an LVEF of 60%, moderate LV hypertrophy, moderate LA enlargement, and grade 2 diastolic dysfunction with no significant valvulopathy. What is the best next step? A Provide reassurance B Refer for gastric bypass C Refer for atrial fibrillation ablation D Start metoprolol and apixaban Answer #10 ExplanationThe correct answer is D – start metoprolol and apixaban.Ms. Hefpeffner has a new diagnosis of atrial fibrillation (AF) and has a significantly elevated risk for embolic stroke based on her CHA2DS2-VASc score of 6 (hypertension, diabetes, heart failure, prior TIA, and female sex). The relationship between AF and HF is complex and the presence of either worsens the status of the other. Managing AF in patients with HFpEF can lead to symptom improvement (Class 2a, LOR C-EO). However, large, randomized trial data are unavailable to specifically guide therapy in patients with AF and HFpEF. Generally, management of AF involves stroke prevention, rate and/or rhythm control, and lifestyle / risk-factor modification. With regards to stroke prevention, patients with chronic HF with permanent-persistent-paroxysmal AF and a CHA2DS2-VASc score of ≥2 (for men) and ≥3 (for women) should receive chronic anticoagulant therapy (Class 1, LOE A). When anticoagulation is used in chronic HF patients with AF, a DOAC is recommended over warfarin in eligible patients (Class 1, LOE A).The decision for rate versus rhythm control should be individualized and reflects both patient symptoms and the likelihood of better ventricular function with sinus rhythm. For patients with HF and symptoms caused by AF, AF ablation is reasonable to improve symptoms and QOL (Class 2a, LOE B-R). However, referring for catheter ablation would be premature before first attempting rate control and instituting anticoagulation therapy. Traditionally, beta-blockers and nondihydropyridine calcium channel blockers are used as first-line agents for rate control in AF. Interestingly, a small open-label trial, RATE-AF in elderly patients with AF and symptoms of HF (mostly with preserved LVEF), compared bisoprolol to digoxin. Although the primary endpoint of quality of life at 6 months was similar between the 2 groups, several secondary QOL endpoints, functional capacity, and reduction in NT-proBNP favored digoxin at 12 months, with similar rate reductions in both groups. More side effects (such as dizziness, lethargy, and hypotension) were seen with bisoprolol than with digoxin. However, digoxin has a narrow therapeutic window and needs to be monitored more closely.Option A (provide reassurance) is inappropriate as this patient has heart failure with preserved EF, defined by signs and symptoms of HF in patients with an LVEF of 50% or more. Echocardiogram hints in this case include LV hypertrophy and diastolic dysfunction. Our patient also has comorbidities frequently associated with HFpEF such as hypertension, diabetes, OSA, and obesity. Other common comorbidities include CAD, CKD, and atrial arrhythmias. When diagnosing HFpEF, care must be taken to rule out mimicking conditions such as pulmonary hypertension or amyloidosis. A large portion of the management of HFpEF includes managing comorbid conditions such as hypertension, OSA, and atrial fibrillation. At this time, she is symptomatic with atrial fibrillation and rapid ventricular response, and warrants both rate control and stroke prophylaxis. Although gastric bypass should be considered for patients with a BMI >35 kg/m2 with comorbidities (such as HTN or diabetes) and patients with a BMI > 40 kg/m2 independent of comorbid conditions, this is not the best next step at this time. First, she should receive anticoagulation to reduce the risk of stroke and achieve better control of her HR and BP. Patients with HFpEF and hypertension should have medication titrated to attain blood pressure targets in accordance with published clinical practice guidelines to prevent morbidity (Class 1, LOE C-LD). Although the optimal BP goal and antihypertensive regimen in patient with HFpEF is not known, HFpEF trials so far have shown that RAAS antagonists including ACEi, ARB, MRA and possibly ARNi could be first-line agents to treat HTN in patients with HFpEF. Beta blockers may be used to treat hypertension in patients with a history ofMI, symptomatic CAD, or AF with rapid ventricular response. These effects need to be balanced with the potential contribution of chronotropic incompetence to exercise intolerance in some patients.Main TakeawayIn patients with HFpEF, the diagnosis and management of comorbidities are very important, especially the treatment of HTN (Class 1, LOE C-LD) and AF (Class 2a, LOE C-EO).Guideline Loc.Section 7.7.1, Figure 12Section 10.2 Decipher the Guidelines: 2022 Heart Failure Guidelines PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron!

Feb 22, 2023

The following question refers to Section 7.6 of the 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure. The question is asked by premedical student and CardioNerds Intern Pacey Wetstein, answered first by Baylor College of Medicine Cardiology Fellow and CardioNerds Ambassador Dr. Jamal Mahar, and then by expert faculty Dr. Nancy Sweitzer. Dr. Sweitzer is Professor of Medicine, Vice Chair of Clinical Research for the Department of Medicine, and Director of Clinical Research for the Division of Cardiology at Washington University School of Medicine. She is the editor-in-chief of Circulation: Heart Failure. Dr. Sweitzer is a faculty mentor for this Decipher the HF Guidelines series. The Decipher the Guidelines: 2022 AHA / ACC / HFSA Guideline for The Management of Heart Failure series was developed by the CardioNerds and created in collaboration with the American Heart Association and the Heart Failure Society of America. It was created by 30 trainees spanning college through advanced fellowship under the leadership of CardioNerds Cofounders Dr. Amit Goyal and Dr. Dan Ambinder, with mentorship from Dr. Anu Lala, Dr. Robert Mentz, and Dr. Nancy Sweitzer. We thank Dr. Judy Bezanson and Dr. Elliott Antman for tremendous guidance. Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. Question #9 Mr. Flo Zin is a 64-year-old man who comes to discuss persistent lower extremity edema and dyspnea with mild exertion. He takes amlodipine for hypertension but has no other known comorbidities. In the clinic, his heart rate is 52 bpm and blood pressure is 120/70 mmHg. Physical exam reveals mildly elevated jugular venous pulsations and 1+ bilateral lower extremity edema. Labs show an unremarkable CBC, normal renal function and electrolytes, a Hb A1c of 6.1%, and an NT-proBNP of 750 (no prior baseline available). On echocardiogram, his LVEF is 44% and nuclear stress testing was negative for inducible ischemia. What is the best next step in management? A Add furosemide BID and daily metolazone B Start empagliflozin and furosemide as needed C Start metoprolol succinate D No change to medical therapy Answer #9 Explanation The correct answer is B – start empagliflozin and furosemide as needed. The patient described here has heart failure with mildly reduced EF (HFmrEF), given LVEF in the range of 41-49%. In patients with HF who have fluid retention, diuretics are recommended to relieve congestion, improve symptoms, and prevent worsening HF (Class 1, LOE B-NR). For patients with HF and congestive symptoms, addition of a thiazide (eg, metolazone) to treatment with a loop diuretic should be reserved for patients who do not respond to moderate or high-dose loop diuretics to minimize electrolyte abnormalities (Class 1, LOE B-NR). Therefore, option A is not correct as he is only mildly congested on examination, and likely would not require such aggressive decongestive therapy, particularly with normal renal function. Adding a thiazide diuretic without first optimizing loop diuretic dosing would be premature. The EMPEROR-Preserved trial showed a significant benefit of the SGLT2i, empagliflozin, in patients with symptomatic HF, with LVEF >40% and elevated natriuretic peptides. The 21% reduction in the primary composite endpoint of time to HF hospitalization or cardiovascular death was driven mostly by a significant 29% reduction in time to HF hospitalization, with no benefit on all-cause mortality. Empagliflozin also resulted in a significant reduction in total HF hospitalizations, decrease in the slope of the eGFR decline, and a modest improvement in QOL at 52 weeks. Of note, the benefit was similar irrespective of the presence or absence of diabetes at baseline. In a subgroup of 1983 patients with LVEF 41% to 49% in EMPEROR-Preserved, empagliflozin, an SGLT2i, reduced the risk of the primary composite endpoint of cardiovascular death or hospitalization for HF. Therefore, in patients with HFmrEF, SGLT2i can be beneficial in decreasing HF hospitalizations and cardiovascular mortality (Class 2a, LOE B-R). Furthermore, by inhibiting glucose reabsorption in the kidney, they have a diuretic effect which may help ease congestion and limit loop diuretic dosing. SGLT2i are beneficial to the vast majority of cardiovascular patients but are contraindicated in patients with type 1 diabetes or prior episodes of diabetic ketoacidosis as they may cause euglycemic DKA. Option C is incorrect. Among patients with current or previous symptomatic HFmrEF (LVEF, 41%–49%), use of evidence-based beta blockers for HFrEF, ARNi, ACEi, or ARB, and MRAs may be considered to reduce the risk of HF hospitalization and cardiovascular mortality, particularly among patients with LVEF on the lower end of this spectrum (Class 2b, LOE B-NR). However, the patient’s heart rate is already low and so initiating a beta blocker would be inappropriate. Switching his calcium channel blocker to ARNi may be considered. Option D is not correct as we can help counsel him on lifestyle and medication changes which can relieve his symptoms and reduce his risk of HF hospitalizations and mortality. Main Takeaway In patients with HFmrEF, diuretics are useful for decongestion and symptomatic improvement (Class 1) and there is a role for GDMT including SGLT2i (Class 2a) and BB, ARNI, ACEi/ARB, MRA (Class 2b). Guideline Loc. Section 7.6.1, Figure 11 Decipher the Guidelines: 2022 Heart Failure Guidelines Page CardioNerds Episode Page CardioNerds Academy Cardionerds Healy Honor Roll CardioNerds Journal Club Subscribe to The Heartbeat Newsletter! Check out CardioNerds SWAG! Become a CardioNerds Patron!

Feb 21, 2023

The following question refers to Section 7.3 of the 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure. The question is asked by Palisades Medical Center medicine resident & CardioNerds Intern Dr. Maryam Barkhordarian, answered first by MedStar Washington Hospital Center cardiology hospitalist & CardioNerds Academy Graduate Dr. Luis Calderon, and then by expert faculty Dr. Gregg Fonarow.Dr. Fonarow is the Professor of Medicine and Interim Chief of UCLA's Division of Cardiology, Director of the Ahmanson-UCLA Cardiomyopathy Center, and Co-director of UCLA's Preventative Cardiology Program.The Decipher the Guidelines: 2022 AHA / ACC / HFSA Guideline for The Management of Heart Failure series was developed by the CardioNerds and created in collaboration with the American Heart Association and the Heart Failure Society of America. It was created by 30 trainees spanning college through advanced fellowship under the leadership of CardioNerds Cofounders Dr. Amit Goyal and Dr. Dan Ambinder, with mentorship from Dr. Anu Lala, Dr. Robert Mentz, and Dr. Nancy Sweitzer. We thank Dr. Judy Bezanson and Dr. Elliott Antman for tremendous guidance.Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. Question #8 Ms. Flo Zinn is a 60-year-old woman seen in cardiology clinic for follow up of her chronic HFrEF management. She has a history of stable coronary artery disease, hypertension, hypothyroidism, and recurrent urinary tract infections. She does not have a history of diabetes and recent hemoglobin A1c is 5.0%. Her current medications include carvedilol, sacubitril-valsartan, eplerenone, and atorvastatin. Her friend was recently placed on an SGLT2 inhibitor and asks if she should be considered for one as well. Which of the following is the most important consideration when deciding to start this patient on an SGLT2 inhibitor? A The patient does not have a history of type 2 diabetes and so does not qualify for SGLT2 inhibitor therapy B While SGLT2 inhibitors improve hospitalization rates for HFrEF, there is no evidence that they improve cardiovascular mortality C Patients taking SGLT2 inhibitors tend to suffer a more rapid decline in renal function than patients not taking SGLT2 inhibitor therapy D Patients may be at a higher risk for genitourinary infections if an SGLT2 inhibitor is started Answer #8 Explanation The correct answer is D – SGLT2 inhibitors have been associated with increased risk of genitourinary infections. Sodium-glucose co-transporter protein 2 (SGLT2) inhibitors have gathered a lot of press recently as the new kid on the block with respect to heart failure management. While they were initially developed as antihyperglycemic medications for treating diabetes, early cardiovascular outcomes trials showed reduced rates of heart failure hospitalization amongst study participants independent of glucose-lowering effects and irrespective of baseline heart failure status – only 10-14% of patients carried a heart failure diagnosis at baseline. This prompted trials to study the effects of SGLT2 inhibitors in patients with symptomatic chronic HFrEF who were already on guideline directed medical therapy irrespective of the presence of type 2 diabetes mellitus. The DAPA-HF and EMPEROR-Reduced trials showed that dapagliflozin and empagliflozin, respectively, both conferred statistically significant improvements in a composite of heart failure hospitalizations and cardiovascular death (Option B). Most interestingly, these effects were seen irrespective of diabetes history. In light of these findings, the 2022 HF guidelines recommend SGLT2 inhibitors in patients with chronic, symptomatic HFrEF with or without diabetes to reduce hospitalization for HF and cardiovascular mortality (Class I, LOE A). The benefits of SGLT2 inhibitors extend beyond cardiovascular health. Analyses of the DAPA-HF and EMPEROR-Reduced trials showed that patients receiving SGLT2 inhibitor therapy had fewer serious renal outcomes and slower rates of decline in eGFR than patients in the control groups. As with all medications, though, SGLT2 inhibitors must be used with an awareness of some potentially serious side effects. SGLT2 inhibitors have been associated with higher rates of genitourinary infections, potentially related to the increased glycosuria associated with sodium-glucose co-transporter 2 inhibition. Trials have shown a 2 to 4-fold increased risk of vulvovaginal candidiasis for patients on SGLT2is compared to placebo. SGLT2 inhibitor use has also been associated with bacterial urinary tract infections, Fournier’s gangrene, and euglycemic ketoacidosis. Main Takeaway SGLT2 inhibitors are now a class I recommendation for patients with chronic symptomatic HFrEF regardless of whether or not they have diabetes. Although SGLT2i increased risk for genital infections, they were otherwise well tolerated in the trials. Guideline Loc. Section 7.3.4 Decipher the Guidelines: 2022 Heart Failure Guidelines PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron!

Feb 15, 2023

The following question refers to Section 7.3.1 of the 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure. The question is asked by Palisades Medical Center medicine resident & CardioNerds Intern Dr. Maryam Barkhordarian, answered first by MedStar Washington Hospital Center cardiology hospitalist & CardioNerds Academy Graduate Dr. Luis Calderon, and then by expert faculty Dr. Robert Mentz. Dr. Mentz is associate professor of medicine and section chief for Heart Failure at Duke University, a clinical researcher at the Duke Clinical Research Institute, and editor-in-chief of the Journal of Cardiac Failure. Dr. Mentz is a mentor for the CardioNerds Clinical Trials Network as lead principal investigator for PARAGLIDE-HF and is a series mentor for this very 2022 heart failure Decipher the Guidelines Series. For these reasons and many more, he was awarded the Master CardioNerd Award during ACC22. Welcome Dr. Mentz! The Decipher the Guidelines: 2022 AHA / ACC / HFSA Guideline for The Management of Heart Failure series was developed by the CardioNerds and created in collaboration with the American Heart Association and the Heart Failure Society of America. It was created by 30 trainees spanning college through advanced fellowship under the leadership of CardioNerds Cofounders Dr. Amit Goyal and Dr. Dan Ambinder, with mentorship from Dr. Anu Lala, Dr. Robert Mentz, and Dr. Nancy Sweitzer. We thank Dr. Judy Bezanson and Dr. Elliott Antman for tremendous guidance. Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. Question #7 Ms. Valarie Sartan is a 55-year-old woman with a history of HFrEF (EF 35%) and well controlled, non-insulin dependent diabetes mellitus who presents to heart failure clinic for routine follow up. She is currently being treated with metoprolol succinate 200mg daily, lisinopril 10mg daily, empagliflozin 10mg daily, and spironolactone 50mg daily. She notes stable dyspnea with moderate exertion, making it difficult to do her yardwork. On exam she is well appearing, and blood pressure is 115/70 mmHg with normal jugular venous pulsations and trace bilateral lower extremity edema. On labs, her potassium is 4.0 mmol/L and creatinine is 0.7 mg/dL with an eGFR > 60 mL/min/1.73m2. Which of the following options would be the most appropriate next step in heart failure therapy? A Increase lisinopril to 40mg daily B Increase spironolactone to 100mg daily C Add sacubitril-valsartan to her regimen D Discontinue lisinopril and start sacubitril-valsartan in 36 hours E No change Answer #7 Explanation The correct answer is D – transitioning from an ACEi to an ARNi is the most appropriate next step in management. The renin-angiotensin aldosterone system (RAAS) is upregulated in patients with chronic heart failure with reduced ejection fraction (HFrEF). Blockade of the RAAS system with ACE inhibitors (ACEi), angiotensin receptor blockers (ARB), or angiotensin receptor neprilysin inhibitors (ARNi) have proven mortality benefit in these patients. The PARADIGM-HF trial compared sacubitril-valsartan (an ARNi) with enalapril in symptomatic patients with HFrEF. Patients receiving ARNi incurred a 20% relative risk reduction in the composite primary endpoint of cardiovascular death or heart failure hospitalization. Based on these results, the 2022 heart failure guidelines recommend replacing an ACEi or ARB for an ARNi in patients with chronic symptomatic HFrEF with NYHA class II or III symptoms to further reduce morbidity and mortality (Option D). This is a class I recommendation with level of evidence of B-R and is also of high economic value. Making no changes at this time would be inappropriate (Option E). While it would be reasonable to increase the dose of lisinopril to 40mg (Option A), this should be pursued only if ARNi therapy is not tolerated. Mineralocorticoid receptor antagonists (MRAs) have a class I (LOE A) recommendation in patients with HFrEF and NYHA class II to IV to reduce morbidity and mortality, provided that eGFR is >30 mL/min/1.73 m2 and serum potassium is <5.0 mEq/L, and there is careful monitoring of potassium, renal function, and diuretic dosing. However, the starting dose of spironolactone (or eplerenone) is 25 mg orally daily, increased to 50 mg daily orally after a month. Higher doses may be appropriate for other indications but are not advocated for HFrEF as the sole indication and so option B is incorrect. Guidance on starting an ARNi While switching from an ACEi to an ARNi, note that ARNi should not be administered concomitantly with ACEi or within 36 hours of the last dose of an ACEi (Class 3 for Harm, LOE B-R). This recommendation comes largely from studies of omapatrilat—a combination ACEi/neprilysin inhibitor. Patients receiving omapatrilat suffered significantly increased risk of angioedema thought secondary to dual suppression of both ACE and neprilysin leading to high concentrations of bradykinin. The current guidelines therefore recommend a washout period of at least 36 hours between the last ACEi dose and the first ARNi dose. If this patient were being transitioned from an ARB such as valsartan, then the first dose of ARNi could simply be given in lieu of the next anticipated dose of ARB. When initiating sacubitril-valsartan, it is important to monitor for signs of hypotension. With this patient’s blood pressure of 115/70 mmHg in clinic, she should have enough blood pressure room to tolerate the new medication; both PARADIGM-HF (ARNi vs ACEi in stable chronic HFrEF) and PIONEER-HF (ARNi vs ACEi in hospitalized patients with ADHF) excluded patients with SBP < 100 mmHg. That said, every patient responds differently, and anticipatory guidance should be given to anybody starting a new drug. In particular, Ms. H.F. should be counseled on symptoms that could reflect low blood pressure, such as lightheadedness or orthostatic syncope, asked to call her provider should she experience anything concerning. Laboratory follow-up should include renal function and potassium levels. ARNis should not be initiated on any patient with a history of angioedema (Class III for Harm, LOE C-LD). While this patient likely does not have this history since she is tolerating and ACEi, it is an important part of any CardioNerd’s checklist when reaching for RAAS inhibitors. Main Takeaway Patients with symptomatic HFrEF who are tolerating ACEi or ARB therapy should be transitioned to ARNi therapy to further reduce morbidity and mortality. Expert Suggestions Offer tips & tricks for initiating and monitoring ARNis in the outpatient setting. Discuss PIONEER-HF & initiation in the inpatient setting. Discuss ACEi & ARB combination therapy. Guideline Loc. Section 7.3.1 Decipher the Guidelines: 2022 Heart Failure Guidelines Page CardioNerds Episode Page CardioNerds Academy Cardionerds Healy Honor Roll CardioNerds Journal Club Subscribe to The Heartbeat Newsletter! Check out CardioNerds SWAG! Become a CardioNerds Patron!

Feb 15, 2023

CardioNerds co-founder Daniel Ambinder joins Cleveland Clinic cardiology fellows, Dr. Essa Hariri, Dr. Anna Scandinaro, and Dr. Beka Bekhdatze, Clinical pharmacist at Cleveland Clinic, Dr. Ashley Kasper, and Dr. Craig Parris from Ohio State University Medical Center for a walk at Edgewater Park in Cleveland, Ohio. Dr. Andrew Higgins (Crtitical Care Cardiology and Advanced HF / Transplant Cardiology at Cleveland Clinic) provides the ECPR for this episode. They discuss the following case involving a rare cause of non-ischemic cardiomyopathy. A young African American male was admitted for cardiogenic shock following an admission a month earlier for treatment resistant psychosis. He was diagnosed with medication-induced non-ischemic cardiomyopathy, which resolved with a remarkable recovery of his systolic function after discontinuation of the culprit medication, Clozapine. Episode notes were drafted by Dr. Essa Hariri. Audio editing by CardioNerds Academy Intern, student doctor Shivani Reddy. Enjoy this case report co-published in US Cardiology Review: Clozapine-induced Cardiomyopathy: A Case Report CardioNerds is collaborating with Radcliffe Cardiology and US Cardiology Review journal (USC) for a ‘call for cases’, with the intention to co-publish high impact cardiovascular case reports, subject to double-blind peer review. Case Reports that are accepted in USC journal and published as the version of record (VOR), will also be indexed in Scopus and the Directory of Open Access Journals (DOAJ). CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls - An Unusual Case of Non-ischemic Cardiomyopathy The diagnosis of drug-induced non-ischemic cardiomyopathy is usually one of exclusion. High clinical suspicion is needed to diagnose drug-induced cardiomyopathy. Missing the culprit medication causing drug-induced cardiomyopathy could be detrimental as there is a high probability of reversing a systolic dysfunction after stopping the offending medication. Clozapine is an effective medication for the treatment-resistant schizophrenia and is associated with reduced suicide risk. Clozapine is reported to cause drug-induced cardiomyopathy and is more common with rapid drug titration. Clozapine is more commonly associated with myocarditis. Close monitoring and vigilance are critical to preventing cardiac complications associated with initiating clozapine. The management of clozapine-associated cardiomyopathy includes clozapine cessation and heart failure guideline-directed medical therapy. Show Notes - An Unusual Case of Non-ischemic Cardiomyopathy We treated a case of clozapine-associated cardiomyopathy presenting in cardiogenic shock. Drug-induced cardiomyopathy is a common yet under-recognized etiology of non-ischemic cardiomyopathy. Clozapine is an FDA-approved atypical antipsychotic medication frequently prescribed for treatment-resistant schizophrenia and the only antipsychotic agent that has been proven to significantly reduce suicide among this patient population. However, Clozapine is reported to be associated with several forms of cardiotoxicity, including myocarditis (most common), subclinical clozapine associated cardiotoxicity, and least commonly, drug-induced cardiomyopathy. Clozapine-associated cardiomyopathy should be considered as a differential diagnosis in schizophrenic patients presenting with signs of acute heart failure. Rapid titration of clozapine is a risk factor for clozapine-associated cardiomyopathy and clozapine-associated myocarditis. To date, there is no evidence or consensus supporting preemptive screening. According to the American Psychiatric Association, whenever clozapine-induced myocarditis or cardiomyopathy is suspected, a cardiology consult is warranted. Experts recommend, when initiating clozapine, to obtain baseline troponin, CRP, and echocardiography upon drug initiation. This is followed by daily symptom assessment and a hemodynamic assessment on every other day. A biochemical assessment of CRP and troponin levels is warranted every 7 days. The authors recommend clozapine caseation if troponin rises above twice the upper normal limit or if CRP levels exceeds 100 mg/L. Because clozapine is a highly effective medication in treating schizophrenia, close monitoring and vigilance is critical to prevent deleterious complications associated with drug cardiotoxicity. Several mechanisms have been proposed to explain the cardiotoxicities reported with clozapine. Most patients with clozapine-associated cardiotoxicity remain asymptomatic, while others may present with typical acute congestive heart failure. The most common presenting symptom was shortness of breath (60%) followed by palpitations (36%), and the main echocardiographic finding in all patients with this disease is systolic dysfunction with reduced ejection fraction. The management of clozapine-associated cardiomyopathy includes clozapine cessation and heart failure guideline-directed medical therapy. Clozapine suspension along with conventional heart failure management have led to a significant improvement in left ventricular function. Decisions regarding resuming clozapine therapy are highly individualized and should consider weighing in the risks and benefits of treatment. Whenever clozapine is rechallenged, very close monitoring and frequent echocardiography may be warranted to prevent subsequent cardiotoxicity. References - An Unusual Case of Non-ischemic Cardiomyopathy 1. Tsao CW, Aday AW, Almarzooq ZI, et al. Heart Disease and Stroke Statistics-2022 Update: A Report from the American Heart Association. Circulation. 2022;145(8). doi:10.1161/CIR.0000000000001052 2. Heidenreich PA, Albert NM, Allen LA, et al. Forecasting the impact of heart failure in the united states a policy statement from the american heart association. Circ Heart Fail. 2013;6(3). doi:10.1161/HHF.0b013e318291329a 3. VanDyck TJ, Pinsky MR. Hemodynamic monitoring in cardiogenic shock. Curr Opin Crit Care. 2021;27(4). doi:10.1097/MCC.0000000000000838 4. Keepers GA, Fochtmann LJ, Anzia JM, et al. The American psychiatric association practice guideline for the treatment of patients with schizophrenia. American Journal of Psychiatry. 2020;177(9). doi:10.1176/appi.ajp.2020.177901 5. Hennen J, Baldessarini RJ. Suicidal risk during treatment with clozapine: A meta-analysis. Schizophr Res. 2005;73(2-3). doi:10.1016/j.schres.2004.05.015 6. Taipale H, Tanskanen A, Mehtälä J, Vattulainen P, Correll CU, Tiihonen J. 20-year follow-up study of physical morbidity and mortality in relationship to antipsychotic treatment in a nationwide cohort of 62,250 patients with schizophrenia (FIN20). World Psychiatry. 2020;19(1):61-68. doi:10.1002/wps.20699 7. Citrome L, McEvoy JP, Saklad SR. A guide to the management of clozapine-related tolerability and safety concerns. Clin Schizophr Relat Psychoses. 2016;10(3). doi:10.3371/1935-1232.10.3.163 8. Knoph KN, Morgan RJ, Palmer BA, et al. Clozapine-induced cardiomyopathy and myocarditis monitoring: A systematic review. Schizophr Res. 2018;199. doi:10.1016/j.schres.2018.03.006 9. Kanniah G, Kumar S. Clozapine associated cardiotoxicity: Issues, challenges and way forward. Asian J Psychiatr. 2020;50. doi:10.1016/j.ajp.2020.101950 10. Curto M, Girardi N, Lionetto L, Ciavarella GM, Ferracuti S, Baldessarini RJ. Systematic Review of Clozapine Cardiotoxicity. Curr Psychiatry Rep. 2016;18(7). doi:10.1007/s11920-016-0704-3 11. Baran DA, Grines CL, Bailey S, et al. SCAI clinical expert consensus statement on the classification of cardiogenic shock: This document was endorsed by the American College of Cardiology (ACC), the American Heart Association (AHA), the Society of Critical Care Medicine (SCCM), and the Society of Thoracic Surgeons (STS) in April 2019. Catheterization and Cardiovascular Interventions. 2019;94(1). doi:10.1002/ccd.28329 12. Alawami M, Wasywich C, Cicovic A, Kenedi C. A systematic review of clozapine induced cardiomyopathy. Int J Cardiol. 2014;176(2). doi:10.1016/j.ijcard.2014.07.103 13. Arzuk E, Karakuş F, Orhan H. Bioactivation of clozapine by mitochondria of the murine heart: Possible cause of cardiotoxicity. Toxicology. 2021;447. doi:10.1016/j.tox.2020.152628 14. Vaddadi KS, Soosai E, Vaddadi G. Low blood selenium concentrations in schizophrenic patients on clozapine. Br J Clin Pharmacol. 2003;55(3). doi:10.1046/j.1365-2125.2003.01773.x 15. Yost BL, Gleich GJ, Fryer AD. Ozone-induced hyperresponsiveness and blockade of M2 muscarinic receptors by eosinophil major basic protein. J Appl Physiol. 1999;87(4). doi:10.1152/jappl.1999.87.4.1272 16. Yuen JWY, Kim DD, Procyshyn RM, White RF, Honer WG, Barr AM. Clozapine-induced cardiovascular side effects and autonomic dysfunction: A systematic review. Front Neurosci. 2018;12(APR). doi:10.3389/fnins.2018.00203 17. Ronaldson KJ, Taylor AJ, Fitzgerald PB, Topliss DJ, Elsik M, McNeil JJ. Diagnostic characteristics of clozapine-induced myocarditis identified by an analysis of 38 cases and 47 controls. Journal of Clinical Psychiatry. 2010;71(8). doi:10.4088/JCP.09m05024yel 18. de Leon J, Tang YL, Baptista T, Cohen D, Schulte PFJ. Titrating clozapine amidst recommendations proposing high myocarditis risk and rapid titrations. Acta Psychiatr Scand. 2015;132(4). doi:10.1111/acps.12421 19. Ronaldson KJ, Fitzgerald PB, Taylor AJ, Topliss DJ, Wolfe R, McNeil JJ. Rapid clozapine dose titration and concomitant sodium valproate increase the risk of myocarditis with clozapine: A case-control study. Schizophr Res. 2012;141(2-3). doi:10.1016/j.schres.2012.08.018 20. Ronaldson KJ,

Feb 12, 2023

Renal replacement therapy (RRT) is routinely utilized in the CICU. Series co-chairs Dr. Eunice Dugan and Dr Karan Desai along with CardioNerds Co-founder Dr. Daniel Ambinder were joined by FIT lead and CardioNerds Ambassador from University of Washington, Dr. Tomio Tran. Our episode expert is world-renowned nephrologist Dr. Joel Topf. Dr. Topf is Medical Director of Research at St. Clair Nephrology, and editor of the Handbook of Critical Care Nephrology. In this episode, we describe a case of cardiogenic shock due to acute myocardial infarction resulting in renal failure, ultimately requiring continuous RRT (CRRT). We discuss the most common causes of AKI within the cardiac ICU, indications for initiating RRT, evidence on the timing of RRT, different modes of RRT, basic management of the RRT circuit, and how to transition patients off of RRT during renal recovery. Episode notes were drafted by Dr. Tomio Tran. Audio editing by CardioNerds Academy Intern, Dr. Maryam Barkhordarian. The CardioNerds Cardiac Critical Care Series is a multi-institutional collaboration made possible by contributions of stellar fellow leads and expert faculty from several programs, led by series co-chairs, Dr. Mark Belkin, Dr. Eunice Dugan, Dr. Karan Desai, and Dr. Yoav Karpenshif. Pearls • Notes • References • Production Team CardioNerds Cardiac Critical Care PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls and Quotes - Approach to Renal Replacement Therapy in the CICU Do not commit “Renalism” - withholding lifesaving treatments from patients with renal impairment due to fear of causing renal injury. Shared decision making is key. In the ICU, most of the time, AKI is caused by ATN due to adverse hemodynamics. Nephrologists can help determine the cause if the patient has an atypical presentation. Late dialysis initiation is non-inferior to early dialysis initiation. Early initiation may lead to higher rates of prolonged time on dialysis. Slow low efficiency daily diafiltration (SLEDD) vs CRRT are equivalent in terms of outcomes and are the preferred methods among patients with hypotension. Intermittent Hemodialysis (iHD) can be used once patients are hemodynamically stable. A “Furosemide Stress Test” can be used to test intact renal function or renal recovery by challenging the nephron to make urine. Show notes - Approach to Renal Replacement Therapy in the CICU What are the risk factors and differential for AKI in the CICU? Start by using the pre-renal vs intrinsic renal vs post-renal framework. Additional considerations in cardiac patients include contrast induced nephropathy, pigment nephropathy, cardiorenal syndrome. Enjoy Episode 262. Management of Cardiorenal Syndrome in the CICU. In the ICU setting, intrinsic renal injury due to ATN is among the most common etiology of AKI. Many risk factors for AKI are not modifiable in the ICU. Optimize renal function by avoiding nephrotoxins, minimizing contrast usage, and keeping the MAP >65-75 mmHg. Contrast nephropathy as an etiology is questionable and may be a marker of a sicker patient population. Avoid “Renalism” - providing substandard care to patients with renal disease due to fear of worsening renal function. Most etiologies are treated with supportive care. What is the approach to timing of renal replacement therapy initiation? Definitions for early vs late vs very late initiation of RRT:Early – Worsening AKI without indications for RRTLate – Worsening AKI with relative indications for RRT Very late – Worsening AKI with strict indications for RRT Late initiation is noninferior in terms of mortality; early initiation is associated with higher rates of prolonged/permanent RRT.1,2,3 Very late initiation associated with worse outcomes.4 In general, start RRT if there are absolute indications (“AEIOU) or the patient is anuric with a high BUN (~140) as delaying RRT much further is associated with worse outcomes. “Furosemide Stress Test” (FST) can be used to predict RRT need.51 mg/kg IV for diuretic naive, 1.5 mg/kg IV if on diuretic Goal = 200 cc urine over 1-2 hours For the non-nephrologists, what are options for RRT acutely and how do they work? There are two principles of RRT:Convection – movement of solutes through semipermeable membrane using pressureUltrafiltration – volume removal using convection; fluid is then replaced to prevent hypovolemiaFluid removed has the same composition of the plasmaNegative fluid balance is the difference between volume removed and replacement fluid; goal usually 25-250 cc/hour Diffusion – movement of solutes from high to low concentrationDialysate runs countercurrent through semipermeable membraneTypical dialysate composition – normal sodium, magnesium, low potassium, no creatinine, no BUN, high bicarbonate Does not remove fluid There are 3 types of RRT: iHD (intermittent hemodialysis), CRRT (continuous renal replacement therapy), SLEDD (slow low efficiency daily diafiltration)None have been shown to be superior in normotensive patientsiHD can remove potassium and toxins more quicklySLEDD and CRRT are equivalent and preferred for hypotensive patients.6SLEDD is less labor intensiveInstitutions usually have a preference of one modality over another Peritoneal dialysis has been used in the ICU in some specialized centers, but is not common. There are 3 methods of CRRT:Continuous hemodialysisRemoves fluid by diffusionUses dialysate, no replacement fluidRemoves small-medium sized moleculesContinuous hemofiltrationRemoves fluid by convectionNo dialysate, needs replacement fluidRemoves large sized molecules Continuous hemodiafiltrationRemoves fluid by diffusion and convection Uses dialysate and replacement fluid What should non-nephrologists understand about daily management of patients on CVVH? CICU clinicians should frequently communicate fluid balance and hemodialysis goals with nephrology and nurses The circuit has 2 pumps: 1 to pull fluid, another to push fluid backMonitor daily pressure trends as deviations may implicate issues with the access Look at I/Os on the circuit to determine fluid balance Ask RN if filter is clotting off because this can cause blood loss anemia due to the amount of blood lost when the circuit needs to be changed Electrolyte management:After 1-2 days of normalizing hyperkalemia, try to keep potassium steady using a 4 K bath CRRT can drop phosphorous precipitously, which may cause cardiac myocyte dysfunction; add Na-Phos if necessary. Very important: frequent line checks to identify infections. If the line is in for several days and begin considering a switch to a tunneled dialysis catheter, especially if longer-term RRT is expected. How does the CICU team monitor for native renal recovery and initiate cardiovascular GDMT? The CICU team should assess daily trends in urine output. Patients may spontaneously make more urine especially as critical illness resolves. Consider trialing diuretics (FST) to assess recovery. Once hemodynamics improves, transition to iHD if there is still a persistent indication for RRT. Temporary dialysis lines are infection prone; consider exchanging for a tunneled iHD line if in place >1 week. Many GDMT medications, often crucial for CV optimization, are considered nephrotoxic and may increase serum potassium. Therefore, it is important to be thoughtful about timing of initiation. Consider initiating GDMT when the Cr is trending towards baseline. Cr is “cosmetic”, and the team should tolerate some Cr increases with life-saving GDMT. Please note that trends in potassium levels is more important than Cr with “nephrotoxic” CV meds. There may be a role for gastrointestinal potassium binders to facilitate GDMT optimization, but the clinical safety and efficacy remains unanswered (trials are underway). It is crucial for patients to get back on GDMT for improved long term cardiac outcomes. References Gaudry S, Hajage D, Schortgen F, et al. Initiation strategies for renal-replacement therapy in the intensive care unit. New England Journal of Medicine. 2016;375(2):122-133. STARRT-AKI Investigators, Canadian Critical Care Trials Group, Australian and New Zealand Intensive Care Society Clinical Trials Group, et al. Timing of initiation of renal-replacement therapy in acute kidney injury. N Engl J Med. 2020;383(3):240-251. Zarbock A, Kellum JA, Schmidt C, et al. Effect of early vs delayed initiation of renal replacement therapy on mortality in critically ill patients with acute kidney injury: the elain randomized clinical trial. JAMA. 2016;315(20):2190. Gaudry S, Hajage D, Martin-Lefevre L, et al. Comparison of two delayed strategies for renal replacement therapy initiation for severe acute kidney injury (AKIKI 2): a multicentre, open-label, randomised, controlled trial. The Lancet. 2021;397(10281):1293-1300. Chawla LS, Davison DL, Brasha-Mitchell E, et al. Development and standardization of a furosemide stress test to predict the severity of acute kidney injury. Crit Care. 2013;17(5):R207. Rabindranath K, Adams J, Macleod AM, Muirhead N. Intermittent versus continuous renal replacement therapy for acute renal failure in adults. Cochrane Database Syst Rev. 2007;(3):CD003773.

Feb 10, 2023

Join CardioNerds to learn about patent ducts arteriosus and Eisenmenger syndrome! Dr. Dan Ambinder (CardioNerds co-founder), ACHD series co-chair Dr. Dan Clark, Dr. Tony Pastor (ACHD fellow, Harvard Medical School), and Dr. Kate Wilcox, Medicine/Pediatrics Resident, Medical College of Wisconsin join Dr. Candice Silversides (Editor-in-chief #JACCAdvances) for this terrific discussion. Notes were drafted by Dr. Kate Wilcox. .Audio editing by CardioNerds Academy Intern, Dr. Maryam Barkhordarian. The CardioNerds Adult Congenital Heart Disease (ACHD) series provides a comprehensive curriculum to dive deep into the labyrinthine world of congenital heart disease with the aim of empowering every CardioNerd to help improve the lives of people living with congenital heart disease. This series is multi-institutional collaborative project made possible by contributions of stellar fellow leads and expert faculty from several programs, led by series co-chairs, Dr. Josh Saef, Dr. Agnes Koczo, and Dr. Dan Clark. The CardioNerds Adult Congenital Heart Disease Series is developed in collaboration with the Adult Congenital Heart Association, The CHiP Network, and Heart University. See more Disclosures: None CardioNerds Adult Congenital Heart Disease PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls - Patent Ductus Arteriosus & Eisenmenger Syndrome The ductus arteriosus, which is formed from the distal portion of the left sixth arch, is key to fetal circulation because it allows blood to bypass the high resistance pulmonary circuit present in utero. After birth there is a significant drop in pulmonary vascular resistance (PVR) which generally leads to functional ductal closure within 48 hours (permanent seal takes 2-3 weeks to form). Risk factors for having a PDA include birth before 37 weeks of gestation, trisomy 21, and congenital rubella. A PDA results in a left to right shunt (qP:qS >1) which over time overloads the left side of the heart and causes pulmonary vascular remodeling. The extra workload on the left side of the heart causes left atrial (can cause atrial arrhythmias) and left ventricular dilation. If left untreated you can eventually have shunt reversal due to very high PVR (Eisenmenger physiology). There are some treatment options at this point (pulmonary vasodilators, etc) but it’s definitely better to close the PDA before this point. One interesting physical exam finding that can stem from shunt reversal in a hemodynamically significant PDA is differential cyanosis (upper body or pre-ductal saturations will be higher than lower body/post-ductal saturations). You can also see clubbing in the toes but not the hands for the same reason. Meet Our Collaborators! Adult Congenital Heart AssociationFounded in 1998, the Adult Congenital Heart Association is an organization begun by and dedicated to supporting individuals and families living with congenital heart disease and advancing the care and treatment available to our community. Our mission is to empower the congenital heart disease community by advancing access to resources and specialized care that improve patient-centered outcomes. Visit their website (https://www.achaheart.org/) for information on their patient advocacy efforts, educational material, and membership for patients and providers CHiP Network The CHiP network is a non-profit organization aiming to connect congenital heart professionals around the world. Visit their website (thechipnetwork.org) and become a member to access free high-quality educational material, upcoming news and events, and the fantastic monthly Journal Watch, keeping you up to date with congenital scientific releases. Visit their website (https://thechipnetwork.org/) for more information. Heart UniversityHeart University aims to be “the go-to online resource” for e-learning in CHD and paediatric-acquired heart disease. It is a carefully curated open access library of educational material for all providers of care to children and adults with CHD or children with acquired heart disease, whether a trainee or a practicing provider. The site provides free content to a global audience in two broad domains: 1. A comprehensive curriculum of training modules and associated testing for trainees. 2. A curated library of conference and grand rounds recordings for continuing medical education. Learn more at www.heartuniversity.org/ CardioNerds Adult Congenital Heart Disease Production Team Amit Goyal, MD Daniel Ambinder, MD

Feb 6, 2023

The Cardiorenal Syndrome is commonly encountered, and frequently misunderstood. Join the CardioNerds team as we discuss the complex interplay between the heart and kidneys with Dr. Elliott Miller (Assistant Professor of Medicine at Yale University School of Medicine and Associate Medical Director of the Cardiac Intensive Care Unit of Yale New Haven Hospital), and Dr. Nayan Arora (Clinical Assistant Professor of Medicine and Nephrologist at the University of Washington Medical Center). We are hosted by FIT lead Dr. Matthew Delfiner (Cardiology Fellow at Temple University), Cardiac Critical Care Series Co-Chairs Dr. Mark Belkin (AHFTC faculty at University of Chicago) and Dr. Karan Desai (Cardiologist at Johns Hopkins Hospital), and CardioNerds Co-Found Dr. Dan Ambinder. In this episode we discuss the definition and pathophysiology of the cardiorenal syndrome, explore strategies for initial diuresis and diuretic resistance, and management of the common heart failure medications in this setting. Show notes were developed by Dr. Matthew Delfiner. Audio editing by CardioNerds Academy Intern, student doctor Akiva Rosenzveig. The CardioNerds Cardiac Critical Care Series is a multi-institutional collaboration made possible by contributions of stellar fellow leads and expert faculty from several programs, led by series co-chairs, Dr. Mark Belkin, Dr. Eunice Dugan, Dr. Karan Desai, and Dr. Yoav Karpenshif. Pearls • Notes • References • Production Team CardioNerds Cardiac Critical Care PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls and Quotes - Management of Cardiorenal Syndrome in the CICU Cardiorenal syndrome (CRS) represents a range of clinical entities in which there is both heart and kidney dysfunction, and can be driven by one, or both, of the organs. CRS is caused by reduced renal perfusion, elevated renal congestion, or a combination of the two. Treatment therefore focuses on increasing perfusion, by optimizing cardiac output and mean arterial pressure, and reducing congestion through diuresis. Patients should be monitored for an adequate response to the initial diuretic dose within 2 hours of administration. If the response is inadequate, the loop diuretic dose should be doubled. Diuretic resistance can be managed via sequential nephron blockade, most commonly with thiazide diuretics, but also with amiloride, high-dose spironolactone, or acetazolamide, as these target different regions of the nephron. In cases of refractory diuretic resistance, hypertonic saline can be considered with the help of an experienced clinician. Continuation or cessation of renin-angiotensin-aldosterone system (RAAS) inhibitors in the setting of CRS should be made on a case-by-case basis. Show notes - Management of Cardiorenal Syndrome in the CICU 1. Cardiorenal syndrome (CRS) is a collection of signs/symptoms that indicate injury to both the heart and kidneys. Organ dysfunction in one can drive dysfunction in the other. Cardiorenal syndrome can be categorized as: Type 1 - Acute heart failure causing acute kidney injury Type 2 - Chronic heart failure causing chronic kidney injury Type 3 - Acute kidney injury causing acute heart failure Type 4 - Chronic kidney injury causing chronic heart failure Type 5 - Co-development of heart and kidney injury by another systemic process. These categories can be helpful for education, discussion, and research purposes, but they do not usually enter clinical practice on a regular basis since different categories of cardiorenal syndrome are not necessarily treated differently. 2. CRS is caused by either reduced renal perfusion, elevated renal congestion, or a combination of the two. When dealing with CRS, note that: CRS can be caused by poor kidney perfusion, though is mostly driven by low renal perfusion pressure. Renal perfusion pressure is the gradient between renal arteries and renal veins, which can be approximated by mean arterial pressure (MAP) minus central venous pressure (CVP) CRS can therefore be treated by reducing CVP (i.e. with diuresis) or increasing MAP or cardiac output 3. Renal decongestion is achieved primarily through diuresis. For diuretic “naïve” patients, furosemide 40 mg IV is a reasonable starting dose For patients already on diuretics prior to admission, increasing their home dose by 2.5x (administered intravenously) usually achieves an adequate initial response Patients should be reassessed 1-2 hours after their initial diuretics dose. If the patient has not made 200 mL of urine, the loop diuretic dose should be doubled. Diuretic dose and urine output have a logarithmic relationship, meaning doubling the dose does not double the urine output. Once you reach a certain dose threshold, you won’t necessarily increase the quantity of diuresis, but rather you will increase the duration of diuresis. 4. It is okay if creatinine rises with diuresis, to a degree. Creatinine elevation with decongestion is more a sign of hemoconcentration and is paradoxically associated with better outcomes. However, if the creatinine rises by more than 30-50% and you are not seeing clinical evidence of decongestion, then that is likely a poor prognostic sign. 5. There are multiple ways to manage diuretic resistance. Diuretic resistance is often due to a variety of mechanisms including increased sodium reabsorption and hypertrophy of the distal convoluted tubule. Sequential nephron blockade can be considered, most commonly with a thiazide diuretic in addition to a loop diuretic, after the loop diuretic dose is sufficiently optimized. Patients with diuretic resistance may also have increased sodium reabsorption in the proximal tubule, so acetazolamide may be helpful in certain cases. Check out the CardioNerds Journal Club on the ADVOR trial! Amiloride and high doses of spironolactone can be used to target the collecting ducts. Finally, hypertonic saline has been used to address persistent diuretic resistance in certain cases, though should be done with an experienced clinician. 6. Decisions regarding cessation versus continuation of renin-angiotensin-aldosterone system (RAAS) inhibitors in the setting of CRS should be made on a case-by-case basis. RAAS inhibitors may not specifically cause harm, but they may make it difficult to discern whether a change in creatinine related to their use versus worsening renal function. On the other hand, there is an increased likelihood that RAAS inhibitors are not resumed when they are held in CRS, which is associated with worse outcomes. Therefore, it is imperative that there is a plan made to resume these medications if they are held. References Jentzer, Bihorac, Brusca et al. “Contemporary Management of Severee Acute Kidney Injury and Refractory Cardiorenal Syndrome: JACC Council Perspectives.” J Am Coll Cardiol. 2020 Sep, 76 (9) 1084-1101. https://www.jacc.org/doi/abs/10.1016/j.jacc.2020.06.070 Rangaswami J., Bhalla V., Blair J.E.A., et al. "Cardiorenal syndrome: classification, pathophysiology, diagnosis, and treatment strategies: a scientific statement from the American Heart Association". Circulation 2019;139:e840-e878: https://www.ahajournals.org/doi/full/10.1161/CIR.0000000000000664 Jentzer J.C., Chawla L.S. "A clinical approach to the acute cardiorenal syndrome". Crit Care Clin 2015; 31:685-703. https://www.criticalcare.theclinics.com/article/S0749-0704(15)00048-2/abstract

Jan 31, 2023

Dr. Filip Ionescu (hematology-oncology fellow at Moffitt Cancer Center in Tampa, FL), Dr. Teodora Donisan (cardiology fellow at the Mayo Clinic in Rochester, MN and CardioNerds House Thomas chief), Dr. Sarah Waliany (internal medicine chief resident at Stanford University in Palo Alto, CA), Dr. Dinu Balanescu (internal medicine chief resident at Beaumont Hospital in Royal Oak, MI) and Dr. Amit Goyal (structural interventional cardiology fellow at the Cleveland Clinic, in Cleveland, OH and CardioNerds Co-Founder), discuss the cardiotoxicities of common cancer treatments with Dr. Susan Dent, a medical oncologist and one of the founders of the field of Cardio-Oncology. Using the recently published ESC Guidelines on cardio-oncology, they cover cardiovascular risk stratification in oncology patients, pretreatment testing, as well as prevention and management of established cardiotoxicity resulting from anthracyclines, trastuzumab, and fluoropyrimidines. They touch on the unique aspects of cardio-oncology encountered in patients with breast cancer, rectal cancer, and lung cancer, who are frequently the recipients of multiple cardiotoxic treatments. Audio editing by CardioNerds Academy Intern, student doctor Chelsea Amo Tweneboah. Access the CardioNerds Cardiac Amyloidosis Series for a deep dive into this important topic. This episode is supported by a grant from Pfizer Inc. This CardioNerds Cardio-Oncology series is a multi-institutional collaboration made possible by contributions of stellar fellow leads and expert faculty from several programs, led by series co-chairs, Dr. Giselle Suero Abreu, Dr. Dinu Balanescu, and Dr. Teodora Donisan. Pearls • Notes • References • Production Team CardioNerds Cardio-Oncology PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls and Quotes - Cancer Therapy-Related Cardiac Dysfunction (CTRCD) – The Oncologist Perspective with Dr. Susan Dent Formal cardiovascular risk stratification must be performed prior to initiating a potentially cardiotoxic anticancer treatment regimen. Considering both drug toxicity and patient-related factors (e.g., age, smoking, hypertension etc) is important. Anthracyclines affect the cardiomyocyte in complex ways which lead to a largely irreversible cardiomyopathy. All patients should have a pretreatment echocardiogram and ECG. Trastuzumab cardiotoxicity, by contrast, is more like stunning the myocardium, which manifests as a reversible decrease in left ventricular ejection fraction which generally normalizes upon discontinuation of the drug. The treatment of chemotherapy-induced cardiomyopathy should involve interdisciplinary discussions and shared decision making with the patient. Beyond guideline-directed medical therapy of heart failure with reduced ejection fraction, management can include temporarily holding or permanently discontinuing the offending agent. Fluoropyrimidine-associated cardiotoxicity manifests as cardiac ischemia from coronary vasospasm. A 5FU infusion is essentially a stress test as it tends to unmask clinically silent atherosclerosis. Show notes What is the basic pretreatment assessment of any oncology patient who is to receive a potentially cardiotoxic regimen? Awareness and management of the cardiovascular toxicity of oncology treatments are of paramount importance to be able to deliver treatment safely and to achieve maximal efficacy guided by an expert multidisciplinary team. Thanks to Dr. Dent and her colleagues’ work, this year we have seen the publication of the first Cardio-Oncology guideline (1). Perhaps the most important recommendation is that cancer patients about to start a cardiotoxic regimen should undergo formal cardiovascular risk stratification by considering both the adverse profile of the planned treatment and patient-related factors (e.g., preexisting heart disease, hypertension, smoking). High-risk patients may be referred early to a cardio-oncologist who can anticipate and mitigate toxicities. In addition to risk stratification, specific treatment modalities may require additional imaging and biochemical testing as outlined next. How does anthracycline-induced cardiotoxicity present and what are the risk factors to consider? Anthracycline-induced cardiotoxicity generally manifests as a permanent decrease in left ventricular ejection fraction (LVEF) caused by direct toxic effect of the cytotoxic chemotherapy on the cardiomyocytes. The risk factors for developing anthracycline-induced cardiotoxicity are cumulative anthracycline dose, advanced age, pretreatment low-normal LVEF, prior cardiovascular disease, as well as other established cardiovascular risk factors (e.g., hypertension, diabetes, obesity, smoking). What is included in the work-up of a patient about to begin an anthracycline-containing regimen? All patients who are about to received anthracyclines require a baseline echocardiogram, ideally with global longitudinal strain, and an electrocardiogram. For patients who are at moderate-to-high risk of developing cardiomyopathy, B-type natriuretic peptide and Troponin can also be helpful for monitoring. How is established anthracycline-induced cardiotoxicity typically managed? When a decrease in LVEF below 50% is detected, management usually involves holding the anthracycline and repeating imaging. At this point, discussion with a cardio-oncologist about the initiation of ACC/AHA guideline-directed medical therapy (GDMT) is warranted. If there is improvement in the LVEF with this approach, the decision to rechallenge is nuanced and often part of a multidisciplinary and shared decision-making process with the patient. What are some proven strategies to prevent or mitigate anthracycline-induced cardiotoxicity? In the case of a rechallenge, two ways to mitigate the risk of cardiac damage are using liposomal doxorubicin, which is a less cardiotoxic anthracycline formulation, and co-administration of dexrazoxane, which is the only FDA-approved cardioprotectant for use in this setting. What is trastuzumab and how does the cardiotoxicity associated with its use differ from that caused by anthracyclines? Trastuzumab is a monoclonal antibody directed against the HER2 receptor molecule expressed on breast cancer cells. The actual mechanism of trastuzumab-associated cardiotoxicity is not clear, but it appears to be more akin to myocardial stunning and is generally reversible. If it occurs, a decrease in LVEF appears early and for most patients withholding the drug is effective in reversing the effect. How is trastuzumab-associated cardiotoxicity managed? For those patients with a nadir LVEF 10% of patients treated with a 5FU infusion (or continuous capecitabine) versus in 3-5% of those who receive the 5FU as a bolus. What is the management of fluoropyrimidine-associated cardiotoxicity? Rechallenge is possible in select patients who take active part in the decision-making process and who are deemed to derive substantially larger benefits than risks from continuing. When done, rechallenges usually take place in an inpatient setting with close monitoring and co-administration of calcium channel blockers and nitrates. Is it possible to rechallenge patients with ischemic symptoms induced by fluoropyrimidine treatment? Generally, presentations are clinically apparent with symptoms of ischemia and management necessarily includes holding the drug and performing an ischemic work-up which may require invasive testing such as coronary angiography. If there is a clear temporal association with fluoropyrimidine use and ischemic symptoms, a multidisciplinary discussion on whether treatment should be continued is warranted. What is unique about the cardiotoxicity of oncology therapy in lung cancer patients?

Jan 22, 2023

CardioNerds Cofounder Dr. Amit Goyal join Dr. Usman Hasnie and Dr. Will Morgan from University of Alabama at Birmingham for a hike up Red Mountain. They discuss the following case: A 75-year-old woman with prior mitral valve ring annuloplasty presented with subacute, intermittent, self-limiting neurologic deficits. Brain MRI revealed multiple subacute embolic events consistent with cardioembolic phenomena. Transesophageal echochardiogram discovered a mobile mass on the mitral valve as the likely cause for cardioembolic stroke. She was taken for surgical repair of the mitral valve. Tissue biopsy confirmed that the mass was an IgG4-related pseudotumor. Expert commentary is provided by Dr. Neal Miller (Assistant Professor of Cardiology, University of Alabama at Birmingham). Audio editing by CardioNerds Academy Intern, student doctor Adriana Mares Check out this published case report here: IgG4-Related Disease Masquerading as Culture-Negative Endocarditis! CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls - Cardioembolic Stroke due to an IgG4-related pseudotumor Surgical indications for endocarditis include severe heart failure, valvular dysfunction with severe hemodynamic compromise, prosthetic valve infection, invasion beyond the valve leaflets, recurrent systemic embolization, large mobile vegetations, or persistent sepsis (in infective endocarditis) despite adequate antibiotic therapy. IgG4 related disease is rare, and likely underrecognized due to the lack of reliable biomarkers. Biopsy and histologic confirmation are imperative to clinch the diagnosis. Cardiac manifestations of IgG4-related disease are rare but are often related to aortopathies. Valvular disease is extremely rare as a manifestation of the disease. Treatment of IgG4 related disease includes steroids as the first line treatment. IgG4 related disease requires a multi-disciplinary approach to both diagnose and treat. Show Notes - Cardioembolic Stroke due to an IgG4-related pseudotumor Notes were drafted by Dr. Hasnie and Dr. Morgan IgG4-related disease has a very diverse presentation including mimicry of infection, malignancy and other autoimmune conditions. It is a fibroinflammatory condition that results in deposition of IgG4 positive plasma cells. It has been described in multiple organ systems including the pancreas, kidneys, lungs and salivary glands. Cardiac manifestations are extremely rare and valvular disease even more so. There are thirteen cases of IgG4 related valvular disease, and of these only two had mitral valve involvement such as this case. The most commonly reported cardiovascular manifestations are related to aortopathies. This disease remains poorly understood at this point. There are no true biomarkers that can be used to risk stratify the diagnosis for clinicians. Biopsy is imperative to the diagnosis. Even serum IgG4 levels are normal in 30% of cases despite meeting histologic criteria on biopsy making the diagnosis incredibly difficult to make. While guidelines have not been developed to guide treatment of IgG4-related disease, steroids are considered the first line treatment option for patients. Often times dosing is 2-4 weeks with a prolonged taper. When looking for glucocorticoid sparing agents, azathioprine, mycophenolate mofetil, and methotrexate are considered alternatives. References - Cardioembolic Stroke due to an IgG4-related pseudotumor 1. Kamisawa T, Funata N, Hayashi Y, et al. A new clinicopathological entity of IgG4- related autoimmune disease. J Gastroenterol 2003;38:982-4. 2. Deshpande V, Zen Y, Chan JK, et al. Consensus statement on the pathology of IgG4-related disease. Mod Pathol. 2012;25(9):1181-1192. doi:10.1038/modpathol.2012.72 3. Dahlgren M, Khosroshahi A, Nielsen GP, Deshpande V, Stone JH. Riedel’s thyroiditis and multifocal fibrosclerosis are part of the IgG4-related systemic disease spectrum. Arthritis Care Res (Hoboken) 2010;62:1312-8. 4. Stone JH, Khosroshahi A, Hilgenberg A, Spooner A, Isselbacher EM, Stone JR. IgG4 related systemic disease and lymphoplasmacytic aortitis. Arthritis Rheum 2009;60:313945. 5. Saeki T, Saito A, Hiura T, et al. Lymphoplasmacytic infiltration of multiple organs with immunoreactivity for IgG4: IgG4-related systemic disease. Intern Med 2006;45:163-7. 6. Kamisawa T, Takuma K, Egawa N, Tsuruta K, Sasaki T. Autoimmune pancreatitis and IgG4-related sclerosing disease. Nat Rev Gastroenterol Hepatol 2010;7:401-9. 7. Shakir A, Wheeler Y, Krishnaswamy G. The enigmatic immunoglobulin G4-related disease and its varied cardiovascular manifestations. Heart. 2021;107(10):790-798. doi:10.1136/heartjnl-2020-318041 8. Tyebally S, Chen D, Bhattacharyya S, Mughrabi A, Hussain Z, Manisty C, et al. Cardiac tumors: JACC cardio oncology state-of-the-art review. J Am Coll Cardiol CardioOnc. 2020;2:293–311 9. Selkane C, Amahzoune B, Chavanis N, et al. Changing management of cardiac myxoma based on a series of 40 cases with long-term follow-up. Ann Thorac Surg. 2003;76(6):1935-1938. doi:10.1016/s0003-4975(03)01245-1 10. Sun JP, Asher CR, Yang XS, et al. Clinical and echocardiographic characteristics of papillary fibroelastomas: a retrospective and prospective study in 162 patients. Circulation. 2001;103(22):2687-2693. doi:10.1161/01.cir.103.22. 11. Stone JH, Zen Y, Deshpande V. IgG4-related disease. N Engl J Med. 2012;366(6):539-551. doi:10.1056/NEJMra1104650 12. Hasnie UA, Herrera LN, Morgan WS, Rodriguez JM, Litovsky S, Chatham WW, Winokur T, Muzny CA. IgG4-Related Disease Masquerading As Culture-Negative Endocarditis. AIM Clinical Cases. 2022;1. doi: 10.7326/aimcc.2022.0075 13. 2016 ASE Guideline: https://www.asecho.org/wp-content/uploads/2016/01/2016_Cardiac-Source-of-Embolism.pdf 14. Shakir A, Wheeler Y, Krishnaswamy G. The enigmatic immunoglobulin G4-related disease and its varied cardiovascular manifestations Heart 2021;107:790-798. 15. Karadeniz H, Vaglio A. IgG4-related disease: a contemporary review. Turk J Med Sci. 2020 Nov 3;50(SI-2):1616-1631. doi: 10.3906/sag-2006-375. PMID: 32777900; PMCID: PMC7672352.

Jan 20, 2023

The following question refers to Section 7.4 of the 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure. The question is asked by New York Medical College medical student and CardioNerds Intern Akiva Rosenzveig, answered first by Cornell cardiology fellow and CardioNerds Ambassador Dr. Jaya Kanduri, and then by expert faculty Dr. Randall Starling.Dr. Starling is Professor of Medicine and an advanced heart failure and transplant cardiologist at the Cleveland Clinic where he was formerly the Section Head of Heart Failure, Vice Chairman of Cardiovascular Medicine, and member of the Cleveland Clinic Board of Governors. Dr. Starling is also Past President of the Heart Failure Society of America in 2018-2019. Dr. Staring was among the earliest CardioNerds faculty guests and has since been a valuable source of mentorship and inspiration. Dr. Starling’s sponsorship and support was instrumental in the origins of the CardioNerds Clinical Trials Program.The Decipher the Guidelines: 2022 AHA / ACC / HFSA Guideline for The Management of Heart Failure series was developed by the CardioNerds and created in collaboration with the American Heart Association and the Heart Failure Society of America. It was created by 30 trainees spanning college through advanced fellowship under the leadership of CardioNerds Cofounders Dr. Amit Goyal and Dr. Dan Ambinder, with mentorship from Dr. Anu Lala, Dr. Robert Mentz, and Dr. Nancy Sweitzer. We thank Dr. Judy Bezanson and Dr. Elliott Antman for tremendous guidance.Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. Question #6 Mr. D is a 50-year-old man who presented two months ago with palpations and new onset bilateral lower extremity swelling. Review of systems was negative for prior syncope. On transthoracic echocardiogram, he had an LVEF of 40% with moderate RV dilation and dysfunction. EKG showed inverted T-waves and low-amplitude signals just after the QRS in leads V1-V3. Ambulatory monitor revealed several episodes non-sustained ventricular tachycardia with a LBBB morphology. He was initiated on GDMT and underwent genetic testing that revealed 2 desmosomal gene variants associated with arrhythmogenic right ventricular cardiomyopathy (ARVC). Is the following statement true or false? “ICD implantation is inappropriate at this time because his LVEF is >35%” True False Answer #6 Explanation This statement is False. ICD implantation is reasonable to decrease sudden death in patients with genetic arrhythmogenic cardiomyopathy with high-risk features of sudden death who have an LVEF ≤45% (Class 2a, LOE B-NR). While the HF guidelines do not define high-risk features of sudden death, the 2019 HRS expert consensus statement on evaluation, risk stratification, and management of arrhythmogenic cardiomyopathy identify major and minor risk factors for ventricular arrhythmias as follows: Major criteria: NSVT, inducibility of VT during EPS, LVEF ≤ 49%. Minor criteria: male sex, >1000 premature ventricular contractions (PVCs)/24 hours, RV dysfunction, proband status, 2 or more desmosomal variants. According to the HRS statement, high risk is defined as having either three major, two major and two minor, or one major and four minor risk factors for a class 2a recommendation for primary prevention ICD in this population (LOE B-NR). Based on these criteria, our patient has 2 major risk factors (NSVT & LVEF ≤ 49%), and 3 minor risk factors (male sex, RV dysfunction, and 2 desmosomal variants) for ventricular arrhythmias. Therefore, ICD implantation for primary prevention of sudden cardiac death is reasonable. Decisions around ICD implantation for primary prevention remain challenging and depend on estimated risk for SCD, co-morbidities, and patient preferences, and so should be guided by shared decision making weighing the possible benefits against the risks, especially in younger patients. Main Takeaway In patients with genetic arrhythmogenic cardiomyopathy with high-risk features of sudden death with LVEF ≤ 45%, implantation of ICD is reasonable. Guideline Loc. Section 7.4 Also: Section 3.10 from “Towbin, J. A., McKenna, W. J., Abrams, D. J., Ackerman, M. J., Calkins, H., Darrieux, F. C. C., Daubert, J. P., de Chillou, C., DePasquale, E. C., Desai, M. Y., Estes, N. A. M., Hua, W., Indik, J. H., Ingles, J., James, C. A., John, R. M., Judge, D. P., Keegan, R., Krahn, A. D., … Zareba, W. (2019). 2019 HRS expert consensus statement on evaluation, risk stratification, and management of arrhythmogenic cardiomyopathy. Heart Rhythm, 16(11), e301–e372. https://doi.org/10.1016/j.hrthm.2019.05.007” Decipher the Guidelines: 2022 Heart Failure Guidelines PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron!

Jan 20, 2023

The following question refers to Section 7.1 of the 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure. The question is asked by New York Medical College medical student and CardioNerds Intern Akiva Rosenzveig, answered first by Cornell cardiology fellow and CardioNerds Ambassador Dr. Jaya Kanduri, and then by expert faculty Dr. Clyde Yancy.Dr. Yancy is Professor of Medicine and Medical Social Sciences, Chief of Cardiology, and Vice Dean for Diversity and Inclusion at Northwestern University, and a member of the AHA/ACC/HFSA Heart Failure Guideline Writing Committee.The Decipher the Guidelines: 2022 AHA / ACC / HFSA Guideline for The Management of Heart Failure series was developed by the CardioNerds and created in collaboration with the American Heart Association and the Heart Failure Society of America. It was created by 30 trainees spanning college through advanced fellowship under the leadership of CardioNerds Cofounders Dr. Amit Goyal and Dr. Dan Ambinder, with mentorship from Dr. Anu Lala, Dr. Robert Mentz, and Dr. Nancy Sweitzer. We thank Dr. Judy Bezanson and Dr. Elliott Antman for tremendous guidance.Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. Question #5 Ms. L is a 65-year-old woman with nonischemic cardiomyopathy with a left ventricular ejection fraction (LVEF) of 35%, hypertension, and type 2 diabetes mellitus. She has been admitted to the hospital with decompensated heart failure (HF) twice in the last six months and admits that she struggles to understand how to take her medications and adjust her sodium intake to prevent this. Which of the following interventions has the potential to decrease the risk of rehospitalization and/or improve mortality? A Access to a multidisciplinary team (physicians, nurses, pharmacists, social workers, care managers, etc) to assist with management of her HF B Engaging in a mobile app aimed at improving HF self-care C Vaccination against respiratory illnesses D A & C Answer #5 The correct answer is D – both A (access to a multidisciplinary team) and C (vaccination against respiratory illness). Choice A is correct. Multidisciplinary teams involving physicians, nurses, pharmacists, social workers, care managers, dieticians, and others, have been shown in multiple RCTs, metanalyses, and Cochrane reviews to both reduce hospital admissions and all-cause mortality. As such, it is a class I recommendation (LOE A) that patients with HF should receive care from multidisciplinary teams to facilitate the implementation of GDMT, address potential barriers to self-care, reduce the risk of subsequent rehospitalization for HF, and improve survival. Choice B is incorrect. Self-care in HF comprises treatment adherence and health maintenance behaviors. Patients with HF should learn to take medications as prescribed, restrict sodium intake, stay physically active, and get vaccinations. They also should understand how to monitor for signs and symptoms of worsening HF, and what to do in response to symptoms when they occur. Interventions focused on improving the self-care of HF patients significantly reduce hospitalizations and all-cause mortality as well as improve quality of life. Therefore, patients with HF should receive specific education and support to facilitate HF self-care in a multidisciplinary manner (Class I, LOE B-R). However, the method of delivery and education matters. Reinforcement with structured telephone support has been shown to be effective. In contrast the efficacy of mobile health-delivered educational interventions in improve self-care in patients with HF remains uncertain. Choice C is correct. In patients with HF, vaccinating against respiratory illnesses is reasonable to reduce mortality (Class 2a, LOE B-NR). For example, administration of the influenza vaccine in HF patients has been shown to reduce all-cause mortality and hospitalizations. Main Takeaway Implementation of multidisciplinary care teams has been proven to reduce rehospitalization and mortality in HF patients. While education on self-care of HF patients is important, not all delivery methods have been shown to be effective. Guideline Loc. Section 7.1 Decipher the Guidelines: 2022 Heart Failure Guidelines PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron!

Jan 15, 2023

The following question refers to Section 4.1 of the 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure. The question is asked by Texas Tech University medical student and CardioNerds Academy Intern Dr. Adriana Mares, answered first by Baylor University cardiology fellow and CardioNerds FIT Trialist Dr. Shiva Patlolla, and then by expert faculty Dr. Eldrin Lewis. Dr. Lewis is an Advanced Heart Failure and Transplant Cardiologist, Professor of Medicine and Chief of the Division of Cardiovascular Medicine at Stanford University. The Decipher the Guidelines: 2022 AHA / ACC / HFSA Guideline for The Management of Heart Failure series was developed by the CardioNerds and created in collaboration with the American Heart Association and the Heart Failure Society of America. It was created by 30 trainees spanning college through advanced fellowship under the leadership of CardioNerds Cofounders Dr. Amit Goyal and Dr. Dan Ambinder, with mentorship from Dr. Anu Lala, Dr. Robert Mentz, and Dr. Nancy Sweitzer. We thank Dr. Judy Bezanson and Dr. Elliott Antman for tremendous guidance. Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. Question #4 Mr. Stevens is a 55-year-old man who presents with progressively worsening dyspnea on exertion for the past 2 weeks. He has associated paroxysmal nocturnal dyspnea, intermittent exertional chest pressure, and bilateral lower extremity edema. Otherwise, Mr. Stevens does not have any medical history and does not take any medications. Which of the following will be helpful for diagnosis at this time? A Detailed history and physical examination B Chest x-ray C Blood workup including CBC, CMP, NT proBNP D 12-lead ECG E All of the above Answer #4 The correct answer is E – All of the above. Mr. Stevens presents with signs and symptoms of volume overload concerning for new onset heart failure. The history and physical exam remain the cornerstone in the assessment of patients with HF. Not only is the H&P valuable for identifying the presence of heart failure but also may provide hints about the degree of congestion, underlying etiology, and alternative diagnoses. As such H&P earns a Class 1 indication for a variety of reasons in patients with heart failure: 1. Vital signs and evidence of clinical congestion should be assessed at each encounter to guide overall management, including adjustment of diuretics and other medications (Class 1, LOE B-NR) 2. Clinical factors indicating the presence of advanced HF should be sought via the history and physical examination (Class 1, LOE B-NR) 3. A 3-generation family history should be obtained or updated when assessing the cause of the cardiomyopathy to identify possible inherited disease (Class 1, LOE B-NR) 4. A thorough history and physical examination should direct diagnostic strategies to uncover specific causes that may warrant disease-specific management (Class 1, LOE B-NR) 5. A thorough history and physical examination should be obtained and performed to identify cardiac and noncardiac disorders, lifestyle and behavioral factors, and social determinants of health that might cause or accelerate the development or progression of HF (Class 1, LOE C-EO) Building on the H&P, laboratory evaluation provides important information about comorbidities, suitability for and adverse effects of treatments, potential causes or confounders of HF, severity and prognosis of HF, and more. As such, for patients who are diagnosed with HF, laboratory evaluation should include complete blood count, urinalysis, serum electrolytes, blood urea nitrogen, serum creatinine, glucose, lipid profile, liver function tests, iron studies, and thyroid-stimulating hormone to optimize management (Class 1, LOE C-EO). In addition, the specific cause of HF should be explored using additional laboratory testing for appropriate management (LOE 1, LOE B-NR). In patients presenting with dyspnea such as Mr. Stevens, measurement of B-type natriuretic peptide (BNP) or N-terminal prohormone of B-type natriuretic peptide (NT-proBNP) is useful to support a diagnosis or exclusion of HF (Class 1, LOE A); and in those with chronic HF, measurements of BNP or NT-proBNP levels are recommended for risk stratification (Class 1, LOE A). In addition to bloodwork, electrocardiography is part of the routine evaluation of a patient with HF and provides important information on rhythm, heart rate, QRS morphology and duration, cause, and prognosis of HF. So for all patients with HF, a 12-lead ECG should be performed at the initial encounter to optimize management (Class 1, LOE C-EO). Imaging is essential in the diagnosis and management of heart failure. In patients with suspected or new-onset HF, or those presenting with acute decompensated HF, a chest x-ray should be performed to assess heart size and pulmonary congestion and to detect alternative cardiac, pulmonary, and other diseases that may cause or contribute to the patient’s symptoms (Class 1, LOE C-LD). Additionally, in those with suspected or newly diagnosed HF, transthoracic echocardiography (TTE) should be performed during the initial evaluation to assess cardiac structure and function (Class 1, LOE C-LD); and when echocardiography is inadequate, alternative imaging (e.g., cardiac magnetic resonance [CMR], cardiac computed tomography [CT], radionuclide imaging) is recommended for assessment of LVEF (Class 1, LOE C-LD). Main Takeaway In patients who present with signs and symptoms of volume overload concerning for new-onset heart failure, it is essential to rule out non-cardiac causes and assess for specific underlying causes of heart failure by using detailed history and physical examination. Once heart failure diagnosis is established, further workup with laboratory testing, ECG, and non-invasive cardiac imaging is warranted to investigate the etiology of heart failure and guide further management. Special attention should be given to detection of signs and symptoms suggesting an advanced stage of disease. Guideline Loc. Section 4.1 Decipher the Guidelines: 2022 Heart Failure Guidelines PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron!

Jan 13, 2023

The following question refers to Section 3.1 of the 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure. The question is asked by Texas Tech University medical student and CardioNerds Academy Intern Dr. Adriana Mares, answered first by Rochester General Hospital cardiology fellow and Director of CardioNerds Journal Club Dr. Devesh Rai, and then by expert faculty Dr. Shelley Zieroth. Dr. Zieroth is an advanced heart failure and transplant cardiologist, Head of the Medical Heart Failure Program, the Winnipeg Regional Health Authority Cardiac Sciences Program, and an Associate Professor in the Section of Cardiology at the University of Manitoba. Dr. Zieroth is a past president of the Canadian Heart Failure Society. She is a steering committee member for PARAGLIE-HF and a PI Mentor for the CardioNerds Clinical Trials Program. The Decipher the Guidelines: 2022 AHA / ACC / HFSA Guideline for The Management of Heart Failure series was developed by the CardioNerds and created in collaboration with the American Heart Association and the Heart Failure Society of America. It was created by 30 trainees spanning college through advanced fellowship under the leadership of CardioNerds Cofounders Dr. Amit Goyal and Dr. Dan Ambinder, with mentorship from Dr. Anu Lala, Dr. Robert Mentz, and Dr. Nancy Sweitzer. We thank Dr. Judy Bezanson and Dr. Elliott Antman for tremendous guidance. Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. Question #3 Which of the following is/are true about heart failure epidemiology? A Although the absolute number of patients with HF has partly grown, the incidence of HF has decreased B Non-Hispanic Black patients have the highest death rate per capita resulting from HF C In patients with established HF, non-Hispanic Black patients have a higher HF hospitalization rate compared with non-Hispanic White patients D In patients with established HF, non-Hispanic Black patients have a lower death rate compared with non-Hispanic White patients E All of the above Answer #3 Explanation The correct answer is “E – all of the above.” Although the absolute number of patients with HF has partly grown as a result of the increasing number of older adults, the incidence of HF has decreased. There is decreasing incidence of HFrEF and increasing incidence of HFpEF. The health and socioeconomic burden of HF is growing. Beginning in 2012, the age-adjusted death-rate per capita for HF increased for the first time in the US. HF hospitalizations have also been increasing in the US. In 2017, there were 1.2 million HF hospitalizations in the US among 924,000 patients with HF, a 26% increase compared with 2013. Non-Hispanic Black patients have the highest death rate per capita. A report examining the US population found the age-adjusted mortality rate for HF to be 92 per 100,000 individuals for non-Hispanic Black patients, 87 per 100,000 for non-Hispanic White patients, and 53 per 100,000 for Hispanic patients. Among patients with established HF, non-Hispanic Black patients experienced a higher rate of HF hospitalization and a lower rate of death than non-Hispanic White patients with HF.Hispanic patients with HF have been found to have similar or higher HF hospitalization rates and similar or lower mortality rates compared with non-Hispanic White patients. Asian/Pacific Islander patients with HF have had a similar rate of hospitalization as non-Hispanic White patients but a lower death rate. These racial and ethnic disparities warrant studies and health policy changes to address health inequity. Main Takeaway Racial and ethnic disparities in death resulting from HF persist, with non-Hispanic Black patients having the highest death rate per capita, and a higher rate of HF hospitalization. Further clinical studies and health policy changes are needed to address these inequalities. Guideline Loc. Section 3.1 Decipher the Guidelines: 2022 Heart Failure Guidelines PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron!

Jan 10, 2023

The following question refers to Section 6.1 of the 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure. The question is asked by Keck School of Medicine USC medical student & CardioNerds Intern Hirsh Elhence, answered first by Mount Sinai Hospital cardiology fellow and CardioNerds FIT Trialist Dr. Jason Feinman, and then by expert faculty Dr. Mark Drazner. Dr. Drazner is an advanced heart failure and transplant cardiologist, Professor of Medicine, and Clinical Chief of Cardiology at UT Southwestern. He is the President of the Heart Failure Society of America. The Decipher the Guidelines: 2022 AHA / ACC / HFSA Guideline for The Management of Heart Failure series was developed by the CardioNerds and created in collaboration with the American Heart Association and the Heart Failure Society of America. It was created by 30 trainees spanning college through advanced fellowship under the leadership of CardioNerds Cofounders Dr. Amit Goyal and Dr. Dan Ambinder, with mentorship from Dr. Anu Lala, Dr. Robert Mentz, and Dr. Nancy Sweitzer. We thank Dr. Judy Bezanson and Dr. Elliott Antman for tremendous guidance. Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. Question #2 A 67-year-old man with a past medical history of type 2 diabetes mellitus, hypertension, and active tobacco smoking presents to the emergency room with substernal chest pain for the past 5 hours. An electrocardiogram reveals ST segment elevations in the anterior precordial leads and he is transferred emergently to the catheterization laboratory. Coronary angiography reveals 100% occlusion of the proximal left anterior descending artery, and he is successfully treated with a drug eluting stent resulting in TIMI 3 coronary flow. Following his procedure, a transthoracic echocardiogram is performed which reveals a left ventricular ejection fraction of 35% with a hypokinetic anterior wall. Which of the following medications would be the best choice to prevent the incidence of heart failure and reduce mortality? A Lisinopril B Diltiazem C Carvedilol D Sacubitril-valsartan E Both A and C Answer #2 The correct answer is E – both lisinopril and carvedilol are appropriate to reduce the incidence of heart failure and mortality. Evidence-based beta-blockers and ACE inhibitors both have Class 1 recommendations in patients with a recent myocardial infarction and left ventricular ejection fraction ≤ 40% to reduce the incidence of heart failure and to reduce mortality. Multiple randomized controlled trials have investigated both medications in the post myocardial infarction setting and demonstrated improved ventricular remodeling as well as benefits for mortality and development of incident heart failure. At this time, there is not sufficient evidence to recommend ARNi over ACEi for patients with reduced LVEF following acute MI. The PARADISE-MI trial randomized a total of 5,661 patients with myocardial infarction complicated by a reduced LVEF, pulmonary congestion, or both to receive either sacubitril-valsartan (97-103mg twice daily) or ramipril (5mg twice daily). After a median follow up time of 22 months, there was no statistically significant difference in the primary outcome of cardiovascular death or incident heart failure. At this time, ARNi have not been included in the guidelines for this specific population. Diltiazem is a non-dihydropyridine calcium channel blocker, a family of drugs with negative inotropic effects and which may be harmful in patients with depressed LVEF (Class 3: Harm, LOE C-LD). Main Takeaway: For patients with recent myocardial infarction and reduced left ventricular function both beta blockers and ACEi have Class 1 recommendations to reduce the incidence of heart failure and decrease mortality. Guideline Location: Section 6.1 Decipher the Guidelines: 2022 Heart Failure Guidelines PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron!

Jan 9, 2023

The following question refers to Section 2.1 of the 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure. The question is asked by Keck School of Medicine USC medical student & CardioNerds Intern Hirsh Elhence, answered first by Mount Sinai Hospital cardiology fellow and CardioNerds FIT Trialist Dr. Jason Feinman, and then by expert faculty Dr. Biykem Bozkurt. Dr. Bozkurt is the Mary and Gordon Cain Chair, Professor of Medicine, Director of the Winters Center for Heart Failure Research, and an advanced heart failure and transplant cardiologist at Baylor College of Medicine in Houston, TX. She is former President of HFSA, former senior associate editor for Circulation, current Editor-In-Chief of JACC Heart Failure. Dr. Bozkurt was the Vice Chair of the writing committee for the 2022 Heart Failure Guidelines. The Decipher the Guidelines: 2022 AHA / ACC / HFSA Guideline for The Management of Heart Failure series was developed by the CardioNerds and created in collaboration with the American Heart Association and the Heart Failure Society of America. It was created by 30 trainees spanning college through advanced fellowship under the leadership of CardioNerds Cofounders Dr. Amit Goyal and Dr. Dan Ambinder, with mentorship from Dr. Anu Lala, Dr. Robert Mentz, and Dr. Nancy Sweitzer. We thank Dr. Judy Bezanson and Dr. Elliott Antman for tremendous guidance. Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. Question #1 A 23-year-old man presents to his primary care physician for an annual visit. His father was diagnosed with idiopathic cardiomyopathy at 40 years of age. His blood pressure in clinic is 146/90 mmHg. He is a personal trainer and exercises daily, including both weightlifting and cardio. He denies any anabolic steroid use. He is an active tobacco smoker, approximately ½ pack per day. Review of systems is negative for symptoms. What stage of heart failure most appropriately describes his current status? A Stage A B Stage B C Stage C D Stage D E None of the above Answer #1 The correct answer is A – Stage A of heart failure. Overall, the ACC/AHA stages of HF were designed to emphasize the development and progression of disease. More advanced stages and progression are associated with reduced survival. Stage A HF is where patients are “at risk for HF”, but without current or previous symptoms or signs of HF, and without structural/functional heart disease or abnormal biomarkers. At-risk patients include those with hypertension, cardiovascular disease, diabetes, obesity, exposure to cardiotoxic agents, genetic variant for cardiomyopathy, or family history of cardiomyopathy. Stage B HF is the “pre-heart failure” stage where patients are without current or previous symptoms or signs of HF but do have at least one of the following: Structural heart disease (i.e., reduced left or right ventricular systolic function, ventricular hypertrophy, chamber enlargement, wall motion abnormalities, and valvular heart disease) Evidence of increased filling pressures Risk factors and increased natriuretic peptide levels or persistently elevated cardiac troponin in the absence of an alternate diagnosis Stage C HF indicates symptomatic heart failure where patients have current or previous symptoms or signs of HF. Stage D HF indicates advanced heart failure with marked HF symptoms that interfere with daily life and with recurrent hospitalizations despite attempts to optimize guideline-directed medical therapy. Therapeutic interventions in each stage aim to modify risk factors (Stage A), treat risk and structural heart disease to prevent HF (stage B), and reduce symptoms, morbidity, and mortality (stages C and D). Given this patient’s family and social histories, along with the clinical finding of elevated blood pressure, he is best classified as having Stage A, or at risk for HF. Were he to have signs of cardiac abnormalities on chest X-ray, ECG, biomarkers, or other testing, he would then be classified as having Stage B, or pre-heart failure. Main Takeaway: It is important to identify patients who are at risk for heart failure (Stage A HF) early to modify risk factors and prevent disease progression. Guideline location: Section 2.1, Figure 1, Table 3 Decipher the Guidelines: 2022 Heart Failure Guidelines PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron!

Jan 8, 2023

Join CardioNerds (Dr. Mark Belkin and Dr. Natalie Tapaskar) as they discuss the 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure with Writing Committee Chair Dr. Paul Heidenreich. They discuss how one gets involved with a guideline writing committee, the nuts and bolts of the guideline writing process, pitfalls and utility of the term “GDMT,” background behind inclusion of “Value Statements,” potential omissions from the document, clinical uptake of recommendations, and anticipated changes for the next iteration. Audio editing by CardioNerds academy intern, Pace Wetstein. This discussion is a prelude to the CardioNerds Decipher The Guidelines Series designed to enhance understanding and uptake of the 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure. We will be using high-impact, board-style, clinical vignette-based questions to highlight core concepts relevant to your practice. We will do so by releasing several short bite-sized Pods with one question per episode. Note that the cases used are hypothetical and created solely to illustrate core concepts. This series was developed by the CardioNerds and created in collaboration with the American Heart Association and the Heart Failure Society of America. It was created by 30 trainees spanning college through advanced fellowship under the leadership of CardioNerds Cofounders Dr. Amit Goyal and Dr. Dan Ambinder, with mentorship from Dr. Anu Lala, Dr. Robert Mentz, and Dr. Nancy Sweitzer. We thank Dr. Judy Bezanson and Dr. Elliott Antman for tremendous guidance. Decipher the Guidelines: 2022 Heart Failure Guidelines PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron!

Jan 6, 2023

The importance of recognition and diagnosis of cardiac amyloidosis is at an all-time high due to its high prevalence and improved therapeutic strategies. Here we discuss what CardioNerds need to know about the manifestations, diagnosis, and management of transthyretin (ATTR) and light chain (AL) cardiac amyloidosis. Join Dr. Dan Ambinder (CardioNerds Cofounder), Dr. Dinu-Valentin Balanescu (Series Cochair, Chief Resident at Beaumont Health, and soon FIT at Mayo Clinic), and Dr. Dan Davies (Episode FIT Lead and FIT at Mayo Clinic) as they discuss cardiac amyloidosis with Dr. Omar Siddiqi, cardiologist at the Boston University Amyloidosis Center and program director for the general cardiovascular fellowship program at Boston University, a CardioNerds Healy Honor Roll Program. Episode notes were drafted by Dr. Dan Davies. Audio editing by CardioNerds Academy Intern, student doctor Chelsea Amo Tweneboah. Access the CardioNerds Cardiac Amyloidosis Series for a deep dive into this important topic. This episode is supported by a grant from Pfizer Inc. This CardioNerds Cardio-Oncology series is a multi-institutional collaboration made possible by contributions of stellar fellow leads and expert faculty from several programs, led by series co-chairs, Dr. Giselle Suero Abreu, Dr. Dinu Balanescu, and Dr. Teodora Donisan. Pearls • Notes • References • Production Team CardioNerds Cardio-Oncology PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls and Quotes Cardiac amyloidosis is no longer considered a rare disease, especially transthyretin amyloidosis in older male patients with HFpEF and aortic stenosis. Echocardiogram is the “gate keeper” of cardiac imaging and provides initial evidence of amyloid infiltration, while cardiac MRI can help refine the presence of an infiltrative cardiomyopathy versus other causes of increased wall thickness. The most clinically important types of amyloid heart disease are transthyretin (ATTR) and light chain (AL) amyloidosis. The workup to differentiate these disorders includes a gammopathy panel to screen for the presence of potentially amyloidogenic light chains (serum and urine electrophoresis WITH immunofixation and serum free light chains), and cardiac scintigraphy with Technetium-99m-labeled bone-seeking tracers (PYP, DPD, etc.) to identify cardiac aTTR infiltration if the gammopathy panel is unrevealing. There is still a role for endomyocardial biopsy in the diagnosis of cardiac amyloidosis! All patients in whom there is concern for cardiac amyloidosis and gammopathy panel indicates the presence of monoclonal light chains should have a biopsy to obtain a tissue diagnosis of likely AL amyloidosis. Alternatively, an endocardial biopsy may prove valuable in patients who have confusing phenotypic features between amyloid types, such as a patient with abnormal monoclonal protein and positive PYP imaging. Be suspicious of heart failure patients that do not tolerate typical medications that lower heart rate. In the restrictive cardiomyopathy of cardiac amyloidosis, patients are reliant on higher heart rates to compensate for the inability to augment stroke volume. Be suspicious of amyloidosis in patients with recurrent left atrial thrombi despite anticoagulation. Show notes CardioNerds Cardiac Amyloid, updated 1.20.21 1. What is cardiac amyloidosis and how common is it? Cardiac amyloidosis is adisorder caused by misfolding of proteins into insoluble forms which are deposited into extracellular spaces of the heart, commonly causing a stiff and thick heart with progressive diastolic dysfunction with restrictive hemodynamics and ensuing heart failure. The two most common types of amyloid protein that affect the heart are transthyretin (ATTR) and light chain (AL). Transthyretin amyloidosis is caused by a misfolded transporter protein produced by the liver, while light chain amyloidosis is caused by a misfolded light chain immunoglobulin produced by clonal plasma cells. ATTR cardiac amyloidosis may be present in 6-17% of older patients with HFpEF and increased wall thickness, as well as in 4-16% of patients undergoing intervention for severe aortic stenosis. AL amyloidosis is much rarer, with a prevalence of about 12 cases per million persons per year. 2. What are some non-cardiac clues to the presence of cardiac amyloidosis? Non-cardiac clinical clues for transthyretin amyloidosis (ATTR) include spinal stenosis, biceps tendon rupture, carpal tunnel syndrome (particularly when bilateral), and peripheral neuropathy. Bilateral carpal tunnel syndrome may be present in up to 60% of ATTR-CA patients with over 40% having a history of biceps tendon rupture. Non-cardiac clinical clues for light chain amyloidosis (AL) include renal disease (esp. nephrotic syndrome), macroglossia, autonomic and peripheral neuropathy, and periorbital purpura (racoon eyes). 3. What are common multimodality imaging features used for the diagnosis of cardiac amyloidosis? For an in-depth discussion about the use of multimodality imaging in the diagnosis of cardiac amyloidosis, enjoy CardioNerds Episode #109 – Nuclear & Multimodality Imaging: Cardiac Amyloidosis. Echocardiography (echo) is among the first test performed in patients for the diagnosis of cardiovascular symptoms and may provide initial clues to the diagnosis. Features of cardiac amyloidosis on echocardiogram include increased left ventricular wall thickness (>12 mm, classically concentric) with abnormal diastolic function, increased right ventricular free wall and interatrial septal thickness, as well as increased valve thickness. There may be a small pericardial effusion. Left ventricular strain is usually abnormal with a characteristic apical sparing pattern. A granular, or sparkling, appearance of the myocardium has been classically described but is poorly predictive. Cardiac magnetic resonance (CMR) imaging is often used for differentiation of increased left ventricular wall thickness (infiltrative cardiomyopathies, hypertrophic cardiomyopathies, etc.) and in patients at increased risk of AL cardiac amyloidosis. Common features specific to CMR include abnormal myocardial nulling (blood pool nulls before the myocardium on inversion recovery sequences), elevated native T1 value, increased extracellular volume (ECV), and late gadolinium enhancement (classically in a diffuse, non-ischemic pattern). Bone scintigraphy (technetium pyrophosphate [PYP] or DPD) is a nuclear imaging study used for the diagnosis of transthyretin amyloidosis. In the absence of an abnormal monoclonal protein, the sensitivity and specificity approach 100%, allowing for the “non-biopsy” diagnosis of ATTR-CA (specifically in the context of a negative gammopathy panel). The 2019 multi-society diagnostic guidelines recommend SPECT imaging be used in combination planar imaging for all cases to improve predictive characteristics. 4. How are heart failure and arrhythmias managed in patients with cardiac amyloidosis? The mainstay of heart failure therapy in cardiac amyloidosis is loop diuretics with or without aldosterone antagonists. Spironolactone was shown to be effective in patients with a phenotype suggesting cardiac amyloidosis in a subgroup analysis of TOPCAT. Patients often have poor tolerance of guideline directed medical therapies for heart failure, including beta blockers and calcium channel blockers, with ACEI/ARB/ARNI frequently limited by hypotension. The SGLT2 inhibitors appear to be tolerated in patients with cardiac amyloidosis but more research is needed to determine impact on cardiovascular outcomes. Rate and rhythm control strategies for atrial arrhythmias can both be successful, but patients may be intolerant of medications. The risk of cardioembolic events in amyloid patients with atrial fibrillations is elevated, independent of CHA2DS2 -VASc score, and therefore all patients should be offered anticoagulation. Be suspicious of amyloidosis in patients with recurrent left atrial appendage thrombi despite anticoagulation. 5. What specific therapies can be used for transthyretin (ATTR) amyloidosis and light chain (AL) amyloidosis? Tafamidis is a transthyretin stabilizer that inhibits tetramer dissociation and reduces amyloid deposition in extracellular tissue. It is the only FDA approved medication for transthyretin cardiac amyloidosis and was shown to be associated with reduced mortality and heart failure hospitalization compared to control in the ATTR-ACT trial. Patisiran is a small interfering RNA that works as a gene silencer for ATTR protein production and is FDA approved for patients with polyneuropathy secondary to hereditary ATTR. Analysis of cardiac outcomes in the APOLLO trial suggest early stabilization of left ventricular wall thickness and reduction in natriuretic peptides in patients with features of concomitant cardiac involvement. Specific therapies for AL amyloidosis are managed by hematologists with the goal of complete hematologic response to prevent further immunoglobulin production and amyloid deposition. These therapies typically include chemotherapy regimens (e.g. cyclophosphamide, bortezomib, dexamethasone [CyBorD]), daratumumab (an anti-CD38 antibody), with or without autologous stem cell transplantation. There are many ongoing trials with novel therapies, with specific interest in treatments targeting removal of systemically deposited amyloid fibrils. References Dorbala, S., Ando, Y., Bokhari, S. et al. ASNC/AHA/ASE/EANM/HFSA/ISA/SCMR/SNMMI expert consensus recommendations for multimodality imaging in cardiac amyloidosis: Part 1 of 2—evidence base and standardized methods of imaging. J. Nucl. Cardiol. 26, 2065–2123 (2019). Link Dorbala, S., Ando,

Jan 1, 2023

This episode is focused on Palliative Care and Shared Decision-Making in the CICU. In this episode, we learn about how the principles of palliative care and shared decision-making apply to our patients across the spectrum of cardiovascular care, especially in the cardiac intensive care unit. We discuss pivotal trials of specialty palliative care and decision aids in cardiology and how they might inform our practice to enhance patient quality of life and improve goal-concordant care. Finally, we discuss practical tips and communication strategies for how to engage patients about end-of-life decisions and topics that can be utilized from outpatient to inpatient to critical care settings. “We need to help patients hope for the best and plan for the worst as time goes on.” Dr. Larry Allen Series co-chairs Dr. Eunice Dugan and Dr. Karan Desai, along with CardioNerds Co-founder Amit Goyal are joined by FIT lead, Dr. Sarah Chuzi. Dr. Chuzi is a Chicagoan and completed her internal medicine residency, cardiology fellowship, AHFTC fellowship and is now Assistant Professor at Northwestern University. Our episode expert is a true national leader in shared decision-making and palliative care in heart failure – Dr. Larry Allen, Medical Director of Advanced Heart Failure and the Co-Director of the Colorado Program for Patient-Centered Decisions at the University of Colorado School of Medicine. Audio editing by CardioNerds Academy Intern, Dr. Christian Faaborg-Andersen. The CardioNerds Cardiac Critical Care Series is a multi-institutional collaboration made possible by contributions of stellar fellow leads and expert faculty from several programs, led by series co-chairs, Dr. Mark Belkin, Dr. Eunice Dugan, Dr. Karan Desai, and Dr. Yoav Karpenshif. Pearls • Notes • References • Production Team CardioNerds Cardiac Critical Care PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls and Quotes - Palliative Care and Shared Decision-Making in the CICU 1. “Much of what we do in cardiology is thinking about how to make people feel better (not just improving cardiac function or length of life). So, on a day-to-day basis we are really providing primary palliative care.” – Dr. Larry Allen 2. “Risk models in cardiology can only be so accurate… While risk models can give us some grounding, we also need to embrace the concept of uncertainty, and help patients understand that there are a variety of things that might happen to them, suggest some things they might plan for, and continue to iteratively come back to the patient and reevaluate what their options are.” – Dr. Larry Allen 3. “Our goal is to help people live happy, healthy, full lives. But, everyone dies. So understanding that death is a part of life and understanding how to help them make those transitions is critical” – Dr. Larry Allen 4. “Having good deaths is a part of good healthcare. We can’t ignore that. We can’t fight against it. We should embrace it. And we have the opportunity to do that.” – Dr. Larry Allen 5. We should still keep in mind the concept of medical futility and determining what options are reasonable for patients. Part of shared decision-making includes discussing what interventions would not be feasible or helpful with patients and families Show notes - Palliative Care and Shared Decision-Making in the CICU Notes drafted by Dr. Sarah Chuzi. 1. How are the basic principles of palliative care relevant to cardiology, and can you define the key concepts of shared decision-making, primary palliative care, specialty (or secondary) palliative care, and hospice care? Throughout medicine, we confront the concepts of symptom control, difficult medical decision-making, and end-of-life. These are the principles of palliative care and they apply very easily across the spectrum of cardiology. Shared decision-making is a meeting between two experts - the patient and the clinician. The patient is the expert in what’s important to them and their hopes, fears, values, goals, and preferences. The clinician is the expert in the medical aspects of care, including care that is not possible, care that might be high value, and the potential trade-offs and range of outcomes involved in a medical decision. Palliative care is defined by the WHO - as care that deals with patient symptoms and quality of life. Increasingly, the terms primary and secondary palliative care are used. Primary palliative care is care provided by a general clinician (or cardiologist), while secondary palliative care is provided by a board-certified palliative care clinician. Hospice care is really a health insurance benefit that provides a certain group of services (e.g. nurses, equipment) for patients who have terminal illness and less than 6 months to live. 2. What have we learned from existing trials looking at specialty palliative care in heart failure? A few large trials (CASA, ENABLE, SWAP-HF, PAL-HF) of specialty palliative care interventions in heart failure have shown mixed results. One of the reasons for this is the heterogeneity in patient and caregiver adjustment/symptoms at baseline. Future trials will need to determine which patients and caregivers are really in need of interventions or assistance surrounding some of these issues. 3. What are some strategies trainees can use to help elucidate a patient’s goals and values and engage in shared decision-making in high intensity, critical care situations? Trying to determine (from the patient or family) whether the patient is a medical maximizer or minimizer can be helpful; i.e., what is his preference for aggressiveness of care. Obtaining collateral from a patient’s power of attorney/next of kin/proxy about prior discussions regarding goals and values is valuable. We should still keep in mind the concept of medical futility and determining what options are reasonable for patients. Part of shared decision-making includes discussing what interventions would not feasible or helpful with patients and families. 4. What is the role of decision aids in the process of deciding whether to pursue LVAD implantation? Decision aids are unique from educational materials in that decision aids discuss alternative treatment options, including what life might be like if a certain treatment option is not pursued. Decision aids encourage patients to reflect on their values and then try to map the decisions in the context of their values. The research group at the University of Colorado developed a decision aid to help patients and their families determine whether an LVAD would be an appropriate medical intervention for them. The decision aid is available online (patientdecisionaid.org) and includes a 26-minute video and an 8-page pamphlet. Currently, they are being disseminated nationally in a large implementation trial. The DECIDE-LVAD trial demonstrated that this decision aid improved values-choice concordance for patients considering LVAD therapy. 5. What are the benefits of hospice for patients with cardiac disease and how does hospice fall short? It’s important to understand what hospice will and will not cover. The hospice benefit is a fixed payment per day. So, it’s important to consider what treatments might be covered and to discuss this with patients and families. For patients with advanced cardiac disease, coverage of inotropes is a common issue that we encounter. It’s important to prepare patients for the fact that inotropes may not be accepted in a given hospice program. Additionally, sometimes clinicians struggle with how to continue to provide care for patients who enter hospice as we try to navigate how to stay involved in their care while respecting their wishes to be at home and not necessarily come to clinic. References - Palliative Care and Shared Decision-Making in the CICU Rogers JG, Patel CB, Mentz RJ, et al. The palliative care in heart failure (PAL-HF) randomized, controlled clinical trial. 2017. J Am Coll Cardiol, 70(3): 331-341. Allen LA, Mcilvennan CK, Thompson JS, et al. Effectiveness of an intervention supporting shared decision making for destination therapy left ventricular assist device: the DECIDE-LVAD randomized clinical trial. 2018. JAMA Intern Med, 178(4): 520-529. Warraich HJ, Patel CB, Kochar A, Rogers JG, Patel MR. Incorporating shared decision making and palliative care into cardiogenic shock pathways. 2010. J Am Coll Cardiol, 74(4): 501-502. Chuzi S, Khan SS, Pak ES. Primary palliative care education in advanced heart failure and transplant cardiology fellowships. 2021. J Am Coll Cardiol, 77(4): 501-505.

Dec 26, 2022

Partial anomalous pulmonary venous return refers to anomalies in which one or more (but not all) of the pulmonary veins connects to a location other than the left atrium. This causes left to right shunting which may have hemodynamic and therefore clinical significance, warranting repair in some patients. Join CardioNerds to learn about partial anomalous pulmonary venous return! Dr. Dan Ambinder (CardioNerds co-founder), Dr. Josh Saef (ACHD FIT at the University of Pennsylvania and ACHD Series co-chair), and Dr. Tripti Gupta (ACHD FIT at Vanderbilt University and episode lead) learn from Dr. Ian Harris (Director of the Adult Congenital Heart Disease program at University of California, San Francisco). Audio editing by CardioNerds Academy Intern, student doctor Shivani Reddy. The CardioNerds Adult Congenital Heart Disease (ACHD) series provides a comprehensive curriculum to dive deep into the labyrinthine world of congenital heart disease with the aim of empowering every CardioNerd to help improve the lives of people living with congenital heart disease. This series is multi-institutional collaborative project made possible by contributions of stellar fellow leads and expert faculty from several programs, led by series co-chairs, Dr. Josh Saef, Dr. Agnes Koczo, and Dr. Dan Clark. The CardioNerds Adult Congenital Heart Disease Series is developed in collaboration with the Adult Congenital Heart Association, The CHiP Network, and Heart University. See more Disclosures: None Pearls • Notes • References • Guest Profiles • Production Team CardioNerds Adult Congenital Heart Disease PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls - Partial Anomalous Pulmonary Venous Return (PAPVR) What is partial anomalous pulmonary venous return (PAPVR)? PAPVR refers to anomalies in which one or more (but not all) of the pulmonary veins connects to a location other than the left atrium. Often, this means one or more pulmonary veins empty into the right atrium or a systemic vein such as the superior vena cava or inferior vena cava. Physiologically, this produces a left-to-right shunt, allowing for already-oxygenated blood to recirculate into the lungs and result in excessive pulmonary blood flow. What are the clinical features of PAPVR?Diagnosis is usually incidental on a cross sectional imaging such as CTA or CMR.The most common associated lesion is an atrial-level defect.It is unusual for a single anomalous pulmonary venous connection of only 1 pulmonary lobe to result in significant shunting. Patients with a significant degree of left to right shunting may have right heart dilatation or symptoms of dyspnea on exertion. When are some strategies for managing patients with PAPVR?A surgical correction is recommended for patients with PAPVR when functional capacity is impaired and RV enlargement is present, there is a net left-to-right shunt sufficiently large to cause physiological sequelae (aka: ratio of pulmonary flow (Qp) to systemic flow (Qs) is > 1.5:1), PA systolic pressure is less than 50% systemic pressure and pulmonary venous resistance is less than one third of systemic venous resistance.Surgical repair involves intracaval baffling of the left atrium (Warden procedure) or direct reimplantation of the anomalous pulmonary vein into the left atrium.Pregnancy is well tolerated in patients with repaired PAPVR. In patients with unrepaired lesion who may have right sided heart dilatation and/or pulmonary hypertension, preconception evaluation and counseling should address how pregnancy may affect mother’s and fetus’s health. Antibiotic prophylaxis for infective endocarditis is typically not needed unless patients are less than 6 months from recent surgery, have residual defect at the patch margin or prior history of infective endocarditis. Show notes - Partial Anomalous Pulmonary Venous Return (PAPVR) Notes (drafted by Dr. Tripti Gupta): 1. What is partial anomalous pulmonary venous return? Anatomically, partial anomalous pulmonary venous return refers to anomalies in which one or more (but not all) of the pulmonary veins connects to a location other than the left atrium. Often, this means one or more pulmonary veins empty into the right atrium or a systemic vein such as the superior vena cava (SVC) or inferior vena cava (IVC).Physiologically, this produces a left-to-right shunt, allowing for already-oxygenated blood to recirculate into the lungs and result in excessive pulmonary blood flow. If all pulmonary veins from both lungs drain to an anomalous site or in an abnormal fashion, then it is identified as a total anomalous pulmonary venous return (TAPVR). Patients with TAPVR often require surgical intervention in childhood. A bit of a nuance in terminology - partial anomalous pulmonary venous return (PAPVR) vs. partial anomalous pulmonary venous connection (PAPVC), requires some explanation. The suffix “return” refers to vessels returning to a chamber (ex: pulmonary vein returns to morphological left atrium after blood functionally mixes with systemic venous return or is redirected via an atrial septal defect) vs. “connection” implies abnormal anatomic attachments. 2. How does this happen? What is the embryological explanation for PAPVR? We know that the pulmonary veins originate from the posterior aspect of the left atrium. Meanwhile, the lung buds that arise from the lung parenchyma canalize as a vessel and gradually connect to the developing pulmonary veins. Some theories say that the lung buds are initially enmeshed in the splanchnic plexus which drains into the cardinal and umbilical vitelline veins (systemic venous system). By week 4 of gestation, the pulmonary veins from the left atrium connects with the superior portion of the splanchnic plexus to form the pulmonary plexus and ultimately loses its connection with the splanchnic plexus. The pulmonary vein is then supposed to divide into 4 branches, 2 on right and 2 on left, each with an orifice at the left atrium. Failure of one or more of the pulmonary veins to separate from the systemic venous systemic results in PAPVC/TAPVC. 3. What are some major clinical findings in PAPVR? PAPVR is typically an incidental diagnosis on CT or MRI in asymptomatic patients when these scans are done for another reason. Many patients with PAPVR may remain asymptomatic throughout childhood and adult life. Physiological changes may depend on degree of left to right shunt, number of veins involved, their sites of connection and associated lesions. 80% of anomalous connections are of the right sided pulmonary veins and 20% affect the left sided pulmonary veins. The most common variants include:Right upper pulmonary vein or right middle pulmonary vein to SVC, azygos vein, or right atrium. This variant is the most common and can be often associated with a sinus venosus defect.Right pulmonary veins to IVC, usually via a single trunk draining caudally and connecting to the IVC near the diaphragm. This variant is sometimes known as Scimitar syndrome. When you look at the descending trunk connecting the right venous return to the right atrium on x-ray or fluoroscopy, it has a crescent-like shape, like a Turkish sword from the Ottoman Empire or a scimitar, hence the name Scimitar syndrome.Left pulmonary vein(s) to the innominate vein via a vertical vein. Left pulmonary veins to the coronary sinus. If more that 50% of a person’s pulmonary venous return drains anomalously to the right side of the heart, there may be right heart enlargement and presentation of symptoms such as dyspnea on exertion earlier in life. Physical exam findings may include prominent right ventricular impulse, a systolic ejection murmur at the left upper sternal border, split S2, and possibly a mid-diastolic rumble. In the absence of an ASD, these findings may not be obvious. On ECG, a RBBB morphology, RAD or first-degree heart block is associated with right ventricular volume enlargement. On echocardiogram, RV enlargement without left heart dysfunction should raise suspicion for anomalous pulmonary venous connection. Other hints can include the presence of a sinus venosus ASD, secundum ASD or RV enlargement that is significantly large for a small ASD/PFO. While left sided pulmonary veins can be visualized on the suprasternal view of transthoracic echocardiogram, right sided veins are more challenging on TTE. A TEE can be used to identify the site and drainage of pulmonary veins. A right heart catheterization is useful to identify the presence and etiology of pulmonary hypertension and quantify flows in pulmonary and systemic system and presence of a shunt. Selective angiography of the right and left pulmonary arteries can confirm the presence and course of pulmonary veins on levophase. A gated cardiac CTA or CMR is helpful and recommended for definitive diagnosis. A CTA offers higher spatial resolution than a CMR at the cost of radiation and iodinated contrast exposure. A CMR offers high resolution for defining vascular anatomy, quantifying chamber dimensions, estimate shunt burden and degree of stenoses using flow quantification techniques. In addition, respiratory-gated 3D whole heart imaging or MRA can be used for multiplanar reconstruction and aid in perioperative planning. Patients with TAPVR present with cyanosis at birth and need urgent surgical correction. 4. What conditions are associated with PAPVR? 80% of patients with PAPVR lesion may have an associated atrial level defect. In particular, a superior sinus venosus defect is frequently associated with right sided anomalous pulmonary venous connections.

Dec 18, 2022

It’s another session of CardioNerds Rounds! In these rounds, Dr. Loie Farina (Advanced Heart Failure and Transplant Fellow at Northwestern University) joins Dr. Jane Wilcox (Chief of the Section of Heart Failure Treatment and Recovery at Northwestern University) to discuss the nuances of HFpEF diagnosis and management. Dr. Wilcox is also the Associate Director of the T1 Center for Cardiovascular Therapeutics in the Bluhm Cardiovascular Institute and Director of the Myocardial Recovery Clinic at Northwestern University. Dr. Wilcox is a prolific researcher, clinician, and thought leader in Heart Failure and we are honored to have her on CardioNerds Rounds! Notes were drafted by Dr. Karan Desai. Audio editing by CardioNerds Academy Intern, student doctor Akiva Rosenzveig. This episode is supported with unrestricted funding from Zoll LifeVest. A special thank you to Mitzy Applegate and Ivan Chevere for their production skills that help make CardioNerds Rounds such an amazing success. All CardioNerds content is planned, produced, and reviewed solely by CardioNerds. Case details are altered to protect patient health information. CardioNerds Rounds is co-chaired by Dr. Karan Desai and Dr. Natalie Stokes. Speaker disclosures: None Challenging Cases - Atrial Fibrillation with Dr. Hugh Calkins CardioNerds Rounds PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Show notes - HFpEF Diagnosis and Management Case #1 Synopsis: A woman in her 80s with a history of HFpEF presented with worsening dyspnea on exertion over the course of a year but significantly worsening over the past two months. Her other history includes prior breast cancer with chemotherapy and radiation therapy, permanent atrial fibrillation with AV node ablation and CRT-P, and CKD Stage III. She presented for an outpatient RHC with exercise to further characterize her HFpEF. Her echo showed normal LV size, no LVH, LVEF of 50%, decreased RV systolic function, severe left atrial enlargement, significantly elevated E/e’ and mild MR. Right heart catheterization showed moderately elevated bi-ventricular filling pressures at rest but with passive leg raise and Stage 1 exercise the wedge pressure rose significantly. We were asked to comment on management. Case #1 Takeaways Amongst the things that were discussed were the role of specific therapies in symptomatic patients with HFpEF. In patients with HFpEF and documented congestion, they will require diuretic therapy for symptomatic relief. But in addition to diuretic therapy, we discussed starting HFpEF-specific therapies. Amongst, those specific therapies mineralocorticoid receptor antagonist (MRA) and sodium-glucose co-transporter 2 (SGLT2) inhibitor. In multiple trials that have included patients with HFPEF, SGLT2i have reduced the risk of hospitalization. This includes the EMPEROR-PRESERVED Trial (see the CardioNerds Journal Club discussion on the trial) in which nearly 6000 patients with NYHA Class II-IV symptoms, EF > 40% and elevated NT-proBNP with a prior HF hospitalization within the past 12 months were randomized to Empagliflozin or placebo. The primary outcome – death from CV causes or hospitalization for Heart Failure – was significantly lower in the SGLT2i arm (13.8% vs 17.1%, 95% CI 0.69-0.90, P 45% to receive either spironolactone or placebo. The primary endpoint (death from CV cause, aborted cardiac arrest, or hospitalization for HF) was not statistically different between treatment arms. Of note, however, there were concerns for regional differences which is outlined well in this NEJM Evidence piece. Case #2 Synopsis: A woman in her 70s with history of hypertension, obesity, and COPD presented to the office for an evaluation of dyspnea. She had noted two years of dyspnea with moderate exercise and had developed lower extremity swelling. She had an echocardiogram that showed normal LV size and function, no LVH, global longitudinal strain at -21% (normal), grade 1 diastolic dysfunction and mild left atrial enlargement. Amongst the initial questions we were asked was how would we approach the diagnostic evaluation of her dyspnea? Case #2 Takeaways There were several things we covered with Dr. Wilcox regarding this patient. One of the things we discussed was whether the patient has HFpEF and then concomitantly, if we suspect and confirm HFpEF, attempting to elucidate an etiology for the patient’s HFpEF. There are diagnostic scores, such as the H2FPEF score that can estimate the probability of HFpEF versus a non-cardiac cause of a patient’s symptoms. There are limitations to the scoring systems – including echocardiographic parameters that may not be available at point of care or prone to error – but it can refine a clinician’s pre-test probability for HFpEF. Amongst other testing, an important note is that coronary artery disease is common in patients with HFpEF and may be a potentially treatable and reversible cause of HFpEF. Thus, evaluation for ischemia is recommended and given a Class IIa recommendation in the 2022 ACC/AHA/HFSA Guideline for the Management of Heart Failure. References - HFpEF Diagnosis and Management Anker SD, Butler J, Filippatos G et al; EMPEROR-Preserved Trial Investigators. Empagliflozin in Heart Failure with a Preserved Ejection Fraction. N Engl J Med. 2021 Oct 14;385(16):1451-1461. doi: 10.1056/NEJMoa2107038. Epub 2021 Aug 27. PMID: 34449189. Heidenreich P, Bozkurt B, Aguilar D, et al. 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure. J Am Coll Cardiol. 2022 May, 79 (17) e263–e421. Pfeffer MA, Claggett B, Assmann SF et al. Regional variation in patients and outcomes in the Treatment of Preserved Cardiac Function Heart Failure with an Aldosterone Antagonist (TOPCAT) trial. Circulation2015; 131:34-42.25406305 Pitt B, Pfeffer MA, Assmann SF, et al. Spironolactone for heart failure with preserved ejection fraction. N Engl J Med2014; 370:1383-1392. 10.1056/NEJMoa1313731 24716680. Reddy YNV, Carter RE, Obokata M et al. A Simple, Evidence-Based Approach to Help Guide Diagnosis of Heart Failure With Preserved Ejection Fraction. Circulation. 2018 Aug 28;138(9):861-870. doi: 10.1161/CIRCULATIONAHA.118.034646. PMID: 29792299; PMCID: PMC6202181. Production Team Karan Desai, MD Natalie Stokes, MD Amit Goyal, MD Daniel Ambinder, MD

Dec 8, 2022

As the burden of cardiovascular disease increases in the United States, the importance of enhanced screening tools, early risk prediction, and prevention strategies grows. Novel risk scoring methods, including polygenic risk scores (PRS), may help identify patients that benefit from early intervention and risk modification. In this episode, we discuss how a PRS is calculated, how to incorporate a PRS into clinical practice, and current barriers to the equitable implementation of risk scores. In terms of frontiers in clinical genetics we also discuss the burgeoning field of pharmacogenetics and how pharmacogenetics may be used to identify responders and non-responders to certain therapies. Join CardioNerds Dr. Jessie Holtzman (CardioNerds Academy Chief and Chief Resident and soon FIT at UCSF), Dr. Alaa Diab (CardioNerds Academy Fellow and Medicine Resident at GBMC), and student doctor Hirsh Elhence (CardioNerds Academy Intern and medical student at USC Keck School of Medicine) as they discuss frontiers in clinical genetics with Dr. Pradeep Natarajan (Director of Preventive Cardiology, Massachusetts General Hospital). Audio editing by CardioNerds Academy Intern, student doctor Akiva Rosenzveig. This episode was developed in collaboration with the American Society of Preventive Cardiology and is supported with unrestricted educational funds from Illumina, Inc. All CardioNerds content is planned, produced, and reviewed solely by CardioNerds. This CardioNerds Cardiovascular Genomics series is a multi-institutional collaboration made possible by contributions of stellar fellow leads and expert faculty from several programs. Pearls • Notes • References CardioNerds Cardiovascular Genomics PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls - Frontiers in Clinical Genetics in Cardiovascular Prevention For common diseases like coronary artery disease, rare mutations may confer a several-fold increased risk of disease – for instance, in familial hypercholesterolemia, a single rare mutation may confer as much as a three-fold increase in risk of coronary artery disease. However, for most common diseases, the overall cumulative impact of several common genetic variants may be greater than that of a monogenetic trait. Family history is a particularly coarse predictor of CV risk, highlighting the need for polygenic risk scores. In particular, younger patients with borderline cardiovascular risk may benefit from the use of a polygenic risk score in the determination of their overall cardiovascular risk profile. A polygenic risk score (PRS) is a weighted sum of several risk-conferring alleles. The weight assigned to an allele is determined by the strength of the association between the allele and CV disease, as determined by genome-wide association studies (GWAS). The data used for genome-wide associated studies in cardiovascular disease have historically included populations primarily of European ancestry. However, more data is being collected from diverse patient cohorts to increase the external validity and broader applicability of such studies. Pharmacogenetic polygenic risk scores may be used to predict drug efficacy and toxicity, as well as to identify biologically plausible drug targets for clinical trial design. Show notes - Frontiers in Clinical Genetics in Cardiovascular Prevention What is a polygenic risk score (PRS)? Monogenic conditions are those in which a variant in a single gene causes a pathological phenotype. For example, familial hypercholesterolemia is often the result of a mutated allele in the LDL receptor gene. In contrast, polygenic risk suggests that there are variants in multiple genes that all confer risk independently, each with a small individual effect size. By aggregating many variants, a risk score may be able to provide an estimate as to the degree of one’s risk of cardiovascular disease. By comparing the allele frequencies of genes between patients with and without cardiovascular disease, risk-conferring alleles may be identified. These studies are called genome-wide association studies (GWAS). From GWAS, PRS can then be calculated by aggregating several risk-conferring alleles. What is the clinical utility of PRS? Current uses of PRSFamily history is a coarse predictor of CV disease. The addition of a PRS to a risk assessment may improve the clinician’s ability to risk stratify patients.Calculating PRS can help identify patients who need early intervention, even in the absence of traditional risk factors (such as hypercholesterolemia or diabetes mellitus). For example, imagine a patient in the top 20th percentile for polygenic risk with a relatively normal LDL. Despite the lack of hyperlipidemia, some evidence may suggest that a statin or aggressive lifestyle modification would lower CV risk in this patient. In particular, for younger patients with borderline CV risk (as measured by traditional risk factors such as blood pressure, age, etc.), a high PRS might promote aggressive lifestyle modification or pharmacotherapy. Potential future uses Pharmacogenomics - Understanding a patient’s genotype may help identify responders and non-responders to certain medications. For example, CYP2C19 is an enzyme that aids in the activation of Clopidogrel. Therefore, patients with a mutation in CYP2C19 may not respond as robustly to Clopidogrel and therefore alternate pharmacotherapy would be recommended. What are the barriers to equity?Historically, GWAS studies largely enrolled patients of European ancestry. As such, the external validity of PRS outside of populations of European descent has been questioned. The NIH has prioritized capturing data from more diverse cohorts, associated with an increase in databases including patients of more varied ancestry. The availability of direct-to-consumer genome sequencing kits may make calculating PRS more feasible for the broader population. However, such tests remain limited in their utility without interpretation by genetic counselors or cardiovascular geneticists. References - Frontiers in Clinical Genetics in Cardiovascular Prevention Khera AV, Chaffin M, Aragam KG, Haas ME, Roselli C, Choi SH, Natarajan P, Lander ES, Lubitz SA, Ellinor PT, Kathiresan S. Genome-wide polygenic scores for common diseases identify individuals with risk equivalent to monogenic mutations. Nat Genet. 2018 Sep;50(9):1219-1224. doi: 10.1038/s41588-018-0183-z. Epub 2018 Aug 13. PMID: 30104762; PMCID: PMC6128408. O'Sullivan JW, Raghavan S, Marquez-Luna C, Luzum JA, Damrauer SM, Ashley EA, O'Donnell CJ, Willer CJ, Natarajan P; American Heart Association Council on Genomic and Precision Medicine; Council on Clinical Cardiology; Council on Arteriosclerosis, Thrombosis and Vascular Biology; Council on Cardiovascular Radiology and Intervention; Council on Lifestyle and Cardiometabolic Health; and Council on Peripheral Vascular Disease. Polygenic Risk Scores for Cardiovascular Disease: A Scientific Statement From the American Heart Association. Circulation. 2022 Aug 23;146(8):e93-e118. doi: 10.1161/CIR.0000000000001077. Epub 2022 Jul 18. PMID: 35862132.

Dec 5, 2022

In this episode, we discuss the utility of veno-arterial extra-corporeal membrane oxygenation (VA-ECMO) for the temporary management of biventricular failure and cardiogenic shock requiring full cardiopulmonary support. Here, we define the types of ECMO and describe the unique physiology of this mechanical circulatory support platform, as well as review the potential complications and management strategies. Most notably, we highlight indications for and contraindications to the use of VA-ECMO and review the importance of patient selection. Lastly, we discuss de-escalation and de-cannulation strategies for patients on VA-ECMO as a bridge to recovery. Join Dr. Amit Goyal (CardioNerds Cofounder and FIT at Cleveland Clinic), Dr. Yoav Karpenshif (Series Co-chair and FIT at University of Pennsylvania), and Dr. Megan Burke (Episode FIT Lead and FIT at University of Pennsylvania) as they learn about how to care for some of our sickest patients from Dr. Ann Gage, interventional and critical care cardiologist at Centennial Heart. At the beginning of the episode, enjoy a message from the very first CardioNerds Scholar, Dr. Katie Vaughan (Chief Resident and soon Cardiology Fellow at BIDMC). Episode notes were developed by Dr. Megan Burke. Audio editing by CardioNerds Academy Intern, Hirsh Elhence. The CardioNerds Cardiac Critical Care Series is a multi-institutional collaboration made possible by contributions of stellar fellow leads and expert faculty from several programs, led by series co-chairs, Dr. Mark Belkin, Dr. Eunice Dugan, Dr. Karan Desai, and Dr. Yoav Karpenshif. Pearls • Notes • References • Production Team CardioNerds Cardiac Critical Care PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls and Quotes - Biventricular Failure and the Use of VA-ECMO Veno-arterial extracorporeal membrane oxygenation (VA-ECMO) is a form of temporary mechanical circulatory support that can do the work of both the heart and lungs. The ECMO circuit is a narcissist, i.e. cannulas are named in reference to the circuit and not the patient (“inflow” vs “outflow”). The decision to utilize ECMO should be made by a multidisciplinary shock team and patient selection is KEY! ECMO physiology rule #1: VA-ECMO increases LV afterload Patients on VA-ECMO should be monitored with a PA catheter and an arterial line in the right arm Show notes - Biventricular Failure and the Use of VA-ECMO Notes drafted by Dr. Megan Burke. 1. What is ECMO and what are the different types? Extracorporeal membrane oxygenation (ECMO) is a temporary form of mechanical life support that comes in two flavors: veno-arterial, or “VA” and veno-venous, or “VV.” VV-ECMO supports extracorporeal gas exchange in the setting of acute respiratory failure VA-ECMO provides full circulatory support in addition to gas exchange, doing the work of both the heart and lungs. 2. What are the components and “anatomy” of the VA-ECMO circuit? The circuit is made up of the following major components: Venous (inflow) cannula Centrifugal Pump Oxygenator (also responsible for CO2 removal) Arterial (outflow) cannula The cannulas are named in reference to the ECMO circuit, not the patient. Dr. Gage suggests that we think of the ECMO circuit (and mechanical circulatory support in general) as narcissistic, i.e. flow is always in reference to the device. Gas exchange happens in the oxygenator. In the oxygenator blood flows through thin filaments that allow for diffusion of oxygen and carbon dioxide. Gas flows in the opposite direction of blood flow to maximize diffusion through the countercurrent effect. Oxygenation is determined by rate of blood flow through the oxygenator and FiO2 delivered. Carbon dioxide removal is determined by rate of countercurrent gas flow, referred to as the sweep speed. 3. What are the indications for VA-ECMO? VA-ECMO is utilized in the setting of severe refractory cardiogenic shock (in the setting of left, right, or biventricular failure) and cardiac arrest. It is a temporary mechanical circulatory support platform, and should be used as a bridge to recovery or a more durable therapy (i.e. durable mechanical support or transplant). Due to lack of randomized data, there are no consensus guidelines for the use of VA-ECMO, and the decision to implement it should be made as part of a multidisciplinary cardiogenic shock team. Common indications include cardiogenic shock, refractory ventricular arrhythmias, massive pulmonary embolism, cardiac arrest, and failure to wean from cardiopulmonary bypass during surgery. The absolute and relative contra-indications to ECMO vary by institution. Given the high mortality rates for patients on VA-ECMO (hospital mortality is approximately 50%, and 6-month survival is as low as 30%), patient selection is key. There are multiple pre VA-ECMO risk factors independently associated with poor outcomes. These include older age, female sex, higher body mass index, and markers of increased severity of illness including laboratory evidence of end-organ dysfunction and longer duration of mechanical ventilation. 4. What are the pathophysiological consequences of VA-ECMO and how do we monitor and treat them? The goal of VA-ECMO is to provide perfusion, however unlike other forms of mechanical circulatory support, it is NOT supporting the heart’s ability to pump blood. In fact, VA-ECMO increases left ventricular afterload, because blood enters the aorta from the outflow cannula somewhere between the aortic root and the diaphragm (depending on cannulation strategy). This creates increased aortic pressure and increased left ventricular volume and afterload, which can lead to pulmonary edema and worsened myocardial demand. In the most extreme cases, the aortic pressure can exceed the left ventricular systolic pressure, thereby preventing blood from ejecting from the LV. This can lead to stasis, thrombus formation, and strokes. For this reason, echocardiography is used frequently to monitor LV ejection. One key marker is the opening of the aortic valve with every beat. Furthermore, hemodynamic monitoring with a pulmonary artery catheter and a RIGHT radial arterial line is essential for management of patient’s on ECMO.The PA catheter allows for an estimation of the filling pressures. Of note, the mixed venous O2 cannot be used to estimate cardiac output when a patient is on VA-ECMO, but low levels still do correlate with poor tissue perfusion and worse outcomes.In general, it is essential to have an arterial catheter in a patient on VA-ECMO to monitor for arterial pulsatility, which is a surrogate for the contribution of the patient’s heart to perfusion. Specifically, a RIGHT radial arterial line is key in these patients because blood from it originates the brachiocephalic artery, which is the closest branch in the aortic arch to the coronary arteries and great vessels of the aortic arch and therefore best estimates the oxygen content in the coronaries and brain. This is key because when a patient is on peripheral VA-ECMO, oxygenated blood arrives to the heart retrograde from the femoral artery. If the left ventricle retains or regains contractility, the poorly oxygenated blood from the lungs (in patients with concurrent significant respiratory failure) is ejected into the proximal aorta. This can lead to the so called “North-south” or “Harlequin” syndrome, where the head and right upper extremity are relatively hypoxic compared to the rest of the body. Arterial blood gases from a right radial arterial line can forewarn of possible coronary and cerebral hypoxia during LV recovery as this syndrome develops and the “mixing” cloud develops. For patients with poor ejection, there are various strategies to decompress, or “vent,” the left ventricle. Strategies include use of medicines to reduce afterload and/or improve inotropy, creation of an atrial septal defect to offload the left heart, and use of temporary mechanical circulatory support devices (IABP or percutaneous LVAD) to allow blood to more easily leave the LV. Treatment of the North-South Syndrome focuses on increasing the oxygenation of blood ejecting from the left ventricle through vent management or adding another venous catheter to pre-oxygenate blood before entering the lungs (VAV-ECMO). Increasing VA-ECMO flow can also shift the mixing zone towards the aortic arch and improve oxygenation, but this will also increase the LV afterload. Other complications of the ECMO circuit include infection, bleeding, and limb ischemia (due to the large bore vascular access), as well as stroke, hemolysis, and thrombus formation (due to the extracorporeal circuitry). 5. How is VA-ECMO weaned? If a patient is on VA-ECMO support as a bridge to recovery, the ability to wean a patient off the circuit relies on invasive hemodynamics, echocardiography, and an assessment of improving end-organ function. The flow of blood out of the circuit can be gradually weaned down to allow for the patient’s native heart to do more of the work of perfusion. Once the patient is thought to be ready for decannulation it is common to perform a turndown study under echocardiographic guidance, where serial evaluations of biventricular function are done at different flow speeds. VA-ECMO is usually decannulated in the operating room to allow for surgical repair of the vasculature in the setting of large bore access. References - Biventricular Failure and the Use of VA-ECMO Papolos AI, Kenigsberg BB, Berg DD, Alviar CL, Bohula E, Burke JA, Carnicelli AP, Chaudhry SP, Drakos S, Gerber DA, Guo J, Horowitz JM, Katz JN, Keeley EC, Metkus TS, Nativi-Nicolau J, Snell JR, Sinha SS, Tymchak WJ, Van Diepen S, Morrow DA,

Nov 30, 2022

The CardioNerds Cardiovascular Genomics Series continues! In this episode Dr. Dan Ambinder (CardioNerds Cofounder and Interventional Cardiologist), Dr. Anjali Wagle (FIT Ambassador at Johns Hopkins) and Dr. James Sampognaro (medicine resident at Johns Hopkins Osler Medicine Residency) learn from Dr. Allison Hays (Associate Professor of Medicine, Division of Cardiology, Johns Hopkins CMR researcher and Medical Director of Echocardiography) and Dr. Cindy James (Associate Professor of Medicine and certified genetic counselor at Johns Hopkins with research focusing on cardiovascular genetic counseling and arrhythmogenic cardiomyopathies). They discuss arrhythmogenic RV cardiomyopathy as the context to learn about genetic counseling and family screening. Episode script and notes were developed by Dr. Anjali Wagle. Audio editing by CardioNerds Academy Intern, student doctor Chelsea Amo Tweneboah. This episode was developed in collaboration with the American Society of Preventive Cardiology and is supported with unrestricted educational funds from Illumina, Inc. All CardioNerds content is planned, produced, and reviewed solely by CardioNerds. This CardioNerds Cardiovascular Genomics series is a multi-institutional collaboration made possible by contributions of stellar fellow leads and expert faculty from several programs. Check out this REVIEW describing the “Multimodality Imaging in Arrhythmogenic Right Ventricular Cardiomyopathy” by Nitin Malik, Allison Hays, and colleagues. For related episodes, please enjoy these case-based discussions: Ep 56. Case Report: Arrhythmogenic Desmoplakin Cardiomyopathy – Northwestern University Ep 74. Case Report: Arrhythmogenic Right Ventricular Cardiomyopathy (ARVC) – Summa Health Pearls • Notes • References CardioNerds Cardiovascular Genomics PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Show notes - Genetic Counseling & Family Screening in Arrhythmogenic Cardiomyopathies Notes (developed by Dr. Anjali Wagle) What is the underlying pathophysiology of arrhythmogenic RV cardiomyopathy (ARVC)? Fibrofatty replacement cardiac myocytes Associated with genetically mediated disruption of desmosomal proteins This leads to thinning and weakness of the heart that can lead to aneurysms and progressive dilatation and failure of the right ventricle (RV) How is ARVC diagnosed? 2010 taskforce criteria (Marcus et al, 2010): RV structural abnormalities including findings seen on echocardiogram, MRI, and RV angiography Pathological criteria Repolarization abnormalities Depolarization/conduction abnormalities Ventricular arrhythmias Genetics and/or family history How does ARVC present? Young, healthy individual will have symptoms of arrhythmias (syncope, pre-syncope, SCD) or heart failure Family screening What are the inheritance and genetic factors of ARVC? Autosomal dominant pattern Low penetrance and variable expressivity Half of patients who are index cases will be found to have a mutation in the desmosomal gene. What are the most common mutations associated with ARVC? Most commonly the genes involved are plakophilin-2 (PKP-2) and desmoplakin. For PKP-2 the most common mutations are truncating mutations. In patients who have inherited two truncating mutations, this will result in neonatal lethality. Is there a difference in the genetic factors of left and right arrhythmogenic cardiomyopathy? ACM is disproportionally a right dominated cardiomyopathy. Left dominated cardiomyopathy has a different genetic profile. Pathogenic variants in desmoplakin disproportionally cause biventricular forms of ACM or left dominated forms. What are the echocardiographic findings in ACM? Wall thinning and aneurysmal dilation in the sub-tricuspid region, RV outflow tract, or base also known as the “triangle of dysplasia.” Progression of disease tends to be from the base to the apex. Why is cardiac MRI the preferred imaging modality in ACM? Higher spatial resolution and improved visualization of the right ventricle Can imaging help define prognosis in ACM? Top two strongest measures of prognostic value in ACM are: RV fractional change area < 33% Tricuspid annular plane systolic exertion < 1.7cm References - Genetic Counseling & Family Screening in Arrhythmogenic Cardiomyopathies Malik, N., Mukherjee, M., Wu, K. C., Zimmerman, S. L., Zhan, J., Calkins, H., James, C. A., Gilotra, N. A., Sheikh, F. H., Tandri, H., Kutty, S., & Hays, A. G. (2022). Multimodality Imaging in Arrhythmogenic Right Ventricular Cardiomyopathy. Circulation. Cardiovascular Imaging, 15(2), e013725. https://doi.org/10.1161/CIRCIMAGING.121.013725 Marcus FI, McKenna WJ, Duane S, Basso C, Bauce B, Bluemke DA, Calkins H, Corrado D, Cox MGPJ, Daubert JP, Fontaine G, Gear K, Hauer R, Nava A, Picard MH, Protonotarios N, Saffitz JE, Sanborn DMY, Steinberg JS, Tandri H, Thiene G, Towbin JA, Tsatsopoulou A, Wichter T, Zareba W. Diagnosis of Arrhythmogenic Right Ventricular Cardiomyopathy/Dysplasia. Circulation. 2010;121:1533–1541.

Nov 28, 2022

Congenital heart disease is the most common birth defect, affecting 1 in 100 babies. Amongst these ventricular septal defects are very common with the majority of patients living into adulthood. In this episode we will be reviewing key features of VSDs including embryologic origin, anatomy, physiology, hemodynamic consequences, clinical presentation and management of VSDs. Dr. Tommy Das (CardioNerds Academy Program Director and FIT at Cleveland Clinic), Dr. Agnes Koczo (CardioNerds ACHD Series Co-Chair and FIT at UPMC), and Dr. Anu Dodeja (Associate Director for ACHD at Connecticut Children’s) discuss VSDs with expert faculty Dr. Keri Shafer. Dr. Shafer is an adult congenital heart disease specialist at Boston Children’s Hospital, and an assistant professor of pediatrics within Harvard Medical School. She is a medical educator and was an invited speaker for the inaugural CardioNerds Sanjay V Desai Lecture, on the topic of growth mindset. Script and notes were developed by Dr. Anu Dodeja. Audio editing by CardioNerds Academy Intern, Shivani Reddy. The CardioNerds Adult Congenital Heart Disease (ACHD) series provides a comprehensive curriculum to dive deep into the labyrinthine world of congenital heart disease with the aim of empowering every CardioNerd to help improve the lives of people living with congenital heart disease. This series is multi-institutional collaborative project made possible by contributions of stellar fellow leads and expert faculty from several programs, led by series co-chairs, Dr. Josh Saef, Dr. Agnes Koczo, and Dr. Dan Clark. The CardioNerds Adult Congenital Heart Disease Series is developed in collaboration with the Adult Congenital Heart Association, The CHiP Network, and Heart University. See more Disclosures: None Pearls • Notes • References • Guest Profiles • Production Team CardioNerds Adult Congenital Heart Disease PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls - Ventricular Septal Defects Most common VSDs: Perimembranous VSD The shunt volume in a VSD is determined largely by the size of the defect and the pulmonary vascular resistance. VSDs cause left to right shunt. The long-term effects are left sided chamber dilation, as is the case with PDAs (post-tricuspid shunts) VSDs can be associated with acquired RVOTO, double chamber right ventricle, LVOTO/sub aortic membrane formation, and aortic regurgitation from aortic valve prolapse. Eisenmenger syndrome results from long-term left-to-right shunt, usually at higher shunt volumes. The resulting elevated pulmonary artery pressure is irreversible and leads to a reversal in the ventricular level shunt, desaturation, cyanosis, and secondary erythrocytosis. Endocarditis prophylaxis is not indicated for simple VSD. It is required for 6 months post VSD closure, in patients post VSD closure with a residual shunt and in Eisenmenger patients with R—>L shunt and cyanosis. Show notes - Ventricular Septal Defects Notes (developed by Dr. Anu Dodeja): What are types OF VSD? (Please note that there are several nomenclatures) Perimembranous VSDMost common type of VSD - 80% of VSDsOccurs in the membranous septum and can be associated with inlet or outlet extensionLocated near the tricuspid and aortic valves, often time can be closed off by tissue from the septal leaflet of the tricuspid valve and associated with abnormalities in the septal leaflet of the tricuspid valve secondary to damage from the left to right shuntCan be associated with acquired RVOTO, double chamber right ventricle, LVOTO/sub aortic membrane formation On TTE, the parasternal short axis view at the base demonstrates this type of VSD at the 10-12 o’clock position. Muscular VSDSecond most common VSD - 15-20% of VSDsCompletely surrounded by muscle, usually restrictive, can be multiple defects These usually close spontaneously by direct apposition of the muscular borders. Supracristal (also known as sub-arterial/sub-pulmonary/conal/juxta-arterial)Represent 5% of VSDsLocated beneath the semilunar valves in the conal or outlet septumDo not usually close spontaneouslyMay be associated with progressive aortic regurgitation due to prolapse of the right aortic cusp and aneurysm of the sinus of Valsalva.Aortic valve prolapse:Prolapsing of the right or non-coronary aortic valve cusp may initially reduce the degree of left-to-right shunt but results in development of aortic regurgitationAortic valve prolapse usually involves the right coronary cusp and less frequently the non-coronary cusp In its early stage: prolapse occurs only in the systolic phase because of the venturi effect resulting from the rapid shunt flow through the defectIn later stages the prolapse also present last with the valve cusps cannot withstand intra-aortic pressure. Eventually the prolapsing aortic valve becomes incompetent because of the significant damage to the valve cusps and annulusAs a prolapsing aortic valve may completely close the ventricular septal defect, shunt physiology may disappear with progressive development of aortic regurgitationSome case reports of aneurysms of sinus of Valsalva indicate that the original defect might be ventricular septal defect complicated by aortic valve prolapse with complete obliteration of the defectRarely the prolapsed valve cusp may perforate with resultant aortic regurgitation into the right ventricle On TTE, the parasternal short axis view at the base demonstrates these VSDs at the 12 to 2 o’clock position Inlet/AV canal typeOccur in the inlet portion of the ventricular septum immediately inferior to the AV valve apparatusCan be associated with a common AV valveMay be associated with AV septal malalignment and straddlingDue to endocardial cushion defect AVSD are the most common CHD in patients with Down syndrome. Malalignment type of VSDsOccur in the output or infundibular septumMalalignment of the outlet septum may occur either anteriorly towards the right ventricle or posteriorly towards the left ventricleThe anterior malalignment of the outlet septum is the most common type of malalignment. In this situation the outlet septum is pulled anteriorly towards the right ventricular outflow tract resulting in a large ventricular septal defect with overriding aortic valve and pulmonary stenosis as seen in Tetralogy of Fallot. Posterior malalignment results in sub-aortic obstruction and can be associated with Coarctation of aorta and IAA. Rarely patients can have a LV-RA shunt known as a Gerbode defectAbsence of the atrioventricular septal tissue resulting in an isolated LV to RA shuntCan occur when the VSDs located slightly more superior to the tricuspid valve apparatusCan also be due to deficient tricuspid valve septal leafletCan occur as a post-operative complication The effective impact of such a shunt is to produce right ventricular volume overload and elevated right atrial pressure and are at increased risk for endocarditis. If VSDs are left to right shunts, why do they cause left sided chamber dilation? The timing of the left to right shunt in ventricular septal defects is predominantly in ventricular systole so the blood goes left to right but is pumped directed out the PA resulting in increased pulmonary venous return to the LA and LV. As such, the RV does not directly see the increased blood volume. There are a few cases in which there maybe RA dilation including: Gerbode defect, Eisenmenger syndrome, and DCRV. What are the indications for VSD repair? Evidence of left ventricular volume overload and hemodynamically significant shunt (Qp: Qs> 1.5:1), if PA pressures are less than 50% systemic and pulmonary vascular resistance is less than 1/3 systemic (2018 ACHD Guidelines) What is the relevance of the conduction system in the approach to VSDs? The nature of the VSD will also allow for understanding the course of the conduction system. Perimembranous defects - the bundle of His runs along the posterior and inferior rim of the VSD. Post-operatively, patients may have a right bundle branch block pattern on ECG. Patients are at risk for surgical CHB which can occur even years post-VSD closure. Inlet type VSD - the bundle of His runs anterior and superior to the defect which can be seen as a northwest axis deviation on EKG (-90 to 180°). Patients are at risk for surgical CHB, which can occur even years post-VSD closure. Surgically induced AV block is less likely with a muscular or supracristal/outlet type of defects because they are distant from the AV nose and bundle of His. What are clinical exam features of VSDs? VSDs cause a holosystolic murmur if pressure in the right ventricle is lower than the left ventricle throughout systole, resulting in a holosystolic left-to-right shunt Small restrictive VSD will have a loud, harsh, holosystolic murmur usually with a thrill in the third or fourth ICS along the LSB Muscular VSDs can have shorter systolic murmurs Absence of VSD murmur, with a loud P2, RV heave is indicative of elevated RV pressures with equalization in ventricular pressures indicating Eisenmenger syndrome. These patents will also have cyanosis, clubbing, over time can have a holosystolic murmur due to functional TR Systolic ejection murmur at the LUSB may be indicative of RVOTO Presence of a diastolic murmur in the RUSB, wide pulse pressure, and prominent carotid pulses indicate AR What are imaging characteristics of VSDs? First and foremost will be location and size of the VSD Parasternal long axis view:Distinct visualization of muscular, membranous, and supracristal/infundibular VSDsPerimembranous and supracristal defects are seen below the aortic valveCan also show aortic cusp prolapse and associated aortic regurgitation

Nov 24, 2022

The field of Cardiovascular Genomics has advanced tremendously over the past two decades, having a significant clinical impact and changing the perception of the role and scope of genetic testing in several cardiovascular domains. To kickstart the Cardiovascular Genomics series, CardioNerds Dr. Sara Coles (FIT at Duke University), Dr. Colin Blumenthal (CardioNerds Academy faculty and FIT at UPenn), and Dr. Karla Asturias (CardioNerds Academy fellow and medicine resident at Pennsylvania Hospital) have a great discussion with Dr. James Daubert, a clinical electrophysiologist at Duke University, with a particular interest in inherited arrhythmia syndromes and sports cardiology. In this episode, we review basic concepts of cardiovascular genomics and genetics in electrophysiology while discussing when to (and when not to!) test our patients and their families and how to approach those results. Audio editing by CardioNerds academy intern, Pace Wetstein. This episode was developed in collaboration with the American Society of Preventive Cardiology and is supported with unrestricted educational funds from Illumina, Inc. All CardioNerds content is planned, produced, and reviewed solely by CardioNerds. This CardioNerds Cardiovascular Genomics series is a multi-institutional collaboration made possible by contributions of stellar fellow leads and expert faculty from several programs. Pearls • Notes • References CardioNerds Cardiovascular Genomics PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls and Quotes - Genetics in Electrophysiology The first step is identifying the right phenotype! Getting the right phenotype is crucial, as genetic testing done in a patient without a clear phenotype (or an incorrect one) would lead to significant anxiety, unnecessary tests and interventions, and potentially misleading and dangerous conclusions for patients and their families. Genetic testing typically should be reserved for patients with a confirmed or suspected diagnosis of an inherited disease or for individuals with a previously diagnosed pathogenic variant in a first-degree relative.1 Discuss with your patient! Genetic counseling is essential and recommended for all patients before and after genetic testing. It should include a thorough discussion of risks, benefits, and possible outcomes, including variants of uncertain significance.2 Cardiovascular genetics is a dynamic and rapidly evolving field. New information can cause a variant of uncertain significance to be reclassified as a pathogenic or likely pathogenic variant or to be downgraded to benign or likely benign as variant databases expand. Another possibility is that new research might identify novel genes for a particular disease, which could warrant retesting, particularly for phenotype-positive and genotype-negative patients.1 Brugada syndrome is an inherited arrhythmogenic disorder characterized by ST-segment elevation in the right precordial leads and malignant ventricular arrhythmias, with occasional conduction disease and atrial arrhythmias. It is diagnosed in patients with ST-segment elevation ≥ 2 mm in ≥ 1 lead among the right precordial leads, with a type I morphology (J-point elevation with slowly descending or concave ST segment elevation merging into a negative T wave), shown in the image below. This pattern can be observed spontaneously or after provocative drug testing (e.g., procainamide). Pathogenic genetic variants in SCN5A that result in loss of function of the cardiac sodium channel are identified in approximately 20% of cases.3,4 Image adapted from Batchvarov VN. The Brugada Syndrome – Diagnosis, Clinical Implications and Risk Stratification. Eur Cardiol Rev. 2014;9(2):82. doi:10.15420/ECR.2014.9.2.82 Measure the QT interval yourself! A correct determination of the QT interval is essential. Although automatic measurements are widely available, the interval can be underestimated or overestimated, particularly in atrial arrhythmias or complex T-wave morphologies. Determining the end of the T-wave can be challenging in this setting, and can be assessed through the tangent method, which determines the end of the T-wave by the intersection between the baseline (U-P segment) and the “tangent” drawn to the steepest last limb of the presumed T-wave.5,6 Image adapted from Postema PG, De Jong JSSG, Van der Bilt IAC, Wilde AAM. Accurate electrocardiographic assessment of the QT interval: teach the tangent. Hear Rhythm. 2008;5(7):1015-1018. doi:10.1016/J.HRTHM.2008.03.037 When encountering a patient with prolonged QT, it is essential to exclude secondary causes like QT-prolonging drugs and electrolyte imbalances. As the acute cause is removed and the acute illness resolves, “see what happens while the dust is settling” and reassess the QT. Show notes - Genetics in Electrophysiology Notes were developed by Dr. Karla Asturias: What are some key basic concepts in clinical genetics? A mutation is defined as a permanent change in the nucleotide sequence, while a polymorphism is a mutation that occurs in more than 1% of a particular population. While both terms are often used, it can lead to confusion due to incorrect assumptions of pathogenicity. Therefore, both terms have been replaced by the term genetic variant, which we now encounter in the literature and guidelines.Proband is the first presenting person in a family that serves as a starting point for a genetic study.The phenotype refers to the clinical syndrome observed in our patients, while the genotype relates to the genetic composition, including the presence or absence of any genetic variants.In the case of Brugada syndrome, the phenotype includes the type I Brugada pattern on ECG and the presence of ventricular arrhythmias. In many cases, the genotype consists of genetic variants in SCN5A that result in the loss of function of the cardiac sodium channel.While particular genotypes can cause disease, the expression of the clinical phenotype can vary, leading to incomplete penetrance, where only a proportion of individuals carrying a specific genetic variant manifest the phenotype.In patients with Brugada syndrome, there is variability in the frequency of ECG abnormalities, even with the same pathogenic variants. Among individuals with an SCN5A pathogenic variant, only 20-30% have an ECG diagnostic of Brugada syndrome, and approximately 80% manifest the characteristic ECG changes when challenged with a sodium channel blocker.4Additionally, the Brugada phenotype has been reported to be 8 to 10 times more common in men than in women.7 Most cardiovascular diseases exhibit genetic heterogeneity, with mutations in multiple genes causing the same condition, meaning multiple genotypes can cause a similar phenotype. In the cases of congenital long QT syndrome and hypertrophic cardiomyopathy, multiple genes have been implicated in these conditions. How do we classify genetic testing results according to the American College of Medical Genetics and Genomics (ACMG) guidelines? The American College of Medical Genetics and Genomics (ACMG) guidelines are internationally accepted and describe standard terminology and methods in clinical genetic testing.8 They classify genetic variants into five different tiers:PathogenicLikely pathogenicVariant of uncertain significance (VUS)Likely benignBenignIt should be noted that, at present, we have no data to support a quantitative assignment of variant certainty to any of the five categories given the heterogenous nature of most diseases.A variant of uncertain significance does not provide a definitive genetic etiology of disease and should not be used for clinical decision-making nor to determine risk for disease in unaffected relatives. 9 Variant interpretation is a dynamic process, and classification may change over time as additional evidence about the variants becomes available. A negative result does not exclude the possibility of genetic disease but indicates that a causative variant could not be identified with the currently available technology and knowledge. What types of genetic testing are available, and when do we use them?3 Sanger sequencing Method of DNA sequencing for a single geneHigh accuracy and low cost, compared to broader genetic testingUsed during cascade family evaluationPanel sequencingTests for a pre-specified “set” of genes related to a particular phenotype or clinical conditionFirst-line diagnostic test for the probandUsually, tests for exons onlyLarger panels may be warranted for overlap or ambiguous phenotypes, with the recognition that larger panels may lead to the identification of more variants of uncertain significanceFor unequivocal phenotypes, targeted panels are preferred, as larger panels are unlikely to increase clinical yield and may introduce ambiguous resultsWhole-exome and whole-genome sequencingComprehensive genetic characterization of coding regions only (exome) or entire genomeTypically reserved for research settings, but can be considered in the evaluation in proband in very heterogenous conditions Non-sequencing testing is also available through PCR for pre-specified variants What is the role of genetic testing in the management of inherited cardiovascular diseases? 9 Genetic testing is used to identify the underlying genetic etiology in a patient with a known or suspected inherited cardiovascular disease. Genetic testing is beneficial when the result alters the treatment, informs about the prognosis, and leads to testing in immediate family members. Common inherited cardiovascular diseases include Brugada syndrome, long QT syndrome, arrhythmogenic cardiomyopathy, dilated cardiomyopathy, hypertrophic cardiomyopathy,

Nov 20, 2022

CardioNerds Cofounder Dr. Amit Goyal is joined by Dr. Douglas Salguero (Internal medicine resident), Dr. Francisco Ujueta (Cardiology fellow), and Dr. Priscilla Wessly (Chief cardiology fellow) from the Columbia University Division of Cardiology at Mount Sinai Medical Center in Miami to discuss a rare case of isolated non-compaction cardiomyopathy. Expert commentary is provided by Dr. Christos Mihos (Director, Echocardiography Laboratory, Columbia University Division of Cardiology, Mount Sinai Medical Center). Audio editing by CardioNerds Academy Intern, Shivani Reddy. CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Case Media - Non-Compaction Cardiomyopathy Episode Schematics & Teaching The etiology has been a constant debate since 1980. It has been debated among researchers and clinicians whether LVNC is a physiologic or a pathologic manifestation. Waning et al., classified 327 unrelated patients into 3 categories: 1) genetic, 2) probably genetic, or 3) sporadic, identifying the most common mutations: MYH7, MYBPC3 and TTN in the genetic LVNC patients, which mostly encode for sarcomere, Z-disc and nuclear-envelope proteins. This supports the hypothesis that the inherited phenotype can arise from a gene mutation possibly during embryogenesis, disrupting the physiologic compaction of normally developing myocardium, which progresses from the base to the apex of the cardiac tissue. It is estimated that genetic LVNC accounts approximately 18-44% of cases, with autosomal dominant transmission being the most common form of inheritance. Physiologic remodeling with prominent trabeculations may be noted in athletes and pregnant women, in comparison to pathologic remodeling which may be encountered in patients with cardiomyopathy (e.g. pressure or volume load). (1) There is no pathognomonic signs or symptoms in LVNC. LVNC patients may encounter various potential clinical characteristics. Presentations are myriad and include heart failure symptoms (HFrEF or HFpEF), ventricular tachycardia (VT/VF), atrial fibrillation, thromboembolism including cerebrovascular accident (CVA), and syncope. In a cohort of 95 probands with LVNC investigated in Europe, as many as 32.3% had an ICD/CRT-D implantation, with 11.8% experiencing a cardiovascular death and 18.2% having an appropriate ICD shock. (2) Imaging plays a key role in diagnosis for LVNC. The identification and diagnosis of LVNC is evaluated using 2D echocardiography. The initial proposed method by Chin et al., evaluated the size of the trabeculation in the center. (3) The most commonly used criteria, Jenni et al. (4), entail the following four finding: Two-layer structure, with a thin compacted layer and a thick non-compacted layer measure at end-systole at the parasternal short-axis view. LVNC is defined by a ratio of N/C > 2 Absence of co-existing cardiac structural abnormalities Prominent, excessive trabeculations and deep intra-trabecular recesses Recesses supplied by intraventricular blood on color doppler Cardiac MRI has increased the diagnostic accuracy in the diagnosis of LVNC. It has been suggested that a NC/C ratio of > 2.3 in diastole distinguished pathological non-compaction, with sensitivity of 86% and a specificity of 99%, respectively. Although studies have shown an increase specificity with cardiac MRI, caution is needed as it may overestimate the presence of LVNC. Late gadolinium enhancement which suggests myocardial fibrosis or scar has been shown to have some prognostic value in LVNC patients. (5) Management for LVNC is multifaceted. As above,LVNC has a variety of presentations and prevailing manifestations will differ among patients. Therefore, the diagnostic and management approach much be personalized for a given patient. Heart failure with reduced ejection fraction is the most common presentation, thus treatment follows guided directed medical therapy, including ACEi/ARB/ARNi, beta-blockers, MRA, SGLT2i, etc. The risk for thromboembolism in patients with LVNC has not been well-established although case-series have noted an increase in clot formation due to the increase in intertrabecular recesses. Although no definitive criteria for anticoagulation have been suggestive in patients with LVNC and atrial fibrillation who meet current recommendations. There is a weak recommendation for anticoagulation in patients with LVNC and LVEF < 40% with or without atrial fibrillation. (6) Arrhythmias in LVNC is frequent. Ambulatory rhythm monitoring may be used to detect atrial fibrillation and ventricular arrhythmias. As with our patient, individuals with LVNC who survive an episode of sustained ventricular tachycardiac or sudden cardiac death, an ICD is indicative as secondary prevention. Otherwise, LVNC in patients with LVEF ≤ 35 percent and NYHA class II to III heart failure, ICD implantation is suggested. (6) Patients should be referred for genetic counseling with testing and subsequent cascade family screening as appropriate. Genetic testing has an important role in the management of LVNC. The identification of genetic LVNC is more predictive of major adverse cardiovascular events in the pediatric population than in adults, based on the finding from Waning et al. It has also been noted that patients with left ventricular dysfunction predicted a higher risk of MACE in carriers of the mutation compared to nongenetic cases. The 2018 Heart Failure Society of America (HFSA) guideline recommends a careful family history for at least three generation and screening of first-degree relatives of all patients with LVNC. Clinical screening should include physical history, echocardiogram, physical examination, electrocardiogram, and creatinine kinase. The HFSA recommends genetic testing for the individual displaying the most affect phenotype of disease. If the individual displays an abnormal disease-causing gene-variant then first degree relatives are recommended to undergo clinical screening for the disease followed by genetic counseling. (7) References - Non-Compaction Cardiomyopathy 1. van Waning JI, Caliskan K, Hoedemaekers YM, et al. Genetics, Clinical Features, and Long-Term Outcome of Noncompaction Cardiomyopathy. J Am Coll Cardiol. 2018;71(7):711-722. doi:10.1016/j.jacc.2017.12.019 https://www.jacc.org/doi/epdf/10.1016/j.jacc.2017.12.019 2. Sedaghat-Hamedani F, Haas J, Zhu F, et al. Clinical genetics and outcome of left ventricular non-compaction cardiomyopathy. Eur Heart J. 2017;38(46):3449-3460. doi:10.1093/eurheartj/ehx545https://academic.oup.com/eurheartj/article/38/46/3449/4364851?login=true#104113970 3. Chin TK, Perloff JK, Williams RG, Jue K, Mohrmann R. Isolated noncompaction of left ventricular myocardium. A study of eight cases. Circulation. 1990;82(2):507-513. doi:10.1161/01.cir.82.2.507https://www.ahajournals.org/doi/10.1161/01.cir.82.2.507 4. Jenni R, Oechslin E, Schneider J, Attenhofer Jost C, Kaufmann PA. Echocardiographic and pathoanatomical characteristics of isolated left ventricular non-compaction: a step towards classification as a distinct cardiomyopathy. Heart. 2001;86(6):666-671. doi:10.1136/heart.86.6.666https://heart.bmj.com/content/heartjnl/86/6/666.full.pdf 5. Dodd JD, Holmvang G, Hoffmann U, et al. Quantification of left ventricular noncompaction and trabecular delayed hyperenhancement with cardiac MRI: correlation with clinical severity. AJR Am J Roentgenol. 2007;189(4):974-980. doi:10.2214/AJR.07.2364https://www.ajronline.org/doi/10.2214/AJR.07.2364 6. Towbin JA, McKenna WJ, Abrams DJ, et al. 2019 HRS expert consensus statement on evaluation, risk stratification, and management of arrhythmogenic cardiomyopathy. Heart Rhythm. 2019;16(11):e301-e372. doi:10.1016/j.hrthm.2019.05.007. https://www.heartrhythmjournal.com/article/S1547-5271(19)30438-2/fulltext 7. Hershberger RE, Givertz MM, Ho CY, et al. Genetic Evaluation of Cardiomyopathy-A Heart Failure Society of America Practice Guideline. J Card Fail. 2018;24(5):281-302. doi:10.1016/j.cardfail.2018.03.004. https://www.onlinejcf.com/article/S1071-9164(18)30101-5/fulltext

Nov 15, 2022

CardioNerds (Dan Ambinder), episode lead Dr. Sarah Fahnhorst (ACHD Cardiologist at Spectrum Health in Grand Rapids, Michigan), and series co-chair Dr. Agnes Koczo (fellow at UPMC) learn about ASD from Dr. Richard Krasuski (ACHD Cardiologist and Director of ACHD at Duke University). Audio editing by CardioNerds Academy Intern, student doctor Adriana Mares An atrial septal defect (ASD) is a common congenital heart disease most often diagnosed in childhood, but initial presentation can be in adulthood. ASDs are abnormal communications between the left and the right atrium. There are four types of ASDs with different embryologic origins. If the defects are large, they will require percutaneous or surgical closure. Unrepaired defects can lead to symptoms of shortness of breath, exercise intolerance, recurrent chest infections, or pulmonary hypertension. This episode of CardioNerds will review the natural history, embryologic origin, diagnostic modalities/findings, indication for closure and long term complications of repaired and unrepaired atrial septal defects. The CardioNerds Adult Congenital Heart Disease (ACHD) series provides a comprehensive curriculum to dive deep into the labyrinthine world of congenital heart disease with the aim of empowering every CardioNerd to help improve the lives of people living with congenital heart disease. This series is multi-institutional collaborative project made possible by contributions of stellar fellow leads and expert faculty from several programs, led by series co-chairs, Dr. Josh Saef, Dr. Agnes Koczo, and Dr. Dan Clark. The CardioNerds Adult Congenital Heart Disease Series is developed in collaboration with the Adult Congenital Heart Association, The CHiP Network, and Heart University. See more Disclosures: None Pearls • Notes • References • Guest Profiles • Production Team CardioNerds Adult Congenital Heart Disease PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls - Atrial Septal Defects It’s a CLASSIC! – On physical exam a wide fixed split S2 along with a systolic ejection murmur due to increased blood flow across the pulmonary valve and potentially a diastolic rumble across the tricuspid valve are CLASSIC findings with atrial septal defects. Atrial septal defects are not all the same. There are four types of atrial septal defects: secundum ASD, primum ASD, sinus venosus and coronary sinus defects (NOTE – the latter are atrial level defects which actually do not involve the interatrial septum). The different types warrant a different approach to closure. Use your tools and if your suspicion is high for an atrial septal defect, keep looking. Sinus venosus defects can easily be missed since the superior vena cava is difficult to image in adults. Diagnostic tools include: history and physical exam (USE the stethoscope), ECG, echocardiogram, cardiac MRI, cardiac CT, and cardiac catheterization.Not all defects NEED to be closed immediately. Moderate-large defects with a shunt greater than 1.5:1 should be closed due to increased risk of pulmonary hypertension and arrhythmias, barring contraindications. Surgery was previously the gold standard for closure of ASDs, but many defects especially secundum atrial septal defects are closed in the cath lab. Show notes - Atrial Septal Defects Notes (developed by Dr. Sarah Fahnhorst What are the four different types of atrial level defects?Secundum atrial septal defectMost common type of atrial septal defect (75%)Located in the center of the atrial septum (fossa ovalis)Hole in the primum septum due to deficiency of the septum secundumPrimum atrial septal defectAccounts for 15-20% of ASDLocated at the inferior portion of the atrial septumIn the spectrum of atrioventricular septal defects/endocardial cushion defectsDefect in the development of the septum primumAssociated with cleft left AV valve, ventricular septal defects, and subaortic stenosisSinus venosus defectAccounts for 5-10% of atrial level defectNot a “septal” defect!Located near the superior vena cava-right atrial junction or very rarely at the mouth of the inferior vena cava80-90% of sinus venosus defects are associated with partial anomalous pulmonary venous returnCoronary sinus defectLeast common 1.5:1) and no signs of pulmonary hypertensionSymptomatic with a large shunt or signs of right heart enlargement or decreased systolic functionPrimum, sinus venosus, and coronary sinus defects will not close spontaneously What are treatment options available for each type of atrial septal defect?Surgical: Primum, sinus venosus, and coronary sinus defects are typically closed surgically. Some centers are closing sinus venosus defects percutaneously if anatomy is suitable particularly when surgery is deemed high risk.If there are additional structural heart defect such as a VSD or cleft mitral valve, then surgical closure is preferred. Transcatheter device closure: Secundum defects can be closed in the cath lab if they have sufficient rims, otherwise they will require surgical closure What are complications of repaired and unrepaired atrial septal defects?Repaired:TranscatheterResidual defectSmall increased risk for atrial arrhythmiasDevice embolizationSurgicalResidual defectSmall increased risk for atrial arrhythmiasUnrepairedPulmonary hypertensionEisenmenger syndromeAtrial arrhythmias (atrial fibrillation or atrial flutter)Right heart failureDecreased exercise and functional capacityIncreased risk of paradoxical embolism leading to risk of thromboembolic stroke References - Atrial Septal Defects Perloff JK. Surgical Closure of Atrial Septal Defect in Adults. New England Journal of Medicine. 1995;333(8):513-514. doi:10.1056/nejm199508243330809Stout KK, Daniels CJ, Aboulhosn JA, et al. 2018 AHA/ACC Guideline for the Management of Adults With Congenital Heart Disease: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines. Circulation. 2019;139(14):e698-e800. doi:doi:10.1161/CIR.0000000000000603Baumgartner H, De Backer J, Babu-Narayan SV, et al. 2020 ESC Guidelines for the management of adult congenital heart disease: The Task Force for the management of adult congenital heart disease of the European Society of Cardiology (ESC). Endorsed by: Association for European Paediatric and Congenital Cardiology (AEPC), International Society for Adult Congenital Heart Disease (ISACHD). Eur Heart J. 2020;42(6):563-645. doi:10.1093/eurheartj/ehaa554Gatzoulis MA, Webb GD, Daubeney PEF. Diagnosis and management of adult congenital heart disease. 3 ed. Elsevier Health Sciences; 2017.Saremi F. Cardiac CT and MR for Adult Congenital Heart Disease. Springer New York; 2013.Allen HD. Moss & Adams' heart disease in infants, children, and adolescents, including the fetus and young adult. 9 ed. Lippincott Williams and Wilkins; 2016. Meet Our Collaborators! Adult Congenital Heart AssociationFounded in 1998, the Adult Congenital Heart Association is an organization begun by and dedicated to supporting individuals and families living with congenital heart disease and advancing the care and treatment available to our community. Our mission is to empower the congenital heart disease community by advancing access to resources and specialized care that improve patient-centered outcomes. Visit their website (https://www.achaheart.org/) for information on their patient advocacy efforts, educational material, and membership for patients and providers CHiP Network The CHiP network is a non-profit organization aiming to connect congenital heart professionals around the world. Visit their website (thechipnetwork.org) and become a member to access free high-quality educational material, upcoming news and events, and the fantastic monthly Journal Watch, keeping you up to date with congenital scientific releases. Visit their website (https://thechipnetwork.org/) for more information. Heart UniversityHeart University aims to be “the go-to online resource” for e-learning in CHD and paediatric-acquired heart disease.

Nov 11, 2022

CardioNerds Cofounder Dr. Amit Goyal is joined by an esteemed group of UCLA cardiology fellows – Dr. Patrick Zakka (CardioNerds Academy Chief), Dr. Negeen Shehandeh (Chief Fellow), and Dr. Adrian Castillo – to discuss a case of primary cardiac angiosarcoma. An expert commentary is provided by Dr. Eric Yang, beloved educator, associate clinical professor of medicine, assistant fellowship program director, and founder of the Cardio-Oncology program at UCLA. Case synopsis: A female in her 40s presents to the ED for fatigue that had been ongoing for approximately 1 month. She also developed night sweats and diffuse joint pains, for which she has been taking NSAIDs. She was seen by her PCP and after bloodwork was done, was told she had iron deficiency so was on iron replacement therapy. Vital signs were within normal limits. She was in no acute distress. Her pulmonary and cardiac exams were unremarkable. Her lab studies showed a Hb of 6.6 (MCV 59) and platelet count of 686k. CXR was without significant abnormality, and EKG showed normal sinus rhythm. She was admitted to medicine and received IV iron (had not consented to receiving RBC transfusion). GI was consulted for anemia work-up. Meanwhile, she developed a new-onset atrial fibrillation with rapid ventricular response seen on telemetry, for which Cardiology was consulted. A TTE was ordered in part of her evaluation, and surprisingly noted a moderate pericardial effusion circumferential to the heart. Within the pericardial space, posterior to the heart and abutting the RA/RV was a large mass measuring approximately 5.5x5.9 cm. After further imaging work-up with CMR and PET-CT, the mass was surgically resected, and patient established care with outpatient oncology for chemotherapy. CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Case Media - primary cardiac angiosarcoma Episode Schematics & Teaching Pearls – primary cardiac angiosarcoma The pericardium is composed of an outer fibrous sac, and an inner serous sac with visceral and parietal layers. Pericardial masses can be primary (benign or malignant) or metastatic. There are other miscellaneous pericardial masses. Imaging modalities for the pericardium include echocardiography, cardiac CT and cardiac MRI. There is also role for PET-CT in pericardial imaging for further characterization of pericardial masses. Cardiac angiosarcomas are extremely rare but are the most common cardiac primary malignant tumors. Evidence-based management if lacking because of paucity of clinical data given the rarity of cardiac angiosarcomas. Surgery is the mainstay of therapy. Radiotherapy and chemotherapy are often used as well. Notes – primary cardiac angiosarcoma Pericardial Anatomy The pericardium is a fibroelastic sac composed of two layers. Outer layer: fibrous pericardium (<2 mm thick) Inner layer: serous pericardium, two-layered sac. Visceral pericardium: adherent to underlying myocardium Parietal pericardium: lines fibrous sac. Between the serous layers, there is the pericardial cavity which normally contains up to 50 cc pericardial fluid. Pericardial Masses Benign Lipoma: slow-growing, collection of adipose cells, thought to arise in AV groove Teratoma: benign germ cell tumors, often right sided. Can cause compressive symptoms of RA, SVC, PA, aortic root. Fibroma: solid mass of connective tissue Hemangioma: vascular mass, often arising from visceral pericardium Malignant Sarcoma: various types including angiosarcoma and liposarcoma. Lymphoma: usually non-Hodgkin B-cell lymphoma, often in immunocompromised patients Mesothelioma: no apparent association with asbestos. Pericardial effusions with nodules/plaques are seen. Metastatic Often associated with hemorrhagic pericardial effusions Breast cancer, lung cancer, melanoma and renal cell carcinoma are most common Pericardial Imaging Echocardiography Advantages: widely available low cost safe can be performed in multiple settings (e.g., HD unstable) Disadvantages: limited view/windows operator dependent technical difficulties (lung disease, obesity, surgical bandages) limited tissue characterization Cardiac Computed Tomography Advantages: Superior tissue characterization compared to echocardiography Can identify extra-cardiac disease Identification of calcification Pre-operative planning High spatial resolution Disadvantages: Use of ionizing radiation and iodinated contrast Difficult gating in patients with tachycardia/arrhythmias; use of breath hold HD stable patients only Cardiac Magnetic Resonance Imaging Advantages: Superior tissue characterization compared to echocardiography/computed tomography Disadvantages: Time consuming, expensive Difficulty gating in patients with tachycardia/arrhythmias; use of breath holds for some sequences Challenges in patients with electronic implants Use of gadolinium contrast Extra-cardiac structures not well visualized; calcifications less well-visualized Positron Emission Tomography/Computed Tomography (PET/CT) Has been shown to be an effective additional imaging modality in patients in whom cardiac mass is suspected to be malignant, and helps provide further confirmation and screening for metastatic disease. Angiosarcoma of the Pericardium Very rare, but most common cardiac primary malignant tumor. Typically right-sided and secondarily involves the pericardium. Primary pericardial angiosarcoma usually occurs in middle-aged, more frequently in males. Often metastatic at time of diagnosis. Clinical presentation Variety of symptoms, and often undetected early on. Symptoms include dyspnea, chest pain, cough, fatigue/malaise, and signs of caval obstruction. Clinical picture rapidly deteriorates as it can eventually result in intractable heart failure and death due to multi-organ failure. Lab/Imaging Tests Tumor marker CA125 elevated. Pericardiocentesis usually reveals bloody fluid (containing RBCs, WBCs). Cytology often misses malignant cells. EKG can show non-specific ST-T wave abnormalities and low QRS voltage. CXR may show an enlarged cardiac silhouette. Transthoracic echocardiography can show pericardial effusion but may fail to show echogenic mass if no good acoustic windows. Large masses in the pericardium may be seen in some patients. CT can show location, size, and extent of mass. CMR can further show tumor necrosis or hemorrhage. Can help characterize and stage tumors. PET/CT can help detect metastasis from pericardial tumors. Definitive diagnosis = biopsy (mediastinoscopy, exploratory pericardiotomy or thoracotomy). Extensive excision is usually recommended. Angiosarcomas histologically are characterized by presence of anastomosing vascular channels that are lined by atypical/malignant endothelial cells showing frequent mitoses. Immunohistochemical staining: endothelial markers (CD31, CD34, vimentin, factor VII). Management Because of rarity there is little clinical evidence-based data for management. Usually responds poorly to chemotherapy and radiation. Surgery is challenging because these tumors are diagnosed late and there is already metastatic disease. Orthotopic cardiac transplantation is sometimes done and has prolonged life, though incidence of metastatic disease limits utility. Could be helpful in patients who have unresectable but locally aggressive tumors without metastasis. Palliative treatment options are usually resorted to because the disease often presents so late. Length of survival after diagnosis ranges between 6-11 months. Ultimately, surgical resection with negative margins is associated with best outcome; there is some benefit to then adding chemotherapy and radiotherapy. References - primary cardiac angiosarcoma Burke A, Tavora F. The 2015 classification of tumors of the heart and pericardium. J Thorac Oncol. 2015; 11(4): 441-452. https://www.jto.org/article/S1556-0864(15)00109-4/fulltext41 Yin H, Mao W, Tan H, et al. Role of 18F-FDG PET/CT imaging in cardiac and pericardial masses. J Nucl Cardiol. 2022; 29(3):1293-1303. https://pubmed.ncbi.nlm.nih.gov/33462788/ -452, APRIL 01, 2016 Xie M, Li Y, Wenfang G. Pericardial angiosarcoma: Status quo. Acc.org 2019. https://www.acc.org/latest-in-cardiology/articles/2019/09/04/06/43/pericardial-angiosarcoma

Nov 3, 2022

It’s another session of CardioNerds Rounds! In these rounds, Dr. Priya Kothapalli (Interventional FIT at University of Texas at Auston, Dell Medical School) joins Dr. Deepak Bhatt (Dr. Valentin Fuster Professor of Medicine and Director of Mount Sinai Heart) to discuss the nuances of antithrombotic therapy. As one of the most prolific cardiovascular researchers, clinicians, and educators, CardioNerds is honored to have Dr. Bhatt on Rounds, especially given that Dr. Bhatt has led numerous breakthroughs in antithrombotic therapy. Come round with us today by listening to the episodes of #CardsRounds! Audio editing by CardioNerds Academy Intern, Dr. Christian Faaborg-Andersen. This episode is supported with unrestricted funding from Zoll LifeVest. A special thank you to Mitzy Applegate and Ivan Chevere for their production skills that help make CardioNerds Rounds such an amazing success. All CardioNerds content is planned, produced, and reviewed solely by CardioNerds. Case details are altered to protect patient health information. CardioNerds Rounds is co-chaired by Dr. Karan Desai and Dr. Natalie Stokes. Speaker disclosures: None Challenging Cases - Atrial Fibrillation with Dr. Hugh Calkins CardioNerds Rounds PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Show notes - Antithrombotic Management with Dr. Deepak Bhatt Case #1 Synopsis: A woman in her early 70s with a history of hypertension, hyperlipidemia, and paroxysmal atrial fibrillation presented with sudden-onset chest pressure and diaphoresis while at rest and was found to have an acute thrombotic 99% mid-LAD occlusion. The patient received OCT-guided PCI with a single drug-eluting stent. We discussed what the appropriate antithrombotic strategy would be for a patient with recent acute coronary syndrome and atrial fibrillation. Case #1Takeaways According to the recent 2021 revascularization guidelines, in patients with atrial fibrillation undergoing PCI and taking oral anticoagulant therapy, it is recommended to discontinue aspirin after 1 to 4 weeks while maintaining P2Y12 inhibitors in addition to a non-vitamin K oral anticoagulant or warfarin.There are two recent trials – AUGUSTUS and the ENTRUST-AF PCI trial – that evaluated regimens of apixaban and edoxaban, respectively, that support earlier findings reporting lower bleeding rates in patients maintained on oral anticoagulant plus a P2Y12 inhibitor compared to triple therapy.Of note, none of these trials were specifically powered for ischemic endpoints, but when pooling data from these trials, rates of death, MI and stent thrombosis with dual therapy were similar to those seen in patients on triple therapy.Additionally, all of these patients enrolled in these trials were briefly treated with triple therapy after PCI before the aspirin was discontinued. In the 2021 guidelines, it is noted that analyses of stent thrombosis suggest that 80% of events occur within 30 days of PCI. Thus, it is reasonable to consider extending triply therapy to 1 month after PCI in high risk patients to reduce risk of stent thromboses.In AUGUSTUS, 90% of patients received clopidogrel as their P2Y12 inhibitor Case #2 Synopsis: A man in his mid-50s with a history of peripheral vascular disease with prior SFA stent for chronic limb ischemia, hyperlipidemia, tobacco use, diabetes, and chronic kidney disease presented with a two day history of “reflux” that was worse with exertion and that improved with rest and associated with diaphoresis. He was diagnosed with an NSTEMI. His LHC revealed 99% mid-RCA thrombotic occlusion with moderate disease in the LAD. He underwent thrombectomy and PCI with a single drug-eluting stent to the RCA. We discussed his short-term and long-term antithrombotic therapy Case #2 Takeaways There were several things discussed regarding the management of this patient’s “poly-vascular disease.” One of the aspects was what to do with his antithrombotic therapy after one year and specifically how the COMPASS trial may apply to this patient.In the COMPASS trial, more than 27,000 patients with stable CAD or peripheral arterial disease (PAD) were randomly assigned to rivaroxaban plus aspirin, rivaroxaban alone, or aspirin alone with a mean follow-up of about 23 months. Of note, the dose of rivaroxaban in the combination arm was 2.5 mg orally twice per day. The patients on combination therapy compared to aspirin alone had a 23% relative risk reduction in CV mortality (1.7 vs. 2.2%; HR 0.78 [95% CI 0.64-0.96]) and nearly 50% reduction in ischemic stroke. As expected, there was high rates of major bleeding in the combination arm (3.1 vs. 1.9%; HR 1.7 [95% CI 1.4-2.05]).As with most decisions in medicine, each clinician would need to balance reducing ischemic events with bleeding risk for each individual patient. However, the COMPASS trial provides further evidence that low-dose oral anticoagulant with rivaroxaban in addition to aspirin can be effective in reducing ischemic events and CV mortality in patients with established atherosclerotic disease. Case #3 Synopsis A man in his early 60s with a history of hypertension and active tobacco use presented to a local hospital with anteroseptal STEMI c/b cardiac arrest with ventricular tachycardia. After multiple defibrillation attempts and CPR, the patient was able to achieve return of spontaneous circulation with intact mental status. The patient was pre-loaded with aspirin, ticagrelor, cangrelor and heparin and brought to the catheterization lab. There was diffuse moderate to severe stenoses in the RCA and a hazy distal LM lesion, but the culprit was a complete occlusion of the proximal LAD to which the patient received a single DES and another to the mid LAD. The patient was then brought to a tertiary care center where consideration was given for elective CABG given the residual disease. We discussed timing of CABG and when/if to pursue it, as well as antithrombotic management in this circumstance Case #3 Takeaways Amongst the things we discussed was the role of cangrelor pre-left heart catheterization. Cangrelor is a potent, short-acting, and reversible intravenous P2Y12 inhibitor with rapid onset of platelet inhibition. And within 1 hour of discontinuation, platelet function can be restored.In the small CANTIC trial, patients undergoing primary PCI pre-treated with crushed 180-mg loading dose of ticagrelor were randomized to cangrelor versus placebo. Within five minutes, cangrelor led to significant P2y12 inhibition which persisted throughout the drug infusion. Of note, there were no drug interactions with ticagrelor given concomitantly with cangrelor at the start of PCI. Thus, in this trial, cangrelor proved to be an effective strategy in bridging latent platelet inhibition that can be seen with oral drugs.This trial was not powered for clinical outcomes, but serves as evidence that cangrelor can be considered for pre-treatment to bridge the gap in platelet inhibitor effects in select patients in whom oral absorption may be compromised or slowed. References Eikelboom JW, Connolly SJ, Bosch J et al. Rivaroxaban with or without Aspirin in Stable Cardiovascular Disease. N Engl J Med. 2017 Oct 5;377(14):1319-1330.Franchi F, Rollini F, Rivas A et al. Platelet Inhibition With Cangrelor and Crushed Ticagrelor in Patients With ST-Segment-Elevation Myocardial Infarction Undergoing Primary Percutaneous Coronary Intervention. Circulation. 2019 Apr 2;139(14):1661-1670.Lopes RD, Heizer G, Aronson R, et al. Antithrombotic therapy after acute coronary syndrome or PCI in atrial fibrillation. N Engl J Med. 2019; 380:1509–1524.Writing Committee Members, Lawton JS, Tamis-Holland JE et al. 2021 ACC/AHA/SCAI Guideline for Coronary Artery Revascularization: Executive Summary: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. J Am Coll Cardiol. 2022 Jan 18;79(2):197-215 Production Team Karan Desai, MD Natalie Stokes, MD Amit Goyal, MD Daniel Ambinder, MD

Oct 23, 2022

CardioNerd (Daniel Ambinder) and series co-chairs Mark Belkin (AHFT Fellow, University of Chicago) and Karan Desai (Cardiologist, Johns Hopkins), join fellow lead, Dr. Pablo Sanchez (FIT, Stanford) for a discussion with Dr. Ryan Tedford (Professor of Medicine at the Medical University of South Carolina) about Right Ventricular (RV) predominant cardiogenic shock. In this episode we explore risk factors, pathophysiology, hemodynamics, and treatment strategies in this common and complex problem. We dissect three cases that epitomize the range of diagnostic dilemmas and management decisions in RV predominant shock, as Dr. Tedford expertly weaves us through the pathophysiology and decision-making involved in managing the “people’s ventricle.” Audio editing by Dr. Gurleen Kaur (Director of the CardioNerds internship program, CardioNerds academy fellow, and IM resident at Brigham and Women’s Hospital). The CardioNerds Cardiac Critical Care Series is a multi-institutional collaboration made possible by contributions of stellar fellow leads and expert faculty from several programs, led by series co-chairs, Dr. Mark Belkin, Dr. Eunice Dugan, Dr. Karan Desai, and Dr. Yoav Karpenshif. Pearls • Notes • References • Production Team CardioNerds Cardiac Critical Care PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls and Quotes - RV Predominant Cardiogenic Shock The degree of RV dysfunction and failure are modulated by stretching its capacity to tolerate insults from deranged afterload, preload, and contractility.Afterload insults are MUCH LESS tolerated than other insults and broadly comprise the most common pathophysiologic cause of both acute and chronic RV failure.RV and left ventricular (LV) function are anatomically and physiologically connected. Progressive derangements in RV function can lead to the deadly “RV spiral,” in which poor RV function causes lower LV preload, leading to hypotension, and thus worsening RV perfusion and function.In RV failure/shock, some basic tenets including treating reversible causes, optimizing preload and afterload, and using inotropes and/or temporary MCS for as limited time as possible.Many acute RV failure patients can recover, but multiorgan injury plays an important role. Therefore, thoughtful and expeditious use of mechanical circulatory support is important. Show notes - RV Predominant Cardiogenic Shock Notes drafted by Dr. Pablo Sanchez. What is the basic difference between RV dysfunction and failure?Dysfunction: Abnormalities in systolic/diastolic function of the RV, but not necessarily to the point of leading to end-organ perfusion defects. RV dysfunction leads to poor outcomes regardless of mechanism.1Failure: Clinical syndrome of inability of RV to maintain adequate output despite adequate preload. 1 How is the RV different from the LV and what impact does it have on pathophysiology and hemodynamics?The LV and RV originate from different embryologic “heart fields.”1,2The RV wall is thinner and more compliant and has only two layers (instead of 3 like the LV).3 Furthermore, unlike the LV which has a significant proportion of endocardial and epicardial transverse myocardial fibers, the RV myocardial fibers are aligned in a longitudinal plane for the most part. Thus, a more significant proportion of RV systolic contraction is longitudinal – base of the ventricle moving towards the apex.The RV is crescent-shaped and has a large surface-to-volume ratio meaning smaller inward motion ejects the same stroke volume. 1Hemodynamically, the RV takes blood from a low-pressure venous system and gives it to a distensible system with low impedance (the normal pulmonary circuit at baseline typically has a resistance one-tenth of the systemic resistance). Therefore, volume loads (preload) are much better handled than pressure (afterload).1 What is RV-PA coupling?As Dr. Tedford noted, RV-PA coupling describes “the interaction of RV contractility and afterload (resistive and pulsatile components). It is the most comprehensive description of RV function and therefore the Gold Standard.” Whether we are referring to the LV or RV, the basic concept of coupling describes the energy transfer between ventricular contractility and arterial afterload.RV-PA coupling has typically been assessed by pressure-volume loops, with ventricular contractility assessed by end-systolic elastance (a load-independent measure of systolic function) and arterial afterload by effective arterial elastance.MODUS OPERANDI: RV dysfunction and eventual failure is modulated by stretching its capacity to tolerate insults from afterload, preload, and contractility. What leads to ACUTE right heart failure?Most commonly results from:1Abrupt increases in afterload (e.g., think PE, hypoxia, and acidemia).Decreased contractility (e.g., think ischemia such as RV infarction, myocarditis, and post-cardiotomy).Volume overload can sometimes lead to acute right heart failure, particularly in the setting of another categorical insult such as septic cardiomyopathy or LVAD support. What leads to CHRONIC right heart failure?This is different than acute right heart failure. Most commonly chronic right heart failure results from:1Gradual increases in afterload (e.g., think pulmonary arterial hypertension).Chronic volume overload (e.g., longstanding tricuspid regurgitation, atrial septal defect, and other congenital lesions like double outlet RV).Contractility (e.g., including the isolated RV cardiomyopathies like arrhythmogenic right ventricular cardiomyopathy or ischemic cardiomyopathy).Other pathologies certainly affect multiple categories (e.g., Ebstein’s anomaly which is a function of contractility and volume overload or single ventricle physiology like post-Fontan patients – for more on these and other ACHD lesions, enjoy the CardioNerds ACHD Series!)MODUS OPERANDI: The cardiovascular system is wholly connected, and acute decompensation leads to progressive derangements in the above levers (including LV function). This phenomenon is called the RV spiral. How do we manage RV failure?The most important and first step is the treatment of reversible causes. For instance, acute coronary syndrome involving the RV requires percutaneous intervention (PCI) or pulmonary embolism requires anticoagulation and/or thrombolytic/device/surgical therapy.PRELOAD OPTIMIZATIONEnsuring that there is adequate preload is a key tenet of diagnosing and treating RV failure. This may require diuresis or judicious volume resuscitation to maintain cardiac output.While guiding fluid management in the setting of RV failure, one should STRONGLY consider invasive hemodynamic monitoring (e.g., over-resuscitation can lead to decreased LV output through septal shift and ventricular interdependence from pericardial constraint).1General target: We could consider a CVP 10-15 mmHg; however, this will be individualized. Another general rule would also be if that a bolus of 500 cc of crystalloid does not result in hemodynamic improvement, further loading should not be continued, especially without invasive hemodynamic guidance.AFTERLOAD OPTIMIZATION The goal should be to correct reversible causes of elevated pulmonary vascular resistance (e.g., acidosis, hypercapnia, hypoxia, and generally in ventilated patients avoid elevated inspiratory pressures > 30mmHg).1With specialized expert guidance, we can consider selective pulmonary vasodilators (acutely and short-term):One example includes inhaled NO, and in observational studies, short-term use lowered PVR and increased RV ejection.4We also have to remember the consequences of reducing RV afterload. Acutely increasing LV preload in a baseline abnormal LV may lead to distention, lowered cardiac output, and pulmonary edema.1Pulmonary vasodilators can act on specific pathways (e.g., nitric oxide, prostacyclin, endothelin-1, and soluble guanylate cyclase stimulators) and come in various forms (oral, inhaled, and intravenous).CONTRACTILITY AUGMENTATION (INOTROPES)We typically utilize inotropes in concert with the prior two but optimize loading so the time we need inotropes is minimal.1Short-term use can improve hemodynamics. Longer-term use will typically increase myocardial O2 consumption and is associated with increased mortality. The RV has coronary perfusion in systole and diastole, so peripheral vasopressors are helpful to maintain perfusion, especially if systolic blood pressure is less than RV systolic pressure.1GOAL: Increase contractility without increasing RV afterload.For those failing to respond to these above measures to optimize preload, afterload, and contractility, there may be a role for temporary mechanical circulatory support (see #10 below). How do we decide between dobutamine and milrinone?BOTH inotropes can lead to hypotension, have similar clinical outcomes, hemodynamic efficacy and arrhythmogenic potential1 (despite the adage that attributes more arrhythmias to dobutamine, studies show the risk is typically the same in both5).Milrinone is a more potent vasodilator (systemic and pulmonary) typically leading to greater decreases in end-diastolic pressures in the ventricles.1 It is renally cleared, has a longer half-life, and acts through a separate mechanism pathway compared to beta-blockade, thus patients can be on milrinone and beta blockers at the same time on a case-by-case basis.1Dobutamine has a shorter half-life, with rapid onset/offset and so may be more ideal in unstable/hypotensive patients.1 What if the patient is hypotensive?In this circumstance, we would need an ino-constrictor or peripheral vasoconstrictor.Vasopressin has almost no impact on PVR, so unlike catecholamines, it does not directly worsen RV afterload.1 What are some important invasive hemodynamic parameters to be aware of?

Oct 13, 2022

CardioNerds (Dr. Patrick Azcarate, Dr. Teodora Donisan, and Amit Goyal) discuss Radiation-Associated Cardiovascular Disease (RACD) with Dr. Eric Yang, cardio-oncologist, assistant professor of medicine, and associate fellowship program director at UCLA. RACD is a consequence of radiation treatment for various mediastinal tumors (breast, lung, lymphoma). It is the second most common cause of morbidity and mortality in patients treated with mediastinal radiation for cancer. While novel techniques decrease radiation exposure during cancer treatment, the incidence is expected to increase because of historical practices and delayed onset of symptoms. The prevalence of RACD is difficult to estimate given under-recognition. Additionally, most of the data comes from patients treated with radiation techniques from decades ago. In this discussion we review every nook and cranny of RACD to help guide you the next time you see a patient with a history of chest radiation. Review this CardioNerds Case Report of radiation associated cardiovascular disease for more: Episode #169. Chest pain in a Young Man – “A Gray (Gy) Area” – UC San Diego. Audio editing by CardioNerds Academy Intern, student doctor Yousif Arif. This episode is supported by a grant from Pfizer Inc. This CardioNerds Cardio-Oncology series is a multi-institutional collaboration made possible by contributions of stellar fellow leads and expert faculty from several programs, led by series co-chairs, Dr. Giselle Suero Abreu, Dr. Dinu Balanescu, and Dr. Teodora Donisan. Pearls • Notes • References • Production Team CardioNerds Cardio-Oncology PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls and Quotes - Radiation-Associated cardiovascular disease Due to the legacy effect, the incidence of RACD will continue to increase in the next few years. When treating patients with a history of mediastinal radiation, we should remember to ask: How much radiation was given? Could the heart have been exposed? Radiation can affect every part of the heart by causing coronary artery disease (CAD), valvulopathy, myocardial disease, conduction disease, and pericardial disease. Exposure to ~25-30 Gy or more significantly increases the risk but RACD can occur at lower doses. Try to delay surgery as much as possible and do all you can in one operation to avoid re-operation in the future. For revascularization, percutaneous coronary intervention (PCI) is typically preferred over coronary artery bypass grafting (CABG) but the choice should be individualized in consultation with a multidisciplinary heart team experienced in the management of RACD. In general, for aortic valve disease, transcatheter replacement is recommended over surgical aortic valve replacement. For mitral valve disease, surgical replacement is recommended over repair. Every decision should be made with a heart team approach and made unique to that specific patient. Show notes - Radiation-Associated cardiovascular disease Notes were drafted by Dr. Patrick Azkarate. 1. Understand the pathophysiology of RACD Ionizing radiation has the potential to damage DNA. Both normal cells and cancer cells get damaged, but cancer has less effective DNA repair mechanisms and therefore malignant cells are more vulnerable to radiation therapy. After radiation causes acute damage, this sets off an inflammatory cascade leading to myofibroblast activation, fibrosis and collagen deposition, and subsequent stiffening of the myocardium and vessels. 2. What may increase one’s risk of developing RACD? Young age ( 30 Gy) or high dose of radiation fractions (>2 Gy/day) Anterior or left chest radiation (breast cancer, lung cancer, lymphoma) Pre-existing cardiovascular disease Tumor in or next to the heart Concomitant chemotherapy (e.g. anthracyclines) 3. What are some techniques being used to reduce radiation exposure? Shielding Respiratory gating techniques (e.g. deep inspiratory breath-hold, activated breathing control) Smaller repeated fractions Narrow tangential beams Proton therapy 4. What are prevention and screening strategies for RACD? Annual history and physical examinationTreat pre-existing conditionsScreen for RACD (myocardial, valvular, pericardial, CAD, or conduction system disease)5 years post-exposure, screen for CAD and consider stress test every 2 years10 years post-exposure, screen for valvular heart disease with an echocardiogram every 2 years1 5. Discuss diagnosis and management of specific complications of RACD CAD The risk of radiation induced CAD (RICAD) is 7.5% per Grey Unit (Gy). The risk is roughly constant, begins several years after exposure, and persists for at least 2-3 decades (>50% of excess ischemic events occurring >10 years after RT).2 Radiation causes inflammatory plaque with high collagen and fibrin content, similar to accelerated atherosclerosis. Angiographic characteristics: Ostial or proximal Anterior and central (predominantly affecting the left anterior descending and the right coronary arteries) Severe, diffuse Long, smooth, concentric, and tubular Treatment: CABG vs PCI While there are no head-to-head trials comparing CABG vs PCI in patients with RICAD, it is known that compared to the general population, following CABG they have worse outcomes (increased risk of wound dehiscence, infection, graft failure, and death).3 The data for PCI is mixed but most recently have shown that patients with RICAD undergoing PCI have similar outcomes compared to patients without radiation exposure.4 Unless there is an additional indication for surgery, PCI for chronic CAD usually preferred. If multi-vessel CAD or higher Syntax score (≥ 22) consider CABG. Other considerations might guide percutaneous vs surgical revascularization Porcelain aorta Fibrotic bypass grafts (internal mammary artery) in the radiation field Multi-valvular disease Valvular disease Radiation causes progressive valve thickening and calcification leading to valve leaflet retraction, followed by regurgitation and then stenosis. Patients usually become symptomatic 1-2 decades after radiation exposure (later than CAD). Prevalence of aortic regurgitation (AR) at 10 years is 4% and at 20 years is 60%. The prevalence of aortic stenosis (AS) at 10 years 0% but at 20 years: 16% Mitral regurgitation (MR) and AR are the most common and occur due to leaflet retraction. These ultimately progress to stenosis. MR is the most common reason for surgery. Echocardiogram is done to evaluate the valves. Surrounding structures may show calcification, such as the annulus, subvalvular apparatus, or aorta-mitral curtain (a hallmark of previous heart irradiation which is associated with mortality in patients undergoing cardiac surgery). Management decisions are complex, depends on the valvular lesion(s) involved, and should be guided by a heart team approach. For aortic valve disease, TAVR is preferred over SAVR (unless there is another indication for surgery or there is excess risk for coronary obstruction or annular rupture). If SAVR is pursued, usually try to replace all valves (even if one is just mild to moderate) to avoid re-operation. For the mitral valve, data is mixed between surgical vs transcatheter approaches. In general, if surgery is indicated then the valve is replaced and not repaired (irradiated valve tissue is fibrotic and calcified) Given increased risk of reoperation, mechanical prostheses may be appealing, especially for younger patients. If there are contraindications to anticoagulation, then a bioprosthesis should be used. General cardiothoracic surgery principles in patients with RACD Worse long-term outcomes compared to age and sex-matched controls undergoing similar procedures Reoperation portends significantly higher risk compared to non-RACD patients Delay surgical intervention as long as possible Address all issues with a complete operation the first time Surgical planning may involve cardiac magnetic resonance imaging (CMR) to look for fibrosis, computer tomography (CT) to identify calcified structures (intra- and extra-cardiac), transthoracic echocardiogram (TTE), right and left heart catheterization to evaluate for restriction vs constriction, coronary angiogram. Myocardial disease In terms of pathophysiology, radiation causes an acute inflammatory cascade, then a pro-fibrotic milieu which leads to myocardial fibrosis and reduced microvascular proliferation and density. RACD-related myocardial dysfunction is defined as >10% decrease in LVEF to a value <50% confirmed by repeated imaging 2-3 weeks after the first diagnostic study or heart failure with preserved ejection fraction (HFpEF) HFpEF is more common than heart failure with reduced ejection fraction (HFrEF). Risk of myocardial disease increases with total radiation dose, fraction size, and volume of heart in the radiotherapy field. Benefit of heart failure pharmacotherapy in subclinical myocardial dysfunction remains unknown, however guideline directed medical therapy is recommended. While transplant is not broadly recommended due to poor outcomes and high risk of recurrent malignancy, this remains a consideration. Conduction system disease The conduction system can sustain direct damage from radiation or can be affected by ischemia or fibrosis. 75% of long-term survivors who received mediastinal radiation have conduction defects on electrocardiogram (ECG). Acutely, we can see transient, nonspecific repolarization abnormalities. Long-term,

Oct 8, 2022

Cardiogenic shock (CS) remains a complex, multifactorial syndrome associated with significant morbidity and mortality. The CardioNerds Critical Care Cardiology Series tackles this important syndrome in a series of several episodes including: LV-predominant Shock, RV-predominant Shock, and Bi-ventricular Shock. In this episode, we review the definitions, pathophysiology, evaluation, and contemporary management, including use of inotropes and mechanical circulatory support, of left ventricular (LV) predominant CS. Series co-chairs Dr. Eunice Dugan and Dr. Karan Desai along with CardioNerds Co-founders Dr. Amit Goyal and Dr. Daniel Ambinder were joined by FIT lead, Dr. Vanessa Blumer, the recipient of the AHA 2021 Laennec Fellow in Training Clinician Award and currently pursuing Advanced Heart Failure and Transplant fellowship at the Cleveland Clinic. Our episode expert is Dr. Shashank Sinha, an Advanced Heart Failure, Mechanical Circulatory Support, and Cardiac Transplant cardiologist, Medical Director of the Cardiac Intensive Care Unit, and Director of the Cardiovascular Critical Care Research Program at INOVA Fairfax Hospital. His illustrious career accomplishments include being a Steering Committee member and site Principal Investigator for the multicenter Cardiogenic Shock Working Group and Critical Care Cardiology Trials Network. Audio editing by CardioNerds academy intern, Anusha Gandhi. The CardioNerds Cardiac Critical Care Series is a multi-institutional collaboration made possible by contributions of stellar fellow leads and expert faculty from several programs, led by series co-chairs, Dr. Mark Belkin, Dr. Eunice Dugan, Dr. Karan Desai, and Dr. Yoav Karpenshif. Pearls • Notes • References • Production Team CardioNerds Cardiac Critical Care PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls and Quotes - LV Predominant Cardiogenic Shock LV-CS is complex! It is important to recognize that the pathophysiology of heart failure-related cardiogenic shock (HF-CS) is distinct from that of acute myocardial infarction (AMI-CS), and also crucial to differentiate between LV-dominant, right ventricular (RV)-dominant and biventricular (BiV)-shock.The SCAI SHOCK Stage Classification provides a unified and standardized vocabulary when assessing severity of CS, and facilitates communication about the diagnosis, presentation, and evolving nature of CS.Norepinephrine is considered the initial vasopressor of choice in most CS patients; the initial inotrope choice is a bit more nuanced!When considering mechanical circulatory support (MCS) for LV shock, high-quality data to guide therapy is lacking but one must always consider “the right patient, for the right device, at the right time” and remember that “pumps pump blood, decisions save lives”.Multidisciplinary, team-based care is paramount to improving survival of the critically ill patient with CS. Show notes - LV Predominant Cardiogenic Shock Notes drafted by Dr. Vanessa Blumer. 1. What tools do you use to define LV CS? CS is a hemodynamically complex and multifactorial syndrome, one of the most common indications for admission to a cardiac intensive care unit, with short-term mortality ranging from 35-50%.It is defined by systemic hypoperfusion and tissue hypoxia due to a primary cardiac insult or dysfunction.Clinical criteria used to define CS typically include evidence of hypotension (classically defined as SBP 90 mmHg) AND evidence of end-organ hypoperfusion (for example, serum lactic acid > 2 mmol/L, acute kidney injury, acute liver injury, altered mental status) in the setting of acute coronary syndrome or acute decompensated heart failure.Laboratory markers, including serum lactic acid, liver function tests, kidney function, and biomarkers including troponin and natriuretic peptides may be helpful. An echocardiogram is an excellent point of care tool to help demonstrate and confirm evidence of LV systolic dysfunction and/or valvular abnormalities. Finally, a right heart catheterization (demonstrating an abnormally low cardiac output and index with elevated filling pressures) may be useful in facilitating the diagnosis and subsequent management. 2. How do HF-CS and AMI-CS lead to different phenotypes? It is important to recognize that HF-CS is now the predominant cause of CS, accounting for more than half of all CS.AMI-CS is characterized by an abrupt presentation due to a primary myocardial ischemic insult leading to necrosis (occurring in 5-10% of AMI patients) and can occur after STEMI or NSTEMI. The canonical clinical course is hypotension due to primary myocardial dysfunction leading to hypoperfusion with congestion as a later clinical or hemodynamic finding.Conversely, a patient with heart failure related shock commonly presents with acutely decompensated heart failure and congestion, leading to hypoperfusion, and culminating in hypotension. 3. How do you distinguish LV-dominant, RV-dominant and BiV shock? LV predominant CS is characterized by high pulmonary capillary wedge pressure (PCWP) and normal or reduced central venous pressure (CVP) in the setting of reduced cardiac output (CO).RV dominant CS is characterized by elevated CVP, normal to low PCWP, and normal to reduced CO.BiV shock is characterized by hypotension, elevated CVP, normal or elevated PCWP, and reduced CO. 4. What is the current role for inotropes, vasodilators, and vasopressors in the management of LV CS? The Acute Cardiovascular Care Association of the European Society of Cardiology published a position statement for the diagnosis and treatment of patients with AMI complicated by CS in 2020. According to this, vasopressors (norepinephrine preferable over dopamine) in the presence of persistent hypotension received a Level of IIb/B recommendation. Intravenous inotropes to increase cardiac output received a IIb/C recommendation.Based on the available evidence and its accompanying limitations, norepinephrine is considered the initial vasopressor of choice in most CS patients. 5. When should we consider management with temporary mechanical circulatory support (t-MCS) devices and how should one strategize device selection? Initiation or escalation of t-MCS largely depends on matching the right device to the right patient at the right time. Because the risk and number of complications increases with duration and type of MCS, these decisions are complex, nuanced, and must consider operator and institutional expertise.When considering type of device (IABP, Impella, ECMO), SCAI Staging and phenotyping (AMI vs HF CS) are absolutely critical. 6. What are treatment goals when following patients with LV CS? Optimize preload, afterload, and contractilityPerform serial reassessment (≤ q 6hr) of hemodynamics & end-organ perfusionAim for timely and tailored treatment escalation/de-escalation Assess for LV and RV recovery (wean t-MCS, vasopressors and inotropes as ableEarly identification of worsening shock: Rising Lactate Increasing pressor requirement Worsening end-organ function CPO 15 and/or PCWP > 15 References - LV Predominant Cardiogenic Shock Abraham J, Blumer V, Burkhoff D, Pahuja M, Sinha SS, Rosner C, Vorovich E, Grafton G, Bagnola A, Hernandez-Montfort JA, Kapur NK. Heart Failure-Related Cardiogenic Shock: Pathophysiology, Evaluation and Management Considerations: Review of Heart Failure-Related Cardiogenic Shock. J Card Fail. 2021 Oct;27(10):1126-1140. doi: 10.1016/j.cardfail.2021.08.010. PMID: 34625131. Kapur NK, Kanwar M, Sinha SS, Thayer KL, Garan AR, Hernandez-Montfort J, Zhang Y, Li B, Baca P, Dieng F, Harwani NM, Abraham J, Hickey G, Nathan S, Wencker D, Hall S, Schwartzman A, Khalife W, Li S, Mahr C, Kim JH, Vorovich E, Whitehead EH, Blumer V, Burkhoff D. Criteria for Defining Stages of Cardiogenic Shock Severity. J Am Coll Cardiol. 2022 Jul 19;80(3):185-198. doi: 10.1016/j.jacc.2022.04.049. PMID: 35835491. CardioNerds Cardiac Critical Care Production Team Karan Desai, MD Dr. Mark Belkin Dr. Yoav Karpenshif Amit Goyal, MD Daniel Ambinder, MD

Oct 6, 2022

It’s another session of CardioNerds Rounds! In these rounds, Dr. Natalie Stokes (Formerly FIT at University of Pittsburgh and now General Cardiology Faculty at University of Pittsburgh) and Dr. Karan Desai (formerly FIT at University of Maryland and now General Cardiology faculty at Johns Hopkins) join Dr. Rick Nishimura (Professor of Medicine at Mayo Clinic) to discuss the nuances of managing mitral regurgitation through real cases. Dr. Nishimura has been an author or Chair of the ACC/AHA valve guidelines going back 20 years and has been recognized internationally as one of the world’s best educators, so you don’t want to miss the #NishFactor on these #CardsRounds! Audio editing by CardioNerds academy intern, Pace Wetstein. This episode is supported with unrestricted funding from Zoll LifeVest. A special thank you to Mitzy Applegate and Ivan Chevere for their production skills that help make CardioNerds Rounds such an amazing success. All CardioNerds content is planned, produced, and reviewed solely by CardioNerds. Case details are altered to protect patient health information. CardioNerds Rounds is co-chaired by Dr. Karan Desai and Dr. Natalie Stokes. Speaker disclosures: None Challenging Cases - Atrial Fibrillation with Dr. Hugh Calkins CardioNerds Rounds PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Show notes - Mitral Regurgitation with Dr. Rick Nishimura Case #1 Synopsis: A man in his 70s with a history of non-ischemic cardiomyopathy (last known LVEF 15-20%) and atrial fibrillation, presented with decompensated heart failure in the setting of moderate to severe mitral regurgitation. He was diuresed, transitioned to GDMT, and referred to cardiac rehabilitation. Over the next 6 months, he continued to have debilitating dyspnea (NHYA Class IIIa) and his outpatient physicians were limited on titrating GDMT further due to hypotension. A TEE was done which demonstrated EF 15%, severe MR by color and quantitation (EROA of 0.5 cm2; Regurgitant Volume of 65 mL), systolic flow reversal in the pulmonary vein and severe tricuspid regurgitation. We were asked how we would approach this case Case #1Takeaways In attempting to keep the evaluation of chronic mitral regurgitation relatively simple, we should ask ourselves three primary questions: (1) What is causing the MR; (2) How much MR is there; and (3) What is the hemodynamic consequence of the MR.To the first question of what is the etiology of the MR – a simple framework is to think of the etiology as an issue of the valve (primary) or an issue of the ventricle/atria (secondary). There is further classification that can be made based on the Carpentier Classification which speaks to the valve leaflet movement and position (normal leaflet motion, excessive leaflet motion [e.g., prolapse], or restricted in systole and/or diastole [e.g., rheumatic heart disease]).During rounds, Dr. Nishimura provided some historical context in that the original valve guidelines had recommendations for intervention on primary mitral regurgitation and not secondary – given that it is considered a disease of the ventricle. Trials like the COAPT trial have greatly shifted our practice in treating secondary mitral regurgitation. Though, we have to be familiar with which patients with secondary MR would truly derive benefit from mitral valve interventionIn regards to the COAPT trial, patients with moderate to severe (3+) or severe (4+) mitral regurgitation who remained symptomatic despite maximally tolerated guideline-directed medical therapy (GDMT) were included. Dr. Nishimura makes the point that about one-third of patients intended to be enrolled in the trial were not included because they improved so much on GDMT. And thus, when evaluating patients for consideration of mitral valve intervention in secondary MR – and specifically transcatheter edge to edge repair (TEER) – every effort to optimize GDMT should be made first before intervening. Other important inclusion and exclusion criteria included that patients had LVEF between 20-50%, LV end-systolic diameter less than or equal to 70 mm, and absence of severe pulmonary hypertension (defined as pulmonary artery systolic pressure > 70 mmHg despite vasodilator therapy) or moderate to severe right ventricular failure.Dr. Nishimura asks our audience if the patient is truly on optimal GDMT and/or optimized? There are basic tools that clue us into optimization including chest x-ray (e.g., is there still pulmonary vascular congestion) and physical examination (e.g., what is the venous pressure).Dr. Nishimura makes an interesting point in correlating our examination with the echocardiographic findings. In patients with largely secondary MR, where the leaflets have poor coaptation and we have a weak ventricle we may not expect to hear a very loud murmur on examination (e.g., there isn’t enough pump to generate the murmur). However, if we hear a significant murmur (e.g., like our patient described in the case with a loud, 3/6, blowing murmur) with presumed secondary MR, our antennae should be up for a possible primary component. Case #2 Synopsis: A man in his early 60s with a history of prior LAD PCI in the setting of an NSTEMI and diabetes presented to your hospital in SCAI Stage C to D Cardiogenic Shock with the background of worsening orthopnea and edema several weeks prior. You are told the patient had a recent echo with LVEF 15%, mild LV dilation, reduced RV function and moderate to severe functional MR. When you meet the patient, he is confused, nauseous and with poor perfusion (e.g., cool extremities and Lactate of 7 mmol/L). The patient is taken for left and right heart catheterization with RHC showing significant elevated filling pressures, large V-waves, and low cardiac index. An IABP is placed and LHC is performed where an acute appearing lesion in the proximal LAD and Mid-RCA are treated with PCI. Over the next week the IABP is weaned and removed and low doses of GDMT started. But once the IABP is removed, nausea returns and lactate starts rising again. Hemodynamics and TEE images are obtained with the IABP at 1:1 and on standby and show significant worsening of the hemodynamics and MR with IABP on standby, with the MR in the severe category, and we are asked to comment on what to do next. Case #2 Takeaways Dr. Nishimura suggests we approach this complex case with a simple question: how much of his shock/congestion is a result of his pump (the LV) versus how much is a result of his valve? Dr. Nishimura notes there is a subset of patients who have dynamic mitral regurgitation, which is primarily related to changes in the structure of the annulus/apparatus that happen with changes in preload/afterload/contractility. These patients can go from mild to severe depending on the loading conditions, as they are exquisitely sensitive to these conditionsDr. Nishimura notes the continuous wave doppler of the mitral regurgitation can give us a rich amount of detail. The MR continuous wave doppler signal reflects the instantaneous doppler between the left ventricle and left atrium. If we pay attention to the signal during isovolumic contraction – if there is a rapid rise in the signal, that suggests that we are generating LV systolic pressure rather quickly and contractility may be preserved (e.g., this refers to dP/dT which has several caveats but qualitatively can be informative us).These patients with dynamic MR who we cannot control the loading conditions, it may be better to treat the MR itself. References Stone GW, Lindenfeld J, Abraham WT, Kar S, Lim DS, Mishell JM, Whisenant B, Grayburn PA, Rinaldi M, Kapadia SR, Rajagopal V, Sarembock IJ, Brieke A, Marx SO, Cohen DJ, Weissman NJ, Mack MJ; COAPT Investigators. Transcatheter Mitral-Valve Repair in Patients with Heart Failure. N Engl J Med. 2018 Dec 13;379(24):2307-2318.Writing Committee Members, Otto CM, Nishimura RA, Bonow RO, Carabello BA, Erwin JP 3rd, Gentile F, Jneid H, Krieger EV, Mack M, McLeod C, O'Gara PT, Rigolin VH, Sundt TM 3rd, Thompson A, Toly C. 2020 ACC/AHA Guideline for the Management of Patients With Valvular Heart Disease: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. J Am Coll Cardiol. 2021 Feb 2;77(4):e25-e197. Production Team Karan Desai, MD Natalie Stokes, MD Amit Goyal, MD Daniel Ambinder, MD

Sep 30, 2022

In this episode, Dr. Carly Fabrizio (Advanced Heart Failure and Transplant Cardiology Physician at Christiana Care Hospital), CardioNerds Critical Care Series Co-Chair Dr. Mark Belkin (Advanced Heart Failure and Transplant Fellow at University of Chicago) and CardioNerds Co-Founder Dr. Amit Goyal (Cleveland Clinic) join Dr. Gavin Hickey (Director of the AHFTC Fellowship and medical director of the left ventricular assist device program at UPMC) and Dr. David Kaczorowski (Surgical Director for the Advanced Heart Failure center, Department of Cardiothoracic Surgery at UPMC) for a discussion on post-cardiotomy shock. Audio editing by CardioNerds Academy Intern, student doctor, Shivani Reddy. Post-cardiotomy shock is characterized by heart failure that results in the inability to wean from cardiopulmonary bypass or develops post cardiac surgery. Patients who develop post-cardiotomy shock typically require inotropic support and may ultimately require temporary mechanical circulatory support. Post-cardiotomy shock carries a high mortality rate. However, early recognition and prevention strategies can help mitigate the risk for developing post-cardiotomy shock. The CardioNerds Cardiac Critical Care Series is a multi-institutional collaboration made possible by contributions of stellar fellow leads and expert faculty from several programs, led by series co-chairs, Dr. Mark Belkin, Dr. Eunice Dugan, Dr. Karan Desai, and Dr. Yoav Karpenshif. Pearls • Notes • References • Production Team CardioNerds Cardiac Critical Care PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls and Quotes - Post-cardiotomy Shock Weaning from cardiopulmonary bypass is an intricate process that includes: rewarming the patient, de-airing the cardiac chambers, ensuring a perfusing heart rhythm, confirming adequate ventilation and oxygenation, removing the intracardiac catheters and cannulas and slowly reducing the blood diverted to the cardiopulmonary circuit and returning it small aliquots to the patient. Much to monitor during the process! Assessing the risk for post-cardiotomy shock prior to going to the OR is important. Consider left ventricular, right ventricular, and valvular function, and don’t forget about the value of hemodynamic assessments (pulmonary artery catheter evaluations) to ensure patients are adequately compensated. Close peri-operative monitoring of hemodynamics, hemo-metabolic derangements, and acid/base status can help identify patients who are failing therapy and may require upgrade to temporary MCS. RV assessment is challenging. Utilizing both imaging and hemodynamic evaluations can help understand which RV’s will require more support. Multi-disciplinary discussions with a heart team approach prior to cardiac surgery are valuable in identifying high risk patients for post cardiotomy shock and discussing contingency plans if issues arise. Show notes - Post-cardiotomy Shock (drafted by Dr. Carly Fabrizio) How can we diagnose post cardiotomy shock?We can diagnose post cardiotomy shock as patients who are undergoing cardiac surgery that develop hypotension and or tachycardia with hypoperfusion and end organ dysfunction. How can assess the risk of developing postcardiotomy shock prior to going to the OR?LV systolic function is not the only evaluation of cardiac functionDon’t ignore the RV!Valvular function must be evaluated in conjunction with LV/RV functionHemodynamics can be helpful prior to going to the ORFilling pressures and CO/CI evaluation --> the more normal range - the less risk of post cardiotomy shockIf going in more deranged --> more complications are likely to occurThink about what options are available post operatively if issues ariseInclude a multi-disciplinary discussions and planning prior to going to the OR Are there any specific pre-operative or intra-operative risk factors that may predispose someone to developing post cardiotomy shock?Many factors can lead to postcardiotomy shock. Some pre-op factors include:Poor pre-operative cardiac function (RV and /or LV function)Entering the OR in cardiogenic shock (inotropes, temporary MCS)Well compensated patients with chronic ventricular dysfunctionIntra-operative factors:Prolonged cross-clamp timeProlonged cardiopulmonary bypass (CPB) times (often seen in complex operations)Inadequate myocardial protectionVentricular distentionTechnical factors What is actually occurring in the OR when weaning from CPB?After the aorta cross clamp is removed- the heart is allowed to re-perfuseRemember that the heart has been ischemic for a considerable amount of timeLungs are re-inflatedTemporary atrial and ventricular pacing wires are placedStable rhythm is achieved and the heart is paced if necessaryAcid / base status and electrolytes (potassium) are optimizedOnce the heart is de-aired, CPB is gradually weanedThe flow of the CPB circuit is gradually reduced and more of the patient’s blood volume is gradually allowed to pass through the heart and lungsTEE is performed while weaning bypassOnce bypass is completely weaned, the cannulas used to establish CPB are removedAnticoagulation is reversedAssess for hemostasisChest tubes are placed, and closure occurs What are the clinical and laboratory parameters which help determine whether vasoactive support alone will be enough vs. when temporary MCS may be needed?Assess perfusion firstBPUrine outputLactic acidPA catheter data / hemodynamic dataCardiac output/index (CO/CI)Pulmonary artery pressures (PAP)Central venous pressures (CVP)Mixed venous oxygen saturationCardiac power output (CPO) and cardiac power index (CPI)CPO consider escalation to temporary MCS Left ventricular assist devices (LVAD) do not support the right ventricle. How can we identify RV failure in these patients and when should you upgrade to RV mechanical circulatory support?Most patient that require left-sided support by nature often have underlying right-sided dysfunction as wellPre-operative - assessment of the RV is important:CVPPAPi (PA systolic pressure- PA diastolic pressure / CVP)CVP: PCWP ratioRV failure can occur in any patientNo great, reliable, and reproducible data on when or how to support the RV following LVAD implantation, or cardiogenic shock in general. More studies are needed. What’s different about how you assess the RV dysfunction in the OR compared to someone who is in the ICU? When do you consider using RV mechanical support upfront in the OR?Intra-operative TEE and direct visualization are both used in the OR to assess RV functionTry to avoid upfront RV mechanical support in the OROptimize with invasive hemodynamic monitoring prior to ORTemporary MCS can be used to optimize patient and help with diuresis pre-operativelyContinue to optimize the RV while in the ORRemove volume through hemoconcentration while on CPB circuit to optimize volume statusConsider temporary MCS for the RV when medical therapy is maximized, and the patient still remains marginal as measured by:LVAD flows, cardiac output/index, mixed venous gases and metabolic parameters Are there any surgical consideration to influence the type of temporary MCS for postcardiotomy shock?Strategize first by asking:What is failing? LV, RV, lungs, or a combinationWhat access is available?Ex: Bi-ventricular failure with hypoxemia and peripheral arterial disease: consider central VA ECMOEx: Pure LV failure but RV and lungs OK --> temporary LV assist device How can we prevent, or decrease the risk, of post-cardiotomy shock ?Optimized hemodynamics going into the OR using a PA catheterMulti-disciplinary discussion with cardiac anesthesia, critical care team, etc. for high-risk casesEnsure adequate end-organ perfusionAvoid pre-operative medications that worsen peri-operative vasoplegiaACE-i/ARB/ARNI, milrinone etc. What is role of advanced therapy evaluations when assessing high risk patients going to the OR?Important to think about options pre-operativelySelection committee discussions to weigh-in on candidacy for LVAD or cardiac transplant and if that may be more beneficial than other cardiac surgical interventions How does team-based care help with decision making?Optimize patients pre procedure and support them peri-procedureInvolving palliative care team and establishing patient goals prior to surgery References - Post-cardiotomy Shock Lorusso, Raffa, Alenizy, et al. “Structured review of post-cardiotomy extracorporeal membrane oxygenation: part 1—Adult patients.” JHLT. 38(11): 1125-1143. 2019.https://www.sciencedirect.com/science/article/pii/S1053249819316328Fukuhara, Takea, Garan, et al. “Contemporary mechanical circulatory support therapy for postcardiotomy shock.” Curr Topics Review Article. 64:183-191. 2016. https://link.springer.com/content/pdf/10.1007/s11748-016-0625-4.pdf CardioNerds Cardiac Critical Care Production Team Karan Desai, MD Dr. Mark Belkin Dr. Yoav Karpenshif Amit Goyal, MD Daniel Ambinder, MD

Sep 23, 2022

In this episode, Daniel Ambinder and Amit Goyal (CardioNerds co-founders), Dr. Gurleen Kaur (medicine resident at Brigham and Women’s Hospital and Director of CardioNerds Internship), student doctor Adriana Mares (medical student at the University of Texas El Paso/Texas Tech University Health Sciences Center El Paso, CardioNerds Academy Intern), and Dr. Teodora Donisan (general cardiology fellow at the Mayo Clinic and CardioNerds Academy Chief) discuss with Dr. Mayra Guerrero (Interventional Cardiologist and Professor of Medicine at the Mayo Clinic) about challenges with diagnosing and treating valve disease in women, as well as ideas on how to increase recruitment for women in cardiology including interventional and structural cardiology. Dr. Guerrero shares her inspiring personal journey and advice for how to navigate becoming a structural cardiologist as an international medical graduate, woman, and mother. Audio editing by CardioNerds Academy Intern, student doctor Adriana Mares. The PA-ACC & CardioNerds Narratives in Cardiology is a multimedia educational series jointly developed by the Pennsylvania Chapter ACC, the ACC Fellows in Training Section, and the CardioNerds Platform with the goal to promote diversity, equity, and inclusion in cardiology. In this series, we host inspiring faculty and fellows from various ACC chapters to discuss their areas of expertise and their individual narratives. Join us for these captivating conversations as we celebrate our differences and share our joy for practicing cardiovascular medicine. We thank our project mentors Dr. Katie Berlacher and Dr. Nosheen Reza. Video Version • Notes • Production Team The PA-ACC & CardioNerds Narratives in Cardiology PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Video version - Structural Heart Disease and LatinX Representation in Cardiology with Dr. Mayra Guerrero https://youtu.be/KvKADqUwUHQ Quoatables - Structural Heart Disease and LatinX Representation in Cardiology with Dr. Mayra Guerrero “Work hard, give it your best, and your work will speak for itself. Don’t be afraid to work hard and you’ll be able to achieve anything you want.”“I’m very fortunate to have had the opportunities that I’ve had, but now it’s my responsibility and the responsibility of many to make sure that we create those opportunities and that we provide mentorship for others who may want to follow the same steps into this field.”“I get angry, it’s normal to have emotions, but what I’ve learned is to transform my anger into something good – think of a project, find a paper, do something good for your career…channel that energy to do something good.”“It’s important that even at young ages you start thinking about how to pay it forward.”“Don’t wait too long to have kids. There’s never a perfect time to be a parent. Once you decide to have a family don’t put a pause on your personal life for your career.” Notes - Structural Heart Disease and LatinX Representation in Cardiology with Dr. Mayra Guerrero Notes (by Dr. Teodora Donisan) Structural valve disease in women and valve care in the global settingHeart disease is the leading cause of death for women. However, the awareness regarding this major public health concern has been declining over the past decade. Valve disease awareness is one of the lowest, at less than 3%.Women have higher mortality than men when they undergo surgical aortic or mitral interventions, mainly because of a higher risk profile. For example, women with severe aortic stenosis usually present at older ages and have many associated comorbidities, however the outcomes are good when they are treated with transcatheter aortic valve replacement (TAVR). Despite this, women are less likely to be referred for aortic valve replacement (AVR) than men. Once women are referred for therapy, they are more likely to be treated with TAVR than surgical aortic valve replacement (SAVR).There is a deficiency in trial enrollment for women which we need to address in order to generate the knowledge we require with regards to treatment. We also need to identify whether there are referral biases when it comes to AVR.Another hypothesis for the disparities in valve disease treatment for women when compared with men might be the decreased number of women in cardiology, especially in interventional cardiology (<10% of interventional cardiologists are women). Of note, <3% of TAVR operators are women (1.5% are surgeons and 1.5% are interventional cardiologists). Diversity and inclusion in interventional cardiologyAbout 8% of interventional cardiologists are women and only 4.2% of cardiologists are Latinx.In order to increase recruitment for WIC, the problem needs to be addressed on multiple levels.Mentorship should be provided to cardiology fellows, and they should be supported in their choice for interventional cardiology. This should be equally offered and tailored to women and underrepresented minorities. Support should be given even earlier in their careers and lives, at school and even with the education they receive at home. Career goals can be achieved with hard work and determination, and this should be an integral part of the education and upbringing from an early age.There is an institutional responsibility to help address this problem. It can start with training to decrease unconscious bias, improvements in workplace conditions (e.g., schedule flexibility, provide maternity/paternity leave, lactation rooms), opening leadership opportunities for women and URiMs, establishing diversity and inclusion committees.The FDA, industry, and societies should have DE&I committees to ensure inclusive representation in clinical trial leadership and to ensure recruitment of women and minorities.Work life harmony as an interventional cardiologistYou must choose your life partner well, caring for your family is teamwork.You might miss moments, but if you work together with your partner and children, it works out.It’s important to provide a strong role model for your family. References Vogel B, Acevedo M, Appelman Y, et al. The Lancet women and cardiovascular disease Commission: reducing the global burden by 2030. Lancet. 2021;397(10292):2385-2438. Production Team Dr. Gurleen Kaur Amit Goyal, MD Daniel Ambinder, MD

Sep 19, 2022

CardioNerds (Amit Goyal and Dan Ambinder), Series Co-Chair Dr. Dinu Balanescu (Academy House Faculty and Chief Resident at Beaumont Hospital), and Episode Lead Dr. Manu Mysore (Former CardioNerds Ambassador and Cardiologist at the University of Maryland) discuss The Need for Cardio-Oncology with Expert Faculty Dr. Bonnie Ky, Director of Penn Cardio-Oncology Translation Center of Excellence and Editor-in-Chief of JACC CardioOncology. Audio editing by CardioNerds Academy Intern, student doctor Yousif Arif. This episode is supported by a grant from Pfizer Inc. Cardio-Oncology is a burgeoning field. There is a need for cardiologists and oncologists to work together in a multidisciplinary fashion using multi-modality imaging and personalized medicine. Cardiologists in particular need to understand basic oncology, anti-cancer therapies, and address risk factors which play an important role in oncologic progression and/or adverse cardiovascular events. The field can only be furthered by research with a focus on specificity of endpoints and multidisciplinary collaboration. The future of the field is in the hands of investigators and clinicians alike. This CardioNerds Cardio-Oncology series is a multi-institutional collaboration made possible by contributions of stellar fellow leads and expert faculty from several programs, led by series co-chairs, Dr. Giselle Suero Abreu, Dr. Dinu Balanescu, and Dr. Teodora Donisan. Pearls • Notes • References • Production Team CardioNerds Cardio-Oncology PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls and Quotes - The Need for Cardio-Oncology with Dr. Bonnie Ky Over 20 million new cancer cases are expected to be added annually to the global burden as novel therapies have improved cancer survivorship. These therapies may be directly associated with cardiotoxicity or may prolong life to allow time for cardiovascular disease to develop in cancer survivors. Hypertension, hyperlipidemia, and obesity are modifiable risk factors that portend a poor prognosis from both an oncologic and cardiovascular perspective. Multi-modality imaging is useful in risk assessment within oncology, with echocardiography (including strain imaging) having a class I indication prior to treatment with many chemotherapeutics. Diverse trial enrollment is essential for furthering the science within Cardio-Oncology to translate clinically into personalized management. There is a need to strengthen a pipeline of young physicians and scientists to further the field of Cardio-Oncology. Show notes - The Need for Cardio-Oncology with Dr. Bonnie Ky Why should cardiologists have familiarity with cancer therapies? By 2030, 23.6 million new cancer cases are expected to be added annually to the global burden.1 Novel therapies and/or combination therapies have improved cancer survivorship but are associated with cardiovascular complications, especially in the elderly and those with pre-existing cardiovascular comorbidities.2 Cardiologists currently lack an understanding of oncologic treatments, with poor knowledge of dosing protocols and cardiotoxicities. This can lead to less aggressive protocols administered, as well as early discontinuation of important treatments for both oncologic and cardiovascular conditions.3 A multidisciplinary collaboration between pharmacists, cardiologists, oncologists, and nurse navigators is needed to improve treatment decision-making for the benefit of cancer patients. Cardiologists should have basic knowledge and understanding of some of the commonly used chemotherapeutic drugs and any adverse events during treatment courses based on clinical trials, FDA reporting, and epidemiological data. JACC Cardio-Oncology seeks to disseminate knowledge through live courses such as Advancing the Care of the Oncology Patient and journal-associated podcasts, with plans to develop a “how-to” series to educate both cardiologists and oncologists. What is the impact of cardiovascular risk factors and morbidity in oncology? In the age of personalized cancer therapies, patients with metastatic disease are living longer and are instead dying from cardiovascular events. Hypertension, obesity, and dyslipidemia are a growing epidemic within the oncologic population. Retrospective analysis by Dr. Sun from the University of Pennsylvania VA suggests that only 68% of men receiving treatment for prostate cancer had a comprehensive cardiovascular risk factor assessment and of those, 54.1% had uncontrolled risk factors!4 Of these, 29.6% were not receiving corresponding cardiac risk-reducing medications.4 Treat the modifiable risk factors aggressively! What type of conditions do cardio-oncologists manage? Cardio-oncologists manage a variety of treatment-associated cardiovascular conditions and adverse events. Common oncologic therapeutics with known cardiotoxicity include anthracyclines, HER-2 receptor antibodies, radiation, tyrosine kinase inhibitors, VEGF-associated tyrosine kinase inhibitors (TKIs), aromatase inhibitors, and even modern treatments including stem cell transplantation and CAR-T therapies. Patients follow-up with the cardio-oncologist before, during, and after treatment sessions. Common cardiovascular events addressed include hypertension, dyslipidemia, arrhythmias, heart failure, coronary artery disease, and obesity. More on these in future episodes! After cancer therapy completion, focus is on addressing cardiovascular and cancer-related risk factors and lifestyle modification. What are strategies for risk assessment of cancer patients in terms of cardiovascular toxicity? Advanced imaging plays a vital role within the field of Cardio-Oncology. The European Society of Medical Oncology gives echocardiography a 1A recommendation that all patients who receive anti-cancer therapy associated with left ventricular dysfunction should have a baseline ejection fraction (EF) assessment. Those who have a reduced EF at baseline are at a higher risk of cardiotoxicity. This can be limited however by body habitus or recent mediastinal surgery.5 Cardiac MRI is a gold standard for measuring left and right ventricular volume and function and is used when there is suboptimal image acquisition. It is particularly useful in the assessment of cardiac masses and inflammatory conditions such as myocarditis.5 Stress echocardiography plays a vital role in the risk stratification of patients undergoing cancer therapies associated with myocardial ischemia, including VEGF inhibitors and TKIs. There is a potential role for assessing diastolic dysfunction as well. Calcium scoring can be determined on non-gated non-contrast CT scans performed for staging of malignancy. Hundley et al. have done remarkable work in understanding if exercise programs will help prevent heart disease with strict cardio-metabolic testing in patients undergoing cancer treatment.6 Large efforts are underway to identify risk calculators to predict cardiotoxicity in a personalized approach. What are monitoring strategies for cardiotoxicity? Consensus statements and expert opinions continue to grow and more of this will be addressed in future episodes. In particular, guidelines are in place for anthracycline use and HER-2 targeted therapy. In August 2022, the European Society of Cardiology released Cardio-Oncology Guidelines, addressing the cardiotoxicity of numerous other classes of anti-cancer therapies and further highlighting the importance of echocardiography and multi-modality imaging for the monitoring of cardiotoxicity in cancer patients.7 What are challenges in designing clinical trials in cardio-oncology? Patients feel vulnerable during the early treatment course with chances of lower trial enrollment. Multi-disciplinary collaboration with a patient-centric focus is needed. Partnership with key stakeholders, including NIH/AHA, is needed. Defining the optimal timing for the initiation of cardio-protective therapy and the duration of such therapy is another challenge. Where do we go from here in Cardio-Oncology? Scientifically, we need to advance personalized medicine to improve patient outcomes. We need to understand the mechanistic overlap between cardiovascular and oncologic disease. We need to leverage technology to assist in the treatment of cancer therapy-related adverse cardiovascular events and oncologic progression. We need to work together to overcome healthcare disparities which play a vital role in Cardio-Oncology. We need to strengthen the pipeline of young investigators and clinicians. References - The Need for Cardio-Oncology with Dr. Bonnie Ky Cancer Statistics (National Institute of Cancer website). https://www.cancer.gov/about-cancer/understanding/statistics. Published 2018. Accessed August 4, 2022. Cardinale D, Biasillo G, Cipolla CM. Curing Cancer, Saving the Heart: A Challenge That Cardioncology Should Not Miss. Curr Cardiol Rep. 2016;18(6):51. Okwuosa TM, Prabhu N, Patel H, et al. The Cardiologist and the Cancer Patient: Challenges to Cardio-Oncology (or Onco-Cardiology) and Call to Action. J Am Coll Cardiol. 2018;72(2):228-232. Sun L, Parikh RB, Hubbard RA, et al. Assessment and Management of Cardiovascular Risk Factors Among US Veterans With Prostate Cancer. JAMA Netw Open. 2021;4(2):e210070. Yu C, Pathan F, Tan TC, Negishi K. The Utility of Advanced Cardiovascular Imaging in Cancer Patients-When, Why, How, and the Latest Developments. Front Cardiovasc Med. 2021;8:728215. Bellissimo MP, Canada JM, Jordan JH, et al. Changes in Physical Activity, Functional Capacity, and Cardiac Function during Breast Cancer Therapy. Cancer Epidemiol Biomarkers Prev.

Sep 16, 2022

CardioNerds (Daniel Ambinder and Amit Goyal) join Dr. Arielle Schwartz (Emory University cardiology fellow), Dr. Joshua Zuniga (former Emory vascular medicine fellow and now USC cardiology fellow), and Dr. Patrick Zakka (UCLA cardiology fellow) from the Emory University School of Medicine. They discuss a case of a young woman with new onset hypertension refractory to 3 antihypertensive agents who is ultimately diagnosed renovascular hypertension due to fibromuscular dysplasia complicated by saccular aneurysm. Dr. Bryan Wells (Director of Vascular Medicine at Emory University) provides the ECPR for this episode. Audio editing by CardioNerds Academy intern, Dr. Christian Faaborg-Andersen. CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Case Media References Gornik HL, Persu A, Adlam D, Aparicio LS, Azizi M, Boulanger M, Bruno RM, de Leeuw P, Fendrikova-Mahlay N, Froehlich J, Ganesh SK, Gray BH, Jamison C, Januszewicz A, Jeunemaitre X, Kadian-Dodov D, Kim ES, Kovacic JC, Mace P, Morganti A, Sharma A, Southerland AM, Touzé E, van der Niepen P, Wang J, Weinberg I, Wilson S, Olin JW, Plouin PF. First International Consensus on the diagnosis and management of fibromuscular dysplasia. Vasc Med. 2019 Apr;24(2):164-189. doi: 10.1177/1358863X18821816. Epub 2019 Jan 16. Erratum in: Vasc Med. 2019 Oct;24(5):475. Erratum in: Vasc Med. 2021 Aug;26(4):NP1. PMID: 30648921. Olin, Circulation. 2014;129:1048-1078. Fibromuscular Dysplasia: State of the Science and Critical Unanswered Questions A Scientific Statement From the American Heart Association S.H.KimMD, MPH†Jeffrey W.OlinDO‡James B.FroehlichMD, MPH§XiaokuiGuMA§J. MichaelBacharachMD‖Bruce H.GrayDO¶Michael R.JaffDO#Barry T.KatzenMD∗∗EvaKline-RogersMS, RN, NP§Pamela D.MaceRN††Alan H.MatsumotoMD‡‡Robert D.McBaneMD§§Christopher J.WhiteMD‖‖Heather L.GornikMD, MHS†. Clinical Manifestations of Fibromuscular Dysplasia Vary by Patient Sex: A Report of the United States Registry for Fibromuscular Dysplasia. JACC. Volume 62, Issue 21, 19–26 November 2013, Pages 2026-2028

Sep 12, 2022

CardioNerds Dr. Josh Saef, Dan Ambinder, join Dr. Jim Kimber and interview experts Dr. Adrienne Kovacs, and Dr. Lauren Lastinger and discuss behavioral health needs and psychosocial wellbeing in the congenital heart disease population. In this episode, our experts tackle issues surrounding mental and behavioral health including anxiety/depression, ADHD, neurodevelopmental disabilities, psychosocial challenges, stressors unique to patients with ACHD and their families, and how the healthcare system can better optimize mental health care for the CHD patient population. Audio editing by CardioNerds Academy Intern, Pace Wetstein. The CardioNerds Adult Congenital Heart Disease (ACHD) series provides a comprehensive curriculum to dive deep into the labyrinthine world of congenital heart disease with the aim of empowering every CardioNerd to help improve the lives of people living with congenital heart disease. This series is multi-institutional collaborative project made possible by contributions of stellar fellow leads and expert faculty from several programs, led by series co-chairs, Dr. Josh Saef, Dr. Agnes Koczo, and Dr. Dan Clark. The CardioNerds Adult Congenital Heart Disease Series is developed in collaboration with the Adult Congenital Heart Association, The CHiP Network, and Heart University. See more Disclosures: None Pearls • Notes • References • Guest Profiles • Production Team CardioNerds Adult Congenital Heart Disease PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls - Congenital Heart Disease and Psychosocial Wellbeing Among patients with congenital heart disease, symptoms of anxiety are more common than symptoms of depression. “Heart-focused anxiety” relates to symptoms attributable to a heart condition including fear of appointments, surgery, or health-uncertainty. It is important to differentiate this from generalized anxiety.Predictors of depression and anxiety include patient-reported physical health status. Defect severity (mild, moderate, great complexity) and physician-diagnosed NYHA class were NOT associated with rates of depression/anxiety [2].Despite CHD, patient self-reported Quality of Life (QoL) is relatively high. Predictors of decreased QoL include older age, lack of employment, never having married, and worse self-reported NYHA functional classImportant treatment strategies include: education for patients and caregivers, early identification and referral to mental health providers, incorporation of providers into CHD teams, and encouraging physical activity and peer-interaction. Show notes - Congenital Heart Disease and Psychosocial Wellbeing Notes (developed by Dr. Jim Kimber) Mental Health Terminology: Adults with CHD face the same mental health challenges as people who don’t have a heart condition. Symptoms of depression and anxiety are the most common: Approximately 1/4 - 1/3 of CHD patients will struggle with clinically significant depression or anxiety at any one point. Up to ½ will meet lifetime diagnostic criteria for these conditions Mood and anxiety disorders differ in that they have separate diagnostic criteria. Importantly, research often uses self-reported symptoms, rather than patients who have formally met diagnostic criteria. Historically, the focus has been on depression. However, elevated symptoms of anxiety are much more common than elevated symptoms of depression. It is important to make the distinction between “Generalized Anxiety,” and “Heart-Focused Anxiety.”Heart-Focused Anxiety: symptoms of anxiety directly related to having a heart condition, such as fear of appointments / worry about a decline in health status, getting an ICD, preparing for surgery, transplants, or having a shortened life expectancy, etc. This may also include a significant component of health uncertainty – the idea that patients are aware of need for a likely intervention but without ability to prognosticate timelines (e.g. need for valve replacement). This component differentiates CHD patients from those with acquired heart disease who have not been surrounded by such uncertainty for significant components of their life.Generalized Anxiety: excessive worry about a lot of factors beyond their control and accompanied by other symptoms like: muscle tension, sleep disturbance. Manifestations of mood and behavioral health problems include: impaired peer relationships, impaired romantic relationships, poor school or work performance, difficulty getting or keeping a job. Persons may struggle with inconsistent medical follow-up, inconsistent compliance, and substance abuse. Predictors & Prevalence of Depression / Anxiety: Defect Severity (mild, moderate, great complexity) was not associated with depression or anxiety. Similarly, physician diagnosed NYHA Class was not associated with depression/anxiety [2]. Known predictors: patient-reported physical health status impacts symptoms of depression/anxiety [2].There is also a link between social wellbeing and psychological well-being. Other studies have highlighted that perceived health status is an important predictor. Risk Stratification All patients with congenital heart disease are at risk for mental health disorders and need to be screened. Those at heightened risk include patients with genetic syndromes (in particular, those with 22q11 deletion, associated with more severe psychiatric disorders), prematurity, longer hospital stays, and those with lower family socioeconomic status. Patients who have undergone cardiopulmonary bypass have higher likelihood of neurologic insults (CVA), but also cognitive dysfunction following surgery. In research, Apolipoprotein E has been predictive of neurodevelopmental dysfunction following cardiac surgery. Other factors, including the number of surgeries, and how often they were separated from peers growing up might also impact mental health well-being in adults. Quality of Life (QoL) and Assessment Approach-IS Study International Study looking at patient-reported outcomes in adults with CHD.Over 4,000 patients from 15 countries were enrolled.Self-Reported Questionnaires administered to gain information on perceived health status, psychological functioning, health behaviors, quality of life (Scale 0-100) [9] Patients have lived with CHD their entire life, and report relatively high QoLOlder age, lack of employment, never having married, and worse NYHA functional class (self- reported) are associated with lower QoL Alternative Assessment for Nonverbal Patients: Concerns may come from caregivers or parentsMay demonstrate behavioral changes: outbursts, changes in feeding/eating habits or weight loss/gain, changes in sleeping patterns, fatigue, low mood, anhedoniaScreening should begin early in childhood (early assessment and diagnosis allows for enrollment in beneficial social / developmental programs)Cardiac Neurodevelopmental Outcome Collaborative (CNOC): recommend screenings for various ages and provide suggested screening algorithms. Transition to Adult Teams: process that occurs during early adolescence Goals: stay in uninterrupted health care throughout their lives, avoid lapses in care, have an established process, allow patients to develop knowledge and skills to assume maximal responsibility for their healthcare management, and adapt information delivery as necessary The I <3 Change Website provides information for people transitioning from pediatric to adult cardiology teamsBeginning in adolescence, pediatric provider is recommended to speak independently with their cardiologist at every visit.Transition is a family process: parents are involved in care and successful transition to help bridge the gap towards independence for the patient Strategies to Ensure Treatment Success Education is Key: Parents and caregivers need an understanding of what CHD concerns are, expected follow up needs, etc.Engage all stakeholders in Medical Home: home health aide, caregiver, primary care physician, etc. Utilize Screening Tools and Implement Routine Screening Refer to Mental Health Provider when Appropriate Embed mental health professional into the Team: identify providers who have an interest in mental health (psychologist / psychiatrist) who are qualified to treat patients with congenital heart disease Improves access and reduces stigmaAllows for ease of access / rapid consultation Encourage appropriate physical activity: exercise and physical activity has physiologic and mental health benefit, improves mood, stress, anxiety, etc. Mental health benefit is present regardless of type / intensity / duration of activity Ask patients if they avoid particular activities and provide reassurance Offer opportunities for peer interaction: patient education sessions, etc. Provide Positive Reinforcement: comment on patients’ resilience and effective coping. Destigmatize It! Practice of carefully worded Key Sentences help to destigmatize mental health disorders: “Does thinking about your health every make you worried or depressed?”“How are you doing from a psychological perspective?”“I know that patients sometimes struggle with low mood or anxiety. If that ever happens to you, let me know, and we can discuss it.” References - Congenital Heart Disease and Psychosocial Wellbeing Gonzalez, V.J., et al., Mental Health Disorders in Children With Congenital Heart Disease. Pediatrics, 2021. 147(2). PubMed CrossRef Kovacs, A.H., et al., Depression and anxiety in adult congenital heart disease: predictors and prevalence. Int J Cardiol, 2009. 137(2): p. 158-64. PubMed CrossRef Gaynor, J.W., et al.,

Aug 31, 2022

CardioNerds (Amit Goyal and Dan Ambinder) join Dr. Radi Zinoviev, Dr. Josh Cohen, and Dr. Tiffany Dong (CardioNerds Ambassador) from the Cleveland Clinic for a day on Edgewater beach. They discuss the following case of the evaluation and management of prosthetic tricuspid valve stenosis in a patient with a history of Ebstein Anomaly. The expert commentary and review (ECPR) is provided by Dr. Jay Ramchand, staff cardiologist with expertise in multimodality cardiovascular imaging at the Cleveland Clinic. Jump to: Case media - Case teaching - References CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Case Media CXR ECG TTE RHC Final TTE TTE 1 TTE 2 TTE 3 Follow up TTE 1 Follow up TTE 2 Episode Schematics & Teaching Pearls - Tricuspid Valve Stenosis Tricuspid stenosis is uncommon ( 60cm.Structural findings that support the presence of severe tricuspid stenosis include a moderately dilated RA and a dilated IVC, though these are not specific.Right heart catheterization hemodynamics that support tricuspid stenosis include a high right atrial pressure and gradual “y” descent.Bioprosthetic tricuspid valves are generally favored over mechanical valves due to risk of thrombosis and longevity of these valves in the tricuspid position. Notes - Tricuspid Valve Stenosis What are causes of tricuspid stenosis? Causes of tricuspid stenosis can be divided into congenital and acquired causes. Congenital causes include tricuspid atresia or stenosis. Acquired causes include rheumatic heart disease, carcinoid syndrome, endocarditis, prior radiation, or fibrosis from endomyocardial procedures or placement of electrical leads. Rheumatic heart disease is the most common cause of tricuspid stenosis and is usually associated with mitral valvulopathy. What are the symptoms and physical exam findings of tricuspid stenosis? Findings revolve around right sided congestion or heart failure symptoms such as peripheral edema, abdominal distension with ascites, hepatomegaly, and jugular venous distension. When examining the jugular vein, you may see prominent a-waves and an almost absent or slow y descent reflective of delayed emptying of the right atrium (in the absence of tricuspid regurgitation). The murmur of tricuspid stenosis includes an opening snap and low diastolic murmur at the left lower sternal border with inspiratory accentuation. Patients may also report fatigue due to decreased cardiac output from obstruction. On echocardiography, what are the features supportive of severe tricuspid stenosis? Qualitatively, the leaflets may be thickened with reduced mobility and there may be diastolic dooming of the valve. Doppler may show high gradients of ≥ 5 mmHg, which may be elevated if there is coexisting tricuspid regurgitation and lower with decreased cardiac output. Associated structural changes include dilated right atrium and inferior vena cava. What is expected on right heart catheterization for tricuspid stenosis? Assuming the patient remains in sinus rhythm, patients with tricuspid stenosis would display high right atrial pressures and a gradual “y” descent. A diastolic gradient may be measured with dual catheters in the right atrium and the right ventricle. What are the treatment options for tricuspid stenosis? Medical management of tricuspid stenosis includes diuretics and addressing the underlying cause. Intervention is indicated for symptomatic severe tricuspid stenosis although the current 2020 ACC/AHA Valve Guidelines do not address tricuspid stenosis. The 2014 ACC/AHA guidelines give a class I indication for tricuspid stenosis surgery during left sided surgery while there is a class I indication for isolated tricuspid stenosis if symptomatic. Percutaneous options include balloon valvotomy while those who are surgical candidates are eligible for valve repair or replacement. Surgical options include repair or replacement with bioprosthetic favored over mechanical given the latter’s susceptibility to thrombosis. References - Tricuspid Valve Stenosis Nishimura, R. A., et al. (2014). "2014 AHA/ACC Guideline for the Management of Patients With Valvular Heart Disease: executive summary: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines." Circulation 129(23): 2440-2492.Otto, C. M., et al. (2021). "2020 ACC/AHA Guideline for the Management of Patients With Valvular Heart Disease: Executive Summary: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines." Circulation 143(5): e35-e71.

Aug 23, 2022

It’s another session of CardioNerds Rounds! In these rounds, Dr. Stephanie Fuentes (EP FIT at Houston Methodist) joins Dr. Hugh Calkins (Professor of Medicine and Director of the Electrophysiology Laboratory and Arrhythmia Service at Johns Hopkins Hospital) to discuss the nuances of atrial fibrillation (AF) management through challenging cases. As an author of several guideline and expert consensus statements in the management of AF and renowned clinician, educator, and researcher, Dr. Calkins gives us many pearls on the management of AF, so don’t miss these #CardsRounds! This episode is supported with unrestricted funding from Zoll LifeVest. A special thank you to Mitzy Applegate and Ivan Chevere for their production skills that help make CardioNerds Rounds such an amazing success. All CardioNerds content is planned, produced, and reviewed solely by CardioNerds. Case details are altered to protect patient health information. CardioNerds Rounds is co-chaired by Dr. Karan Desai and Dr. Natalie Stokes. Speaker disclosures: None Challenging Cases - Atrial Fibrillation with Dr. Hugh Calkins CardioNerds Rounds PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Show notes - Challenging Cases - Atrial Fibrillation with Dr. Hugh Calkins Case #1 Synopsis: A woman in her mid-60s presents with symptomatic paroxysmal atrial fibrillation (AF). An echocardiogram has demonstrated that she has a structurally normal heart. Her primary care doctor had started Metoprolol 50 mg twice a day but she has remained symptomatic. In office, an EKG confirms AF, but she converts to sinus while there. She is seeking advice to prevent further episodes and in general wants to avoid additional medications Case #2 Takeaways We discussed several potential options for treatment. Amongst the first things we discussed was amiodarone. In a patient of this nature without structural heart disease and under the age of 70, Dr. Calkins discussed that he would probably consider amiodarone as a 2nd line option. While amiodarone may be effective in maintaining sinus rhythm in comparison to other antiarrhythmic medications like sotalol, flecainide, and propafenone, it does have significant toxicity.If antiarrhythmic drugs (AAD) were to be considered, we also discussed the options of dofetilide versus sotalol. Dofetilide typically requires inpatient initiation due to the risk of QT prolongation and Torsades. Since women tend to have longer corrected QT (QTc) intervals, high dose dofetilide may be more proarrhythmogenic in women. Though, Dr. Calkins noted that many patients don’t tolerate sotalol due to fatigue and generally dofetilide is well tolerated.When it comes to the “pill in the pocket” approach, Dr. Calkins noted that its utility is more so in patients with persistent AF that is known to not stop on its own. For instance, an individual who has AF a few times a year that is persistent may benefit from flecainide or propafenone (“in the pocket”) instead of being brought in for an electrical cardioversion. In this scenario, the first time one of these agents is used, the patient ought to be closely monitored. For our patient, her episodes were too frequent and self-terminating for a “pill in the pocket” approach to be effective.Current guideline recommendations for catheter ablation include a Class IA recommendation for patients with paroxysmal AF refractory to AADs, and a Class IIA recommendation as first-line therapy for patients with paroxysmal AF.In the 2020 ESC Atrial Fibrillation Guidelines, catheter ablation is given a Class IA recommendation to improve symptoms of AF recurrences in patients who have failed or are intolerant of one Class I or III AADs. For patients who have failed or have been intolerant of beta blocker alone for rhythm control, catheter ablation is given a Class IIA recommendation. As first-line therapy in paroxysmal AF, catheter ablation is given a Class IIA recommendation as well.Of note, three recent trials have demonstrated catheter ablation as first line therapy is reasonable and newer guidelines will reflect this. Specifically, EARLY-AF compared ablation (cryoablation) vs AAD (mainly with flecainide/propafenone) as a first line therapy. The cryoablation arm showed significantly less recurrence of AF at one yearThe guidelines clearly state that aligning the treatment plan with the patient’s goals and risk tolerance are paramount. Catheter ablation does have potential complications such as pericardial effusion or access-related issues, though these are rare. Furthermore, as time has passed, catheter ablation success rates have improved.Up and coming techniques such as electroporation may be game-changing with regards to success rate and safety. Waiting times for a procedure may be an issue, so one could consider an AAD, such as flecainide, as a standing dose awaiting the procedure.Regarding predictors of success for catheter ablation, Dr. Calkins noted that the key factor was type of AF. With paroxysmal AF there is roughly 70-80% success rate with the 1st procedure, 50-70% with persistent AF, and 30-50% with longstanding persistent AF. Other predictors of success include BMI (higher BMI associated with a lower success rate and a higher rate of complications), left atrial size (with a linear dimension of ≥ 5.5 cm indicating less likelihood of success), age, and obstructive sleep apnea.One of the questions that was raised was screening for structural heart disease before starting flecainide/propafenone. Typically, an EKG and TTE are done, and if they are not suggestive of structural heart disease, Dr. Calkins noted it would be reasonable to use these agents. With increasing age, there’s increased risk of subclinical CAD, though it is not in the guidelines to perform functional testing or anatomic imaging prior to starting these agents.Finally, Dr. Calkins noted as an aside that in patients with sick sinus syndrome, management in the past has involved placing a permanent pacemaker (PPM) followed by AAD agents. However, catheter ablation may be a better option because it treats AF and improves the sinus rate because of its effect on the autonomic system, eliminating pauses that would have otherwise warranted a pacemaker. After ablation, the resting HR can improve 10-30 bpm and this can be a marker of successful catheter ablation. Case #2 Synopsis: A man in his mid-60s with a history of surgically placed bioprosthetic AVR, CAD with prior CABG, newly diagnosed ischemic cardiomyopathy with LVEF 20-25% with imaging revealing reversible ischemia in multiple coronary territories, presented to the clinic with dyspnea in the setting of persistent AF now 6 weeks after multi-vessel PCI. Other relevant information is that he appears congested in clinic and his EKG demonstrates a left bundle branck block (LBBB) with QRS at 172 ms. He seeks your opinion for management options. Case #2 Takeaways Dr. Calkins discussed that the only safe AAD in this circumstance would be Amiodarone, and that the risk of developing complete heart block (CHB) in a patient with LBBB placed on amiodarone is not high enough to preclude its use. One strategy would be to give this patient an amiodarone load followed by direct current cardioversion (DCCV). Following DCCV, if the patient maintains sinus rhythm, one could consider continuing with amiodarone at a lower dose or pursuing catheter ablation as a next strategy.Dr. Calkins emphasized understanding the temporal relationship between AF and HF in patients with reduced ejection fraction. In patients with new-onset AF and reduced EF, aggressive rhythm control with catheter ablation would be warranted because there is a higher likelihood of improving the cardiomyopathy.Another option to consider in patients with HFrEF and permanent atrial fibrillation that remain symptomatic or who have had hospitalizations with HF is AV node ablation with cardiac resynchronization therapy, though for a patient like this other viable treatment options remain to be tested. Regarding an ICD, the patient may recover their EF post-revascularization and implementation of guideline-directed therapy. Thus, with ischemic cardiomyopathy post revascularization, the decision to place an ICD should wait 90 days. Furthermore, the EF may improve with control of the AF. Case #3 Synopsis: A woman in her mid-80s with hypertension and recent COVID-19 pneumonia is admitted to the hospital with hypoxia, reduced LVEF and found to have AF with rapid ventricular response. The patient’s underlying conditions were treated and attempts at ventricular rate control were attempted but limited by blood pressure. A DCCV with amiodarone loading was also attempted but failed to maintain sinus rhythm. Case #3 Takeaways Some feasible options in this circumstance include further loading with amiodarone and reconsidering another DCCV versus an AV node ablation with permanent pacemaker implantation if medical therapies are limited or failing.Digoxin use for rate control alone in critically ill patients is typically discouraged. This is because we now know that its mechanism of action involves raising vagal tone and acutely ill patients typically have low vagal tone so it may not be helpful. However, in patients with rapid AF and HF, it is reasonable to use it. When used in combination with amiodarone, one may reduce the dose of digoxin in half given its drug-drug interaction Production Team Karan Desai, MD Natalie Stokes, MD Amit Goyal, MD Daniel Ambinder, MD

Aug 17, 2022

In this episode, Daniel Ambinder (CardioNerds Co-Founder), Dr. Gurleen Kaur (Director of CardioNerds Internship and medicine resident at Brigham and Women’s Hospital), Dr. Eunice Dugan (Cardiology fellow at Cleveland Clinic) and Dr. Zarina Sharalaya (Interventional and Structural Cardiologist at North Texas Heart) learn from the Dr. Sheila Sahni (Interventional Cardiologist and Director of The Women’s Heart Program at The Sahni Heart Center) regarding radiation safety in the cath lab and methods of reducing radiation exposure to the operator. She also discusses radiation safety for the pregnant interventional cardiologist and how to safely manage pregnancy during the gestational period. We hear her inspirational journey as a female interventional cardiologist and her experience in starting the Women’s Heart Program at Sahni Heart Center. Special message by Dr. Jeff Lander, New Jersey ACC Chapter Governor. Audio editing by CardioNerds Academy Intern, Pace Wetstein. The PA-ACC & CardioNerds Narratives in Cardiology is a multimedia educational series jointly developed by the Pennsylvania Chapter ACC, the ACC Fellows in Training Section, and the CardioNerds Platform with the goal to promote diversity, equity, and inclusion in cardiology. In this series, we host inspiring faculty and fellows from various ACC chapters to discuss their areas of expertise and their individual narratives. Join us for these captivating conversations as we celebrate our differences and share our joy for practicing cardiovascular medicine. We thank our project mentors Dr. Katie Berlacher and Dr. Nosheen Reza. Video Version • Notes • Production Team Claim free CME just for enjoying this episode! There are no relevant disclosures for this episode. The PA-ACC & CardioNerds Narratives in Cardiology PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Video version - Radiation Safety & Women in Interventional Cardiology with Dr. Sheila Sahni https://youtu.be/iIwnsu6qJ4k Tweetorial - Radiation Safety & Women in Interventional Cardiology with Dr. Sheila Sahni https://twitter.com/gurleen_kaur96/status/1563608232211296256?s=21&t=iay5zosSBDjPBLWJ4kWIAw Quoatables - Radiation Safety & Women in Interventional Cardiology with Dr. Sheila Sahni “Having anyone who can believe in you when you are really passionate about something is really all you need… the passion is what’s going to carry you through. It’s not about being male or female or pregnant or not pregnant, it’s about what you love to do and how can you master it.” “Our careers can wait, but family planning cannot. If you are fortunate enough to have the opportunity to start a family even if it’s during your training, you should”. Notes - Radiation Safety & Women in Interventional Cardiology with Dr. Sheila Sahni What are procedural techniques to utilize during a heart catheterization to reduce radiation exposure to the operator? Decrease number and length of cine acquisitions and fluoroscopy timeDecrease the frame rate - halving the frame rate reduces radiation dose by 50%Decrease the distance between the image intensifier and the patientLimit steep LAO angulationsApply collimation as much as possible which reduces overall patient dose and scatter radiationLimit digital magnification which can increase skin dose exposure by 50% What are the important dose limits to consider for a pregnant female and her fetus in the cath lab? The US Nuclear Regulatory Commission (NRC) regulatory equivalent dose limit is 5mSv during the entire pregnancy of the declared pregnant woman.The annual natural background radiation dose in the US is 3mSv.The average under-lead dose to a working pregnant interventionalist over the entire gestation is ~0.3mSv.The fetus of a working pregnant interventionalist is estimated to receive ~0.09mSv over an entire gestation. What are the ways in which pregnant women can protect themselves and the fetus from radiation exposure in the cath lab? Disclose (confidentially if desired) pregnancy to the radiation safety office to ensure fetal protectionWear an additional dosimeter underneath the lead apron at waist level to track fetal radiation doseDecrease occupational exposure via radiation protection measures as summarized below What are important considerations for lead apron use in the cath lab to maximize radiation protection? Make sure your lead fits!Do not sit in your lead- sitting in lead can lead to cracks which can decrease protectionHang up your lead when not being usedConsider shoulder pads/arm sleeve addition to lead apron to protect breast tissueEnsure that your lead apron is undergoing periodic screening to monitor for defectsConsider lead thickness - 0.5mm thickness attenuates 98-99.5% of scattered radiation, 0.35mm thickness attenuates 95-96% of scattered radiation References Sahni S, Chieffo A, Balter S. Women as one. Radiation Safety in the Practice of Cardiology. https://rad.womenasone.org/. Accessed March 31, 2022. Production Team Dr. Gurleen Kaur Amit Goyal, MD Daniel Ambinder, MD

Aug 14, 2022

The modern CICU has evolved to include patients with complex pulmonary mechanics requiring more non-invasive and mechanical ventilation. Series co-chairs Dr. Eunice Dugan and Dr. Karan Desai along with CardioNerds Co-founder Dr. Amit Goyal were joined by FIT lead, Dr. Sam Brusca, who has completed his NIH Critical Care and UCSF Cardiology fellow and currently faculty at USCF. We were fortunate enough to have two expert discussants: Dr. Burton Lee, Head of Medical Education and Global Critical Care within the National Institutes of Health Critical Care Medicine Department and master clinician educator with the ATS Scholar’s Critical Care for Non-Intensivists program, and Dr. Chris Barnett, ACC Critical Care Cardiology council member and Section Chair of Critical Care Cardiology at UCSF. In this episode, these experts discuss the basics of mechanical ventilation, including the physiology/pathophysiology of negative and positive pressure breathing, a review of ventilator modes, and a framework for outlining the goals of mechanical ventilation. They proceed to apply these principles to patients in the CICU, specifically focusing on patients with RV predominant failure due to pulmonary hypertension and patients with LV predominant failure. Audio editing by CardioNerds Academy Intern, student doctor, Shivani Reddy. The CardioNerds Cardiac Critical Care Series is a multi-institutional collaboration made possible by contributions of stellar fellow leads and expert faculty from several programs, led by series co-chairs, Dr. Mark Belkin, Dr. Eunice Dugan, Dr. Karan Desai, and Dr. Yoav Karpenshif. Pearls • Notes • References • Production Team CardioNerds Cardiac Critical Care PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls and Quotes - Positive Pressure Ventilation in the CICU Respiratory distress, during spontaneous negative pressure breathing can lead to high transpulmonary pressures and potentially large tidal volumes. This will increase both RV afterload (by increasing pulmonary vascular resistance) and LV afterload (by increasing LV wall stress). An analogy for the impact of negative pleural pressure during spontaneous respiration on LV function is that of a person jumping over a hurdle. The height of the hurdle does not increase, but the ground starts to sink, so it is still harder to jump over. Intubation in patients with right ventricular failure is a tenuous situation, especially in patients with chronic RV failure and remodeling (increased RV thickness, perfusion predominantly during diastole, RV pressure near or higher than systemic pressure). The key tenant to safe intubation is avoiding hypotension, utilizing induction agents such as ketamine or etomidate, infusing pressors, and potentially even performing awake intubations. Non-invasive positive pressure ventilation in HFrEF has hemodynamic effects similar to a cocktail of IV inotropes, dilators, and diuretics. CPAP decreases pulmonary capillary wedge pressure (LV preload), decreases systemic vascular resistance (afterload), and increases cardiac output. Airway pressure during mechanical ventilation is based on the “equation of motion”: Pressure = Volume/Compliance + Flow*Resistance + PEEP. Our goals of oxygenation on mechanical ventilation include achieving acceptable PaO2/Sat with the lowest FiO2 possible (avoiding oxygen toxicity) and optimal PEEP (which increases oxygenation but can have detrimental impact on cardiac output) Our goals of ventilation on mechanical ventilation include achieving acceptable pH and PaCO2 while preventing ventilator induced lung injury and avoiding auto-PEEP. We prevent lung injury by reducing tidal volume (ideally 65 mmHg, >92-94%), whilst avoiding inspired oxygen toxicity (FiO2 > 60%) - Oxygenation is primarily impacted by FiO2 and PEEP. PEEP can be titrated to aide in reducing FiO2, though can have negative impacts on cardiac output by reducing venous return 4. What are the Ventilation Goals of Mechanical Ventilation? - To achieve acceptable PCO2 and pH without causing harm (ventilator induced lung injury) - We avoid ventilator induced lung injury by reducing tidal volume (ideal < 8 cc/kg), reducing mechanical power (respiratory rate), reducing plateau pressure (< 30 cmH20), reducing driving pressure (< 15 cmH20), and reducing repeated alveolar opening/closing (by having adequate lung recruitment) - Ventilation is primarily impacted by TV and respiratory rate, which equate to minute ventilation 5. How can we calculate Airway Pressure using the Equation of Motion as related to Mechanical Ventilation? Airway Pressure = V/C + FxR + PEEP V/C = TV/Compliance and represents the alveolar pressure of the lung generated by a given TV at a given static lung compliance FxR = Flow x Resistance and is akin to Ohm’s law (V=IR), representing the pressure due to dynamic/resistive forces in the larger airways PEEP is the pressure stating point at the beginning of the inspiration 6. What considerations need to be taken when intubating a patient with RV Failure/Pulmonary Hypertension? - Intubation should be avoided if possible (though notably, respiratory distress and spontaneous breathing is not necessarily preferable, especially in the setting of respiratory acidosis or excessively low lung volumes) - Reliable vascular access and in-line pressors are key to avoiding hypotension during induction - Rapid sequence intubation (RSI) drugs such as etomidate and ketamine are preferred to propofol - Awake intubation is safest if feasible References - Positive Pressure Ventilation in the CICU 1. Alviar CL, Miller PE, McAreavey D, et al. Positive Pressure Ventilation in the Cardiac Intensive Care Unit. J Am Coll Cardiol. Sep 25 2018;72(13):1532-1553. doi:10.1016/j.jacc.2018.06.074 2. Barnett CF, O'Brien C, De Marco T. Critical care management of the patient with pulmonary hypertension. Eur Heart J Acute Cardiovasc Care. Jan 12 2022;11(1):77-83. doi:10.1093/ehjacc/zuab113 3. Bradley TD, Holloway RM, McLaughlin PR, Ross BL, Walters J, Liu PP. Cardiac output response to continuous positive airway pressure in congestive heart failure. Am Rev Respir Dis. Feb 1992;145(2 Pt 1):377-82. doi:10.1164/ajrccm/145.2_Pt_1.377 4. Esteban A, Frutos-Vivar F, Ferguson ND, et al. Noninvasive positive-pressure ventilation for respiratory failure after extubation. N Engl J Med. Jun 10 2004;350(24):2452-60. doi:10.1056/NEJMoa032736 5. Girardis M, Busani S,

Aug 4, 2022

CardioNerds (Amit and Dan) join join Dr. Andrew Dicks (Vascular medicine physician at Prisma Health, former fellow at Mass General Vascular) and Dr. Prateek Sharma (Vascular interventional & medicine fellow at MGH) for an ice-cold drinks at the Esplanade in Boston, MA to discuss a case about a patient who developed a pulmonary embolism and masterfully discuss the diagnosis and management of of pulmonary emboli. Dr. Ido Weinberg (Director, Vascular Medicine Fellowship at MGH) provides the ECPR for this episode. Case Abstract: A 59-year-old Spanish-speaking man with no significant past medical history presents after falling 15-20 feet from a ladder and landing on his back. He was found to have an L1 fracture and left radial fracture and underwent T12-L2 fusion with neurosurgery on hospital day 1 and ORIF of left radial fracture with orthopedic surgery on hospital day 2. On hospital day 5, he develops acute onset tachycardia with HR in the 130s bpm with new O2 requirement associated with mild shortness of breath at rest without any chest discomfort. His labs were notable for an elevated troponin and proBNP. He underwent CTPA which demonstrated acute bilateral occlusive pulmonary emboli (PE) extending in the right and left main pulmonary arteries. TTE demonstrated right ventricle dilation. The patient was started on a heparin infusion and a PE response team (PERT) meeting was held to discuss treatment options. Given recent surgery, use of thrombolytic therapy was felt to be too risky and thus he was taken for percutaneous thrombectomy in the cath lab. PA pressure prior to intervention was 51/21 mmHg. The patient underwent suction thromboembelectomy with the Flow Triever device with extraction of thrombus and improvement in PA pressure to 19/11 mmHg. He was treated with anticoagulation thereafter and discharged home two days after the procedure. Jump to: Case media - Case teaching - References CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Case Media Acute bilateral occlusive and nonocclusive pulmonary emboli extending from the right and left main pulmonary arteries to the lobar and segmental arteries of all the lobes. Moderate right heart strain including the right atrium and the right ventricle. RV/LV ratio > 1.0. Right ventricular cavity is dilated (RV size at the base measures to 45mm). Right ventricular systolic function is moderately decreased. Right ventricular free wall is hypokinetic with sparing of the right ventricular apex consistent with acute right ventricular strain Pulmonary angiography demonstrated extensive proximal bilateral PEs Caption: Post-procedure TTE demonstrated resolution of RV strain with normalization of RV size and function. Episode Schematics & Teaching Pearls While there are markers to suggest PE, such as ECG findings or evidence of RV dilatation, a PE cannot be confirmed without imaging.Elevation of cardiac biomarkers and evidence of RV dysfunction are used to risk stratify PE, not the degree of thrombus burden or locale of thrombus.Enoxaparin is the preferred anticoagulant to initiate at time of PE diagnosis if comorbidities allow.Optimal treatment of intermediate risk PE remains uncertain as there is little data about long-term outcomes. Aggressive treatment should be used judiciously and chosen on a case-by-case basis.PE response teams (PERT) allow for multidisciplinary expert opinion in the face of scarce evidence to determine what is felt to be the best management strategy. Notes 1. What is a PERT team and why is it helpful? We have several tools and approaches for the management of PE. There are also many subspecialities involved in the care of patients with PE, including vascular medicine, intervention cardiology, hematology, pulmonology, cardiac surgery, radiology, emergency department, intensive care, and more. As such, the best treatment plan for a given patient with PE can be challenging, especially if the services involved in treatment of the PE function in silos.PERT, or PE Response Team, was built to address this concern. It is a multidisciplinary team that originated at MGH whose goal is to coordinate care for high-risk PE patients and advance PE-related care in the institution.PERT allows for multidisciplinary expert opinion in the face of scarce evidence to determine what is felt to be the best management strategy. 2. How do we risk stratify patients with PE? Risk stratification is largely dependent on the hemodynamic significance caused by the PE. In addition to vital sign derangement, patients with PE should also be evaluated for evidence of cardiac strain due to PE by checking for evidence of RV dilatation on CT or TTE and for elevation of cardiac biomarkers. The combination of this information is used to risk stratify patients. Additionally, risk stratification tools, such as the PESI and sPESI scores, are used to guide risk stratification.Based on the ESC 2019 guidelines, PEs are stratified into high risk, intermediate-high risk, intermediate-low risk, or low risk.High risk: evidence of hemodynamic instability as defined by hypotension or shock.Intermediate-high risk: evidence of both RV dysfunction on imaging AND elevated cardiac biomarkers in the absence of HD instabilityIntermediate-low risk: evidence of either RV dysfunction on imaging OR elevated cardiac biomarkers in the absence of HD instabilityLow risk: no evidence of cardiac dysfunction on imaging or labs and no evidence of HD instability.Risk stratification is important as it helps guide medical management of patients. Important factors that have not been associated with PE severity include degree of thrombus burden and location of clot. 3. What do we know about optimal management of patients with intermediate risk PE? Unfortunately, data is fairly limited with regards to the optimal management strategy for patients with intermediate risk PE, namely whether anticoagulation alone is sufficient versus if a patient would benefit from more advanced therapies. All patients should be started on anticoagulation, preferably SQ enoxaparin if comorbidities allow, as soon as possible (if there are no contraindications to anticoagulation). However, choosing which patients would benefit from more advanced therapies remains limited.Thrombolysis has been associated with lower all-cause mortality in patients with intermediate-risk PE when compared to anticoagulation alone. However, not surprisingly, thrombolysis was also associated with more major bleeding, including intracranial hemorrhage. In the ULTIMA trial, catheter directed thrombolysis was shown to improve RV dysfunction more quickly compared to anticoagulation at 24 hours. However, at 90 days, there was no difference in degree of RV dysfunction between the two groups.Percutaneous thrombectomy devices have been shown to be safe and effective at reducing RV size. However, there are no head-to-head comparisons of these modalities versus anticoagulation or thrombolysis and data is limited regarding the long-term efficacy.Choosing the correct patient to proceed with advanced therapies remains challenging and the decision is often made on a case-by-case basis. There are ongoing randomized control trials that will hopefully assist in guiding this decision making. 4. What about management for those with high-risk PE? High risk PEs mandate aggressive and rapid treatment.Thrombolysis has been shown to have a mortality benefit compared to anticoagulation. Catheter directed thrombolysis can be considered in high-risk PE; however, rapid implementation needs to be available.VA-ECMO has also been demonstrated to reduce mortality in these patients. 5. What additional treatment options are available for patients with PE who are not improving on anticoagulation and have a contraindication to thrombolytic therapy? There are several contraindications to thrombolytic therapy, including recent surgery, CVA, or bleeding. Percutaneous and surgical thrombectomy should be considered in these patients.Surgical thrombectomy is effective but does require significant anticoagulation during the surgery while the patient is on cardiac bypass. For this reason, patients that have a contraindication to thrombolysis might not be able to tolerate the high levels of anticoagulation required for the surgery and thus a surgical thrombectomy might not be a feasible option.There are several percutaneous thrombectomy devices on the market currently which have been shown to be safe and effective at reducing the RV size in the acute period. Because these devices do not require thrombolytic agents, the risk of bleeding is lower and there is less ICU utilization. However, there have not been head-to-head comparisons between these devices and other treatment modalities. References Konstantinides SV, Meyer G, Becattini C, et al. 2019 ESC Guidelines for the diagnosis and management of acute pulmonary embolism developed in collaboration with the European Respiratory Society (ERS). Eur Heart J. 2020;41(4):543-603. doi:10.1093/eurheartj/ehz405Robertson L, Jones LE. Fixed dose subcutaneous low molecular weight heparins versus adjusted dose unfractionated heparin for the initial treatment of venous thromboembolism. Cochrane Database Syst Rev. 2017;2:CD001100. doi:10.1002/14651858.CD001100.pub4Meyer G, Vicaut E, Danays T, et al. Fibrinolysis for patients with intermediate-risk pulmonary embolism. N Engl J Med. 2014;370(15):1402-1411. doi:10.1056/NEJMoa1302097Chatterjee S, Chakraborty A, Weinberg I, et al. Thrombolysis for pulmonary embolism and risk of all-cause mortality, major bleeding, and intracranial hemorrhage: a meta-analysis. JAMA. 2014;311(23):2414-2421. doi:10.1001/jama.

Jul 31, 2022

CardioNerds (Daniel Ambinder) and ACHD series co-chair Dr. Dan Clark discuss advanced heart failure therapies including mechanical circulatory support (MCS) and heart transplantation (HT) in patients with adult congenital heart disease (ACHD) with Dr. Rafael Alonso-Gonzalez, cardiologist and director of Adult Congenital Heart Disease program at the University of Toronto and ACHD fellow Dr. Andy Pistner (University of Washington). They cover epidemiology of heart failure in ACHD, outcomes after HT, unique challenges of HT in this population, impact of allocation policies on access to transplantation, and regionalization of advanced heart failure care. They also discuss a practical approach to advanced heart failure therapy evaluation in ACHD. Audio editing by CardioNerds Academy Intern, student doctor Adriana Mares. The CardioNerds Adult Congenital Heart Disease (ACHD) series provides a comprehensive curriculum to dive deep into the labyrinthine world of congenital heart disease with the aim of empowering every CardioNerd to help improve the lives of people living with congenital heart disease. This series is multi-institutional collaborative project made possible by contributions of stellar fellow leads and expert faculty from several programs, led by series co-chairs, Dr. Josh Saef, Dr. Agnes Koczo, and Dr. Dan Clark. The CardioNerds Adult Congenital Heart Disease Series is developed in collaboration with the Adult Congenital Heart Association, The CHiP Network, and Heart University. See more Disclosures: None Pearls • Notes • References • Guest Profiles • Production Team CardioNerds Adult Congenital Heart Disease PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls - Advanced Heart Failure Therapies (MCS/HT) Among ACHD Patients Heart failure is a major comorbidity and the leading cause of death in adults with congenital heart disease.Identification of advanced heart failure in ACHD is challenging. ACHD patients do not always self-identify exercise limitations or exertional dyspnea. Cardiopulmonary exercise testing is a useful tool in evaluating these patients.Patients with ACHD awaiting heart transplantation are less likely than non-ACHD patients to receive a heart transplant, and ACHD patients have an increased risk of death or delisting while awaiting heart transplantation.Evaluation of transplant candidacy and potential need for multi-organ transplantation in complex congenital heart disease (i.e., Fontan palliation) requires a multidisciplinary approach.Regionalization of care improves outcomes for ACHD patients with advanced heart failure. High volume transplant centers have better early survival for ACHD patients after heart transplant, and the highest volume ACHD transplant centers in each UNOS region have better early survival. Show notes - Advanced Heart Failure Therapies (MCS/HT) Among ACHD Patients 1. How many ACHD patients have heart failure? Patients with ACHD are a large and heterogeneous group. The signs and symptoms of heart failure vary widely depending on the underlying congenital heart disease. Patients with D-transposition of the great arteries repaired with an arterial switch operation have low rates of heart failure (~3%)1 compared to those patients Fontan palliation for single ventricle physiology (40%)2. Heart failure is the leading cause of death in patients with ACHD3,4. 2. How many patients with ACHD end up receiving a heart transplant or mechanical circulatory support? Heart transplantation for congenital heart disease in adults has been increasing in frequency since the late 1980s. Between 2010 and 2012, this accounted for 4% of all adult heart transplants in the United States5. This represents a small fraction compared to the number of adults who die due to complications of heart failure related to congenital heart disease. In a recent study of the INTERMACs registry, 126 patients with ACHD from a total of 16,000 patients over a 10-year period underwent placement of durable mechanical support devices (ventricular assist device)6. 3. Why are these numbers low relative to the number of ACHD patients with heart failure? Identification of those patients with ACHD who are at risk for adverse outcomes related to heart failure is challenging. The symptoms of heart failure reported in these patients is often different from what is described in patients with acquired heart failure. Similarly, having grown up with reduced aerobic capacity, many of these patients do not self-identify exercise limitations or exertional dyspnea7. The organ allocation policies that are used to prioritize patients for transplant also contribute to this situation. Patients with ACHD on the heart transplant wait-list are less likely than their non-ACHD counterparts to receive a transplant. This difference persists regardless of initial urgency listing status8. Secondly, patients with ACHD are more likely to die or be delisted (presumably due to clinical deterioration) while awaiting heart transplantation9. The US heart allocation policies have recently been updated, which may improve access to heart transplantation in this population. Other barriers to heart transplantation in patients with ACHD include allosensitization (development of antibodies against potential donor antigens), donor-recipient size matching, psychosocial barriers, and anatomic or other surgical challenges. Lastly, there are few providers with training in both advanced heart failure and adult congenital heart disease to integrate the evaluations necessary to identify suitable candidates for transplantation. 4. How do patients with ACHD do after heart transplantation? Patients with ACHD have a worse early mortality after heart transplant (up to 1 year) compared to those patients without ACHD10. However, early survival after heart transplantation in ACHD has been improving over the past 20 years11. Additionally, those patients with ACHD who survive past the first year after heart transplantation have improved survival compared to patients without congenital heart disease. More recently, we have found that that patients with ACHD undergoing heart transplant at high-volume centers (>38 transplants per year) have improved early survival compared to low-volume centers (<14 transplants per year)12. Overall survival is also improved when heart transplantation is performed at the highest volume ACHD transplant center in the UNOS region when compared to all the other transplant centers13. This idea of regionalization of care holds promise for transplant outcomes in this population. References - Advanced Heart Failure Therapies (MCS/HT) Among ACHD Patients Khairy P, Clair M, Fernandes SM, et al. Cardiovascular outcomes after the arterial switch operation for D-transposition of the great arteries. Circulation. Jan 22 2013;127(3):331-9. doi:10.1161/CIRCULATIONAHA.112.135046 Piran S, Veldtman G, Siu S, Webb GD, Liu PP. Heart failure and ventricular dysfunction in patients with single or systemic right ventricles. Circulation. Mar 12 2002;105(10):1189-94. doi:10.1161/hc1002.105182 Verheugt CL, Uiterwaal CS, van der Velde ET, et al. Mortality in adult congenital heart disease. Eur Heart J. May 2010;31(10):1220-9. doi:10.1093/eurheartj/ehq032 Oechslin EN, Harrison DA, Connelly MS, Webb GD, Siu SC. Mode of death in adults with congenital heart disease. The American Journal of Cardiology. 2000;86(10):1111-1116. doi:10.1016/s0002-9149(00)01169-3 Maxwell BG, Wong JK, Sheikh AY, Lee PH, Lobato RL. Heart transplantation with or without prior mechanical circulatory support in adults with congenital heart disease. Eur J Cardiothorac Surg. May 2014;45(5):842-6. doi:10.1093/ejcts/ezt498 Cedars A, Vanderpluym C, Koehl D, Cantor R, Kutty S, Kirklin JK. An Interagency Registry for Mechanically Assisted Circulatory Support (INTERMACS) analysis of hospitalization, functional status, and mortality after mechanical circulatory support in adults with congenital heart disease. J Heart Lung Transplant. May 2018;37(5):619-630. doi:10.1016/j.healun.2017.11.010 Gratz A, Hess J, Hager A. Self-estimated physical functioning poorly predicts actual exercise capacity in adolescents and adults with congenital heart disease. Eur Heart J. Feb 2009;30(4):497-504. doi:10.1093/eurheartj/ehn531 Everitt MD, Donaldson AE, Stehlik J, et al. Would access to device therapies improve transplant outcomes for adults with congenital heart disease? Analysis of the United Network for Organ Sharing (UNOS). J Heart Lung Transplant. Apr 2011;30(4):395-401. doi:10.1016/j.healun.2010.09.008 Alshawabkeh LI, Hu N, Carter KD, et al. Wait-List Outcomes for Adults With Congenital Heart Disease Listed for Heart Transplantation in the U.S. J Am Coll Cardiol. Aug 30 2016;68(9):908-17. doi:10.1016/j.jacc.2016.05.082 Menachem JN, Schlendorf KH, Mazurek JA, et al. Advanced Heart Failure in Adults With Congenital Heart Disease. JACC Heart Fail. Feb 2020;8(2):87-99. doi:10.1016/j.jchf.2019.08.012 Riggs KW, Zafar F, Radzi Y, Yu PJ, Bryant R, 3rd, Morales DLS. Adult Congenital Heart Disease: Current Early Expectations After Cardiac Transplantation. Ann Thorac Surg. Feb 2020;109(2):480-486. doi:10.1016/j.athoracsur.2019.06.067 Menachem JN, Lindenfeld J, Schlendorf K, et al. Center volume and post-transplant survival among adults with congenital heart disease. J Heart Lung Transplant. Nov 2018;37(11):1351-1360. doi:10.1016/j.healun.2018.07.007 Nguyen VP, Dolgner SJ, Dardas TF, Verrier ED, McMullan DM, Krieger EV. Improved Outcomes of Heart Transplantation in Adults With Congenital Heart Disease Receiving Regionalized Care. J Am Coll Cardiol. Dec 10 2019;74(23):2908-2918. doi:10.1016/j.jacc.2019.09.062 Meet Our Collaborators!

Jul 26, 2022

CardioNerds (Amit Goyal), Dr. Colin Blumenthal (CardioNerds Academy House Faculty Leader and FIT at the University of Pennsylvania), and Dr. Anjali Wagle (CardioNerds Ambassador and FIT at Johns Hopkins University), discuss the baseline assessment of stroke and bleeding risk in patients with atrial fibrillation (AF) with Dr. Elaine Hylek. Dr. Hylek is a professor of medicine at the Boston University School of Medicine and is the Director of the Thrombosis and Anticoagulation Service at Boston Medical Center. Stroke is a potentially devastating and preventable complication of AF. Understanding the balance between stroke and bleeding risk is crucial in determining who should be on anticoagulation. Join us to discuss this topic! In the next episode of the series, we will discuss situational risk assessment in the context of peri-cardioversion, peri-procedural status, triggered atrial fibrillation, and more. Audio editing by CardioNerds Academy Intern, Pace Wetstein. This CardioNerds Atrial Fibrillation series is a multi-institutional collaboration made possible by contributions of stellar fellow leads and expert faculty from several programs, led by series co-chairs, Dr. Kelly Arps and Dr. Colin Blumenthal. This series is supported by an educational grant from the Bristol Myers Squibb and Pfizer Alliance. All CardioNerds content is planned, produced, and reviewed solely by CardioNerds. We have collaborated with VCU Health to provide CME. Claim free CME here! Disclosures: Dr. Hylek discloses grant and research support from Medtronic and Janssen, and honoraria and/or consulting fees from Boehringer Ingelheim, and Bayer. CardioNerds Atrial Fibrillation PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls and Quotes - Atrial Fibrillation: Assessment of Stroke & Bleeding Risk The CHA2DS2-VASc should be used to determine stroke risk in all patients. It was updated from the CHADS2 score to better separate patients into high and low risk and a score of 0 has a very low risk of a stroke. Understanding a given model’s derivation is key to application for any risk model. Understanding who was and was not included when a risk score was derived helps determine how to clinically use it. For example, mechanical valves, hypertrophic cardiomyopathy, cardiac amyloidosis, and moderate to severe MS were all excluded or poorly represented and should receive AC in AF regardless of CV. The HAS-BLED score should be used to identify modifiable risk factors for bleeding and address them. It is less useful to determine when we should stop AC. Factors that go into the score are dynamic and the intention was to alert the provider of potentially modifiable factors that could be addressed to lower bleeding risk (such as better BP control). Fear the clot. Patients should be on AC unless there is a serious contraindication as embolic strokes can be devastating with a high mortality (~24% mortality at 30 days) “What am I saying by not writing the prescription... I am saying that it’s OK to have an ischemic stroke.” Survey data shows that patients are willing to experience 3.5 GI bleeds on average before 1 stroke, so favoring AC is often a patient centered approach Notes - Atrial Fibrillation: Assessment of Stroke & Bleeding Risk Notes drafted by Dr. Anjali Wagle 1. Why do strokes happen in atrial fibrillation? Why is reducing stroke risk so important? Atrial fibrillation is associated with a significantly increased risk of stroke. The mortality of strokes related to AF have been estimated to be around 25% at 30 days in early studies which included either persistent or permanent AF, though of note, these studied were biased towards larger strokes since the diagnosis was based on physical exam and not high resolution imaging. AF promotes thrombogenesis through Virchow’s triad which includes: Abnormal blood flow Endothelial damage Hypercoagulability In atrial fibrillation, patients usually have a dilated left atrium and decreased blood flow through the atrial appendage which contribute to thrombogenesis. Multiple risk scores have been derived (i.e., CHA2DS2VASc) for estimation of stroke risk in patient with AF to identify whom to treat with anticoagulation to reduce the stroke risk. 2. How were CHADS2 and CHA2DS2VASc (CV) created and validated? The CHADS2 score was derived in 2001 by Gage et al from data including hospitalized patients with nonrheumatic AF who were not prescribed warfarin at hospitalized discharge. The CHADS2 score assigns one point to congestive heart failure, hypertension, age ≥ 75 years, and diabetes mellitus and two points to a previous history of stroke or transient ischemic attack (TIA) for a total of 6 points. Stroke rate per 100 patient-years rose by a factor of 1.5 for each 1-point increase in the CHADS2 score. However, it was found that there were several limitations associated with the CHADS2 score including that more than half of the patients were classified as moderate risk, making it unclear if antiplatelet or anticoagulation should be used in this population. Additionally, there were other “minor” risk factors (female sex, CAD, age 65-74) that were not included in the score. In 2010, Lip et al proposed the CHA2DS2VASc score that included these three additional factors: female gender, vascular events, and age 65-74. These additions to the original CHADS2 score allowed the CHA2DS2VASc score to reclassify patients in the moderate risk group into either the high or low risk groups (CV 2), making the decision of when to start anticoagulation easier. Some weaknesses of the CV score include that the individual factors are binary. For example, one point for diabetes does not discriminate risk based on if the patient’s A1c is 14 vs. 7. Similarly, the score is static and assumes the risk from each risk factor doesn’t change over time even though the endothelial dysfunction caused by a specific disease state isn’t fixed. Additionally, the C-statistic for the CV score is only 0.6 with newer scores that are more accurate including such as GARFIELD-AF (but these newer scores are less user friendly). That being said, the score still does a very good job of differentiating between high and low risk patients, which is the most important clinical question when deciding if someone needs anticoagulation. 3. Which populations were not studied in the validation of the CV score? Many of these studies have woefully low enrollment of racially diverse populations. Additionally, patients with amyloidosis, moderate-severe MS, and HOCM have a baseline higher risk of stroke were excluded from these studies. Patients with bioprosthetic valves were also excluded from the original derivation though there is now limited data showing use of the CV is reasonable. 4. How does AF burden affect stroke risk? Is there a temporal association between AF and stroke? Early trials did not find a temporal association between AF and stroke, though these trials often used physical exam definitions for stroke and current technology like implantable loop recorders (ILRs) didn’t exist to monitor 24/7. More modern studies like the TREND and KP-RHYTHM trials showed that stroke risk is related to AF burden. Longer episodes of AF seem to clearly be associated with stroke, but shorter episodes of AF aren’t as temporally related to stroke. In the LOOP trial use of ILRs to detect episodes of AF longer than 6 minutes led to a 3-fold increase in AF detection and initiation of AF, but did not reduce the number of strokes. This could indicate that there is some amount of AF that doesn’t require AC or that short runs of AF are associated with atrial myopathy that could be causing the strokes. It remains unclear what is the “chicken and egg” in this scenario. 5. How can we assess bleeding risk for patients with atrial fibrillation? How can we use these scores in our clinical practice? Developed and published in 2010 by Pisters et al., the HAS-BLED (hypertension, abnormal renal/liver function, stroke, bleeding history or predisposition, labile INR, elderly [age >65], medication predisposing to bleeding, excessive alcohol use) score aimed to create an easy to calculate and clinically meaningful score to estimate bleeding risk. It was validated using 3,978 patients from the Euro Heart Survey on AF and had good predictive accuracy (C-statistic 0.72). Of note, the score uses the less severe ISTH definition for a major hemorrhage, which doesn’t require as severe bleeding as the TIMI major bleeding definition. Many of the factors that go into the score are dynamic (for example HTN is SBP > 160 and not a history of HTN). The intention was to alert the provider of potentially modifiable factors that could be addressed to lower bleeding risk (such as better BP control). This would reduce the patients HAS-BLED score and therefore their bleeding risk. There is no absolute cutoff where anticoagulation in AF would be considered prohibitive. 6. What is the approach for patients with borderline stroke risk with a CV of 1 in men or 2 in women? Patients with a CV of 1 have between a 0.6% and a 0.9% risk of stroke/TIA/systemic embolism in a given year. That means even with a CV of 1 they have close to a 1/100 risk of an event in a given year. Given the high mortality and morbidity with embolic strokes and the lower incidence of major bleeding with modern DOACs, should have shared decision-making conversation with patients about starting AC at this risk level. One can consider other risk factors not in CV like LA function, appendage morphology, AF burden etc to help as tie breakers. References - Atrial Fibrillation: Assessment of Stroke & Bleeding Risk Pisters R, Lane DA, Nieuwlaat R, de Vos CB, Crijns HJ,

Jul 17, 2022

With the advent and rapid evolution of contemporary percutaneous coronary intervention (PCI), the early invasive management of acute myocardial infarction (AMI) has become a mainstay in therapy with significant impact on patient outcomes. However, despite modern advances in technology and system-based practices, AMI presenting with cardiogenic shock (CS) continues to portend a high risk of morbidity and mortality. Few randomized controlled clinical trials are available to guide decision-making in this uniquely challenging patient population. Understanding the pathophysiologic mechanism by which injury occurs and propagates the shock cycle can be instrumental in selecting an appropriate strategy for revascularization and left ventricular unloading. In this episode we are joined by Dr. Venu Menon, The Mehdi Razavi Endowed Chair and Professor of Medicine at the Cleveland Clinic Lerner College of Medicine, section head of clinical cardiology, fellowship program director, and director of the Cardiac intensive care unit at the Cleveland Clinic. Dr. Menon shares his wealth of knowledge and experience to help us review the contemporary data available for AMI CS management in a case-based discussion. We are also joined by Dr. Priya Kothapalli, star chief fellow and future interventionalist from University of Texas at Austin, series co-chair Dr. Yoav Karpenshif, and CardioNerds Co-founders Amit Goyal and Daniel Ambinder. Audio editing by CardioNerds Academy Intern, Dr. Christian Faaborg-Andersen. The CardioNerds Cardiac Critical Care Series is a multi-institutional collaboration made possible by contributions of stellar fellow leads and expert faculty from several programs, led by series co-chairs, Dr. Mark Belkin, Dr. Eunice Dugan, Dr. Karan Desai, and Dr. Yoav Karpenshif. Pearls • Notes • References • Guest Profiles • Production Team CardioNerds Cardiac Critical Care PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls and Quotes - Approach to Acute Myocardial Infarction Cardiogenic Shock with Dr. Venu Menon The H&P does matter! Age, location of infarction, heart rate, systolic blood pressure, and heart failure symptoms all carry weight in determining prognosis and risk of mortality.Define functional status, comorbid conditions, and life expectancy to help guide clinical decision-making. Do a quick bedside echocardiogram if possible to elucidate the predominant mechanism driving CS and rule out mechanical complications.Act with urgency! Get to the catheterization lab to characterize coronary anatomy and revascularize the culprit vessel as soon as possible.Minimize/avoid the use of vasopressors; if needed, wean as quickly as possible to avoid worsening myocardial ischemia. Consider mechanical circulatory support early!Despite dramatic advances in AMI management, data is limited in AMI CS management. Ask the important questions, get involved in the scientific inquiry as a trainee! Show notes - Approach to Acute Myocardial Infarction Cardiogenic Shock with Dr. Venu Menon 1. Why is it important to recognize AMI complicated by CS? AMI CS occurs in 7-10% of patients presenting with AMI and has a higher prevalence among elderly patients.The SHOCK trial (1999) showed significant survival benefit at 6 months with early revascularization with balloon angioplasty compared to medical therapy alone in AMI CS.Registry data suggests that early revascularization is beneficial in AMI CS even in elderly patients. Decision-making should be guided using a holistic view of the patient’s overall biology.Despite advances in revascularization techniques and availability of mechanical support, AMI CS portends a 40-45% risk of 30-day mortality in the modern era.Significant variation in management strategy exists between centers and data to guide decision-making is limited.The Society for Cardiovascular Angiography and Intervention (SCAI) classification system of shock stage may be helpful in characterizing patient risk and guiding clinical decision-making. 2. Which patients with AMI CS should undergo invasive monitoring and revascularization? What should be the timing of any intervention? In viable patients presenting with AMI CS, the primary goal should be to get to the catheterization laboratory to characterize the anatomy and revascularize the culprit vessel as soon as possible.Patient history, physical exam, laboratory exam, and echocardiography, if available, are critical pieces of information that should be obtained without delaying catheterization laboratory transfer.Patients presenting in SCAI shock stages C-E may require stabilization pre-procedure while minimizing delays to revascularization.Anticipating potential sequelae (such as acute pulmonary edema with respiratory failure requiring intubation) is crucial to minimizing delays.Maintain adequate perfusion pre-procedure (goal mean arterial blood pressure of >65mmHg). Minimize use and avoid escalation of vasopressor or inotropic therapy, as these agents worsen myocardial ischemia.The prevalence of multivessel disease, left main or proximal left anterior descending artery disease in AMI CS is high. Revascularization with restoration of TIMI 3 flow as soon as possible should be the primary goal, regardless of strategy. 3. When should mechanical circulatory support (MCS) be used in AMI CS? Immediate MCS may be beneficial in patients with persistent hemodynamic or electrical instability or patients at high risk for developing instability. MCS should be placed early and maintained until the shock cycle is reversed.If the primary mechanism for CS is left ventricular failure, an intra-aortic balloon pump (IABP) or transvalvular axial flow pump (Impella) may be considered. Additional strategies include venoarterial extracorporeal membrane oxygenation with left ventricular venting strategy or TandemHeart percutaneous assist device.There is limited data regarding the role of MCS in AMI; this is an area of active clinical investigation. Mechanistically, MCS provides the obvious benefits of supporting systemic perfusion while reducing cardiac workload; risks include bleeding, thrombosis, hemolysis, limb ischemia, and other vascular complications.MCS should be weaned slowly using multiple clinical and hemodynamic parameters, including Swan Ganz catheter data.If unable to wean MCS due to insufficient myocardial recovery despite support over a prolonged period in the setting of adequate revascularization, additional options such as durable MCS, heart transplantation, or palliative care should be considered. 4. What is the current evidence base for culprit-only vs. complete revascularization in AMI CS? The CULPRIT-SHOCK trial showed an increased 30-day and 1-year risk of a composite of all-cause mortality and need for renal replacement therapy in patients that underwent culprit and immediate non-culprit vessel revascularization in AMI CS.While there is no definitive data to support complete revascularization in AMI CS, this strategy may be considered in patients with multiple possible culprit lesions or subtotal non-culprit lesions with reduced TIMI grade flow corresponding with wall motion abnormality and normal wall thickness suggestive of viable myocardium. References - Approach to Acute Myocardial Infarction Cardiogenic Shock with Dr. Venu Menon Tehrani BN, Truesdell AG, Psotka MA, et al. A Standardized and Comprehensive Approach to the Management of Cardiogenic Shock. JACC Hear Fail. 2020;8(11):879-891. doi:10.1016/j.jchf.2020.09.005Kapur NK, Davila CD. Timing, timing, timing: the emerging concept of the ‘door to support’ time for cardiogenic shock. Eur Heart J. 2017;38(47):3532-3534. doi:10.1093/eurheartj/ehx406Hochman JS, Sleeper LA, Webb JG, et al. Early Revascularization in Acute Myocardial Infarction Complicated by Cardiogenic Shock. N Engl J Med. 1999;341(9):625-634. doi:10.1056/NEJM199908263410901Ibanez B, Halvorsen S, Roffi M, et al. Integrating the results of the CULPRIT-SHOCK trial in the 2017 ESC ST-elevation myocardial infarction guidelines: viewpoint of the task force. Eur Heart J. 2018;39(48):4239-4242. doi:10.1093/eurheartj/ehy294Shah AH, Puri R, Kalra A. Management of cardiogenic shock complicating acute myocardial infarction: A review. Clin Cardiol. 2019;42(4):484-493. doi:10.1002/clc.23168Basir MB, Kapur NK, Patel K, et al. Improved Outcomes Associated with the use of Shock Protocols: Updates from the National Cardiogenic Shock Initiative. Catheter Cardiovasc Interv. 2019;93(7):ccd.28307. doi:10.1002/ccd.28307Doll JA, Ohman EM, Patel MR, et al. A team-based approach to patients in cardiogenic shock. Catheter Cardiovasc Interv. 2016;88(3):424-433. doi:10.1002/ccd.26297Thiele H, Ohman EM, de Waha-Thiele S, Zeymer U, Desch S. Management of cardiogenic shock complicating myocardial infarction: an update 2019. Eur Heart J. 2019;40(32):2671-2683. doi:10.1093/eurheartj/ehz363Thiele H, Akin I, Sandri M, et al. PCI Strategies in Patients with Acute Myocardial Infarction and Cardiogenic Shock. N Engl J Med. 2017;377(25):2419-2432. http://www.nejm.org/doi/10.1056/NEJMoa1710261. Accessed April 10, 2021.Van Diepen S, Katz JN, Albert NM, et al. Contemporary Management of Cardiogenic Shock: A Scientific Statement from the American Heart Association. Circulation. 2017;136(16):e232-e268. doi:10.1161/CIR.0000000000000525Henry, Timothy D., et al. “Invasive Management of Acute Myocardial Infarction Complicated by Cardiogenic Shock: A Scientific Statement from the American Heart Association.” Circulation, vol. 143, no. 15, 2021, doi: 10.1161/cir.0000000000000959. Guest Profiles Dr. Venu Menon Dr. Venu Menon earned his medical degree from Jawaharlal Institute of Postgraduate Medical Education and Research in Pondicherry, India.

Jul 14, 2022

It’s another session of CardioNerds Rounds! In these rounds, Co-Chair, Dr. Karan Desai (previous FIT at the University of Maryland Medical Center, and now faculty at Johns Hopkins) joins Dr. Ryan Tedford (Professor of Medicine and Chief of Heart Failure and Medical Directory of Cardiac Transplantation at the Medical University of South Carolina in Charleston, SC) to discuss the nuances of managing pulmonary hypertension in the setting of left-sided heart disease. Dr. Tedford is an internationally-recognized clinical researcher, educator, clinician and mentor, with research focuses that include the hemodynamic assessment of the right ventricle and its interaction with the pulmonary circulation and left heart. This episode is supported with unrestricted funding from Zoll LifeVest. A special thank you to Mitzy Applegate and Ivan Chevere for their production skills that help make CardioNerds Rounds such an amazing success. All CardioNerds content is planned, produced, and reviewed solely by CardioNerds. Case details are altered to protect patient health information. CardioNerds Rounds is co-chaired by Dr. Karan Desai and Dr. Natalie Stokes. Speaker disclosures: None Cases discussed and Show Notes • References • Production Team CardioNerds Rounds PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Show notes - Challenging Cases - Nuances in Pulmonary Hypertension Management with Dr. Ryan Tedford Case #1 Synopsis: A woman in her late 30s presented to the hospital with 4 weeks of worsening dyspnea. Her history includes dilated non-ischemic cardiomyopathy diagnosed in the setting of a VT arrest around 10 years prior. Over the past 10 years she has been on guideline-directed medical therapy with symptoms that had been relatively controlled (characterized as NYHA Class II), but without objective improvement in her LV dimensions or ejection fraction (LVEF 15-20% by TTE and CMR and LVIDd at 6.8 cm). Over the past few months she had been noting decreased exercise tolerance, worsening orthopnea, and episodes of symptomatic hypotension at home. When she arrived to the hospital, she presented with BP 95/70 mmHg, increased respiratory effort, congestion and an overall profile consistent with SCAI Stage C-HF shock. In the case, we go through the hemodynamics at various points during her hospitalization and discuss options for management including medical therapy and mechanical support. The patient was eventually bridged to transplant with an Impella 5.5. Initial Hemodynamics Right Atrium (RA) Pressure Tracing: Right Ventricle (RV) Pressure Tracing: Pulmonary Artery (PA) Pressure Tracing: Pulmonary Capillary Wedge Pressure (PCWP) Tracing: Case 1 Rounding Pearls One of the first points that Dr. Tedford made was thinking about our classic frameworks of characterizing acute decompensated heart failure, specifically the “Stevenson” classification developed by Dr. Lynne Stevenson that phenotypes patients along two axes: congestion (wet or dry) and perfusion (warm or cold). Dr. Tedford cautioned that young patients may not fit into these classic boxes well, and that a normal lactate should not re-assure the clinician that perfusion is normal.In reviewing the waveforms, Dr. Tedford took a moment to note that besides just recording the absolute values of the pressures transduced in each chamber or vessel, it is critical to understand the morphology of the tracings themselves. For instance, with the RA pressure tracing above, there is no respiratory variation in the mean pressure. This is essentially a “resting Kussmaul’s sign,” which is typically indicative of significant RV dysfunction. Thus, even though our echocardiogram in this case did not necessarily show a significantly dilated RV with mildly reduced longitudinal function (TAPSE), hemodynamically the patient is demonstrating significant RV compromise.If we compare the RA pressure tracing to the PCWP, we see that there is respiratory variation in the PCWP tracing. We typically think of pronounced respiratory variation in the RA or PCWP tracing in the setting of obesity or lung disease, but loading conditions can also lead to significant respiratory variation.As was noted during the case discussion, irreversible pulmonary hypertension is considered an absolute contraindication to heart transplantation though there is variation on the absolute threshold above which transplantation is contraindicated. Generally, a pulmonary vascular resistance (PVR) of 3 Woods Units is considered a contraindication to isolated cardiac transplantation. Testing for reversibility of an elevated PVR with a vasodilator like nitroprusside is common in this patient population.In a study by Dr. Steven Hsu and colleagues, Pulmonary Artery Pulsatility Index (PAPi) was shown to be the hemodynamic factor that best correlated with intrinsic RV myocyte dysfunction in patients with advanced heart failure (using a cutoff of PAPi of 1.85). Dr. Tedford made note to remember that PAPi is highly influenced by RA pressure (the denominator in the ratio). Case #2 Synopsis: A woman in her late 40s presented to clinic for another opinion regarding her PH management. In regards to her history, in the 1990s she underwent a mechanical mitral valve replacement (MVR) for mixed mitral valve disease in the setting of rheumatic fever as well as a single vessel CABG (SVG to the RCA). In the early 2000s, she had developed severe and symptomatic tricuspid regurgitation (TR) and underwent redo sternotomy for TV repair (TVr). She had generally done well until the past year when she started developing dyspnea on light exertion, abdominal fullness, lower extremity edema and over the course of a year she had four hospitalizations for heart failure. Over her hospitalizations, she was also diagnosed with hemolytic anemia. Diagnostic work-up revealed pre and post-capillary PH. Dr. Tedford reviews the subsequent hemodynamic evaluation and provides insight on managing PH post valvular intervention. She was ultimately diagnosed with mitral paravalvular regurgitation treated with transcatheter PVL closure. Initial Hemodynamics RA Pressure Tracing RV Pressure Tracing PA Pressure Tracing PCW Pressure Tracing Left Ventricular (LV) Pressure Tracing PCW and LV Simultaneous Pressure Tracing Case 2 Rounding Pearls: The patient had been placed on sildenafil for persistent PH post-valve intervention. Dr. Tedford briefly mentioned the SIOVAC trial which was designed to evaluate treatment with sildenafil (40 mg TID) compared with placebo amongst patients with persistent PH (mean PA pressure ≥ 30 mmHg) 1 year after valvular replacement or repair (majority of whom were patients that had mitral valve intervention). In this study, sildenafil was associated with worse functional status, specifically heart failure or dyspnea compared to placebo (34% vs. 20%, p = 0.04).Dr. Tedford briefly touched upon the prognostic value of the diastolic pulmonary gradient (DPG, calculated as diastolic PA pressure subtracted by PCWP) in patients being considered for cardiac transplantation. We commonly use PVR and transpulmonary gradient (TPG) to characterize the degree of pre-capillary PH and suitability for transplantation. However, these markers are not ideal surrogates for pulmonary vascular remodeling and differentiating between fixed remodeling versus reversible changes. For instance, the TPG can be elevated not only as a result of pulmonary vascular remodeling but elevated LA pressures passively transmitted back to the pulmonary vasculature leading to elevations in the diastolic PA pressure.The DPG was thought to potentially define higher risk left heart failure patients with clinically significant pre-capillary PH. However, in Dr. Tedford’s 2014 analysis, the DPG did not delineate higher risk among patients with elevated TPG and PVR undergoing cardiac transplantation. There could be several explanations including that the cutoff for abnormal DPG is low (≥7) and thus small errors in measurement could have significant influence on what is characterized as abnormal. Furthermore, the diastolic PA pressure measurement is particularly prone to ringing artifact. References - Challenging Cases - Nuances in Pulmonary Hypertension Management with Dr. Ryan Tedford Aslam MI, Jani V, Lin BL, et al. Pulmonary artery pulsatility index predicts right ventricular myofilament dysfunction in advanced human heart failure. Eur J Heart Fail. 2021 Feb;23(2):339-341. doi: 10.1002/ejhf.2084. Epub 2021 Jan 5. PMID: 33347674; PMCID: PMC8574988.Bermejo J, Yotti R, García-Orta R, et al., on behalf of the Sildenafil for Improving Outcomes after VAlvular Correction (SIOVAC) investigators. Sildenafil for improving outcomes in patients with corrected valvular heart disease and persistent pulmonary hypertension: a multicenter, double-blind, randomized clinical trial.Mehra MR, Canter CE, Hannan MM, et al; International Society for Heart Lung Transplantation (ISHLT) Infectious Diseases, Pediatric and Heart Failure and Transplantation Councils. The 2016 International Society for Heart Lung Transplantation listing criteria for heart transplantation: A 10-year update. J Heart Lung Transplant. 2016 Jan;35(1):1-23. doi: 10.1016/j.healun.2015.10.023. PMID: 26776864.Tedford RJ, Beaty CA, Mathai SC et al. Prognostic value of the pre-transplant diastolic pulmonary artery pressure-to-pulmonary capillary wedge pressure gradient in cardiac transplant recipients with pulmonary hypertension. J Heart Lung Transplant. 2014 Mar;33(3):289-97. doi: 10.1016/j.healun.2013.11.008. Epub 2013 Nov 28. Erratum in: J Heart Lung Transplant. 2019 Feb;38(2):233. PMID: 24462554; PMCID: PMC3955214.Thibodeau JT, Drazner MH.

Jul 12, 2022

The following question refers to Section 6.2 of the 2021 ESC CV Prevention Guidelines. The question is asked by Dr. Christian Faaborg-Andersen, answered first by Houston Methodist medicine resident Dr. Najah Khan, and then by expert faculty Dr. Jaideep Patel. Dr. Patel recently graduated from Virginia Commonwealth University cardiology fellowship and is now a preventive cardiologist at the Johns Hopkins Hospital. The CardioNerds Decipher The Guidelines Series for the 2021 ESC CV Prevention Guidelines represents a collaboration with the ACC Prevention of CVD Section, the National Lipid Association, and Preventive Cardiovascular Nurses Association. Question #18 A 60-year-old Black woman with a history of hypertension and heart failure with reduced ejection fraction (EF 40%) presents to clinic for follow-up. She is currently doing well with NYHA class II symptoms. She is taking carvedilol 25 mg BID, sacubitril/valsartan 97/103 mg BID, and spironolactone 25 mg daily, all of which have been well tolerated. In clinic, her BP is 125/80 mmHg, and her HR is 55 bpm. Routine labs are within normal limits including Cr of 1.0, K of 4.0, and HbA1c of 6.0. What is the most appropriate next step in her management? A. No change in management B. Reduce beta blocker C. Add an SGLT2 inhibitor (dapagliflozin or empagliflozin) D. Add vericiguat E. Add hydralazine/isosorbide dinitrate Answer #18 The correct answer is C – Add an SGLT2 inhibitor (dapagliflozin or empagliflozin) For patients with symptomatic HFrEF, neurohormonal antagonists (ACEi, ARB, ARNI; BB; MRA) improve survival and reduce the risk of HF hospitalization. This patient is already on these agents. The addition of an SGLT2 inhibitor on top of neurohormonal blockade reduces the risk of CV death and worsening HF in patients with symptomatic HFrEF and is the next best step for this patient (Class I, LOE A). Vericiguat may be considered in patients with symptomatic HFrEF with HF worsening despite already being on maximally tolerated neurohormonal blockade (Class IIb, LOE B), but first-line therapies should be started first. Hydralazine/Isosorbide dinitrate should be considered in self-identified Black patients or people who have EF ≤ 35% or <45% with dilated LV with class III-IV symptoms despite maximally tolerated neurohormonal blockade (Class IIa, LOE B), but is not the next best step here. She is tolerating the beta blocker without adverse effects so there is no reason to decrease the dosage. Main Takeaway In patients with symptomatic HFrEF (EF ≤ 40%), SGLT2 inhibitors are considered first line therapy in addition to ACE-I/ARB/ARNI, BB, and MRAs to reduce the risk of HF hospitalization and death. Importantly this is irrespective of presence of diabetes. Guideline Location Section 6.2, page 3295-3296 Figure 13 page 3278; recommendation table page 3279. CardioNerds Decipher the Guidelines - 2021 ESC Prevention Series CardioNerds Episode Page CardioNerds Academy Cardionerds Healy Honor Roll CardioNerds Journal Club Subscribe to The Heartbeat Newsletter! Check out CardioNerds SWAG! Become a CardioNerds Patron!

Jul 7, 2022

The following question refers to Section 4.9 of the 2021 ESC CV Prevention Guidelines. The question is asked by Dr. Christian Faaborg-Andersen, answered first by UCSD fellow Dr. Patrick Azcarate, and then by expert faculty Dr. Melissa Tracy. Dr. Tracy is a preventive cardiologist, former Director of the Echocardiography Lab, Director of Cardiac Rehabilitation, and solid organ transplant cardiologist at Rush University. The CardioNerds Decipher The Guidelines Series for the 2021 ESC CV Prevention Guidelines represents a collaboration with the ACC Prevention of CVD Section, the National Lipid Association, and Preventive Cardiovascular Nurses Association. Question #17 A 74-year-old man with a history of hypertension, chronic kidney disease, and gastroesophageal reflux presents with chest pain and is found to have an NSTEMI due to an obstructive lesion in the proximal LAD. One drug-eluting stent is placed, and he is started on dual antiplatelet therapy with aspirin and clopidogrel. He is concerned about the risk of bleeding from his gastrointestinal tract. What would you recommend to reduce his risk of bleeding? A. Lansoprazole, a proton pump inhibitor B. Famotidine, a histamine-2 blocker C. Calcium carbonate, an antacid D. None, proton pump inhibitors are contraindicated. Answer #17 The correct answer is A. The ESC recommends that patients at high risk for GI bleeding who are receiving antiplatelet therapy take proton pump inhibitors (Class I, LOE A). High risk for bleeding includes patients who are age ≥65, history of peptic ulcer disease, Helicobacter pylori infection, dyspepsia or GERD symptoms, chronic renal failure, diabetes mellitus, and concomitant use of other antiplatelet agents, anticoagulants, nonsteroidal anti-inflammatory drugs, or steroids. Coadministration of proton pump inhibitors that specifically inhibit CYP2C19 (omeprazole or esomeprazole) may reduce the pharmacodynamic response to clopidogrel. Although this interaction has not been shown to affect the risk of ischemic events, coadministration of omeprazole or esomeprazole with clopidogrel is not recommended. Main Takeaway In patients with high gastrointestinal bleeding risk who are receiving antiplatelet therapy, proton pump inhibitors are recommended. Omeprazole and esomeprazole may reduce the efficacy of clopidogrel and should not be used concomitantly with clopidogrel. Guideline Location Section 4.9.3, Page 3291 Figure 13 page 3278; recommendation table page 3279. CardioNerds Decipher the Guidelines - 2021 ESC Prevention Series CardioNerds Episode Page CardioNerds Academy Cardionerds Healy Honor Roll CardioNerds Journal Club Subscribe to The Heartbeat Newsletter! Check out CardioNerds SWAG! Become a CardioNerds Patron!

Jul 5, 2022

The following question refers to Section 4.6 and Figure 13 of the 2021 ESC CV Prevention Guidelines. The question is asked by student doctor Shivani Reddy, answered first by NP Carol Patrick, and then by expert faculty Dr. Roger Blumenthal. Dr. Roger Blumenthal is professor of medicine at Johns Hopkins where he is Director of the Ciccarone Center for the Prevention of Cardiovascular Disease. He was instrumental in developing the 2018 ACC/AHA CV Prevention Guidelines. The CardioNerds Decipher The Guidelines Series for the 2021 ESC CV Prevention Guidelines represents a collaboration with the ACC Prevention of CVD Section, the National Lipid Association, and Preventive Cardiovascular Nurses Association. Question #16 True or False: For patients with established ASCVD, secondary prevention entails adding a PCSK9 inhibitor if goal LDL is not met on maximum tolerated doses of a statin and ezetimibe. Answer #16 The correct answer is True. The ultimate on-treatment LDL-C goal of <55 mg/dL (<1.4 mmol/L) and a reduction of at least ≥50% from baseline should be considered for primary prevention of persons <70 years of age at very high risk (Class IIa) and in those with established ASCVD (Class I). It is recommended that a high-intensity statin is prescribed up to the highest tolerated dose to reach these LDL-C goals (Class I). The combination of statin with ezetimibe brings a benefit that is in line with meta-analyses showing that LDL-C reduction has benefits independent of the approach used. The beneficial effect of ezetimibe is also supported by genetic studies. Together, these data support the position that ezetimibe should be considered as second-line therapy, either on top of statins when the therapeutic goal is not achieved (Class I), or when a statin cannot be prescribed (Class IIa). PCSK9 inhibitors (monoclonal antibodies to PCSK9) decrease LDL-C by up to 60%, either as monotherapy or in addition to the maximum tolerated dose of statin and/or other lipid-lowering therapies, such as ezetimibe. Their efficacy appears to be largely independent of background therapy. Among patients in whom statins cannot be prescribed, PCSK9 inhibition reduced LDL-C levels when administered in combination with ezetimibe. Both alirocumab and evolocumab effectively lower LDL-C levels in patients who are at high or very high CVD risk, including those with DM, with a large reduction in future ASCVD events. Therefore, for those who do not meet LDL-C goals with maximally tolerated doses of both a statin and ezetimibe, combination therapy including a PCSK9 inhibitor may be considered for primary prevention of patients at very high risk but without familial hypercholesterolemia (Class IIa) and is recommended for secondary prevention for those with established ASCVD (Class I). In addition, for very-high-risk FH patients (that is, with ASCVD or with another major risk factor) who do not achieve their goals on a maximum tolerated dose of a statin and ezetimibe, combination therapy including a PCSK9 inhibitor is recommended (Class I). Main Takeaway Statins, ezetimibe, and PCSK9 inhibitors should be used in a stepwise approach to achieve target lipid lowering goals in accordance with their risk profile. Guideline Location Page 3279, Sections 4.6.3.1.4, 4.6.3.1.5 Figure 13 page 3278; recommendation table page 3279. CardioNerds Decipher the Guidelines - 2021 ESC Prevention Series CardioNerds Episode Page CardioNerds Academy Cardionerds Healy Honor Roll CardioNerds Journal Club Subscribe to The Heartbeat Newsletter! Check out CardioNerds SWAG! Become a CardioNerds Patron!

Jul 5, 2022

The following question refers to Section 4.3 of the 2021 ESC CV Prevention Guidelines. The question is asked by CardioNerds Academy Intern Dr. Maryam Barkhordarian, answered first by pharmacy resident Dr. Anushka Tandon and then by expert faculty Dr. Kim Williams. Dr. Williams is Chief of the Division of Cardiology and is Professor of Medicine and Cardiology at Rush University Medical Center. He has served as President of ASNC, Chairman of the Board of the Association of Black Cardiologists (ABC, 2008-2010), and President of the American College of Cardiology (ACC, 2015-2016). The CardioNerds Decipher The Guidelines Series for the 2021 ESC CV Prevention Guidelines represents a collaboration with the ACC Prevention of CVD Section, the National Lipid Association, and Preventive Cardiovascular Nurses Association. Question #15 Your patient mentions that she drinks “several” cups of coffee during the day. She also describes having a soda daily with lunch and occasionally a glass of wine with dinner. Which of the following recommendations is appropriate? A. Coffee consumption is not harmful and may even be beneficial, regardless of the number of drinks per day. B. Drinking two glasses of wine/day is safe from a cardiovascular prevention standpoint. C. Soft drinks (and other sugar-sweetened beverages) must be discouraged. D. None of the above Listen to this podcast episode! Answer #15 The correct answer is C. Soft drinks (and other sugar-sweetened beverages) must be discouraged. Sugar-sweetened beverages have been associated with a higher risk of CAD and all-cause mortality. The ESC guidelines give a class I recommendation for restriction of free sugar consumption (in particular sugar-sweetened beverages) to a maximum of 10% of energy intake. This is a class IIa recommendation in the ACC/AHA guidelines. Choice A is incorrect because: the consumption of nine or more drinks a day of non-filtered coffee (such as boiled, Greek, and Turkish coffee and some espresso coffees) may be associated with an up to 25% increased risk of ASCVD mortality. Moderate coffee consumption (3-4 cups per day) is probably not harmful, and perhaps even moderately beneficial. Choice B is incorrect: It is a class I recommendation to restrict alcohol consumption to a maximum of 100 g per week. The standard drink in the US contains 14 g of alcohol, so 100 mg of alcohol translate to: o 84 ounces of beer (5% alcohol) o Or 56 – 63 ounces of malt liquor (75% alcohol) or o Or 35 ounces of wine (12% alcohol) or ONE 5 fl oz glass of wine/day. o Or 31.5 ounces of distilled spirits (40% alcohol). The ACC/AHA guidelines recommended limiting alcohol consumption only for the management of hypertension to: ≤2 drinks daily for men and: ≤1 drink daily for women. Main Takeaway The main takeaway: ASCVD risk reduction can be achieved by restricting sugar-sweetened beverages to a maximum of 10% of energy intake. Guideline Location Section 4.3.2, Page 3271 CardioNerds Decipher the Guidelines - 2021 ESC Prevention Series CardioNerds Episode Page CardioNerds Academy Cardionerds Healy Honor Roll CardioNerds Journal Club Subscribe to The Heartbeat Newsletter! Check out CardioNerds SWAG! Become a CardioNerds Patron!

Jul 1, 2022

The following question refers to Sections 3.3-3.4 of the 2021 ESC CV Prevention Guidelines. The question is asked by student Dr. Adriana Mares, answered first by early career preventive cardiologist Dr. Dipika Gopal, and then by expert faculty Dr. Allison Bailey. Dr. Bailey is a cardiologist at Centennial Heart. She is the editor-in-chief of the American College of Cardiology's Extended Learning (ACCEL) editorial board and was a member of the writing group for the 2018 American Lipid Guidelines. The CardioNerds Decipher The Guidelines Series for the 2021 ESC CV Prevention Guidelines represents a collaboration with the ACC Prevention of CVD Section, the National Lipid Association, and Preventive Cardiovascular Nurses Association. Question #14 Ms. Soya M. Alone is a 70-year-old woman of Bangladeshi ethnicity with a history of anxiety and depression. She currently lives at home by herself, does not have many friends and family that live nearby, and has had a tough year emotionally after the passing of her husband. She spends most of her time in bed with low daily physical activity and has experienced more weakness and exhaustion over the past year along with loss of muscle mass. Which of the following are potential risk modifiers in this patient when considering her risk for CVD?A. Bangladeshi ethnicity B. Psychosocial factorsC. Frailty D. History of anxiety and depressionE. All of the above Answer #14 The correct answer is E – All of the above.Traditional 10-year CVD risk scores do not perform adequately in all ethnicities. Therefore, multiplication of calculated risk by relative risk for specific ethnic subgroups should be considered (Class IIa, LOE B). Individuals from South Asia have higher CVD rates. The ESC guidelines recommend using a correction factor by multiplying the predicted risk by 1.3 for Indians and Bangladeshis, and 1.7 for Pakistanis. These correction factors are derived from data from QRISK3. In the UK, the QRISK calculator algorithm has been derived and validated in 2.3 million people to estimate CVD risk in different ethnic groups and unlike other calculators, it counts South Asian origins as an additional risk factor. The reasons for such differences remain inadequately studied, as do the risks associated with other ethnic backgrounds. Barriers to developing accurate risk prediction tools include the wide heterogeneity amongst the population.The 2019 ACC/AHA guidelines also list high-risk race/ethnicities such as South Asian ancestry as a risk-enhancing factor. However, there is no separate pooled cohort equation for different ethnicities, and consideration should be given that the pooled cohort equations will underestimate ASCVD risk in South Asians.Psychosocial stress including loneliness and critical life events are associated, in a dose-response pattern, with the development and progression of ASCVD, with relative risks between 1.2 and 2.0. Conversely, indicators of mental health, such as optimism and a strong sense of purpose, are associated with lower risk. While there is not a specific way proposed by the guidelines for psychosocial factors to improve risk classification, it is important to screen patients with ASCVD for psychological stress, and clinicians should attend to somatic and emotional causes of symptoms as well. The ESC guidelines give a Class IIa (LOE B) recommendation for assessment of stress symptoms and psychosocial stressors.This patient should also be formally screened for frailty, which is not the same as aging but includes factors such as slowness, weakness, low physical activity, exhaustion and shrinking, and makes her more vulnerable to the effect of stressors and is a risk factor for both high CV and non-CV morbidity and mortality. However, the ability of frailty measures to improve CVD risk prediction has not been formally assessed, so the guidelines do not recommend integrating it into formal CVD risk assessment. Frailty may however, influence treatment as it can help build an individualized care plan.Mental disorders such as anxiety and depression are associated with the development of CVD as well. Detrimental effects may be potentially caused by unhealthy lifestyle, increased exposure to socioeconomic stressors, and cardiometabolic side-effects of medications. The ESC guidelines give a Class 1 (LOE C) recommendation that mental disorders with either significant functional impairment or decreased use of healthcare systems be considered as influencing total CVD risk.Main TakeawayPsychosocial stress and frailty are associated with risk of ASCVD and should be assessed in patients when considering CVD risk. In addition, current risk scores may under-or over-estimate CVD risk in different ethnic minority groups.Guideline LocationSection 3.3.1, 3.3.2, 3.3.4, 3.4.10, page 3258 – 3259, 3265 – 3266 CardioNerds Decipher the Guidelines - 2021 ESC Prevention SeriesCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor RollCardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron!

Jun 30, 2022

The following question refers to Section 3.2 of the 2021 ESC CV Prevention Guidelines. The question is asked by student Dr. Hirsh Elhence, answered first by Mayo Clinic Fellow Dr. Teodora Donisan, and then by expert faculty Dr. Eugene Yang. Dr. Yang is professor of medicine of the University of Washington where he is medical director of the Eastside Specialty Center and the co-Director of the Cardiovascular Wellness and Prevention Program. Dr. Yang is former Governor of the ACC Washington Chapter and current chair of the ACC Prevention of CVD Section. The CardioNerds Decipher The Guidelines Series for the 2021 ESC CV Prevention Guidelines represents a collaboration with the ACC Prevention of CVD Section, the National Lipid Association, and Preventive Cardiovascular Nurses Association. Question #13 You are seeing a 45-year-old woman with a past medical history of hypertension, overweight status, hyperlipidemia, and active tobacco use disorder. Her BMI is 27 kg/m2, BP is 150/75, HbA1C is 5.8%, total cholesterol is 234 mg/dL, HDL is 59 mg/dL, and LDL is 155 mg/dL. She is from Romania, a country with very high CVD risk. Which of the following statements is CORRECT? A. LDL-C needs to be decreased by at least 50%, as small absolute LDL-C reductions would not provide clinical benefit B. Hypertension is not an important CVD risk factor in our patient, as she is young. C. Prediabetes is not a significant CV risk factor for our patient, as she is not yet diabetic. D. Smoking confers a higher CVD risk for women than for men. E. Her weight does not increase her CVD risk, as she is overweight rather than obese Answer #13 The correct answer is D – Smoking confers a higher CVD risk for women than for men. Prolonged smoking increases the CVD risk more in women than in men. Our patient is 45 years old. CVD risk in smokers < 50 years-old is 5x higher than in non-smokers. Of note, smoking is responsible for 50% of all avoidable deaths in smokers and a lifetime smoker will lose 10 years of life, on average. Secondhand smoke and smokeless tobacco can also increase the CVD risk. Option A is incorrect. The SCORE2 risk chart for populations at very high CVD risk places her at a 14% (very high) 10-year risk for myocardial infarction, stroke, or cardiovascular death. She would derive benefit even from incremental reductions in LDL-C values. The absolute benefit of lowering LDL-C depends on both the absolute risk of ASCVD and the absolute reduction in LDL-C, so even a small absolute reduction in LDL-C may be beneficial in high- or very-high-risk patients. Furthermore, the reduction in CVD risk is proportional to the decrease in LDL-C, irrespective of the medications used to achieve such change. This remains true even when lowering LDL-C values to < 55 mg/dl. Option B is incorrect. Hypertension is a major cause of CVD regardless of age, and the risk of death from either CAD or stroke increases linearly from BP levels as low as 90 mmHg systolic and 75 mmHg diastolic upwards. Particularly relevant for our patient, lifetime BP evolution differs in women compared to men, potentially resulting in an increased CVD risk at lower BP thresholds. Option C is incorrect. Type 1 DM, type 2 DM, and prediabetes are all independent risk factors for ASCVD. Of note, it would be important to address this risk factor with our patient, as women who develop type 2 diabetes have a particularly high risk for stroke. Option E is incorrect. All-cause mortality is lowest at a BMI on 20-25 kg/m2 in apparently healthy patients. Even overweight patients are at increased CVD risk. There is a linear relationship between BMI and mortality in non-smokers and a J-shaped relationship in ever-smokers. In patients with heart failure, a lower mortality risk has been observed with higher BMI – the “obesity paradox.” It would be important to evaluate the waist circumference in our patient, as both BMI and waist circumference are associated with ASCVD risk. Main Takeaway The main ASCVD risk factors are hyperlipidemia (elevated apolipoprotein-B-containing lipoproteins, of which LDL-C is most abundant), hypertension, cigarette smoking, diabetes, and adiposity. Identifying patients who will benefit most from ASCVD risk factor treatment is central to ASCVD prevention efforts. In general, the higher the absolute CVD risk, the higher the absolute benefit of risk factor treatment, and thus the lower the number needed to treat to prevent one CVD event during a period of time. Guideline Location Section 3.2.1., pages 3236, 3242, 3243. CardioNerds Decipher the Guidelines - 2021 ESC Prevention Series CardioNerds Episode Page CardioNerds Academy Cardionerds Healy Honor Roll CardioNerds Journal Club Subscribe to The Heartbeat Newsletter! Check out CardioNerds SWAG! Become a CardioNerds Patron!

Jun 27, 2022

CardioNerds (Dr. Kelly Arps, Dr. Colin Blumenthal, Dr. Dan Ambinder, and Dr. Teodora Donisan) discuss the screening, detection, and diagnosis of atrial fibrillation (AF) with Dr. Ben Freedman. AF is frequently undiagnosed and its first manifestation can be a debilitating stroke. European and American guidelines differ slightly with regards to guidelines for AF screening in asymptomatic individuals. There are multiple methods available to screen for AF; the setting and the clinical scenario can help guide the choice. Consumer-led screening has its own challenges, as it can detect AF in a younger population where we should prioritize aggressive management of risk factors and comorbidities. There is uncertainty regarding the minimum AF burden that increases thromboembolic risk, however a high CHAD2S2-VASc score remains the strongest predictor of stroke risk independent of AF burden. Perioperative AF associated with non-cardiac surgery has increased risk of future stroke and adverse cardiac outcomes and should likely be treated as a new diagnosis of chronic AF. This CardioNerds Atrial Fibrillation series is a multi-institutional collaboration made possible by contributions of stellar fellow leads and expert faculty from several programs, led by series co-chairs, Dr. Kelly Arps and Dr. Colin Blumenthal. This series is supported by an educational grant from the Bristol Myers Squibb and Pfizer Alliance. All CardioNerds content is planned, produced, and reviewed solely by CardioNerds. We have collaborated with VCU Health to provide CME. Claim free CME here! Disclosures: Dr. Ben Freedman disclosed that he has received grant or research support from Pfizer. Pearls • Notes • References • Guest Profiles • Production Team CardioNerds Atrial Fibrillation PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls and Quotes - Screening, Detection, and Diagnosis of Atrial Fibrillation “Stroke is a poor early sign of AF.” AF remains frequently undiagnosed and there remains uncertainty about the optimal target population and screening methodology. “We have to tailor AF screening to the purpose we’re using it for” If in a primary care setting, check the pulse. If the goal is to exclude high-risk AF – handheld ECG for heart rhythm snapshots are appropriate. If the goal is to identify or exclude AF with a high level of certainty, continuous monitors are necessary for greater sensitivity. Consumer-led screening is performed by (mostly young) individuals using commercial monitors and smart watches, facilitating earlier recognition of paroxysmal AF in this population. In these cases, we should prioritize aggressive management of risk factors and comorbidities to reduce the risk of progression to persistent AF. There is no specific cutoff for AF duration which has been identified to predict elevated stroke risk; AF is likely both a risk factor and a risk marker for stroke, suggesting an underlying atrial myopathy. Non-cardiac surgeries and procedures can be considered “AF stress tests.” If AF occurs in these settings, it is usually more clinically significant and has a higher risk of stroke and death than AF associated with cardiac surgeries. Notes - Screening, Detection, and Diagnosis of Atrial Fibrillation Notes drafted by Dr. Teodora Donisan and reviewed by Dr. Kelly Arps 1. Why is it important to screen for AF and who should be screened? AF is frequently undiagnosed and its first manifestation can be a debilitating stroke or death. Let’s go over a few numbers: 15% of people with AF are currently undiagnosed and 75% of those individuals would be eligible for anticoagulation.1 10-38% of individuals with ischemic strokes are found to have AF as a plausible cause, and the true proportion may be even higher, given difficulties in detecting intermittent AF.2 Current guideline recommendations: European guidelines: opportunistic screening for AF is recommended for individuals ≥65 years old.3 American guidelines: AF screening is recommended in patients with cryptogenic strokes and those with device-recorded atrial high-rate episodes.4 Opportunistic screening for AF can be done by checking the pulse or noticing the irregular heart rate on blood pressure monitors. When AF is found by opportunistic screening at a single time point, it is usually persistent AF. Continuous ambulatory heart rhythm monitoring can identify shorter episodes of paroxysmal AF, perhaps earlier in the AF disease course. In patients with unexplained stroke we have different ways to search for occult AF: In the hospital: all patients should have 72h of ECG monitoring. There is evidence that nurse-led ECG surveillance detects more paroxysmal AF earlier and more frequently than 24-hour Holter recordings.5 After discharge: if clinical suspicion for occult AF is high (e.g., cerebral imaging concerning for cardioembolic source, evidence of left atrial enlargement, elevated BNP), consider more prolonged monitoring via cutaneous patches, multiple Holter recordings, or implantable cardiac monitors. 2. What tools are currently available to screen for AF? There are multiple tools available for AF screening: pulse palpation, oscillometry, and ambulatory heart rhythm ECG monitoring with external or subcutaneous devices. Handheld ECG devices are very convenient options, as they can diagnose AF in 30 seconds directly, whereas other methods such as oscillometry would ultimately require ECG confirmation. If in the office for a quick screen: check the pulse; If you’re looking for high-burden AF: handheld one-time ECG; If you’re looking to identify or rule out AF with a high degree of certainty: continuous monitoring with transcutaneous patch or implantable monitor. 3. How should commercial monitor/smart watch data be incorporated into clinical practice? We need to be aware of the population who have access to and more often use these modern technologies; use is unequally distributed around the world and across the age span.6 These devices are most often used by people who are 35-40 years old, not the typical population for whom AF screening may be more impactful. If we do identify AF in these younger individuals, starting anticoagulation may not be indicated. It is important, however, to emphasize more aggressive management of risk factors and comorbidities (e.g., weight loss, diet, exercise, alcohol reduction, hypertension control, screening for and treating prediabetes and diabetes, screening for obstructive sleep apnea, and assessing thyroid function) to reduce the risk of AF progression. 4. How much atrial fibrillation is clinically relevant? There is uncertainty regarding the minimum AF burden that increases the thromboembolic risk above an individual’s baseline risk, with studies exploring durations of ≥ 5 minutes to ≥ 24 hours.7,8 Several studies show that there isn’t a clear temporal relationship between device-detected high-rate episodes and strokes either, with only a small number of patients experiencing arrhythmia in the month before a stroke.9 The CHA2DS2-VASc score is very important when discussing thromboembolic risk: if it is low, then the risk of stroke is low; if it is high, risk of stroke is higher, even if there is a low burden of AF. AF is likely both a risk factor and a risk marker for stroke, suggesting an underlying atrial myopathy. This would explain why a specific cutoff point for AF duration is not necessarily relevant to predict stroke risk. 5. How should clinicians approach peri-operative AF? Perioperative AF is associated with increased perioperative morbidity, higher stroke rates, more readmissions, and lower survival.10 The significance of AF is different depending on the type of surgery: With AF after cardiac surgery (which involves opening the pericardium and direct irritation of the atria), the incidence of perioperative AF is greater (20-30%). Roughly 25% of patients with AF after CABG experience asymptomatic recurrent AF episodes during the first month after the procedure.11 Many individuals with AF after cardiac surgery do not go on to have chronic AF. With AF after general surgery, the chance of chronic AF and future risk of adverse events are significantly elevated, as AF should not be a direct result of the procedure itself and instead likely represents a previously undiagnosed atrial myopathy. Consider noncardiac procedures as an “AF stress test”. Give this information, we should strongly consider anticoagulation after identifying AF associated with non-cardiac surgeries or procedures, when indicated by the CHA2DS2-VASc score. We should start anticoagulation in individuals with AF associated with cardiac surgeries only if there are other risk factors or clini Opportunistic screening for AF can be done by checking the pulse or noticing the irregular heart rate on blood pressure monitors. When AF is found by opportunistic screening at a single time point, it is usually persistent AF. Continuous ambulatory heart rhythm monitoring can identify shorter episodes of paroxysmal AF, perhaps earlier in the AF disease course. In patients with unexplained stroke we have different ways to search for occult AF: In the hospital: all patients should have 72h of ECG monitoring. There is evidence that nurse-led ECG surveillance detects more paroxysmal AF earlier and more frequently than 24-hour Holter recordings.5 After discharge: if clinical suspicion for occult AF is high (e.g., cerebral imaging concerning for cardioembolic source, evidence of left atrial enlargement, elevated BNP), consider more prolonged monitoring via cutaneous patches, multiple Holter recordings, or implantable cardiac monitors. References - Screening, Detection,

Jun 19, 2022

CardioNerds Tommy Das (Program Director of the CardioNerds Academy and cardiology fellow at Cleveland Clinic), Rick Ferraro (cardiology fellow at the Johns Hopkins Hospital), and Dr. Xiaoming Jia (Cardiology Fellow at Baylor College Medicine) take a closer look at the mechanism of icosapent ethyl in triglyceride lowering and ASCVD risk reduction with Dr. Michael Shapiro, the Fred M. Parrish professor of cardiology at Wake Forest University and Director of the Center for Preventative Cardiology at Wake Forest Baptist Health. Audio editing by CardioNerds Academy Intern, student doctor Akiva Rosenzveig. This episode is part of the CardioNerds Lipids Series which is a comprehensive series lead by co-chairs Dr. Rick Ferraro and Dr. Tommy Das and is developed in collaboration with the American Society For Preventive Cardiology (ASPC). Relevant disclosures: None Pearls • Notes • References • Guest Profiles • Production Team CardioNerds Cardiovascular Prevention PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls - Icosapent Ethyl Eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) are two major Omega-3 fatty acids found in fish oil. While both have been shown to lower triglycerides, only purified EPA formulations have been shown to reduce ASCVD risk.Mechanisms of triglyceride (TG) lowering by icosapent ethyl are multiple and include reduction of hepatic VLDL production, stimulation of lipoprotein lipase activity, increased chylomicron clearance, reduced lipogenesis, increased beta oxidation, and reduced delivery of fatty acids to the liver.There was only modest reduction of triglycerides in REDUCE-IT and JELIS despite association with significant reduction in cardiovascular outcome events, suggesting likely mechanisms outside of triglyceride lowering that may contribute to ASCVD reduction.While there was an increased signal for peripheral edema and atrial fibrillation associated with icosapent ethyl in prior trials, overall side effect rates were very low.Icosapent ethyl is considered to be cost-effective based on cost-effective analysis. Show notes - Icosapent Ethyl EPA and DHA have differing biological properties that may explain differences in ASCVD risk reduction observed in cardiovascular outcome trials 1.The REDUCE-IT trial, which enrolled secondary prevention and high-risk primary prevention patients with elevated triglycerides who were on statin therapy, showed significant reduction of major adverse cardiovascular events in the icosapent ethyl group compared with a mineral oil placebo2. Only modest reductions of TG were seen in the REDUCE-IT and JELIS trials despite association with significant reduction in events 2,3. Potential mechanisms contributing favorable effects of EPA on ASCVD risk reduction include inhibition of cholesterol crystal formation, stabilization of membrane structures, reversal of endothelial dysfunction, inhibition of lipoprotein and membrane lipid oxidation 4.Pleotropic effects of EPA include influence on platelet aggregation, lower thromboxane activity, increased prostaglandin level, and effects on blood pressure, insulin resistance and inflammation.Triglycerides are a surrogate for triglycerides-rich lipoproteins, which are likely causally associated with ASCVD 5.There is increased signal for bleeding, lower extremity edema, and atrial fibrillation with icosapent ethyl but overall side effect rates are very low 2.In order to ensure higher rates of medication access and adherence, clinicians must be cognizant of the cost to the patient. In practice, it is important to have a structured approach to improve insurance approval rate for medications that require prior authorizationsWith icosapent ethyl, cost effectiveness analyses have shown the medication is cost-effect for ASCVD risk reduction in secondary prevention patients and high-risk diabetic patients6.While moderate hypertriglyceridemia (150-499mg/dL) is likely a marker for increased residual risk for ASCVD, those with severe hypertriglyceridemia (>=500mg/dL) are also at risk for acute pancreatitis. Remember that these are fasting levels and post-prandial levels are likely much higher (i.e., in the thousands).In most scenarios, hypertriglyceridemia is driven by a combination of environmental and genetic factors. Environmental factors to consider when treating these patients include diet, alcohol intake, metabolic syndrome, diabetes, hypothyroidism, nephrotic syndrome, CKD, medications (ie. anti-rejection medications, steroids, thiazides).Hypertriglyceridemia is very amenable to lifestyle modification – diet, weight loss, exercise, diabetes control, etc.Equations for estimating LDL-C are generally not accurate when TG is severely elevated. In these circumstances we can instead use direct LDL-C, non-HDL-C, or apoB.We are entering an exciting era of preventative cardiology with many new therapeutics in the pipeline. References - Icosapent Ethyl Mozaffarian D, Wu JH. Omega-3 fatty acids and cardiovascular disease: effects on risk factors, molecular pathways, and clinical events. J Am Coll Cardiol. 2011;58(20):2047-2067.Bhatt DL, Steg PG, Miller M, et al. Cardiovascular Risk Reduction with Icosapent Ethyl for Hypertriglyceridemia. N Engl J Med. 2019;380(1):11-22.Yokoyama M, Origasa H, Matsuzaki M, et al. Effects of eicosapentaenoic acid on major coronary events in hypercholesterolaemic patients (JELIS): a randomised open-label, blinded endpoint analysis. Lancet. 2007;369(9567):1090-1098.Jia X, Koh S, Al Rifai M, Blumenthal RS, Virani SS. Spotlight on Icosapent Ethyl for Cardiovascular Risk Reduction: Evidence to Date. Vasc Health Risk Manag. 2020;16:1-10.Wall R, Ross RP, Fitzgerald GF, Stanton C. Fatty acids from fish: the anti-inflammatory potential of long-chain omega-3 fatty acids. Nutr Rev. 2010;68(5):280-289.Weintraub WS, Bhatt DL, Zhang Z, et al. Cost-effectiveness of Icosapent Ethyl for High-risk Patients With Hypertriglyceridemia Despite Statin Treatment. JAMA Netw Open. 2022;5(2):e2148172. Guest Profiles Dr. Michael Shapiro Dr. Michael Shapiro the Fred M. Parrish professor of cardiology at Wake Forest University and leader in the field of cardiovascular prevention. He is the Director of the Center for Preventative Cardiology at Wake Forest Baptist Health and has published widely in the field of atherosclerosis imaging and cardiovascular health. Dr. Xiaoming Jia Dr. Xiaoming Jia is a cardiology fellow at Baylor College of Medicine CardioNerds Lipids Production Team Tommy Das, MD Dr. Rick Ferraro Amit Goyal, MD Daniel Ambinder, MD

Jun 15, 2022

CardioNerd (Amit Goyal), ACHD series co-chair Dr. Agnes Koczo (UPMC), and episode FIT lead, Dr. Logan Eberly (Emory University, incoming ACHD fellow at Boston Adult Congenital Heart) join Dr. Peter Ermis (Program Director of the Adult Congenital Heart Disease Program at Texas Children's Heart Center), and Dr. Scott Cohen (Associate Professor and Director of the Adult Congenital Heart Disease Program at the Medical College of Wisconsin) for a discussion about transitions of care in congenital heart disease. Audio editing by Dr. Gurleen Kaur (Director of the CardioNerds Internship and CardioNerds Academy Fellow). Congenital heart disease (CHD) is the most common clinically significant congenital defect, occurring in approximately 1 in 100 live births. With modern advances in pediatric cardiology and cardiac surgery, over 90% of children born in the developed world with CHD will now survive into adulthood, and there are currently more adults than children living with CHD in the United States1. As these children become adults, they will need to transition their care from pediatric to adult-centered care. Unfortunately, during this transition period, there is often delayed or inappropriate care, improper timing of the transfer of care, and undue emotional and financial stress on the patients, their families, and the healthcare system. At its worst, patients are lost to appropriate follow-up. In this episode, we review the current climate in transitions of care for CHD patients from child-centered to adult-centered care, discuss the difficulties that can occur during the transitions process. We further discuss how to mitigate them, and highlight the key elements to the successful transitions of care. The CardioNerds Adult Congenital Heart Disease (ACHD) series provides a comprehensive curriculum to dive deep into the labyrinthine world of congenital heart disease with the aim of empowering every CardioNerd to help improve the lives of people living with congenital heart disease. This series is multi-institutional collaborative project made possible by contributions of stellar fellow leads and expert faculty from several programs, led by series co-chairs, Dr. Josh Saef, Dr. Agnes Koczo, and Dr. Dan Clark. The CardioNerds Adult Congenital Heart Disease Series is developed in collaboration with the Adult Congenital Heart Association, The CHiP Network, and Heart University. See more Disclosures: None Pearls • Notes • References • Guest Profiles • Production Team CardioNerds Adult Congenital Heart Disease PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls - Transitions of Care in Congenital Heart Disease There is a clear distinction between the TRANSFER of care and TRANSITION of care. Transfer is merely moving from a pediatric to adult provider. Transition involves the continuing education of the patient with regards to their congenital heart disease, the importance of longitudinal follow up, and leading patients toward more autonomous medical care. Transition begins in the pediatric cardiology clinic prior to the transfer of care and is an ongoing process that continues well after the physical transfer of care. A critical aspect of the transition and transfer of care is cultivating trust—that is, the new adult congenital heart disease (ACHD) provider must earn the trust of the patient and family. A failure to do so will inevitably prevent an optimal transition of care. During transition, parents are transitioning along with their children. With transition to adult care, there is also a goal to transition responsibility for medical care from the parent to the child. Setting goals and expectations can help both the parents and the child effectively make this transition. Loss to follow up is one of the most concerning complications of poor transition. Interestingly, there does not appear to be a strong association between complexity of congenital heart disease and the likelihood of loss to follow up. ACHD providers should not assume that patients with complex ACHD are less likely to be lost to follow up. For example, approximately 25-30% of Fontan patients have lapses or gaps in care. Effective transition of care is essential for all severity levels of ACHD. It is recommended in the 2018 AHA/ACC Guideline for the Management of Adults With Congenital Heart Disease2, as well as in the 2011 AHA Scientific Statement on Best Practices in Managing Transition to Adulthood for Adolescents With Congenital Heart Disease3. Show notes - Transitions of Care in Congenital Heart Disease 1. What is the current climate in transitions of care for patients from child-centered to adult-centered care, and what are some of the difficulties on the side of the provider as well as the patient during this process? Transition is a complex process, and there is no “one size fits all” approach to the effective transition of ACHD patients.Many patients live far away from an ACHD centers of excellence.There are also currently not enough ACHD cardiologists to care for ACHD patients.Due to these challenges, there can be anxiety with regards to transferring care to an ACHD provider from the perspective of both the patient and the pediatric cardiologist.This time in a young person’s life is not just a time of transition of medical care; there are many simultaneous immense life transitions as well. There may be a loss of focus on the importance of ongoing follow up in medical care. 2. What topics should be addressed at the first ACHD visit? The ACHD program and its relationship to both the pediatric and adult hospital should be thoroughly explained, and the patient needs to be informed where both inpatient and outpatient care take place.ACHD providers should ask open-ended questions to determine the patient’s understanding of their congenital heart disease and then provide education as needed.The first ACHD visit should focus on laying out a detailed, long-term plan of care for the patient. Patients should be advised what specifically will be monitored going forward (such as valve function, cardiac chamber size, arrhythmias, etc.), as well as what future diagnostic testing (echo, MRI/CT, stress testing, etc.) is to be expected. For female patients, contraception and the safety of pregnancy should be addressed starting in the first visit.One of the primary goals of the first ACHD visit is also to build trust. To this end, an ACHD provider should try to avoid any major changes to medical therapy at the first visit unless deemed absolutely necessary. 3. What are advantages and disadvantages of different models of transitions of care? There is no “one size fits all” model to transition, but there certainly are some guiding principles.Formal transition programs are important. They can help normalize transition and eliminate the sentiment that the patient is being “kicked out” of pediatric cardiology clinic. Additionally, formal transitions programs can reduce unexpected cardiac hospitalizations for ACHD patients2. This decreases the unnecessary utilization of hospital resources.An ACHD program that remains within a children’s hospital has the benefit that the patients are already familiar with the site, and they may also be less likely to be lost to follow up. However, there is the drawback that non-cardiology providers in a children’s hospital are often unfamiliar with the management of adult medical problems, which necessitates forming relationships with adult providers at partner institutions, and this can be challenging.Ultimately, ACHD patients can be cared for effectively at either a children’s hospital-based or adult hospital-based program. The model that is most effective for a particular institution is dependent upon the resources available and the investment of a supportive multi-disciplinary team. 4. What is the role of the parents in the transition process? Parents play a vital role in the transition process. They are often quite informed of their child’s history, so the new ACHD provider needs to carefully review the patient’s history prior to the first visit. Having thorough knowledge of a patient's medical history will help build trust with patients and their families.ACHD providers should involve the parents in the transition process and should set goals and expectations. They should ask the parents to empower their child with regards to their medical care (such as encouraging them to manage their own medications, schedule their own medical appointments, etc.)ACHD providers need to have patience when working with parents during the transition process. Providers need to acknowledge that the parents have been the primary manager of their child’s medical care for many years, and it is often difficult to give up this role and to allow their child to be autonomous.It’s important to remember that parents are also transitioning. They transition from being the primary manager of their child’s health to being co-managers, before ultimately relinquishing the responsibility to their child. 5. What are some negative sequelae of a poor transition of care? The worst possible outcome is loss to follow up. This can result in potentially preventable medical complications.Inadequate or poor transition can lead to parental and/or patient distrust of the ACHD provider, which in turn increases the risk of being lost to follow up.Suboptimal transition increases the risk that the patient will engage in high-risk behaviors that can be harmful to their health.Patients who are not transitioned properly tend to utilize more hospital resources. 6. How should female ACHD patients be counseled on women’s health issues? In general, cardiologists are not well trained in addressing issues such as sexual health and contraception.

Jun 3, 2022

CardioNerds (Amit Goyal and Daniel Ambinder), join Dr. Gurleen Kaur (Director of CardioNerds Internship and medicine resident at Brigham and Women’s Hospital), Dr. Victoria Thomas (Cardionerds Ambassador, Vanderbilt University Medical Center) Dr. Katie Berlacher (Cardiology program director, University of Pittsburgh Medical Center), and Dr. Julie Damp (Vanderbilt University Medical Center Cardiovascular disease fellowship program director) to discuss becoming & thriving as a fellowship program director and more in this installment of the Narratives in Cardiology Series. Special message by Tennessee ACC State Chapter Governor, Dr. John L Jefferies. Audio editing by CardioNerds Academy Intern, student doctor Akiva Rosenzveig. The PA-ACC & CardioNerds Narratives in Cardiology is a multimedia educational series jointly developed by the Pennsylvania Chapter ACC, the ACC Fellows in Training Section, and the CardioNerds Platform with the goal to promote diversity, equity, and inclusion in cardiology. In this series, we host inspiring faculty and fellows from various ACC chapters to discuss their areas of expertise and their individual narratives. Join us for these captivating conversations as we celebrate our differences and share our joy for practicing cardiovascular medicine. We thank our project mentors Dr. Katie Berlacher and Dr. Nosheen Reza. Video Version • Notes • Production Team Claim free CME just for enjoying this episode! There are no relevant disclosures for this episode. The PA-ACC & CardioNerds Narratives in Cardiology PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Tweetorial - Becoming & Thriving as a Fellowship Program Director with Dr. Katie Berlacher and Dr. Julie Damp https://twitter.com/gurleen_kaur96/status/1542620967733805056?s=21&t=AMSKElEz4oZZTA9nVbWBCA Video version - Becoming & Thriving as a Fellowship Program Director with Dr. Katie Berlacher and Dr. Julie Damp https://youtu.be/E-C-SSV7LZg Notes - Becoming & Thriving as a Fellowship Program Director with Dr. Katie Berlacher and Dr. Julie Damp Drafted by Dr. Victoria Thomas. 1. What does it mean to be a big “E” when people say they are a clinician Educator? It can mean teaching students directly at bedside. However, it is also a sacrifice of daily mentoring and listening to students’ challenges and difficulties.Being a clinician educator is just as much of a calling as is serving in medicine.Clinician Educators focus on medicine but also the science and best practices of teaching the art of doctoring. 2. What is physician burnout? Why is this important for to CardioNerds? Physician burnout is a syndrome of chronic workplace stress that leads to emotional exhaustion and a sense of dissatisfaction and disconnection personally and professionally. 30-45% of cardiologists have reported physician burnout. 3. What factors affect physician burnout? Emotional and physical exhaustion often lead to physician burnout. First year of training as an intern or fellow and first year of serving as an attending are particularly high-risk periods. This is largely due to learning a new system and responsibilities mixed with a sense of decreased accomplishment.The sense of decreased accomplishment can lead to physicians suffering from impostor syndrome.Grit can be defined as a perseverance for long-term goals. The level of grit was not associated with burnout among first-year Internal Medicine residents. 4. What are some of the solutions to prevent or address physician burnout? Physicians need to feel a sense of belonging and should be supported and celebrated when they have accomplished something by their colleagues and administrators. Fellows and attendings want to feel listened to and supported.Destigmatizing this idea of “perfection in medicine”. Physician should share with each other their accomplishments but also their mistakes to create a community of personal and professional connection and acceptance.Practicing mini acts of gratitude such as exercise or therapy can help with burnout.Delegation of work tasks and taking breaks have been shown to improve mental well-being. 5. What support do program directors have to help prevent burnout for themselves? Many local graduate medical education (GME) offices will have some resources for program directors depending on the size and funding. The Accreditation Council for Graduate medical Education (ACGME) had developed an on-line series to help new program directors understand their new roles. It is also recommended to network and create community of program directors to work with and bounce ideas from. 6. What are some of the differences found among cardiology program directors regarding support from leadership? 45% of men versus 29% of women program directors felt adequate support from leadership. 56% of late-career versus 35% mid-career and early-career program directors felt adequate support from leadership.There is no evidence to support this, however, but contributing factors may include the documented history of gender bias, wage inequality, and program size. References Team Cullen, M. W., Damp, J. B., Soukoulis, V., Keating, F. K., Abudayyeh, I., Auseon, A., ... & Weissman, G. (2021). Burnout and well-being among cardiology fellowship program directors. Journal of the American College of Cardiology, 78(17), 1717-1726.Mehta, L. S., Lewis, S. J., Duvernoy, C. S., Rzeszut, A. K., Walsh, M. N., Harrington, R. A., ... & American College of Cardiology Women in Cardiology Leadership Council. (2019). Burnout and career satisfaction among US cardiologists. Journal of the American College of Cardiology, 73(25), 3345-3348.Peckham C. Physician burnout: it just keeps getting worse. Medscape; 2015.Klein, A. J., Grau, T., Spagnoletti, C. L., Rothenberger, S. D., & Berlacher, K. (2021). Grit Does Not Predict Burnout among First-Year Internal Medicine Residents. Southern Medical Journal, 114(5), 272-276.Edwards, S. T., Helfrich, C. D., Grembowski, D., Hulen, E., Clinton, W. L., Wood, G. B., ... & Stewart, G. (2018). Task delegation and burnout trade-offs among primary care providers and nurses in Veterans Affairs Patient Aligned Care Teams (VA PACTs). The Journal of the American Board of Family Medicine, 31(1), 83-93.Shanafelt, T. D., & Noseworthy, J. H. (2017, January). Executive leadership and physician well-being: nine organizational strategies to promote engagement and reduce burnout. In Mayo Clinic Proceedings (Vol. 92, No. 1, pp. 129-146). Elsevier. Production Team Dr. Gurleen Kaur Amit Goyal, MD Daniel Ambinder, MD

May 29, 2022

CardioNerds (Amit and Dan) join Dr. Omid Amidi (CardioNerds Academy Graduate) and Dr. Marwah Shahid from the UCLA Cardiology Fellowship program along with Dr. Evelyn Song (CardioNerds Academy House Faculty and Heart Failure Hospitalist at UCSF) to discuss a complex case focused on management of severe coronary artery disease in a patient with Glanzmann thrombasthenia. Dr. Rushi Parikh (Interventional cardiologist, UCLA) provides the ECPR for this episode. Audio editing by CardioNerds Academy Intern, student doctor Akiva Rosenzveig. Glanzmann Thrombasthenia is a bleeding disorder due to impairment of platelet aggregation secondary to a mutation in the GPIIB/IIIA receptor. This case is focused on work up of stable coronary artery disease followed by a discussion on duration of dual antiplatelet therapy post percutaneous coronary intervention in a patient with Glanzmann thrombasthenia. Check out this published case in JACC: Case Reports Jump to: Case media - Case teaching - References CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Case Media See the published case in JACC: Case Reports Episode Schematics & Teaching Pearls 1. Patients with Glanzmann thrombocytopenia (GT) may have a higher risk of bleeding, depending on their disease phenotype. 2. It is unclear whether the mechanism of GT protects patient against stent thrombosis in the setting of PCI. Additionally, there is little data on the use of antiplatelet agents in patients with GT. 3. Short-term DAPT may be a reasonably safe option for patients with GT undergoing PCI. 4. We report a successful case of percutaneous coronary intervention in a patient with GT with no complications at a 1 year follow up. Notes 1. What is Glanzmann thrombasthenia? GT is an inherited platelet disorder that is characterized by spontaneous bleeding with phenotypic variability ranging from minimal bruising to potentially fatal hemorrhaging. GT is caused by autosomal recessive inheritance of quantitative or qualitative deficiencies of functional αIIbβ3 integrin coded by ITGA2B or ITGB3 genes for αIIb and β3, respectively. As a result, platelets may be stimulated, but the platelet glycoprotein IIb/IIIa receptor is unable to bind fibrinogen to cross-link platelets, rending them potentially ineffective. In platelet aggregation studies, there is lack of response to collagen, epinephrine, arachidonic acid, and ADP stimulation. Thus, platelet aggregation is impaired. 2. What is known about PCI and antiplatelet therapy in the setting of Glanzmann thrombasthenia? To the best of our knowledge, this is the first case report of percutaneous coronary intervention in the setting of GT. It is unclear if the mechanism of GT alone provides sufficient antiplatelet activity and whether antiplatelet therapy leads to significantly increased bleeding risk. The use of antiplatelet therapy is not well studied in the GT population. What we do know is that the mechanism of GT prevents platelet aggregation—the final step in platelet-related thrombosis—while oral antiplatelet therapy affects platelet activation, thus, in our patient we felt that short term DAPT was reasonable. It is important to note that in the event of an active bleed requiring platelet transfusion, donor platelets possess functional glycoprotein IIb/IIIa receptors and thus exponentially increase the risk of stent thrombosis. Therefore, unlike our case, if a patient is not maintained on chronic oral antiplatelet therapy, initiation of oral or intravenous antiplatelet therapy should be considered to prevent stent thrombosis at the time of platelet transfusion. Like any other patient with a high bleeding risk, it is important to have clear indications to conduct a coronary angiogram in patients with GT. Shared decision making is vital in regard to the benefits and risk of an angiogram in relation to the patient’s presentation, symptoms and history. The same is true in regard to coronary revascularization in these patients. Besides functional stress testing, coronary CTA is a viable option to evaluate coronary anatomy to identify high risk anatomy in these patients. References Truong Katie P., Zhang Jessica J., Shahid Marwah, et al. Management of high-grade coronary artery disease and concomitant glanzmann thrombasthenia. JACC: Case Reports. 2021;3(14):1625-1629.Lawton Jennifer S., Tamis-Holland Jacqueline E., et al. 2021 acc/aha/scai guideline for coronary artery revascularization. Journal of the American College of Cardiology. 2022;79(2):e21-e129.Gulati Martha, Levy Phillip D., et al. 2021 aha/acc/ase/chest/saem/scct/scmr guideline for the evaluation and diagnosis of chest pain. Journal of the American College of Cardiology. 2021;78(22):e187-e285.

May 27, 2022

CardioNerds (Amit Goyal and Daniel Ambinder), Dr. Ahmed Ghoneem (CardioNerds Academy Chief of House Taussig and medicine resident at Lahey Hospital), and Dr. Gurleen Kaur (Director of CardioNerds Internship and medicine resident at Brigham and Women’s Hospital) discuss family history of premature ASCVD with Dr. Ann Marie Navar, Preventive Cardiologist and Associate Professor in the Departments of Internal Medicine and Population and Data Sciences at UT Southwestern Medical Center. They discuss the art of soliciting a nuanced family history, refining cardiovascular risk using risk models and novel markers, counseling patients with elevated risk, and more. Show notes were drafted by Dr. Ahmed Ghoneem and reviewed by Dr. Gurleen Kaur. Audio editing was performed by CardioNerds Intern, student Dr. Adriana Mares. For related teaching, check out this Tweetorial about CAC by Dr. Gurleen Kaur, the Family History of Premature ASCVD Infographic by Dr. Ahmed Ghoneem, and the CardioNerds Cardiovascular Prevention Series. CardioNerds Cardiovascular Prevention PageCardioNerds Episode Page Show notes - Family History of Premature ASCVD with Dr. Ann Marie Navar Patient summary: Mr. B is a 51-year-old gentleman who is referred to CardioNerds Prevention Clinic by his PCP. He does not have a significant past medical history. He is a former smoker but quit 2 years ago. His BP in clinic today is 138/84; he is not on any antihypertensives. His most recent lipid profile 2 weeks prior showed a total cholesterol level of 250 mg/dL, a TG level of 230 mg/dL, an LDL cholesterol of 174 mg/dL, and an HDL cholesterol of 30 mg/dL. He tells us that his father had a “heart attack” at the age of 52, and he would like to further understand his own risk. We calculate his ASCVD risk score, and it is 9.8%. 1. What constitutes a positive family history (FHx) of premature ASCVD? What is an approach to the art of soliciting the FHx from our patients? Definition of family history of premature ASCVD: the history of an atherosclerotic event (e.g., myocardial infarction or stroke) in a male first degree relative before the age of 55 or a female first degree relative before the age of 65. Dr. Navar’s approach to soliciting a family history:Lead with a general question such as “what do you know about any medical conditions that run in your family?”.Then ask more specific questions about the parents and siblings, such as “Is your mother still alive? How long did she live? Has she ever had a heart attack or stroke?”If the answer is yes, ask about how old they were at the time of the event.A challenging aspect of the FHx can be eliciting the difference between atherosclerotic events and sudden cardiac death. While atherosclerotic diseases are a much more common cause of unexplained sudden death, it's important that we don't miss the opportunity to identify inherited cardiomyopathies, channelopathies, inherited aortopathies or other heritable SCD syndromes. 2. Is the “dose” of family history important (for example: the number of affected relatives, the closeness of those relationships, the age of onset)? While conducting studies to test this may be difficult, the few studies that have looked at the number of affected relatives have found a dose-response type relationship, where increasing number of relatives affected increases the risk of heart disease.1,2 3. How does a family history affect cardiovascular risk stratification? FHx of premature ASCVD does not improve the predictive ability of the Pooled Cohort Equations (PCE) at a population level. Therefore, it does not factor into the ASCVD risk calculation utilizing the PCE. However, it enhances the patient’s risk at an individual level. The ACC/AHA guidelines recognize FHx of premature ASCVD as a risk-enhancing factor [together with CKD, chronic inflammatory conditions such as psoriasis, primary hypercholesterolemia, high-risk ethnicity such as South Asian ancestry, metabolic syndrome, history of premature menopause (before age 40 y) and history of pregnancy-associated conditions that increase later ASCVD risk, such as preeclampsia].3 Dr. Navar’s advice is to think of the PCE as a starting point during risk assessment, followed by searching for the other risk-enhancing factors, to come up with a more tailored risk assessment for that individual patient. 4. After we explained to our patient the enhanced risk, he tells us that he feels like his fate is sealed and that nothing he can do would improve his outcomes because it's in his genes. We have data though, that shows that healthy lifestyles reduce the risk of coronary artery disease and individuals at high genetic risk of CAD.4 How would you handle this challenging conversation and counsel our patient? We should always think about how risk conversations can affect our patients emotionally. Many patients come to CV prevention clinic because they want to know what they can do about their risk. A “scared straight” approach can be de-motivating for these patients.“It's never too late to start cardiovascular prevention. And there are never patients that are too high risk that we can't do anything to lower their risk of heart disease” can be a reassuring beginning to the conversation.Reinforce any work that the patient has already done to lower their risk of heart disease such as quitting smoking. This shows the patients that they have already started making a difference.This can then be followed by discussing the available tools to lower this patient’s risk: diet modification, exercise, weight management, control of diabetes, control of blood pressure, statins, etc. 5. In addition to lifestyle management, would you recommend a statin for Mr. B, who has an intermediate CVD risk and risk enhancing factors such as positive family history? Dr. Navar’s short answer is YES. Even though the patient is at intermediate risk, his actual risk is higher given his family history. “The cornerstone of long-term risk prevention for this patient is going to be a statin”.Dr. Navar usually approaches this conversation using a simple yet effective analogy: “imagine that you're out shopping, and there's a vitamin that will lower your risk of heart disease over your lifetime by 30 to 50%, depending on your cholesterol level and how much your cholesterol is lowered. It's very safe. It has minimal side effects and it's all of $3 a month. But unlike vitamins, we actually have randomized control trial data that show that they make a difference. Would you take it?”.It’s important to identify the LDL goal for each patient before prescribing a statin. 6. Our patient is still uncertain about starting a statin mainly because he's asymptomatic and doesn't feel that his family history is a strong enough reason for him to have to take a daily medication for the rest of his life. The ACC/AHA guidelines highlight the importance of shared decision making with our patients. They also recommend measuring the coronary artery calcium or CAC score in intermediate risk patients to help facilitate a more informed risk discussion. Would a CAC score be of benefit in our patient’s case? The initial step in this decision-making process is to identify what are the patient’s thoughts on taking statins, i.e where they are on the “Statin Spectrum” as Dr. Navar eloquently described. It is important to discuss the current evidence for the benefit of statins, and that the relative risk reduction we see per degree of LDL lowering is actually highest in the youngest and lowest risk groups.Some patients are engaged and interested in taking statins from the beginning. It may not be beneficial to measure CAC scores in these patients.Other patients, like our patient, remain uncertain about statins. These patients are great candidates for CAC score, which acts as a “tie-breaker” in this situation. Being aware of the presence of CAC in their arteries can be a strong motivator for these patients to start statin therapy.In non-smoking patients with CAC=0, it would be reasonable to hold statin therapy and repeat a CAC score in five years (assuming no major change in other risk factors such as diabetes, return to smoking, etc.).5It is important to recognize the caveats of CAC scores:The ACC/AHA guidelines identify some patients whom clinicians should not de-risk despite a CAC=0, such as active smokers.CAC is less prevalent in young people, and less prevalent in women compared to men, raising the possibility of false reassurance.CAC testing involves a small, but not insignificant, amount of radiation exposure.It is often not covered by insurance. 7. There've been a lot of interest in novel lipid biomarkers such as lipoprotein(a) and Apolipoprotein B, and how elevated blood levels of these markers may be associated with ASCVD risk and are recognized as risk enhancing factors. How do you incorporate testing for Lp(a) and ApoB into your practice? Lipoprotein (a)It is a type of cholesterol particle that looks like an LDL particle, but it has an additional protein on it on the surface. It doesn't correlate with LDL levels or any of the traditional risk factors for ASCVD, and Lp(a) levels are very consistent throughout lifetime. Moreover, it is genetically determined, and elevated Lp(a) levels usually run in families.The guidelines recommend measuring Lp(a) in patients with family history of premature ASCVD.3There are no commercially available treatments at this time that lower Lp(a), however a number of novel therapies are currently in clinical trials.Despite that fact, several preventive cardiologists (such as Dr. Navar) may measure Lp(a) to identify patients at increased risk, and subsequently target lower LDL levels in these patients (LDL<70, and in patients with multiple risk factors or established CVD, LDL<55). Apolipoprotein BIt reflects the total number of atherogenic lipoprotein particles,

May 24, 2022

It’s another session of CardioNerds Rounds! In these rounds, Co-Chairs, Dr. Karan Desai and Dr. Natalie Stokes and Dr. Tiffany Dong (FIT at Cleveland Clinic) joins Dr. Randall Starling (Professor of Medicine and Director of Heart Transplant and Mechanical Circulatory Support at Cleveland Clinic) to discuss the nuances of guideline directed medical therapy (GDMT) through real cases. As a past president of the Heart Failure Society of America (HFSA) and author on several guidelines, Dr. Starling gives us man pearls on GDMT. Come round with us today by listening to the episodes and joining future sessions of #CardsRounds! This episode is supported with unrestricted funding from Zoll LifeVest. A special thank you to Mitzy Applegate and Ivan Chevere for their production skills that help make CardioNerds Rounds such an amazing success. All CardioNerds content is planned, produced, and reviewed solely by CardioNerds. Case details are altered to protect patient health information. CardioNerds Rounds is co-chaired by Dr. Karan Desai and Dr. Natalie Stokes. Speaker disclosures: None Cases discussed and Show Notes • References • Production Team CardioNerds Rounds PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Show notes - CardioNerds Rounds: Challenging Cases - Modern Guideline Directed Therapy in Heart Failure with Dr. Randall Starling Case #1 Synopsis: A man in his 60s with known genetic MYPBC3 cardiomyopathy and heart failure with a reduced ejection fraction of 30% presents with worsening dyspnea on exertion over the past 6 months. His past medical history also included atrial fibrillation with prior ablation and sick sinus syndrome with pacemaker implantation. Medications are listed below. He underwent an elective right heart catheterization prior to defibrillator upgrade for primary prevention. At the time of right heart catheterization, his blood pressure was 153/99 with a heart rate of 60. His RHC demonstrated a RA pressure of 15mmHg, RV 52/16, PA 59/32 (mean 41), and PCWP 28 with Fick CO/CI of 2.8 L/min and index of 1.2 L/min/m2. His SVR was 1900 dynes/s/cm-5. He was admitted to the cardiac ICU and started on nitroprusside that was transitioned to a regimen of Sacubitril-Valsartan and Eplerenone. His final RHC numbers were RA 7, PA 46/18/29, PCWP 16 and Fick CO/CI 6.1/2.6. His discharge medications are shown below. Takeaways from Case #1 Unless there are contraindications (cardiogenic shock or AV block), continue a patient’s home beta blocker to maintain the neurohormonal blockade benefits. A low cardiac index should be interpreted in the full context of the patient, including their symptoms, other markers of perfusion (e.g., urine output, mentation, serum lactate), and mean arterial pressure before holding or stopping beta blockade. Carvedilol, metoprolol succinate and bisoprolol are all evidence-based options for beta blockers in heart failure with reduced ejection fraction.If there is concern of lowering blood pressure too much with Sacubitril/Valsartan, one method is to trial low dose of valsartan first and then transition to Sac/Val. Note, in the PARADIGM-HF trial, the initial exclusion criteria for starting Sac/Val included no symptomatic hypotension and SBP ≥ 100. At subsequent up-titration visits, the blood pressure criteria was decreased to SBP ≥ 95.In multiple studies, protocol-driven titration of GDMT has shown to improve clinical outcomes, yet titration remains poor. The following image from Greene et al. in JACC shows that in contemporary US outpatient practices that GDMT titration is poor with few patients reaching target dosing. Case #2 Synopsis: A 43 year-old male with a past medical history of familial dilated cardiomyopathy requiring HVAD placement two years prior now comes in with low flow alarms. He is feeling well otherwise with chronic dyspnea on exertion. A CT chest and abdomen with contrast for showed outflow graft occlusion. Given a TTE showed LV recovery that correlated with invasive hemodynamics, his LVAD was decommissioned. He was tried on a low dose Sacubitril/Valsartan but was unable to tolerate it due to hypotension. He was discharged on carvedilol 3.125mg BID and lisinopril 5mg daily. Over the next 10 months in clinic, his GDMT was titrated to carvedilol 25mg BID, spironolactone 25mg daily and Sacubitril/Valsartan 49-51mg BID. Takeaways Case #2 In patients with ventricular assist devices, the differential for low flow alarms includes hypovolemia, arrhythmias, RV failure, cardiac tamponade and inflow cannula obstruction. A careful history, exam (with particular attention to the JVD), and bedside echocardiogram can help differentiate the cause.EF recovery occurs in about 5% of patients in large LVAD registries. Favorable prognostic factors for EF recovery include female sex and nonischemic cardiomyopathy of short duration.In the TRED-HF trial, patients were randomly assigned to phased withdrawal or continuation of GDMT over 6 months. The primary endpoint was relapse defined as a reduction in LVEF of more than 10% and to less than 50%, an increase in LVEDV by more than 10% and to higher than the normal range, a two-fold rise in NT-pro-BNP and to more than 400 ng/L or clinical evidence of heart failure. While a small trial (51 patients were enrolled), over the first 6 months, 44% of patients assigned to treatment withdrawal met the primary endpoint of relapse compared with none assigned to continue treatment (estimated of event rate 45.7% [95% CI 28.5-67.2]; p=0.0001).We still do not have great predictors of relapse, and thus for most patients with HFrecEF, GDMT should continue indefinitely. References - CardioNerds Rounds: Challenging Cases - Modern Guideline Directed Therapy in Heart Failure with Dr. Randall Starling Halliday BP, Wassall R, Lota AS, et al. Withdrawal of pharmacological treatment for heart failure in patients with recovered dilated cardiomyopathy (TRED-HF): an open-label, pilot, randomised trial. Lancet. 2019 Jan 5;393(10166):61-73. doi: 10.1016/S0140-6736(18)32484-X. Epub 2018 Nov 11. PMID: 30429050; PMCID: PMC6319251.Greene SJ, Fonarow GC, DeVore AD, et al. Titration of Medical Therapy for Heart Failure With Reduced Ejection Fraction. J Am Coll Cardiol. 2019 May 21;73(19):2365-2383. doi: 10.1016/j.jacc.2019.02.015. Epub 2019 Mar 4. PMID: 30844480; PMCID: PMC7197490.McMurray JJ, Packer M, Desai AS, et al. Angiotensin-neprilysin inhibition versus enalapril in heart failure. N Engl J Med. 2014 Sep 11;371(11):993-1004. doi: 10.1056/NEJMoa1409077. Epub 2014 Aug 30. PMID: 25176015. Production Team Karan Desai, MD Natalie Stokes, MD Amit Goyal, MD Daniel Ambinder, MD

May 20, 2022

Atrial fibrillation may reach pandemic proportions in the next 2-3 decades. Factors that drive this phenomenon have been studied in predominantly White populations, leading to a significant underrepresentation of certain racial/ethnic groups in atrial fibrillation epidemiological studies. Most atrial fibrillation epidemiology studies suggest that the non-Hispanic Black population has a lower incidence/prevalence of atrial fibrillation, despite a higher risk factor burden (“Afib paradox”). At the same time, non-Hispanic Blacks have worse outcomes compared to the White population and underrepresented populations and women are less likely than White men to receive optimal guideline-based therapies for atrial fibrillation. In this episode, CardioNerds Dr. Kelly Arps (Co-Chair Atrial Fibrillation series, Cardiology fellow at Duke University), Dr. Colin Blumenthal (Co-Chair Atrial Fibrillation series, CardioNerds Academy House Faculty Leader for House Jones, Cardiology fellow at the University of Pennsylvania), and Dr. Dinu-Valentin Balanescu (CardioNerds Academy Faculty for House Jones, rising internal medicine chief resident at Beaumont Hospital), discuss with Dr. Larry Jackson (cardiac electrophysiologist and Vice Chief of Diversity, Equity, and Inclusion in the Division of Cardiology at Duke University) about atrial fibrillation epidemiology and health equity, challenges and possible solutions to improving diversity in clinical trials, and race/ethnicity/sex/gender differences in the detection, management, and outcomes of atrial fibrillation. Audio editing by CardioNerds Academy Intern, student doctor Akiva Rosenzveig. This CardioNerds Atrial Fibrillation series is a multi-institutional collaboration made possible by contributions of stellar fellow leads and expert faculty from several programs, led by series co-chairs, Dr. Kelly Arps and Dr. Colin Blumenthal. This series is supported by an educational grant from the Bristol Myers Squibb and Pfizer Alliance. All CardioNerds content is planned, produced, and reviewed solely by CardioNerds. We have collaborated with VCU Health to provide CME. Claim free CME here! Disclosure: Larry R. Jackson II, MD, MHs, has the following relevant financial relationships:Advisor or consultant for: Biosense Webster Inc.Speaker or a member of a speakers bureau for: Biotronik Inc.; Medtronic Inc. Pearls • Notes • References • Guest Profiles • Production Team CardioNerds Atrial Fibrillation PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls and Quotes - Atrial Fibrillation: Epidemiology, Health Equity, & The Double Paradox Atrial fibrillation confers an enormous public health burden. It is estimated that it will reach pandemic proportions over the next 30 years, with potentially 100-180 million people worldwide suffering from this condition.Large epidemiological atrial fibrillation registries have very small populations of underrepresented groups. More diverse enrollment in clinical trials is essential and may be obtained by increasing diversity among research staff, principal investigators, and steering committees, and use of mobile/telehealth technologies to remove bias related to differences in presentation. The CardioNerds Clinical Trials Network specifically aims pair equitable trial enrollment with trainee personal and professional development.Most atrial fibrillation epidemiology studies suggest that the non-Hispanic Black population has lower incidence/prevalence of atrial fibrillation, despite higher risk factor burden. This “paradox” is likely due to a multifactorial process, with clinical differences, socioeconomic factors, and genetic factors contributing.Underrepresented populations are less likely than White patients to receive optimal guideline-based management of atrial fibrillation. Though there is a higher incidence of intracranial bleeding on vitamin K antagonists in this population, they are less likely to receive optimal anticoagulation for stroke prevention with direct oral anticoagulants. Also, despite overall worse outcomes, they are less likely to be prescribed rhythm control strategies or offered catheter-based ablation despite known data with improved outcomes with early rhythm control.Gender-based differences in atrial fibrillation epidemiology, management, and outcomes also exist. Compared to men, women have a lower incidence/prevalence of atrial fibrillation but are more likely to be symptomatic. They are also more likely to receive rate instead of rhythm control strategies and suboptimal stroke reduction therapies Overall, women have worse outcomes than men. “I want to differentiate [equitable care] from equal care. I think this idea of equity means that we have to take into account the myriad of differences that we see between people of different races, ethnicities, genders, sexes, regions, whether they’re citizens or not, whether they’re disabled or not […] and make sure that we’re thinking about those in terms of prescriptions and discussion and communication, and offering our patients therapy, […] it's not [enough] to offer different people the same therapy because they may have different barriers that may prevent them from uptaking that therapy or utilizing that.” Dr. Larry Jackson Notes - Atrial Fibrillation: Epidemiology, Health Equity, & The Double Paradox Drafted by Dr. Dinu-Valentin Balanescu and reviewed by Dr. Colin Blumenthal. 1. What factors contribute to the atrial fibrillation epidemic and where do we expect to be over the next 20-30 years? The current global prevalence of atrial fibrillation is unclear. It is estimated that over the next 30 years, the prevalence of atrial fibrillation may reach pandemic proportions, with potentially 100-180 million people worldwide suffering from this condition.1Factors that drive this increase:Classic: heart failure, coronary artery disease, hypertension, diabetes, tobacco use, obesity.Novel risk factors: obstructive sleep apnea, metabolic syndrome, left ventricular hypertrophy, left atrial enlargement.Novel markers (inflammatory, biochemical): B-type natriuretic peptide, CRP.Many of the above factors have been determined by studying predominantly White populations. 2. There is conflicting data regarding the incidence of atrial fibrillation across race and ethnicity, with most studies suggesting a higher incidence in the non-Hispanic White population compared to non-Hispanic Black or Hispanic individuals, while some suggest a similar prevalence. How is this discrepancy explained? The discrepancy may stem from various rates of clinical detection, rather than incidence or prevalence, of atrial fibrillation between different race/ethnicity groups (“ascertainment bias”).Conflicting data persists even when detection is adjusted for. A cohort of the MESA study showed that the prevalence among race and ethnicity was similar when the diagnosis was made using Holter monitor data.2 Data from the ASSERT trial suggest that when using implantable loop recorders, the incidence of atrial fibrillation among the non-Hispanic Black population was lower than a European White population.3There is a substantial need for further study on the epidemiology of atrial fibrillation across race/ethnicity. 3. Non-Hispanic Black populations have a higher risk factor burden for atrial fibrillation than White patients, but as described above most studies demonstrate a lower incidence – how is this “paradox” explained? The “atrial fibrillation paradox” is a double paradox, as Dr. Jackson explains: despite a higher risk factor burden, non-Hispanic Blacks have a lower incidence/prevalence of atrial fibrillation. At the same time, non-Hispanic blacks have worse outcomes compared to the white population.4This is likely due to a multifactorial process, with clinical differences, socioeconomic factors, and genetic factors contributing.5 Specifically:Ascertainment bias. Certain racial/ethnic groups may have access issues preventing them from seeking medical attention for rhythm assessment and/or may be less likely to be prescribed rhythm monitors for objective assessment. Additionally, it has been shown that the non-Hispanic Black population has more paroxysmal symptoms, which could lead to difficulties in diagnosis.Survival bias. Non-Hispanic Whites have a longer life expectancy compared to underrepresented racial/ethnic groups, which may lead to a greater risk of developing atrial fibrillation over time.Genetic/epigenetic differences. Stronger European ancestry within non-Hispanic Blacks is associated with a higher risk of atrial fibrillation. Genome-wide association studies suggest that non-Hispanic Blacks may have protective genes compared to whites. 4. What are barriers to the diagnosis of atrial fibrillation in understudied populations and how can inclusion in research studies be improved? Large epidemiological registries have traditionally included very small proportions of underrepresented groups. A more diverse enrollment in clinical trials is essential.Clinical trial participation of marginalized populations may be achieved by:Using mobile/telehealth technologies to recruit and follow patients.Increasing diversity and heterogeneity among research staff, principal investigators, steering committees, which has been shown to improve study diversity.From a clinical standpoint, barriers may be removed by:Educating patients on atrial fibrillation, its complications, its treatments, and its outcomes.Involving family and other social communities as part of decision-making support. The CardioNerds Clinical Trials Network specifically aims pair equitable trial enrollment with trainee personal and professional development 5.

May 16, 2022

CardioNerds Tommy Das (Program Director of the CardioNerds Academy and cardiology fellow at Cleveland Clinic), Rick Ferraro (cardiology fellow at the Johns Hopkins Hospital), and Dr. Aliza Hussain (cardiology fellow at Baylor College Medicine) take a deep dive on the REDUCE-IT trial with Dr. Peter Toth, director of preventive cardiology at the CGH medical center in Sterling, Illinois, clinical professor in family and community medicine at the University of Illinois School of Medicine, and past president of the National Lipid Association and the American Board of Clinical Lipidology. Special introduction to CardioNerds Clinical Trialist Dr. Jeff Wang (Emory University). Audio editing by CardioNerds academy intern, Shivani Reddy. This episode is part of the CardioNerds Lipids Series which is a comprehensive series lead by co-chairs Dr. Rick Ferraro and Dr. Tommy Das and is developed in collaboration with the American Society For Preventive Cardiology (ASPC). Relevant disclosures: None Pearls • Notes • References • Guest Profiles • Production Team CardioNerds Cardiovascular Prevention PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls - REDUCE-IT The Reduction of Cardiovascular Events with EPA-Intervention Trial (REDUCE-IT) trial was a large randomized controlled trial that showed a significant reduction in atherosclerotic cardiovascular disease (ASCVD) events with use of icosapent ethyl ester in secondary prevention patients and high risk primary prevention patients with diabetes and residual elevated triglycerides between 135 to 499 mg/dL on top of maximally tolerated statin therapy1. Despite the use of high intensity statin therapy, considerable residual risk for future atherosclerotic cardiovascular disease exists in patients with ASCVD.Elevated triglycerides (TGs) are an important marker of increased residual ASCVD risk2.There are two primary types of Omega-3 fish oils: eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA). Omege-3 fish oils have been shown to lower triglyceride levels.Low-dose combination EPA and DHA has not exhibited incremental cardiovascular benefit in either primary prevention and secondary prevention patients on top of statin therapy3-5.REDUCE-IT showed the use of high dose EPA in patients with either ASCVD or DM and one additional risk factor, and relatively well-controlled LDL-C levels on maximally tolerated statin therapy and residual hypertriglyceridemia (TG 135-499 mg/dL) results in significant reductions in cardiovascular events over a median follow-up period of 4.9 years1. Show notes - REDUCE-IT Multiple epidemiologic and Mendelian randomization studies have established elevated triglyceride (TG) levels as an important risk factor for atherosclerotic cardiovascular events6-8. However previous clinical trials using TG-lowering medication such as niacin, fibrates and low dose omega-3 fish oil have not shown to reduce cardiovascular events when added to statin therapy in patients with or without ASCVD,9,10.The JELIS trial first demonstrated a significant reduction in cardiovascular events when 1.8g daily of eicosapentaenoic acid (EPA) was added to low-intensity statin therapy in patients with ASCVD and hypercholesterolemia, However, the trial was limited due to open label design without placebo, use of low doses of background statin therapy, and geographic/demographic limitations to participants in Japan11.In a large international multicenter randomized controlled trial, the Reduction of Cardiovascular Events with Icosapent Ethyl–Intervention Trial (REDUCE-IT) randomized 8,179 patients with established atherosclerotic heart disease or diabetes and an additional risk factor, on maximally tolerated statin therapy, to 4 gm/day of icosapent ethyl (a highly purified and stable EPA ethyl ester) or mineral oil1. Over a median follow up of 4.9 years, the use of icosapent ethyl ester was associated with significant reductions in major cardiovascular events (cardiovascular death, nonfatal MI, nonfatal stroke, coronary revascularization, or unstable angina) compared to placebo, with an absolute risk reduction of 4.8% and NNT of 21.There were similar reductions in the key components of the primary endpoint, including a 20% relative risk reduction in cardiovascular death with icosapent ethyl.Median TG levels were reduced by 18% in the icosapent ethyl group and rose by 2.2% in the placebo group. LDL levels increased in both groups, although to a lesser degree in the icosapent ethyl group.There was a trend towards increased bleeding (2.7% with icosapent ethyl versus 2.1% with placebo, p=0.06) and a modest but significant increase in hospitalizations for atrial fibrillation or flutter with icosapent ethyl (3.1% versus 2.1%).Since the publication of REDUCE-IT, several clinical practice guidelines, including those of the American Diabetes Association (ADA), National Lipid Association (NLA) and the European Society of Cardiology (ESC)/European Atherosclerosis Society (EAS), have endorsed the use of icosapent ethyl in their recommendations to further reduce ASCVD risk in select patients. References - REDUCE-IT Bhatt DL, Steg PG, Miller M, et al. Cardiovascular risk reduction with icosapent ethyl for hypertriglyceridemia. N Engl J Med. 2019;380(1):11-22. doi: 10.1056/NEJMoa1812792. https://www.nejm.org/doi/full/10.1056/nejmoa1812792Libby P. Triglycerides on the rise: Should we swap seats on the seesaw? Eur Heart J. 2015;36(13):774-776. doi: 10.1093/eurheartj/ehu500. https://academic.oup.com/eurheartj/article/36/13/774/475534Dietary supplementation with n-3 polyunsaturated fatty acids and vitamin E after myocardial infarction: Results of the GISSI-prevenzione trial. gruppo italiano per lo studio della sopravvivenza nell'infarto miocardico. Lancet. 1999;354(9177):447-455. doi: S0140673699070725. https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(99)07072-5/fulltextRisk and Prevention Study Collaborative Group, Roncaglioni MC, Tombesi M, et al. N-3 fatty acids in patients with multiple cardiovascular risk factors. N Engl J Med. 2013;368(19):1800-1808. doi: 10.1056/NEJMoa1205409. https://www.nejm.org/doi/10.1056/NEJMoa1205409?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub%20%200www.ncbi.nlm.nih.govASCEND Study Collaborative Group, Bowman L, Mafham M, et al. Effects of n-3 fatty acid supplements in diabetes mellitus. N Engl J Med. 2018;379(16):1540-1550. doi: 10.1056/NEJMoa1804989. https://www.nejm.org/doi/10.1056/NEJMoa1804989?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub%20%200www.ncbi.nlm.nih.govTriglyceride Coronary Disease Genetics Consortium and Emerging Risk Factors Collaboration, Sarwar N, Sandhu MS, et al. Triglyceride-mediated pathways and coronary disease: Collaborative analysis of 101 studies. Lancet. 2010;375(9726):1634-1639. doi: 10.1016/S0140-6736(10)60545-4. https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(10)60545-4/fulltextDo R, Willer CJ, Schmidt EM, et al. Common variants associated with plasma triglycerides and risk for coronary artery disease. Nat Genet. 2013;45(11):1345-1352. doi: 10.1038/ng.2795. https://www.nature.com/articles/ng.2795Sarwar N, Danesh J, Eiriksdottir G, et al. Triglycerides and the risk of coronary heart disease: 10,158 incident cases among 262,525 participants in 29 western prospective studies. Circulation. 2007;115(4):450-458. doi: CIRCULATIONAHA.106.637793. https://www.ahajournals.org/doi/10.1161/CIRCULATIONAHA.106.637793?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub%20%200pubmedKeech A, Simes RJ, Barter P, et al. Effects of long-term fenofibrate therapy on cardiovascular events in 9795 people with type 2 diabetes mellitus (the FIELD study): Randomised controlled trial. Lancet. 2005;366(9500):1849-1861. doi: S0140-6736(05)67667-2. https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(05)67667-2/fulltextACCORD Study Group, Ginsberg HN, Elam MB, et al. Effects of combination lipid therapy in type 2 diabetes mellitus. N Engl J Med. 2010;362(17):1563-1574. doi: 10.1056/NEJMoa1001282. https://www.nejm.org/doi/full/10.1056/nejmoa1001282Yokoyama M, Origasa H, Matsuzaki M, et al. Effects of eicosapentaenoic acid on major coronary events in hypercholesterolaemic patients (JELIS): A randomised open-label, blinded endpoint analysis. Lancet. 2007;369(9567):1090-1098. doi: S0140-6736(07)60527-3. https://www.thelancet.com/article/S0140-6736(07)60527-3/fulltextNicholls SJ, Lincoff AM, Garcia M, et al. Effect of high-dose omega-3 fatty acids vs corn oil on major adverse cardiovascular events in patients at high cardiovascular risk: The STRENGTH randomized clinical trial. JAMA. 2020;324(22):2268-2280. doi: 10.1001/jama.2020.22258. https://doi.org/10.1001/jama.2020.22258. . Guest Profiles Dr. Peter Toth Dr. Peter Toth is the Director of Preventive Cardiology at CGH Medical Center in Sterling, IL, and Professor of Clinical Family and Community Medicine at the University of Illinois College of Medicine in Peoria, and adjunct associate professor of medicine, Johns Hopkins University School of Medicine. He received his medical degree from Wayne State University School of Medicine in Detroit, MI, and PhD in Biochemistry from Michigan State University in East Lansing. He has written extensively on the topic of lipids and is Co-Editor of twenty textbooks in preventive cardiology, diabetes, hypertension, and lipidology. Additionally, Dr. Toth is the President of the American Society of Preventive Cardiology, past President of the National Lipid Association, as well as incoming chair of the American Heart Association’s Council on Lipoproteins, Lipid Metabolism, and Thrombosis. Dr. Aliza Hussain Dr. Aliza Hussain is a cardiology fellow at Baylor College of Medicine.

May 13, 2022

The following question refers to Section 4.11 of the 2021 ESC CV Prevention Guidelines. The question is asked by Dr. Christian Faaborg-Andersen, answered first by UCSF resident Dr. Jessie Holtzman, and then by expert faculty Dr. Laurence Sperling. Dr. Laurence Sperling is the Katz Professor in Preventive Cardiology at the Emory University School of Medicine and Founder of Preventive Cardiology at the Emory Clinic. Dr. Sperling was a member of the writing group for the 2018 Cholesterol Guidelines, serves as Co-Chair for the ACC's Cardiometabolic and Diabetes working group, and is Co-Chair of the WHF Roadmap for Cardiovascular Prevention in Diabetes. The CardioNerds Decipher The Guidelines Series for the 2021 ESC CV Prevention Guidelines represents a collaboration with the ACC Prevention of CVD Section, the National Lipid Association, and Preventive Cardiovascular Nurses Association. Question #12 Medically supervised cardiac rehabilitation programs after ASCVD events and for patient with heart failure carries a Class I recommendation. However, placement of referrals, uptake and enrollment after referral, and rigor of rehabilitation all remain inconsistent. What minimum cumulative duration of cardiac rehabilitation has been chosen as a threshold of effectiveness for cardiac rehabilitation by the European Society of Cardiology? A. 100-300 minutes, 10 sessions B. 300-500 minutes, 16 sessions C. 500-700 minutes, 22 sessions D. 700-1000 minutes, 28 sessions E. >1000 minutes, 36 sessions Answer #12 The correct answer is E: >1000 minutes across 36 sessions. Cardiac rehabilitation is a comprehensive, multidisciplinary intervention not just including exercise training and physical activity counselling, but also education, risk factor modification, diet/nutritional counselling, and vocational and psychosocial support. A broad evidence base demonstrates that multidisciplinary cardiac rehabilitation and prevention programs after ASCVD events or revascularization reduce recurrent cardiovascular hospitalizations, myocardial infarction, and cardiovascular mortality. In patients with chronic HF (mainly HFrEF), exercise based cardiac rehabilitation (EBCR) may improve all-cause mortality, reduce hospital admissions, and improve exercise capacity and quality of life. Such programs include a wide array of activities including physical activity, risk factor modification, psychosocial support, nutrition counseling, and more. Despite the heterogenous design of clinical trials, cardiac rehabilitation has been shown to be a cost-effective intervention. Based upon the available review data, the European Association of Preventive Cardiology and the European Society of Cardiology proposed minimum standards for secondary prevention cardiac rehabilitation programs. Based upon a comprehensive review of the literature, ESC recommends that cardiac rehabilitation be multidisciplinary, supervised by health professionals, and start as soon as possible after a cardiovascular event. Cardiac rehabilitation should include both aerobic and muscular resistance tailored to the fitness level of the participant, should carry a duration of >1000 minutes in total, and should exceed 36 sessions total. While uptake remains limited, electronic prompts within the medical record and automatic referrals should be considered to enhance referral and participation. Future research should continue to explore the benefit of home-based cardiac rehabilitation with or without telemonitoring. Lastly, studies have shown that uptake remains lower among women, and targeted programs should be undertaken to address such disparities. Main Takeaway Current European Society of Cardiology guidelines provide a Class I (LOE A) recommendation for the participation in multidisciplinary cardiac rehabilitation programs for the secondary prevention of ASCVD events including revascularization and in individuals with heart failure (mainly HFrEF) to improve patient outcomes. Guideline Location Section 4.11, Page 3292. CardioNerds Decipher the Guidelines - 2021 ESC Prevention Series CardioNerds Episode Page CardioNerds Academy Cardionerds Healy Honor Roll CardioNerds Journal Club Subscribe to The Heartbeat Newsletter! Check out CardioNerds SWAG! Become a CardioNerds Patron!

May 12, 2022

The following question refers to Section 6.1 of the 2021 ESC CV Prevention Guidelines. The question is asked by Dr. Christian Faaborg-Andersen, answered first by UCSD cardiology fellow Dr. Harpreet Bhatia, and then by expert faculty Dr. Eugenia Gianos. Dr. Gianos specializes in preventive cardiology, lipidology, cardiovascular imaging, and women’s heart disease; she is the director of the Women’s Heart Program at Lenox Hill Hospital and director of Cardiovascular Prevention for Northwell Health. The CardioNerds Decipher The Guidelines Series for the 2021 ESC CV Prevention Guidelines represents a collaboration with the ACC Prevention of CVD Section, the National Lipid Association, and Preventive Cardiovascular Nurses Association. Question #11 A 70-year-old man with a history of hypertension, diabetes, hyperlipidemia, peptic ulcer disease with a prior upper GI bleed, as well as coronary artery disease presents to clinic. About one year ago he suffered an NSTEMI treated with percutaneous coronary intervention to the mid LAD. He is feeling well and able to walk 1 mile daily with no anginal symptoms. He is currently taking aspirin 81 mg daily, ticagrelor 90 mg BID, atorvastatin 40 mg daily, metoprolol 25 mg BID, lisinopril 5 mg daily, and lansoprazole 15mg daily. He has a preserved ejection fraction. His BP in clinic is 110/70 and HR is 65 bpm. His LDL is 50 mg/dL. What do you recommend for his further management? A. Switch ticagrelor to clopidogrel, continue indefinitelyB. Stop ticagrelor, continue aspirin indefinitelyC. Continue aspirin + ticagrelor indefinitelyD. Stop ticagrelor, start rivaroxaban 2.5 mg BIDListen to the podcast episode! Answer #11 The correct answer is B – stop ticagrelor, continue aspirin indefinitely.Twelve months of DAPT is recommended for acute coronary syndromes (Class I, LOE A). Long-term secondary prevention with dual anti-thrombotic therapy (DAPT > 12 months with a P2Y12 inhibitor and low-dose aspirin or low-dose rivaroxaban 2.5mg BID with low-dose aspirin) may be considered for patients who are at high ischemic risk without high risk of bleeding (Class IIa, LOE A). However, this patient is at increased bleeding risk (peptic ulcer disease with prior GI bleeding) and has no ischemic symptoms, and so neither would be recommended.Main TakeawayIn summary, 12 months of DAPT is recommended after ACS. Prolonged DAPT or low-dose rivaroxaban may be considered with high ischemic risk and low bleeding risk.Guideline LocationSection 6.1, Pages 3294-3295. CardioNerds Decipher the Guidelines - 2021 ESC Prevention SeriesCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor RollCardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron!

May 11, 2022

The following question refers to Section 4.6 of the 2021 ESC CV Prevention Guidelines. The question is asked by student Dr. Shivani Reddy, answered first by NP Carol Patrick, and then by expert faculty Dr. Eileen Handberg. Dr. Handberg is an Adult Nurse Practitioner, Professor of Medicine, and Director of the Cardiovascular Clinical Trials Program in the Division of Cardiovascular Medicine at the University of Florida. She has served as Chair of the Cardiovascular Team Section and the Board of Trustees with the ACC and is the President Elect for the PCNA. The CardioNerds Decipher The Guidelines Series for the 2021 ESC CV Prevention Guidelines represents a collaboration with the ACC Prevention of CVD Section, the National Lipid Association, and Preventive Cardiovascular Nurses Association. Question #10 Ms. DW is a 67-year-old woman with a history of coronary artery disease and prior percutaneous coronary intervention in 2019 with a drug-eluting stent to the proximal left anterior descending artery. They have transitioned to your clinic from a previous provider, and their LDL is 134 mg/dL. What would be the ESC recommended goal LDL-C level for this patient? A. <30 mg/dL B. <55 mg/dL C. <70 mg/dL D. <100 mg/dL Answer #10 The correct answer is B. The ESC guidelines outline a robust LDL-C reduction goal of <55mg/dL (<1.4mmol/L) and ≥50% reduction from baseline in those with known atherosclerotic cardiovascular disease, with the highest possible Class I (LOE A) recommendation for this goal. A goal LDL-C <55mg/dL with ≥50% reduction from baseline should also be considered in apparently healthy persons <70 years of age who are at very high risk (Class IIa, LOE C). To achieve these goals, the guidelines recommend a stepwise approach to treatment including dietary, lifestyle, and medical management. Recognizing that lower LDL-C is better, the guidelines recommend liberal intensification of treatment especially if using submaximal doses of generic or low-cost statins and side effects are not apparent. High-intensity statin is recommended to be prescribed to the highest tolerated dose to reach LDL-C goals set for each specific risk group (Class I, LOE A). If these goals are not achieved with the maximum tolerated dose of a statin, combination therapy with ezetimibe is recommended (Class I, LOE B). Choice A is incorrect. An LDL-C <30mg/dL is a more significant reduction than that recommended by the guidelines, even for patients with known ASCVD. Notably, for patients with ASCVD who experience a second vascular event within 2 years while taking maximum tolerated statin-based therapy, an LDL-C goal of <1.0 mmol/L (40 mg/dL) may be considered. Choice C is incorrect. The ESC prevention guidelines recommend considering a goal of <70mg/dL for patients in the primary prevention setting at high risk who are <70 years of age (Class IIa, LOE C). (Recall again that for those at very high risk the primary prevention recommendation is target LDL-C <55 mg/dL). Choice D is incorrect. LDL-C <100mg/dL was a frequently cited goal in older iterations of various prevention and lipid guidelines. As the data has shifted to support lower LDL-C goals, this is not a noted goal within the 2021 ESC prevention guidelines for patients <70 years of age. Main Takeaway Lower is better when it comes to LDL-C For those with known atherosclerotic cardiovascular disease, liberal intensification of lipid lowering treatment is recommended. Guideline Location Section 4.6.2.1, page 3276-3279, Figure 6 on page 3252, Figure 7 on page 3253 CardioNerds Decipher the Guidelines - 2021 ESC Prevention Series CardioNerds Episode Page CardioNerds Academy Cardionerds Healy Honor Roll CardioNerds Journal Club Subscribe to The Heartbeat Newsletter! Check out CardioNerds SWAG! Become a CardioNerds Patron!

May 10, 2022

The following question refers to Section 4.3 of the 2021 ESC CV Prevention Guidelines. The question is asked by Dr. Maryam Barkhordarian, answered first by pharmacy resident Dr. Anushka Tandon, and then by expert faculty Dr. Noreen Nazir. Dr. Noreen Nazir is Assistant Professor of Clinical Medicine at the University of Illinois at Chicago, where she is the director of cardiac MRI and the preventive cardiology program. The CardioNerds Decipher The Guidelines Series for the 2021 ESC CV Prevention Guidelines represents a collaboration with the ACC Prevention of CVD Section, the National Lipid Association, and Preventive Cardiovascular Nurses Association. Question #9 Mr. A is a 28-year-old man who works as an accountant in what he describes as a “desk job” setting. He shares that life got “a little off-track” for him in 2020 between the COVID-19 pandemic and a knee injury. His 2022 New Years’ resolution is to improve his overall cardiovascular and physical health. He has hypertension and a family history of premature ASCVD in his father, who died of a heart attack at age 50. Prior to his knee injury, he went to the gym 3 days a week for 1 hour at a time, split between running on the treadmill and weightlifting. He has not returned to the gym since his injury and has been largely sedentary, although he is trying to incorporate a 20-minute daily walk into his routine. Which of the following exercise-related recommendations is most appropriate? A. A target of 75-150 minutes of vigorous-intensity or 150-300 minutes of moderate-intensity aerobic physical exercise weekly is recommended to reduce all-cause mortality, CV mortality, and morbidity. B. Bouts of exercise less than 30 minutes are not associated with favorable health outcomes. C. Exercise efforts should be focused on aerobic activity, since only this type of activity is associated with mortality and morbidity benefits. D. Light-intensity aerobic activity like walking is expected to have limited health benefits for persons with predominantly sedentary behavior at baseline. Answer #9 The correct answer is A. There is an inverse relationship between moderate-to-vigorous physical activity and CV morbidity/mortality, all-cause mortality, and incidence of type 2 diabetes, with additional benefits accrued for exercise beyond the minimum suggested levels. The recommendation to “strive for at least 150-300 min/week of moderate-intensity, or 75-150 min/week of vigorous-intensity aerobic physical activity, or an equivalent combination thereof” is a Class 1 recommendation per the 2021 ESC guidelines, and a very similar recommendation (at least 75 minutes of vigorous-intensity or 150 minutes of moderate-intensity activity) is also Class 1 recommendation per 2019 ACC/AHA primary prevention guidelines. Both the ESC and ACC/AHA provide examples of activities grouped by absolute intensity (the amount of energy expended per minute of activity), but the ESC guidelines also offer suggestions for measuring the relative intensity of an activity (maximum/peak associated effort) in Table 7, which allows for a more individualized, customizable approach to setting activity goals. Importantly, individuals who are unable to meet minimum weekly activity recommendations should still be encouraged to stay as active as their abilities and health conditions allow to optimize cardiovascular and overall health. Choice B is incorrect, as data suggests physical activity episodes of any duration, including <10 min, are associated with favorable outcomes like all-cause mortality benefit. The duration of a single exercise bout is less correlated with health benefits than the total physical activity time accumulated per week. Choice C is incorrect. Per the ESC guidelines, it is a class 1 recommendation to perform resistance exercise, in addition to aerobic activity, on 2 or more days per week to reduce all-cause mortality. Data indicate that the addition of resistance exercise to aerobic activity is associated with lower risks of total CV events and all-cause mortality, so it’s expected that a combination of weightlifting and aerobic activity may be more beneficial for than either type of activity alone. The 2019 ACC/AHA prevention guidelines do not make a formal recommendation regarding resistance exercise; they do note that it has multiple health benefits (e.g., BP-lowering, improved glycemic control) though state its association with ASCVD risk reduction is unclear. Choice D is incorrect: sedentary time is independently associated with greater risk for several major chronic diseases and mortality. Reducing sedentary time for inactive adults and adding in light-intensity physical activity (as little as 15 minutes daily) is a class 1 recommendation to reduce all-cause and CV mortality and morbidity. The 2019 ACC/AHA guidelines suggest that reduced sedentary behavior may be “reasonable for ASCVD risk reduction” (Class 2b). Assuming our patient has had predominantly sedentary behavior, starting with a 20-minute daily walk can provide initial health benefits while working up to more and higher-intensity activity. Main Takeaway Physical activity should be individually assessed and prescribed in terms of frequency, intensity, time (duration), type, and progression. Guideline Location Section 4.3.1, Pages 3268-3269, Table 7 CardioNerds Decipher the Guidelines - 2021 ESC Prevention Series CardioNerds Episode Page CardioNerds Academy Cardionerds Healy Honor Roll CardioNerds Journal Club Subscribe to The Heartbeat Newsletter! Check out CardioNerds SWAG! Become a CardioNerds Patron!

May 9, 2022

This question refers to Sections 3.1 of the 2021 ESC CV Prevention Guidelines. The question is asked by CardioNerds Academy Intern, student Dr. Hirsh Elhence, answered first by internal medicine resident at Beaumont Hospital and soon to be Mayo Clinic cardiology fellow and Dr. Teodora Donisan and then by expert faculty Dr. Eugene Yang.Dr. Yang is professor of medicine of the University of Washington where he is medical director of the Eastside Specialty Center and the co-Director of the Cardiovascular Wellness and Prevention Program. Dr. Yang is former Governor of the ACC Washington Chapter and current chair of the ACC Prevention of CVD Section.The CardioNerds Decipher The Guidelines Series for the 2021 ESC CV Prevention Guidelines represents a collaboration with the ACC Prevention of CVD Section, the National Lipid Association, and Preventive Cardiovascular Nurses Association. Question #8 Please read the following patient vignettes and choose the FALSE statement.A. A 39-year-old man who comes for a regular physical, has normal vitals and weight, denies any significant past medical or family history – does not need systematic cardiovascular disease (CVD) assessment.B. A 39-year-old woman who comes for a regular physical, has normal vitals and weight, and has a history of radical hysterectomy (no other significant past medical or family history) – could benefit from systematic or opportunistic CVD assessment.C. A 39-year-old woman who comes for a regular physical, has normal vitals except for a BMI of 27 kg/m2 and a family history of hypertension – requires a systematic global CVD assessment.D. A 39-year-old man who comes for a regular physical, has normal vitals and weight, and has a personal history of type I diabetes – requires a systematic global CVD assessment. Answer #8 The correct answer is C.Option A is an accurate statement, as systematic CVD risk assessment is not recommended in men 40 years-old and women > 50 years-old or postmenopausal, even in the absence of known ASCVD risk factors. (Class IIb, level C)Option C is a false statement and thus the correct answer, as the recommendations for global screening in this patient are not as strong and would require shared decision making. Opportunistic screening of blood pressure can be considered in her, as she is at risk for developing hypertension. Blood pressure screening should be considered in adults at risk for the development of hypertension, such as those who are overweight or with a known family history of hypertension. (Class IIa, level B)Option D is an accurate statement, as systematic global CVD risk assessment is recommended in individuals with any major vascular risk factor (i.e., family history of premature CVD, familial hyperlipidemia, CVD risk factors such as smoking, arterial hypertension, DM, raised lipid level, obesity, or comorbidities increasing CVD risk). (Class I, level C)Additional learning points:Do you know the difference between opportunistic and systematic CVD screening?Opportunistic screening refers to screening without a predefined strategy when the patient presents for different reasons. This is an effective and recommended way to screen for ASCVD risk factors, although it is unclear if it leads to benefits in clinical outcomes.Systematic screening can be done following a clear strategy formally evaluating either the general population or targeted subpopulations (i.e., type 2 diabetics or patients with significant family history of CVD). Systematic screening results in improvements in risk factors but has no proven effect on CVD outcomes.Main TakeawaySystematic CVD risk assessment in the general population without CV risk factors does not seem to be cost effective and has unclear benefits on outcomes, although it does lead to increased detection of potentially actionable CV risk factors. Risk assessment is not a one-time event and should be repeated (e.g., every 5 years), but there is no clear data to guide intervals.Guideline LocationSection 3.1, page 3236; Table on page 3242. CardioNerds Decipher the Guidelines - 2021 ESC Prevention SeriesCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor RollCardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron!

May 8, 2022

The following question refers to Section 3.4 of the 2021 ESC CV Prevention Guidelines. The question is asked by student Dr. Adriana Mares, answered first by early career preventive cardiologist Dr. Dipika Gopal, and then by expert faculty Dr. Michael Wesley Milks. Dr. Milks is a staff cardiologist and assistant professor of clinical medicine at the Ohio State University Wexner Medical Center where he serves as the Director of Cardiac Rehabilitation and an associate program director of the cardiovascular fellowship. He specializes in preventive cardiology and is a member of the American College of Cardiology's Cardiovascular Disease Prevention Leadership Council. The CardioNerds Decipher The Guidelines Series for the 2021 ESC CV Prevention Guidelines represents a collaboration with the ACC Prevention of CVD Section, the National Lipid Association, and Preventive Cardiovascular Nurses Association. Question #7 While you are on holiday break visiting your family, your aunt pulls you aside during the family gathering to ask a few questions about your 70-year-old uncle. He has hypertension, hyperlipidemia, type 2 diabetes mellitus, and moderate chronic obstructive pulmonary disease. His medications include Fluticasone/Salmeterol, Tiotropium, Albuterol, Lisinopril, Simvastatin, and Metformin. She is very concerned about his risk for heart disease as he has never had his “heart checked out.” She asks if the presence of COPD increases his chance of having heart disease. Which of the following statements would best answer her question? A. Systemic inflammation and oxidative stress caused by COPD promote vascular remodeling and a paradoxical ‘anticoagulant’ state affecting all vasculature types. B. Although chronic COPD is associated with increased cardiovascular events, individual exacerbations have no impact on risk of cardiovascular events. C. Patients with mild-moderate COPD are 8-10x more likely to die from atherosclerotic cardiovascular disease than respiratory failure. D. Cardiovascular mortality increases proportionally with an increase in forced expiratory volume in 1 second (FEV1) Answer #7 The correct answer is C. Patients with mild-moderate COPD are 8-10x more likely to die from atherosclerotic cardiovascular disease than respiratory failure. Patients with COPD have a 2-3-fold increased risk of CV events compared to age-matched controls even when adjusted for tobacco smoking, a shared risk factor. This can be partly explained by other common risk factors including aging, hypertension, hyperlipidemia, and low physical activity. Interestingly, CVD mortality increases proportionally with a decrease (rather than increase) in FEV1, making answer choice D wrong (28% increase CVD mortality for every 10% decrease in FEV1). Additionally, COPD exacerbations and related infections are associated with a 4x increase in CVD events, making answer choice B incorrect. COPD has several effects on the vasculature which creates a ‘procoagulant’ not ‘anticoagulant’ effect on all vascular beds. This is associated with increased risk of cognitive impairment due to cerebral microvascular damage as well as increased risk of ischemic and hemorrhagic stroke. Main Takeaway The presence of COPD (even mild to moderate) has a significant impact on the incidence of non-fatal coronary events, stroke, and cardiovascular mortality mediated by inherent disease process and progression, risk factors (smoking, aging, hypertension, and hyperlipidemia), and systemic inflammation altering vasculature creating a ‘procoagulant’ effect. The ESC gives a Class I indication (LOE C) to investigate for ASCVD and ASCVD risk factors in patients with COPD. Guideline Location 3.4.5, Page 3264. CardioNerds Decipher the Guidelines - 2021 ESC Prevention Series CardioNerds Episode Page CardioNerds Academy Cardionerds Healy Honor Roll CardioNerds Journal Club Subscribe to The Heartbeat Newsletter! Check out CardioNerds SWAG! Become a CardioNerds Patron!

May 6, 2022

CardioNerds (Amit Goyal, Daniel Ambinder) and special co-host Dr. Mark Belkin, join the Journal of Cardiac Failure Family to discuss the 2022 AHA/ACC/HFSA Guideline for The Management of Heart Failure. The JCF Editor-In-Chief Dr. Robert Mentz, Deputy Editor Dr. Anu Lala, and FIT editors -- Dr. Vanessa Bluemer, Dr. Ashish Corrhea, and Dr. Quinton Youmans -- share their hot takes and practical takeaways from the guidelines. At JCF, we’re privileged to share this important document that will support improved care for those living with heart failure,” stated Editor-in Chief Dr. Robert J. Mentz and Deputy Editor Anu Lala. “The 2022 guidelines convey patient-centered updates regarding the language we use to communicate disease considerations (e.g., stages of HF) and practice-changing guidance around the diagnosis and management of HF including newer therapeutics (e.g., SGLT2i). There is an emphasis not only on managing HF but also on how to treat important comorbidities as part of the holistic care for patients living with HF." 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure Executive Summary A Clinician's Guide to the 2022 ACC/AHA/HFSA Guideline for the Management of Heart Failure by Dr. Michelle Kittleson CardioNerds Heart Success Series PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Guideline Top 10 Take-Home Messages - Guideline for The Management of Heart Failure 1. Guideline-directed medical therapy (GDMT) for heart failure (HF) with reduced ejection fraction (HFrEF) now includes 4 medication classes that include sodium-glucose cotransporter-2 inhibitors (SGLT2i). 2. SGLT2i have a Class of Recommendation 2a in HF with mildly reduced ejection fraction (HFmrEF). Weaker recommendations (Class of Recommendation 2b) are made for ARNi, ACEi, ARB, MRA, and beta blockers in this population. 3. New recommendations for HFpEF are made for SGLT2i (Class of Recommendation 2a), MRAs (Class of Recommendation 2b), and ARNi (Class of Recommendation 2b). Several prior recommendations have been renewed including treatment of hypertension (Class of Recommendation 1), treatment of atrial fibrillation (Class of Recommendation 2a), use of ARBs (Class of Recommendation 2b), and avoidance of routine use of nitrates or phosphodiesterase-5 inhibitors (Class of Recommendation 3: No Benefit). 4. Improved LVEF is used to refer to those patients with previous HFrEF who now have an LVEF >40%. These patients should continue their HFrEF treatment. 5.Value statements were created for select recommendations where high-quality, cost-effectiveness studies of the intervention have been published. 6. Amyloid heart disease has new recommendations for treatment including screening for serum and urine monoclonal light chains, bone scintigraphy, genetic sequencing, tetramer stabilizer therapy, and anticoagulation. 7. Evidence supporting increased filling pressures is important for the diagnosis of HF if the LVEF is >40%. Evidence for increased filling pressures can be obtained from noninvasive (e.g., natriuretic peptide, diastolic function on imaging) or invasive testing (e.g., hemodynamic measurement). 8. Patients with advanced HF who wish to prolong survival should be referred to a team specializing in HF. A HF specialty team reviews HF management, assesses suitability for advanced HF therapies, and uses palliative care including palliative inotropes where consistent with the patient's goals of care. 9. Primary prevention is important for those at risk for HF (stage A) or pre-HF (stage B). Stages of HF were revised to emphasize the new terminologies of “at risk” for HF for stage A and pre-HF for stage B. 10.Recommendations are provided for select patients with HF and iron deficiency, anemia, hypertension, sleep disorders, type 2 diabetes, atrial fibrillation, coronary artery disease, and malignancy.

May 4, 2022

CardioNerds (Amit Goyal and Daniel Ambinder) join Dr. Phoo Pwint Nandar (former FIT Ambassador), Dr. Deep Shah (current FIT Ambassador), and Dr. Sugat Wagle from the Summa Health Cardiology Department for an afternoon at Cuyahoga National Valley Park. We discuss a case of a post-partum woman who presented with ventricular fibrillation arrest due to SCAD. She had ongoing advanced cardiac life support (ACLS) for nearly 60 minutes before obtaining return of spontaneous circulation. We discuss the broad differential of VF arrest, including acute coronary syndrome and spontaneous coronary artery dissection (SCAD) – among many others. We also go over the etiology and management of SCAD as well the complications. Pregnancy is a crucial stressor to the cardiovascular system and understanding its hemodynamic changes is crucial to all physicians. The E-CPR segment is provided by Dr. Grace Ayafor, Interventional cardiology faculty, Summa Health. Jump to: Case media - Case teaching - References CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Case Media Episode Schematics & Teaching - SCAD Pearls - SCAD SCAD remains underdiagnosed. It has a wide range of clinical presentations, including chest pain, ACS, VT/VF arrest, and cardiogenic shock.Underlying etiologies of SCAD include autoimmune diseases, connective tissue disorders, fibromuscular dysplasia, external stressors, and pregnancy.There are 3 types of SCAD, and coronary angiogram is the gold standard for diagnosis.Common areas of involvement of SCAD include left anterior descending and left circumflex arteries; however, SCAD can manifest in any coronary artery as well as simultaneously in multiple coronary arteries. Left main trunk involvement is rare, more likely to be associated with the peri-partum state, and requires complex management decisions guided by a heart team approach.Most SCAD cases are benign and treated conservatively, however, some require intervention (PCI or CABG) depending on clinical severity and course.Recurrent SCAD has been reported in 10-30% of the patients and aggressive management of hypertension is recommended.Guidelines regarding SCAD management are largely based on expert consensus due to a dearth of high-quality data. Efforts to raise awareness and study this syndrome are of paramount importance. Notes - SCAD 1. What is SCAD and how does it present? Spontaneous coronary artery dissection (SCAD) is defined as an epicardial coronary dissection that is not associated with atherosclerosis or instrumentation.This occurs with hematoma formation within the tunica media, thereby potentially compressing the arterial true lumen leading to ischemia.There are two proposed mechanisms of hematoma formation: “inside-out” and “outside-in”. The inside-out hypothesis posits that the hematoma arises from the true lumen via a dissection flap – an endothelial-intimal disruption. Conversely the outside-in hypothesis posits that the hematoma arises de novo within the media through disruption of traversing microvessels.There is a wide range of clinical presentation for SCAD varying in severity including asymptomatic / benign presentation, anginal syndromes, acute myocardial infarction, VT/VF arrest, and cardiogenic shock. Our patient presented with VF arrest and ACS.SCAD epidemiology is confounded by a lack of awareness. A high index of suspicion is warranted. Diagnosis can be missed in young or mid-life without CV risk factors who would present with atypical/mild chest pain. 2. What are the etiologies of SCAD? SCAD is associated with the peripartum state (presumed due to combination of hormonal mediated vessel wall integrity changes and hemodynamic stressors), illicit substance use, autoimmune disorders, connective tissue disorders, fibromuscular dysplasia, and vigorous external stressors.Many patients recall extreme physical or emotional stress preceding the event. Men are more likely to present in the setting of a physical stressor whereas women are more likely to report an emotional stressor.Pregnancy-associated SCAD is most common in the first week after delivery like our patient.Genetic evaluation for connective tissue disorders and aortopathy syndromes (i.e., Marfan, Loeys-Dietz, and Ehlers-Danlos) should be considered.Arterial imaging to identify significant extracoronary vascular abnormalities is recommended since there is the association of SCAD with fibromuscular dysplasia. 3. What is the gold standard to diagnose SCAD? Coronary angiography performed by an experienced interventional cardiologist is the gold standard to diagnose SCAD. The left anterior descending artery is most commonly affected, and most cases of SCAD occur in the mid-distal arteries.There are 3 angiographic variants SCAD.Type 1 is with evident with the contrast dye staining the arterial wall with multiple radiolucent lumen.Type 2 (majority of the cases including the present case) is diffuse stenosis of varying severity with subtle abrupt changes in arterial caliber (long smooth narrowing).Type 3 mimics atherosclerosis and is often difficult to differentiate from it. 4. What is the management of SCAD in acute setting? Management of SCAD depends on clinical severity. Thrombolytics should be avoided. Most cases are benign and treated conservatively with work up for secondary causes. 95% of conservatively treated patients with mild SCAD such as minimal ongoing ischemia with preserve coronary flow will heal within 30 days. More severe cases of SCAD require intervention such as PCI or CABG. Surgical approaches are preferred in left main involvement, long segments, and with diffuse coronary artery involvement like in our case. Utilizing vein grafts is preferred as most SCAD cases heal with eventual graft closure. Off note, PCI in SCAD is associated with higher complication rates and suboptimal outcomes, including risk of iatrogenic dissection or propagation of hematoma. 5. What is the management of SCAD in pregnant patient? The management strategy of SCAD during pregnancy is similar to that in the nonpregnant state, with additional considerations to optimize maternal and fetal outcomes. After 20 weeks gestation, recommend left lateral recumbent positioning whenever possible to reduce aortocaval compression and optimize venous return. If necessary, consider maternal stabilization and optimization of cardiac status followed by planned delivery under controlled conditions. For more, enjoy Episode #167 – Cardiac Interventions During Pregnancy with Dr. Michael Luna. 5. What is the prognosis of SCAD and long-term management? Recurrent SCAD has been reported in 10-30% of patients. Post-SCAD chest pain is common and may persist for many months. Due to iatrogenic risk from invasive angiography, serial electrocardiography and biomarker assessment, and noninvasive cardiac computed tomography angiography should be considered. Standard heart failure medications are indicated for left ventricular dysfunction, and hypertension should be treated. 6. How to prevent recurrent SCAD? The factors associated with recurrence remain poorly understood. After SCAD, further pregnancy should perhaps be discouraged and contraception should be discussed. Women who strongly desire pregnancy should receive thorough preconception counseling. References Macaya, F., Salinas, P., Gonzalo, N., Fernández-Ortiz, A., Macaya, C., & Escaned, J. (2018). Spontaneous coronary artery dissection: contemporary aspects of diagnosis and patient management. Open Heart, 5(2), e000884. Hayes, S. N., Kim, E. S. H., Saw, J., Adlam, D., Arslanian-Engoren, C., Economy, K. E., Ganesh, S. K., Gulati, R., Lindsay, M. E., Mieres, J. H., Naderi, S., Shah, S., Thaler, D. E., Tweet, M. S., & Wood, M. J. (2018). Spontaneous Coronary Artery Dissection: Current State of the Science: A Scientific Statement From the American Heart Association. Circulation, 137(19). McGrath-Cadell, L., McKenzie, P., Emmanuel, S., Muller, D. W. M., Graham, R. M., & Holloway, C. J. (2016). Outcomes of patients with spontaneous coronary artery dissection. Open Heart, 3(2), e000491. Alonso-Fernández-Gatta, M., Uribarri, A., Diego-Nieto, A., & Sánchez, P. L. (2017). Progressive spontaneous coronary artery dissection secondary to fibromuscular dysplasia requiring mechanical circulatory support. Journal of Cardiology Cases, 16(6), 216–218. Cepas-Guillén, P. L., Flores-Umanzor, E. J., Sabate, M., & Masotti, M. (2019). Multivessel spontaneous coronary artery dissection involving the left main coronary artery: a case report. European Heart Journal - Case Reports, 3(1). Tweet, M. S., Eleid, M. F., Best, P. J. M., Lennon, R. J., Lerman, A., Rihal, C. S., Holmes, D. R., Jr, Hayes, S. N., & Gulati, R. (2014). Spontaneous Coronary Artery Dissection. Circulation: Cardiovascular Interventions, 7(6), 777–786. Hayes SN, Tweet MS, Adlam D, et al. Spontaneous Coronary Artery Dissection: JACC State-of-the-Art Review. J Am Coll Cardiol 2020;76:961-984.

May 3, 2022

CardioNerds (Daniel Ambinder), ACHD series co-chairs, Dr. Josh Saef (ACHD fellow, University of Pennsylvania) Dr. Daniel Clark (ACHD fellow, Vanderbilt University), and ACHD FIT lead Dr. Jon Kochav (Columbia University) join Dr. Eric Krieger (Director of the Seattle Adult Congenital Heart Service and the ACHD Fellowship, University of Washington) to discuss multimodality imaging in congenital heart disease. Audio editing by CardioNerds Academy Intern, Dr. Maryam Barkhordarian. Special introduction to CardioNerds Clinical Trialist Dr. Shiva Patlolla (Baylor University Medical Center). In this episode we discuss the strengths and weaknesses of the imaging modalities most commonly utilized in the diagnosis and surveillance of patients with ACHD. Specifically, we discuss transthoracic and transesophageal echocardiography, cardiac MRI and cardiac CT. The principles learned are then applied to the evaluation of two patient cases – a patient status post tetralogy of Fallot repair with a transannular patch, and a patient presenting with right ventricular enlargement of undetermined etiology. The CardioNerds Adult Congenital Heart Disease (ACHD) series provides a comprehensive curriculum to dive deep into the labyrinthine world of congenital heart disease with the aim of empowering every CardioNerd to help improve the lives of people living with congenital heart disease. This series is multi-institutional collaborative project made possible by contributions of stellar fellow leads and expert faculty from several programs, led by series co-chairs, Dr. Josh Saef, Dr. Agnes Koczo, and Dr. Dan Clark. The CardioNerds Adult Congenital Heart Disease Series is developed in collaboration with the Adult Congenital Heart Association, The CHiP Network, and Heart University. See more Disclosures: None Pearls • Notes • References • Guest Profiles • Production Team CardioNerds Adult Congenital Heart Disease PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls - Cardiovascular Multimodality Imaging in Congenital Heart Disease Transthoracic echocardiography (TTE) is the first line diagnostic test for the diagnosis and surveillance of congenital heart disease due to widespread availability, near absent contraindications, and ability to perform near comprehensive structural, functional, and hemodynamic assessments in patients for whom imaging windows allow visualization of anatomic areas of interest.Transesophageal echocardiography (TEE) use in ACHD patients is primarily focused on similar indications as in acquired cardiovascular disease patients: the assessment of endocarditis, valvular regurgitation/stenosis severity and mechanism, assessment of interatrial communications in the context of stroke, evaluation for left atrial appendage thrombus, and for intraprocedural guidance. When CT or MRI are unavailable or contraindicated, TEE can also be used when transthoracic imaging windows are poor, or when posterior structures (e.g. sinus venosus, atrial baffle) need to be better evaluated.Cardiac MRI (CMR) with MR angiography imaging is unencumbered by imaging planes or body habitus and can provide comprehensive high resolution structural and functional imaging of most cardiac and extracardiac structures. Additional key advantages over echocardiography are ability to reproducibly quantify chamber volumes, flow through a region of interest (helpful for quantifying regurgitation or shunt fraction), assess for focal fibrosis via late gadolinium enhancement imaging, and assess the right heart.Cardiac CT has superior spatial resolution in a 3D field of view which makes it useful for clarifying anatomic relationships between structures, visualizing small vessels such as coronary arteries or collateral vessels, and assessing patency of larger vessels (e.g branch pulmonary arteries) through metallic stents which may obscure MR imaging. Downsides relative to CMR include requirement of nephrotoxic contrast for imaging of intracardiac/intravascular structures, and while gated images can be obtained throughout the cardiac cycle similarly to CMR, this is particularly costly from an ionizing radiation standpoint.When working up an unknown congenital lesion, it is critical to communicate the differential diagnosis when ordering a test so that the imager can protocol the study accordingly. Not all echocardiograms, CT or MRI scans are the same. Show notes - Cardiovascular Multimodality Imaging in Congenital Heart Disease What are the key strengths and weaknesses of transthoracic echocardiography? STRENGTHS: (1) “Most important ability is availability”: Transthoracic echocardiography is the first line imaging modality in the assessment of patients with congenital heart disease because it is widely available at significantly lower cost with no contraindications or risks to the patient. (2) Versatility: A wide array of echo approaches can be employed to provide comprehensive structural and physiological data. 2D echo techniques are most useful for visual assessment of cardiac structural abnormalities. Color doppler provides qualitative data regarding flow, and spectral doppler (inclusive of tissue doppler imaging) provides quantitative data defining intracardiac hemodynamics. 3D echo can be applied to optimize imaging planes for valve area planimetry and quantify chamber volumes as well as global contractile function. Strain imaging using 2D speckle tracking techniques can be employed to evaluate regional contractility. (3) High temporal resolution: High temporal resolution makes echocardiography a superior modality for imaging fast-moving structures (e.g., valvular vegetations or intracardiac masses). WEAKNESSES: (1) “You can’t study what you can’t see”: Suboptimal ultrasound penetration can limit transthoracic imaging quality in patients with large body habitus, or patients in the post-operative state. Furthermore, imaging planes are limited by sonographic windows - many anatomic cardiac (e.g., sinus venosus and coronary sinus defects, anomalous coronary arteries) and extracardiac (e.g., aortic dilation/coarctation, anomalous venous return) abnormalities are often incompletely evaluated by echocardiography in adult patients. This is a major limitation as many ACHD conditions are associated with aortopathy and anomalous pulmonary or systemic venous return which may necessitate dedicated cross-sectional imaging. Finally, right ventricular imaging is limited by near field artifact and complex chamber geometry; and similarly anterior structures such as right ventricular to pulmonary arterial conduits are poorly evaluated with transthoracic echocardiography. What differentiates a congenital echocardiogram from a standard adult protocol? Congenital echocardiograms obtain more comprehensive anatomic evaluation to visualize structural anomalies that might not be evident in standard imaging planes. Most congenital echo protocols begin with a subcostal short axis and long axis sweep to determine segmental anatomy, visceral and atrial situs, cardiac position, cardiac looping, and arterial situs. Additional views are attempted from the suprasternal position to better characterize major venous and arterial connections and anatomy (bidirectional Glenn, etc.). Sweeps are often obtained between views within the same window to clarify the relationships between anatomic structures and identify abnormalities (e.g. inter-chamber connections) not apparent in the standard imaging planes. What is the role of transesophageal echocardiography in adult congenital cardiology imaging? In adult patients with acquired cardiovascular disease, transesophageal echocardiography (TEE) is most commonly employed for the assessment of endocarditis, valvular regurgitation/stenosis severity and mechanism, assessment of interatrial communications in the context of stroke, evaluation for left atrial appendage thrombus, and for intraprocedural guidance. Each of these indications are also commonly encountered in an ACHD population. In congenital cardiology, improved spatial resolution of posterior heart structures can similarly be leveraged to image pathology not well visualized by a transthoracic approach such as for identifying sinus venosus defects, characterizing secundum atrial septal defects to determine feasibility of percutaneous closure, or for assessment of baffle leak on Fontan or atrial switch D-TGA patients. Additionally, TEE increasingly plays a critical role in the perioperative setting (e.g., examining physiology pre- and post-bypass) and for monitoring and guidance of percutaneous interventions in the cardiac catheterization lab. What are the key strengths and weaknesses of Cardiac MRI? STRENGTHS: (1) Unencumbered imaging planes: Unlike echocardiography, for which views are limited by echocardiographic windows, cardiac MRI technicians can prescribe unlimited imaging planes for a more complete coverage of both intracardiac and extracardiac anatomy – particularly with addition of MR angiography. This allows for improved assessment of anterior structures (e.g., the RV, RV-PA conduits), posterior structures (e.g., atrial baffles, sinus venosus or coronary sinus defects), and extracardiac anomalies (e.g., anomalous venous return, aortopathies, pulmonary arterial stenoses), which are usually poorly imaged by echocardiography in adults. Additionally, imaging is generally unaffected by body habitus, and may be used as the primary imaging modality for patients with poor transthoracic windows. (2) Reproducible volumetric quantification: Cardiac MRI is the gold standard for chamber volume assessment. Chamber volumes are obtained from endocardial contouring of Cine-CMR short axis stacks,

Apr 27, 2022

CardioNerds (Amit Goyal and Daniel Ambinder), join Dr. Kara Denby (Interventional cardiology fellow, Cleveland Clinic), Dr. Tony Pastor (ACHD fellow, Harvard Medical School), Dr. Katie Berlacher (Cardiology program director, UPMC), and Dr. Stephen Cook (ACHD cardiologist, Indiana University) to discuss empowering the LGBTQIA+ community of cardiovascular patients & professionals and more in this installment of the Narratives in Cardiology Series. This episode features the Indiana ACC Chapter. Episode introduction and audio editing by CardioNerds Academy Intern, Pace Wetstein. This discussion was inspired by this perspective piece on ACC.org titled: Finding Our Voices: Building an LGBTQIA+ Community Within Cardiology. To learn more about diversity and equity among the LGBTQIA+ population, check out this webinar organized by the ACC. The PA-ACC & CardioNerds Narratives in Cardiology is a multimedia educational series jointly developed by the Pennsylvania Chapter ACC, the ACC Fellows in Training Section, and the CardioNerds Platform with the goal to promote diversity, equity, and inclusion in cardiology. In this series, we host inspiring faculty and fellows from various ACC chapters to discuss their areas of expertise and their individual narratives. Join us for these captivating conversations as we celebrate our differences and share our joy for practicing cardiovascular medicine. We thank our project mentors Dr. Katie Berlacher and Dr. Nosheen Reza. Video Version • Notes • Production Team Claim free CME just for enjoying this episode! There are no relevant disclosures for this episode. The PA-ACC & CardioNerds Narratives in Cardiology PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Tweetorial - Empowering the LGBTQIA+ Community of Cardiovascular Patients & Professionals https://twitter.com/Gurleen_Kaur96/status/1526334939830034432?s=20&t=wMk75ORn1_KJtMTOY1IAdw Video version - Empowering the LGBTQIA+ Community of Cardiovascular Patients & Professionals Coming soon Production Team Dr. Gurleen Kaur Amit Goyal, MD Daniel Ambinder, MD

Apr 24, 2022

CardioNerds (Amit Goyal and Daniel Ambinder) join Dr. Sonu Abraham (Cardiology fellow, Lahey Hospital and Medical Center), Dr. Amitoj Singh (Internal Medicine Resident, Lahey Hospital and Medical Center), Dr. Ahmed Ghoneem (Internal Medicine Resident, Lahey Hospital and Medical Center, CardioNerds Academy Chief) and Dr. Aanika Balaji (Internal Medicine Resident, Johns Hopkins) for a scrumptious meal on the Boston Harbor as they discuss a case of a young woman with metastatic melanoma on immune checkpoint inhibitors presenting with dyspnea. The presentation, risk factors, work up and management of patients with immune checkpoint inhibitor induced myocarditis are described. The E-CPR segment is provided by Dr. Sarju Ganatra, the founding director of the cardio-oncology program at Lahey Clinic. CardioNerds Clinical Trialist Dr. Carrie Mahurin (University of Vermont Medical Center) is introduced at the beginning of the episode. A 41-year-old woman presented with mild dyspnea on exertion and non-productive cough. She had a history of Hashimoto thyroiditis, nodular thyroid s/p resection on levothyroxine, and metastatic melanoma on immune checkpoint inhibitor therapy with ipilimumab and nivolumab. She also had a history of obesity and underwent gastric bypass surgery several years prior. Though she lost weight after the surgery, she regained a significant amount and was 244 lbs with a BMI of 42. Her exam findings were remarkable for tachycardia, bilateral pulmonary rales, elevated JVP, and symmetric pedal edema. Investigations revealed a mild troponin elevation, non-specific EKG changes, and TTE with severely reduced left ventricular function (EF 15%) and a low GLS. Cardiac MRI showed patchy delayed myocardial enhancement in a non-ischemic distribution with marked global hypokinesis and EF of 11%. Endomyocardial biopsy confirmed the diagnosis of immune checkpoint inhibitor (ICI) associated myocarditis. The ICI therapy was discontinued and she was treated with high dose intravenous corticosteroids followed by a prolonged oral steroid taper with clinical improvement and complete recovery of left ventricular function. Jump to: Case media - Case teaching - References CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Case Media - immune checkpoint inhibitor myocarditis Episode Schematics & Teaching CardioNerds Myocarditis, updated 1.20.21 Pearls - immune checkpoint inhibitor myocarditis ICI-associated myocarditis has a high mortality rate necessitating a high degree of clinical suspicion. When in doubt, check it out! The initial 4 diagnostic pillars include EKG, troponin, BNP and TTE. Cardiac MRI and endomyocardial biopsy help to confirm the diagnosis.Left ventricular function is normal in 50% of these patients with ICI-associated myocarditis, so the ejection fraction is not a sensitive test for ruling this out.Endomyocardial biopsy should be considered in patients with a high clinical suspicion but negative or ambiguous non-invasive imaging.Early initiation of corticosteroids within 24 hours of presentation is associated with better outcomes.ICIs should be discontinued indefinitely in those with Grade 3 or 4 disease. Notes - immune checkpoint inhibitor myocarditis 1. Immune checkpoint inhibitors – What are they and why should we as cardiologists know about them? Immune checkpoint inhibitors (ICI) boost the host immune response against tumor cells by inhibiting the intrinsic brakes of the immune response.There are currently 7 FDA approved drugs in this group: one CTLA-4-blocking antibody called ipilimumab; three PD-1-blocking antibodies [nivolumab, pembrolizumab, and cemiplimab]; and three PD-L1-blocking antibodies [atezolizumab, avelumab, and durvalumab].Like a car, T-cells have an ignition switch, gas pedals, and brakes.T-cells become activated when receptors on the surface of the T-cell bind to an antigen on the surface of the invading cells like cancer cells.Think of the T-cell receptor as the ignition switch and the antigen as the key.Antigen presenting cells patrol the body and pick up evidence of foreign antigens like cancer which they present to T-cells in the lymph nodes via the T-cell receptor.Like gas pedals, there are co-stimulatory signals like CD 28 which interact with proteins on the antigen presenting cells. With these “gas pedal” stimuli, T-cells get activated, multiply, and hunt for the cancer and finally kill the cancer cells.The T-cells also have “breaks” or “checkpoints” to down-regulate the immune response.The Cytotoxic T-lymphocyte antigen 4, also called the CTLA-4, acts to slow down the activation of T-cells.Further down the line, there is another checkpoint called the Programmed cell death 1 or PD-1. PD-1 is a molecule on the surface of T-cells which acts as another set of brakes.When a T cell with PD-1 on its surface interacts with another cell which has a PD-1 ligand (PD-L1), the T-cell activity is down-regulated.Many cancer cells overexpress PD-L1 to fight back against the T cells, by putting a “brake” on their immune response.By removing these brakes, we can augment the T-cells’ immune response against cancer cells.But if the T-cells mount an exaggerated response against normal host cells, then an autoimmune process ensues leading to “immune-related adverse events” (irAEs) like ICI-associated myocarditis. 2. Who are at risk of developing ICI-associated myocarditis? Anti-CTLA 4 therapy is associated with a higher prevalence of cardiotoxicity than the PD-1 and PD-L1 inhibitors.Combination therapy (i.e., when 2 or more ICIs are given together) increase the risk of irAEs.Preexisting diabetes, obesity, and autoimmune disease have been found to be independent risk factors.An association of preexisting cardiovascular risk factors like hypertension and smoking with the development of ICI-induced myocarditis has been suggested. 3. What are the prevalence and prognosis of ICI-associated myocarditis? Immune checkpoint inhibitors have various forms of cardiotoxicities, but ICI-associated myocarditis is the most feared complication.The overall prevalence is 1.2% to 2.4% when using combination ICI therapy. However, the estimated rate of mortality in ICI associated myocarditis is 38 to 46%.Approximately 50% of these patients with myocarditis may develop heart failure, cardiogenic shock, complete heart block, cardiac arrest, and ventricular arrhythmias. 4. What is the differential diagnose for ICI-associated myocarditis? The differential diagnoses are acute coronary syndrome, stress cardiomyopathy, other forms of myocarditis, pericarditis, pneumonitis, viral myocarditis, endocrinopathies, cardiac sarcoidosis and other causes of cardiomyopathy and heart failure including prior cardiotoxic therapy. 5. What are the initial investigations to be done for ICI-associated myocarditis? EKG, troponin, BNP, and TTE (as needed) are the basic 4 pillars of testing in patients with suspected ICI induced myocarditis.Nearly all patients with myocarditis have an abnormal EKG. These are however non-specific findings like sinus tachycardia, QRS or QT prolongation, conduction abnormalities, diffuse T-wave inversion, abnormal Q waves, atrial or ventricular arrhythmias, local or diffuse ST elevation.Troponins are elevated in most cases, up to 94% in one study. The implications of the level of troponin elevation are not completely clear but there is data that suggests that higher levels of troponin elevation are associated with worse cardiovascular outcomes.BNP can be elevated if the patient is in heart failure or volume overloaded. However, it lacks sensitivity and specificity for ICI associated myocarditis and is not always helpful.Even patients with fulminant myocarditis can present with a normal left ventricular function. Around 50% of patients with ICI induced myocarditis have been found to have a normal LV function. Also, among those who had major adverse cardiac events, 38% had a normal EF. 6. How do you grade severity? The American Society of Clinical Oncology broadly categorized the intensity of disease into 4 groups: G1 – Mildly abnormal screening tests and no symptomsG2 – Abnormal screening tests with mild symptomsG3 – Moderately abnormal screening tests (arrhythmia, cardiac biomarker > upper limits of normal and significant echocardiographic findings) and symptoms with mild activity.G4 – Moderate to severe decompensation, hemodynamic instability, cardiac biomarker > 3 upper limit of normal, requiring intravenous medications or interventions. To summarize, G1 and G2 are considered stable and minimally symptomatic and G3 and G4 are very symptomatic or unstable patients and will need to be admitted. 7. What are the treatment options? Prompt initiation of immunosuppressive therapy is critical for these patients.The first line agents are corticosteroids.Start with high dose corticosteroids within 24 hours of presentation. Typically, we start with intravenous methylprednisolone 1000 mg daily for 3 days, followed by oral prednisone 1 mg/kg/day.The steroids should then be tapered slowly over at least 4–6 weeks only after resolution of symptoms, normalization of LVEF or stabilization of arrhythmias.If unresponsive to steroids, tacrolimus, mycophenolate mofetil, anti-thymocyte globulin, iv gamma globulin and plasmapheresis are alternative therapies. 8. Is it safe to restart ICIs after treatment? The current recommendation is a definite discontinuation of ICI in case of grade 3 (severe) or life threatening (grade 4) immune related adverse events.May consider re-challenge in those with milder disease and complete cardiac recovery – individualized and multidisciplinary team approach. References

Apr 6, 2022

The CardioNerds Academy Class of 2021 graduation ceremony kicked off the inaugural Sanjay V Desai Lecture: Growth Mindset, Power of Yet, & Pursuit of Mastery. Join us as Dr. Tommy Das (CardioNerds Academy Program Director), and Dr. Saman Nematollahi (CardioNerds Academy Director of Research) discuss Growth Mindset with Dr. Keri Shafer and Dr. David Hirsh. Terrific acting by Dr. Patrick Zakka, Dr. Teodora Donisan, Dr. Ahmed Ghoneem, and Dr. Jessie Holtzman. Dr. Sanjay V Desai serves as the Chief Academic Officer, The American Medical Association and is the former Program Director of the Osler Medical Residency at The Johns Hopkins Hospital. Dr. Keri Shafer is an adult congenital heart disease specialist at Boston Children’s Hospital, and an assistant professor of pediatrics within Harvard Medical School. She completed internal medicine residency at Beth Israel Deaconess Medical Center, before completing cardiology fellowship at UT Southwestern and Adult Congenital and Pulmonary Hypertension subspecialty training at Boston Children’s and BWH. Dr. David Hirsh is an associate professor of Medicine within Harvard Medical School, as well as the director of the HMS Academy fellowship in medical education and the associate dean of undergraduate medical education. Relevant disclosures: None CardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron!

Apr 1, 2022

CardioNerds, Amit Goyal, Dr. Tommy Das (Program Director of the CardioNerds Academy and Cardiology fellow at Cleveland Clinic), Dr. Rick Ferraro (Director of CardioNerds Journal Club and Cardiology fellow at the Johns Hopkins Hospital), Dr. Patrick Zakka (CardioNerds Academy Chief fellow of House Jones and Cardiology fellow at UCLA) discuss omega-3 fatty acids & the battle of the oils with Dr. Pam Taub, Director of Step Family Foundation Cardiovascular Rehabilitation and Wellness Center and Professor of Medicine at UC San Diego. Learn all about the different types of omega-3 fatty acids and the differences between prescription omega-3 fatty acids and dietary supplement fish oils. Audio editing by CardioNerds Academy Intern, Shivani Reddy. This episode is part of the CardioNerds Lipids Series which is a comprehensive series lead by co-chairs Dr. Rick Ferraro and Dr. Tommy Das and is developed in collaboration with the American Society For Preventive Cardiology (ASPC). Relevant disclosures: None Pearls • Notes • References • Guest Profiles • Production Team CardioNerds Cardiovascular Prevention PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls - Omega-3 Fatty Acids & The Battle Of The Oils Coming soon! Show notes - Omega-3 Fatty Acids & The Battle Of The Oils Coming soon! References - Omega-3 Fatty Acids & The Battle Of The Oils Arnett DK, Blumenthal RS, Albert MA, et al. 2019 ACC/AHA Guideline on the Primary Prevention of Cardiovascular Disease: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines [published correction appears in Circulation. 2019 Sep 10;140(11):e649-e650] [published correction appears in Circulation. 2020 Jan 28;141(4):e60] [published correction appears in Circulation. 2020 Apr 21;141(16):e774].Grundy SM, Stone NJ, Bailey AL, et al. 2018 AHA/ACC/AACVPR/AAPA/ABC/ACPM/ADA/AGS/APhA/ASPC/NLA/PCNA Guideline on the Management of Blood Cholesterol: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines [published correction appears in Circulation. 2019 Jun 18;139(25):e1182-e1186]. Circulation. 2019;139(25):e1082-e1143.Authors/Task Force Members; ESC Committee for Practice Guidelines (CPG); ESC National Cardiac Societies. 2019 ESC/EAS guidelines for the management of dyslipidaemias: Lipid modification to reduce cardiovascular risk [published correction appears in Atherosclerosis. 2020 Jan;292:160-162] [published correction appears in Atherosclerosis. 2020 Feb;294:80-82]. Atherosclerosis. 2019;290:140-205.Bhatt D, Steg P, Miller M et al., 2019. Cardiovascular Risk Reduction with Icosapent Ethyl for Hypertriglyceridemia. The New England journal of medicine, 380(1), pp.11–22.Budoff M, Bhatt D, Kinninger A et al. Effect of icosapent ethyl on progression of coronary atherosclerosis in patients with elevated triglycerides on statin therapy: final results of the EVAPORATE trial. Eur Heart J. 2020;41(40):3925-3932.Nicholls S, Lincoff A, Garcia M et al. Effect of High-Dose Omega-3 Fatty Acids vs Corn Oil on Major Adverse Cardiovascular Events in Patients at High Cardiovascular Risk: The STRENGTH Randomized Clinical Trial. JAMA. 2020;324(22):2268-2280. Guest Profiles Dr. Pam Taub Dr. Pam Taub, Professor of Medicine, is the founding director of the StepFamily Foundation Cardiac Rehabilitation and Wellness Center at the University of California, San Diego. Dr. Taub is a leader in preventive cardiology and has authored over one hundred publications, abstracts and book chapters. Dr. Taub is a leader in multiple professional societies, including board membership for the American Society of Preventive Cardiology. Dr. Patrick Zakka Dr. Patrick Zakka completed his medical school at the American University of Beirut in Lebanon, followed by internal medicine residency and a chief resident year at Emory University. He is currently a first year cardiology fellow at UCLA and graduated as a CardioNerds fellow in House Taussig and is now the Chief Fellow of House Jones. CardioNerds Lipids Production Team Tommy Das, MD Dr. Rick Ferraro Amit Goyal, MD Daniel Ambinder, MD

Mar 27, 2022

In this episode we discuss cardiogenic shock due to valvular heart disease. Join Dr. Pranoti Hiremath (Interventional cardiology fellow, Johns Hopkins), Dr. Karan Desai (CN Critical Care Series Co-Chair, Cardiology fellow, University of Maryland), Dr. Yoav Karpenshif (CN Critical Care Series Co-Chair, Chief cardiology fellow, University of Pennsylvania), and Amit Goyal (CardioNerds Co-Founder) as they interview Dr. Paul Cremer (Associate Director of the Cardiac Intensive Care Unit and Associate Director of the Cardiovascular Fellowship at the Cleveland Clinic) in this broad overview of valvular shock. We discuss the nuances in diagnosis, differing presentations and how physical exam, multi-modality imaging, and invasive hemodynamics can inform management. Audio editing by Dr. Gurleen Kaur (Director of the CardioNerds Internship and CardioNerds Academy Fellow). The CardioNerds Cardiac Critical Care Series is a multi-institutional collaboration made possible by contributions of stellar fellow leads and expert faculty from several programs, led by series co-chairs, Dr. Mark Belkin, Dr. Eunice Dugan, Dr. Karan Desai, and Dr. Yoav Karpenshif. Pearls • Notes • References • Guest Profiles • Production Team CardioNerds Cardiac Critical Care PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls and Quotes - Cardiogenic Shock and Valvular Heart Disease Shock due to valve disease is the result of a structural abnormality that may be temporized with medical therapy and circulatory support devices. However, it is ultimately best treated with a structural solution in the form of either percutaneous valvular therapies or cardiac surgery.When treating a patient with cardiogenic shock with normal or hyperdynamic ventricular function, we should keep a high index of suspicion for valvular disease. The cardiac output may be reduced due to a stenotic lesion “blocking” forward flow or regurgitant lesion causing backward flow.Acute mitral and aortic regurgitation will typically not manifest as a loud murmur on physical exam. The combination of hypotension and rapid flow of regurgitant blood on an “unprepared” cardiac chamber results in rapid equalization of chamber pressures, shortening the intensity and duration of the murmur. On transthoracic echocardiogram, for instance with acute MR, color Doppler may not show a large turbulent jet, and thus the MR may be underestimated or not appreciated at all.Echocardiography is critical to understand the etiology and severity of valvular shock, and invasive hemodynamics are often needed to guide medical and mechanical interventions.In multi-valve disease with severe aortic stenosis and functional mitral regurgitation, we typically treat the aortic stenosis first, since the mitral regurgitation may improve from the reduction in afterload associated with treating aortic stenosis. Show notes - Cardiogenic Shock and Valvular Heart Disease 1. Shock due to valve disease arises due to a structural problem that may be temporized with medical therapy and circulatory support devices, but is ultimately best treated with a structural solution in the form of either percutaneous valvular therapies or cardiac surgery. Stabilizing therapies for acute mitral regurgitation include afterload reduction with vasodilators, diuresis as needed to reduce pulmonary edema, and mechanical circulatory support including intra-aortic balloon pumps.Therapies for acute aortic regurgitation are typically more limited and include vasopressors such as epinephrine. Bradycardia should be avoided with agents such as dobutamine or temporary pacing to reduce time in diastole. Temporary mechanical circulatory support options are limited in the setting of acute AR, though case reports of techniques such as LAVA ECMO (left atrial venoarterial extracorpeal membrane oxygenation) as a bridge to definitive therapy have been reported.There are several factors to consider in patients with aortic stenosis and cardiogenic shock.In some patients with aortic stenosis and LV dysfunction, the shock is a result of LV pressure overload potentially leading to congestion, the high afterload introduced on the LV by the stenotic aortic valve, and increased systemic vascular resistance (compensatory for the failing LV). In these patients, acute vasodilators (specifically nitroprusside) can relieve the additive afterload on the LV imposed by increased SVR as a bridge to definitive therapy.In other patients with severe AS, the LV faces high afterload at the level of the aortic valve but the SVR is relatively low (as well as the pressures in the aortic root which can reduce coronary perfusion), and thus these patients may require a pure alpha agonist (e.g., phenylephrine) to reduce the afterload mismatch and reduce myocardial ischemia.Furthermore, when patients have high LV filling pressures, they are reliant on longer diastole times and an atrial kick to promote LV filling and thus rapid atrial fibrillation can be highly detrimental. In both phenotypes, mechanical circulatory support may be needed as a bridge to valve surgery or TAVR.Percutaneous balloon valvuloplasty of the aortic valve may be utilized as a bridge to definitive therapy in select patientsIn scenarios of valvular disease and cardiogenic shock, right heart catheterization can be helpful to guide and titrate medical therapy and inform decisions to escalate to mechanical circulatory support.Percutaneous therapies (e.g., TAVR or Transcatheter Edge to Edge Repair with MitraClip) are increasingly being utilized as a “primary” therapy on a case by case basis for patients in cardiogenic shock with valvular disease. More data is needed to inform patient phenotypes who would benefit from such a strategy without futility. 2. What is the differential diagnosis for cardiogenic shock with normal or hyperdynamic left ventricular function? One framework to approach cardiogenic shock with normal or hyperdynamic left systolic function is to consider (1) pericardial failure with constriction or tamponade; (2) myocardial failure with severe restrictive disease (3) electrical failure with new arrhythmia, or (4) valvular failure.In this scenario, we should have a high index of suspicion for valvular disease. The cardiac output may be reduced due to a stenotic lesion blocking forward flow or regurgitant lesion causing backward flow. 3. If I don’t hear a significant murmur on examination, does that rule out an acute regurgitant valvular disease as a cause of shock? Acute mitral and aortic regurgitation may not manifest as a loud murmur on physical exam. In severe, acute AR, a murmur may not be audible if the diastolic pressure in the LV and aorta equilibrate quickly. Similarly, in acute, severe MR, there can be a rapid rise in LA Pressure reducing the driving pressure across the mitral valve.On transthoracic echocardiogram, the same pathophysiology can explain why acute regurgitant lesions may not be readily apparent. For instance, with acute MR, color Doppler may not show a large turbulent jet, and thus the MR may be underestimated or not appreciated at all. In patients with sudden hemodynamic instability after myocardial infarction with hyperdynamic LV function by TTE, for instance, and no other cause for deterioration, TEE can be helpful in evaluating for Acute MR due to papillary muscle or chordal rupture. 4. Echocardiography and guidance with right heart catheterization is helpful to understand the etiology and severity of valvular shock. Echocardiography can help determine whether valve dysfunction is primary (e.g. leaflet perforation due to endocarditis) versus secondary (e.g. dilated left ventricle leading to functional mitral regurgitation), as well as provide clues to the chronicity of valve disease.A right heart catheterization can help inform whether valvular disease is the primary insult or if other factors are contributing, inform an initial management strategy (e.g., medical therapies alone vs. mechanical circulatory support), and assess response to therapy. 5. In multi-valve disease, what is the best way to differentiate which lesion is the culprit? These scenarios are not uncommon and require clinicians to use a multi-modal approach, from patient history, exam, echocardiography, other imaging modalities, and invasive hemodynamics. Identifying the “primary” lesion can still be difficult even after multiple data points.Empiric therapy and assessment of subsequent hemodynamic response may be one way to practically approach multi-valve disease.One scenario covered on the episode was patients with severe aortic stenosis and severe mitral regurgitation. The MR in this scenario may be partly functional due to high LV systolic pressures and may improve with intervention on the aortic valve. Thus, one approach would be to treat AS and evaluate if the MR improves. References - Cardiogenic Shock and Valvular Heart Disease Erlebach M, Lange R. Multivalvular Disease: Percutaneous Management in 2019 and Beyond. Interv Cardiol. 2019;14(3):142-146. Published 2019 Nov 18. doi:10.15420/icr.2019.13.R1 Khot UN, Novaro GM, Popović ZB, Mills RM, Thomas JD, Tuzcu EM, Hammer D, Nissen SE, Francis GS. Nitroprusside in critically ill patients with left ventricular dysfunction and aortic stenosis. N Engl J Med. 2003 May 1;348(18):1756-63. doi: 10.1056/NEJMoa022021. PMID: 12724481. Otto CM, Nishimura RA, Bonow RO, et al. 2020 ACC/AHA Guideline for the Management of Patients With Valvular Heart Disease: Executive Summary: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines [published correction appears in Circulation. 2021 Feb 2;143(5):e228] [published correction appears in Circulation. 2021 Mar 9;143(10):e784]. Circulation.

Mar 25, 2022

The following question refers to Section 4.8 of the 2021 ESC CV Prevention Guidelines. The question is asked by CardioNerds Academy Intern student Dr. Christian Faaborg-Andersen, answered first by UCSF resident Dr. Jessie Holtzman, and then by expert faculty Dr. Melissa Tracy. Dr. Tracy is a preventive cardiologist, echocardiographer, Director of Cardiac Rehabilitation, and solid organ transplant cardiologist at Rush University. The CardioNerds Decipher The Guidelines Series for the 2021 ESC CV Prevention Guidelines represents a collaboration with the ACC Prevention of CVD Section, the National Lipid Association, and Preventive Cardiovascular Nurses Association. Question #6 A 62-year-old man with a history of non-obstructive coronary artery disease, heart failure with reduced ejection fraction (EF 30-35%), stage III chronic kidney disease, and type II diabetes mellitus presents to your clinic to establish care. His only medications are aspirin 81 mg daily and metformin 1000 mg BID, which he has taken since being diagnosed with diabetes mellitus 5 years ago. His hemoglobin A1c is 6.8%. What changes would you recommend to his medications at this time?A. Start glipizideB. Start saxagliptinC. Start empagliflozinD. No changes Answer #6 The correct answer is C – start empagliflozin.The Trials involving SGLT-2 inhibitors and GLP-1R agonists have shown cardiovascular benefits independent of glycemic control and metformin use.The ADA recommends metformin as a first-line therapy for all patients with type 2 DM. The ESC also recommends metformin as first-line therapy but only in patients without ASCVD, CKD, or HF (Class I, LOE B). If a patient has ASCVD, metformin can be considered (Class IIa, LOE B). Rather, for those patients with type 2 DM and ASCVD, the ESC recommends the use of GLP-1R agonist or SGLT-2 inhibitors with proven outcome benefits to reduce CV and/or cardiorenal outcomes (Class I, LOE A). Additionally, for those with type 2 DM and either CKD or HFrEF, the ESC recommends the use of SGLT-2 inhibitor to improve outcomes (Class I, LOE A).In contrast to the ADA, the view of the ESC is that metformin should be considered but is not mandatory first-line treatment in patients with diabetes and ASCVD or evidence of target organ damage. The initiation of metformin in such patients should not forego or delay the initiation of evidence-based SGLT2 inhibitors or GLP-1RAs.Therefore, the next best step for our patient is to start an SGLT-2 inhibitor given his history of CAD, HF, and CKD. While this patient’s A1c goal is within the range recommended for patients with Type 2 DM and ASCVD (<7%), given his CAD, HF, and CKD an SGLT-2 inhibitor should still be added.Saxagliptin is a DPP-4 inhibitor, a class of drugs that showed no effect of MACE but increased risk of HF hospitalization in patients with DM and existing.Lifestyle management is a top priority for ASCVD prevention and management of DM. Lifestyle intervention lowers future microvascular and macrovascular risks as well as mortality in the longer term. Intensive lifestyle changes with low-calorie diets and mean weight losses in the region of 10 kg leads to remission of type 2 DM in around 46% of cases at 1 year and 36% by 2 years. Smoking cessation, a diet low in saturated fat and high in fiber, aerobic physical activity, strength training, and reduction in energy intake for weight optimization are all recommended for patient with diabetes mellitus (Class I).Main TakeawayIn patients with Type 2 DM and ASCVD or end organ dysfunction, SGLT-2 inhibitors or GLP-1R agonists should be recommended regardless of background therapy or glycemic control. For patients with type 2 diabetes mellitus and CKD or HFrEF, SGLT-2 inhibitor is recommended.Guideline LocationSection 4.8.1, Pages 3289-90. CardioNerds Decipher the Guidelines - 2021 ESC Prevention SeriesCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor RollCardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron!

Mar 25, 2022

The following question refers to Section 4.10 of the 2021 ESC CV Prevention Guidelines. The question is asked by CardioNerds Academy Intern student Dr. Christian Faaborg-Andersen, answered first by UCSD fellow Dr. Patrick Azcarate, and then by expert faculty Dr. Laurence Sperling. Dr. Laurence Sperling is the Katz Professor in Preventive Cardiology at the Emory University School of Medicine and Founder of Preventive Cardiology at the Emory Clinic. Dr. Sperling was a member of the writing group for the 2018 Cholesterol Guidelines, serves as Co-Chair for the ACC's Cardiometabolic and Diabetes working group, and is Co-Chair of the WHF Roadmap for Cardiovascular Prevention in Diabetes. The CardioNerds Decipher The Guidelines Series for the 2021 ESC CV Prevention Guidelines represents a collaboration with the ACC Prevention of CVD Section, the National Lipid Association, and Preventive Cardiovascular Nurses Association. Question #5 The European Society of Cardiology Prevention guidelines currently recommend that low-dose colchicine (0.5mg/day) may be considered for the primary prevention of cardiovascular disease.A. TrueB. False Answer #5 The correct answer is False. The correct answer is False.The European Society of Cardiology recommends that low-dose colchicine may be considered as an adjunctive therapy for secondary rather than primary prevention of cardiovascular disease in individuals whose risk factors are otherwise insufficiently controlled (Class IIb, LOE A). A broad evidence base currently supports that inflammation has pro-atherosclerotic effects and that reducing inflammation may reduce atherogenesis in high-risk patients.The initial LoDoCo trial in 2013 first demonstrated a 10.7% absolute risk reduction in acute coronary syndrome, out of hospital cardiac arrest, and non-cardioembolic ischemic stroke with daily low-dose colchicine; however, results were clouded by small sample size. Subsequently, the CANTOS trial in 2017 demonstrated a 15% relative reduction in non-fatal myocardial infarction, non-fatal stroke, and cardiovascular death with Canakinumab, an anti-inflammatory monoclonal antibody inhibitor of interleukin-1. More recently, the COLCOT trial in 2019 studying patients with recent AMI and LoDoCo2 trial in 2021 studying patients with stable chronic CAD both demonstrated reductions in myocardial infarction, cardiovascular mortality, CVA, and ischemia-driven revascularization with colchicine 0.5mg/day. In the LoDoCo2 trial, stable CAD was defined either angiographically, by coronary CT, CAC >400, or history of CABG >10 years prior with evidence of failed grafts or angioplasty since that time.In high-risk individuals with stable ischemic heart disease, the most recent evidence suggests that once daily low dose colchicine may reduce myocardial infarction and other ischemic events. Future studies may assess the biochemical markers including the trend of lipids and inflammatory markers to identify subpopulations that may benefit most from this therapy.Main Takeaway:Based upon the 2021 ESC Prevention Guidelines, clinicians may consider initiating low-dose colchicine (0.5mg/day) for secondary prevention of cardiovascular disease, particularly if other risk factors are insufficiently controlled or if recurrent CVD events occur despite optimal therapy.Guideline Location: Section 4.10, page 3291. CardioNerds Decipher the Guidelines - 2021 ESC Prevention SeriesCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor RollCardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron!

Mar 24, 2022

The following question refers to Section 4.7 and figure 16 of the 2021 ESC CV Prevention Guidelines. The question is asked by CardioNerds Academy Intern Student Dr. Shivani Reddy, answered first by Fellow at Johns Hopkins Dr. Rick Ferraro, and then by expert faculty Dr. Roger Blumenthal.Dr. Roger Blumenthal is professor of medicine at Johns Hopkins where he is Director of the Ciccarone Center for the Prevention of Cardiovascular Disease. He was instrumental in developing the 2018 ACC/AHA CV Prevention Guidelines. Dr. Blumenthal has also been an incredible mentor to CardioNerds from our earliest days.The CardioNerds Decipher The Guidelines Series for the 2021 ESC CV Prevention Guidelines represents a collaboration with the ACC Prevention of CVD Section, the National Lipid Association, and Preventive Cardiovascular Nurses Association. Question #4 Ms. K.M. is a 40-year-old woman presenting to the outpatient clinic for a routine physical exam required for her employment as an airline stewardess. She states she has been in her usual good health but does experience occasional headaches and lightheadedness while in flight. On exam her BP was noted to be 170/90. The diagnosis of hypertension is confirmed during a subsequent clinic visit. What would be the most appropriate initial therapy recommendation(s) for Ms. K.M.?A. Initiate single drug therapy with a beta-blocker.B. Discuss and initiate lifestyle interventionsC. Initiate two-drug combination therapy with a thiazide-like diuretic, BB, CCB, or an ARB.D. Both B and C Answer #4 The correct answer is D. Both B (lifestyle interventions) and C (initial combination therapy) are appropriate at this time. Lifestyle interventions are indicated for all patients with high-normal BP or hypertension because they can delay the need for drug treatment or complement the BP-lowering effect of drug treatment (Class 1). Moreover, most lifestyle interventions have health benefits beyond their effect on BP. Single-drug therapy will rarely achieve optimal BP control. Therefore, initial antihypertensive therapy with a combination of two drugs, preferably as a single-pill combination, is recommended for the management of HTN (Class 1). The only exceptions would be patients with a baseline BP close to the recommended target, who might achieve that target with a single drug, or very old (>80 years) or frail patients who may better tolerate a gentler reduction of BP. Five major classes of BP-lowering drug therapy have shown benefit in reducing CV events; angiotensin-converting enzyme (ACE) inhibitors, angiotensin receptor blockers (ARBs), beta-blockers, calcium channel blockers (CCBs), and thiazide or thiazide-like diuretics. A combination of an ACE inhibitor or ARB with a CCB or thiazide/thiazide-like diuretic is the preferred initial therapy for most patients with hypertension (Class 1). For those in whom treatment requires escalation to three drugs, a combination of an ACE inhibitor or ARB with a CCB and a thiazide/thiazide-like diuretic should be used (Class 1). Resistant hypertension is defined as BP being uncontrolled despite treatment with optimal or best-tolerated doses of three or more drugs including a diuretic, and confirmed by ABPM or HBPM. Spironolactone is the most effective drug for lowering BP in resistant hypertension when added to existing treatment; however, the risk of hyperkalaemia is increased in patients with CKD. When spironolactone is not tolerated, amiloride, alpha-blockers, beta-blockers, or centrally acting drugs, such as clonidine, have evidence supporting their use. Renal denervation and device-based therapy may be considered for specific cases. Beta-blockers should be used when there is a specific indication (e.g. angina, post myocardial infarction, arrythmia, HFrEF, or as an alternative to an ACE inhibitor or ARB in women of child-bearing potential). Combinations of an ACE inhibitor and an ARB are not recommended because of no added benefit on outcomes and increased risk of harm (Class III). The diagnosis and treatment of hypertension in women is similar to that in men, except for women of child-bearing potential or during pregnancy, because of potential adverse effects of some drugs on the fetus, especially in the first trimester. In addition, the effect of oral contraceptive pills on the risk of developing or worsening hypertension should be considered. Main Takeaway: Combination drug therapies are more effective in lowering BP than monotherapy. BP management in women is similar to men with the exception of child-bearing potential given potential teratogenicity of some agents. Guideline Location: 4.7.5.1-4, Page 3288 Figure 16, pg. 3287 CardioNerds Decipher the Guidelines - 2021 ESC Prevention SeriesCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor RollCardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron!

Mar 23, 2022

The following question refers to Section 4.3 of the 2021 ESC CV Prevention Guidelines. The question is asked by CardioNerds Academy Intern Dr. Maryam Barkhordarian, answered first by medicine resident CardioNerds Academy House Chief Dr. Ahmed Ghoneem, and then by expert faculty Dr. Kim Williams. Dr. Williams is Chief of the Division of Cardiology and is Professor of Medicine and Cardiology at Rush University Medical Center. He has served as President of ASNC, Chairman of the Board of the Association of Black Cardiologists (ABC, 2008-2010), and President of the American College of Cardiology (ACC, 2015-2016). The CardioNerds Decipher The Guidelines Series for the 2021 ESC CV Prevention Guidelines represents a collaboration with the ACC Prevention of CVD Section, the National Lipid Association, and Preventive Cardiovascular Nurses Association. Question #3 Mrs. B is a 56-year-old African American woman with a past medical history significant for type 2 diabetes (HbA1C 7.6) and hypercholesterolemia. Her calculated ASCVD risk score today is 12.5% and her BMI is 24kg/m2. She is concerned about her high cholesterol levels despite being on a statin and feels that her diet is “not healthy enough.” She is interested in making dietary changes to help reduce her ASCVD risk. Which of the following recommendations is appropriate?A. Sodium restriction to <3g /day will be of no benefit because she is not hypertensive.B. Isocaloric substitution of saturated fat with polyunsaturated fat is associated with reduction of CHD risk.C. Dietary fiber intake is associated with GI benefits but has no CV risk reduction benefit.D. Supplementing diet with vitamins A, B, C and E helps reduce ASCVD risk. Answer #3 The correct answer is B.Risk of CHD is reduced when dietary saturated fats are replaced with other foods having similar caloric values. The greatest reduction was observed when saturated fats were isocalorically replaced with polyunsaturated fats (↓25%), followed by monounsaturated fats (↓15%) and carbohydrates from whole grains (↓9%). This is a class 1a recommendation in the ESC guidelines and a class IIa recommendation in the 2019 ACC/AHA guidelines. Conversely, increased trans fatty acid intake is associated with increased CHD risk. A regulation of the European Union (EU) Commission has set the upper limit of trans fats to 2 g per 100 g of fat. The ACC/AHA guidelines recommend that the intake of trans fats should be avoided (a class III: harm).Choice A is incorrect because dietary sodium restriction is recommended not only for control of blood pressure, but also for reduction of ASCVD risk. In a meta-analysis, salt reduction of 2.5 g/day resulted in a 20% reduction of ASCVD events (RR 0.80). Reduction of salt intake is a class 1 recommendation in the ESC guidelines compared to a class IIa recommendation in the 2019 ACC/AHA guidelines.Choice C is incorrect because a 10 g/day higher fiber intake was associated with a 16% lower risk of stroke (RR 0.84) and a 6% lower risk of type 2 DM (RR 0.94). A high fiber intake may reduce postprandial glucose responses after carbohydrate-rich meals and also lower triglyceride levels. The Mediterranean diet is rich in fiber (it includes high intakes of fruits, vegetables, pulses and wholegrain products) and is a class I recommendation.Choice D is incorrect because while vitamin supplementation has been associated with reduction in ASCVD risk in observational studies, intervention trials have failed to show any benefit. Main Takeaway:A healthy diet is recommended as a cornerstone of CVD prevention in all individuals, independent of their underlying co-morbidities. Replacing saturated with unsaturated fats, reducing salt intake, and choosing a more plant-based diet that is rich in fiber can lower risk of CVD.Guideline LocationSection 4.3.2, Page 3270 CardioNerds Decipher the Guidelines - 2021 ESC Prevention SeriesCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor RollCardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron!

Mar 22, 2022

The following question refers to Section 3.3 of the 2021 ESC CV Prevention Guidelines. The question is asked by CardioNerds Academy Intern student Dr. Adriana Mares, answered first by Brigham & Women’s medicine intern & Director of CardioNerds Internship Dr. Gurleen Kaur, and then by expert faculty Dr. Allison Bailey.Dr. Bailey is an advanced heart failure and transplant cardiologist at Centennial Heart. She is the editor-in-chief of the American College of Cardiology's Extended Learning (ACCEL) editorial board and was a member of the writing group for the 2018 American Lipid Guidelines. The CardioNerds Decipher The Guidelines Series for the 2021 ESC CV Prevention Guidelines represents a collaboration with the ACC Prevention of CVD Section, the National Lipid Association, and Preventive Cardiovascular Nurses Association. Question #2 Mr. Early M. Eye is a 55-year-old man with a history of GERD who is seeing you in clinic as he is concerned about his family history of early myocardial infarction and would like to discuss if he should be taking a statin for cardiovascular prevention. He has never smoked tobacco. His 10-year CVD risk is estimated to be 8%. Which imaging modality is recommended by the ESC guidelines to reclassify his CVD risk?A. Coronary Artery Calcium (CAC) scoringB. Echocardiography C. Ankle brachial index D. Contrast enhanced computed tomography coronary angiography (CCTA)E. None of the above Answer #2 The correct answer is A.Coronary artery calcium (CAC) scoring can reclassify CVD risk upwards and downwards and should specifically be considered in patients with calculated risk scores that are around decision thresholds. CAC scores which are high-than-expected for age and sex increase estimated future CVD risk. Notably, CAC scoring may also be used to “de-risk” if CAC is absent or lower-than-expected. The 2021 ESC Prevention Guidelines give a Class IIb (LOE B) recommendation to consider CAC scoring to improve risk classification around treatment decision thresholds. However, one limitation of CAC is that it does not provide direct information on total plaque burden or stenosis severity. In addition, there is also a Class IIb (LOE B) recommendation to use plaque detection by carotid ultrasound as an alternative when CAC scoring is unavailable or not feasible. Plaque assessed through carotid ultrasound is defined as presence of wall thickening that is >50% greater than the surrounding vessel wall or a focal region with intima-media thickness measurement >1.5mm that protrudes into the lumen.Similar to the ESC Prevention Guidelines, the 2019 ACC/AHA guidelines on primary prevention of CVD also have a Class IIa recommendation for using CAC score, and explicitly mention its use for adults at intermediate risk (>7.5% to 100 Agatson units to reclassify risk upwards and CAC of 0 to reclassify risk downwards. However, the guidelines also mention that clinicians should not down-classify risk in patients who have CAC of 0 if they are current smokers, have diabetes, have a family history of ASCVD, or have chronic inflammatory conditions. Furthermore, the 2018 ACC/AHA Cholesterol guidelines have a Class IIa recommendation that if CAC is 0, it is reasonable to withhold statin therapy and reassess risk in 5 to 10 years, as long as higher risk conditions that we just discussed are absent. If CAC is 1-99, it is reasonable to initiate statin therapy for patients ≥ 55 years of age.Choice B is incorrect. Echocardiography is not recommended to improve CV risk prediction due to lack of convincing evidence that it improves CVD risk reclassification.Choice C is incorrect. While the 2013 ESC guidelines mentioned that ABI may be considered as a risk modifier in CVD risk estimation, the newer 2021 guidelines state that ankle brachial index has limited potential in terms of reclassification risk, though an individual patient data meta-analysis showed there may be utility for women at intermediate risk. 12-27% of middle-aged individuals can have an abnormal ankle brachial index, defined as less than 0.9, of which 50-89% may not have typical claudication symptoms. Conversely, the 2019 ACC/AHA guidelines include ABI <0.9 as a risk-enhancing factor.Choice D is incorrect. Coronary computed tomographic angiography (CCTA) has been shown in studies such as SCOT-HEART to have utility in predicting cardiac events in patients with stable chest pain and can identify coronary stenosis. It is not currently recommended by ESC guidelines for prognostic value or risk classification in asymptomatic patients.According to the ESC guidelines, routine vascular testing or imaging other than CAC scoring or carotid ultrasound for plaque determination are not recommended (Class III, LOE B).In terms of this patient’s family history of premature CVD, the ESC guidelines describe that even though family history is significantly associated with CVD in studies, it only marginally improves the prediction of CVD risk beyond conventional ASCVD risk factors. However, family history should still be obtained regularly when seeing patients, and if there is a positive family history of ASCVD, a comprehensive CVD risk assessment is warranted. Importantly, family history is not binary and those with a greater “dose” of family history (more relatives affected at earlier ages) may be at greater risk.Main TakeawayWhen a patient without established ASCVD has an estimated 10-year risk around treatment decision thresholds, CAC scoring is the best-established imaging modality to improve CVD risk stratification.Guideline LocationSection 3.3.3, page 3259 CardioNerds Decipher the Guidelines - 2021 ESC Prevention SeriesCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor RollCardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron!

Mar 21, 2022

This question refers to Sections 3.2 and 3.3 of the 2021 ESC CV Prevention Guidelines. The question is asked by CardioNerds Academy Intern, student Dr. Hirsh Elhence, answered first by Ohio State University Cardiology Fellow Dr. Alli Bigeh, and then by expert faculty Dr. Eugene Yang. Dr. Yang is professor of medicine of the University of Washington where he is medical director of the Eastside Specialty Center and the co-Director of the Cardiovascular Wellness and Prevention Program. Dr. Yang is former Governor of the ACC Washington Chapter and current chair of the ACC Prevention of CVD Section. The CardioNerds Decipher The Guidelines Series for the 2021 ESC CV Prevention Guidelines represents a collaboration with the ACC Prevention of CVD Section, the National Lipid Association, and Preventive Cardiovascular Nurses Association. Question #1 A 48-year-old Pakistani woman with rheumatoid arthritis comes to your clinic asking how she can reduce her risk of ASCVD. Her mother died of an MI at age 45, her father is healthy at age 79. Her calculated 10-year risk based on SCORE2 is 3%. SBP is 120 mmHg, LDL is 120 mg/dL. What is the next best step? A. Order an echocardiogram B. Schedule a follow-up appointment in 1 year C. Discuss initiating a statin D. Repeat lipid panel in 3-5 years Answer #1 Answer: C. Discuss Initiating a statin The absolute benefit derived from risk factor modification depends on the absolute risk of CVD and the absolute improvements in each risk factor category. Risk factor treatment recommendations are based on categories of CVD risk (“low-to-moderate”, “high”, and “very high”). The cut-off risk levels for these categories are numerically different for various age groups to avoid undertreatment in the young and to avoid overtreatment in the elderly. As age is a major driver of CVD risk, but lifelong risk factor treatment benefit is higher in younger people, the risk thresholds for considering treatment are lower for younger people as per the ESC guidelines. Treatment decisions should be made with shared decision-making valuing patient preference. Option A is INCORRECT- there is a lack of convincing evidence that echocardiography improves CVD risk reclassification, and it is NOT recommended to improve CV risk prediction. (Class III, LOE B) Option B is INCORRECT- simply doing nothing is not appropriate for this patient with elevated CVD risk. Option C is CORRECT- This patient has a seemingly low 10-year CVD risk based on SCORE 2 of 3% and her SBP is controlled; however, given her age she is considered as having high CVD risk, therefore treatment should be considered. Stepwise approach involves targeting LDL 20%. Guideline Location Table 5 and Figure 5, Page 32513.2.3.4, Page 32533.2.3, Figure 6 page 32523.3, Pages 3258-3259 CardioNerds Decipher the Guidelines - 2021 ESC Prevention SeriesCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor RollCardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron!

Mar 20, 2022

CardioNerds (Amit Goyal and Daniel Ambinder) and guest host, Dr. Priya Kothapalli (UT Austin fellow and CardioNerds Ambassador), join SUNY Downstate cardiology fellows, Dr. Eric Kupferstein and Dr. Gautham Upadhya to discuss a case about a patient who had coronary artery bypass grafting that was complicated by a LIMA grafted to the great cardiac vein. Dr. Alan Feit (Professor of Medicine, SUNY Downstate) provides the E-CPR for this episode. Dr. Moritz Wyler von Ballmoos (Director, robotic cardiac and vascular surgery for Houston Methodist Cardiovascular Surgery Associates) provides a special perspective regarding coronary artery bypass grafting as it relates to this case. Episode introduction with CardioNerds Clinical Trialist Dr. Jana Lovell (Johns Hopkins). Left Internal Mammary Artery (LIMA) to Left Anterior Descending (LAD) artery anastomosis is the cornerstone of Coronary Artery Bypass Graft (CABG) surgery. Anastomosis of the LIMA to the Great Cardiac Vein (GCV) is a known but rare complication of the surgery. Currently there are no clear guidelines in regard to further management. We report a case of a LIMA to GCV anastomosis managed with a drug eluting stent (DES) to the mid LAD after ruling out a significant left to right heart shunt. Jump to: Case media - Case teaching - References CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Case Media - Coronary Artery Bypass Grafting: An Iatrogenic Left to Right Cardiac Shunt Angiography Episode Schematics & Teaching - Coronary Artery Bypass Grafting: An Iatrogenic Left to Right Cardiac Shunt Pearls - Coronary Artery Bypass Grafting: An Iatrogenic Left to Right Cardiac Shunt Listen to the patient's story. The patient determines when the angina is no longer stable angina.The placebo effect of our interventions should not be discounted.LIMA to GCV anastomosis creates a left to right cardiac shunt. A Qp:Qs greater than 1.5 signifies a significant shunt.Increasing the pressure in the coronary sinus may actually be beneficial to the patient.LIMA-LAD is remains the most efficacious and long lasting graft but why not other arterial grafts? Notes - Coronary Artery Bypass Grafting: An Iatrogenic Left to Right Cardiac Shunt Iatrogenic anastomosis of the LIMA to the GCV is a rare but noted complication of CABG surgery. Review of the literature has reported under 40 such cases of arteriovenous fistula formation in the coronary system. Detection of the anastomosis generally stems from recurrent angina which can be attributed to unresolved ischemia or coronary steal syndrome but also can be detected with new heart failure (namely right sided heart failure due to left to right shunting). Diagnosis is usually made with coronary angiography, but CT coronary angiography has also been reported. Due to the rarity of this complication, no clear guidelines are in place directing the management leaving it to the discretion of the various Heart Teams. Evaluating for signs of heart failure and/or ischemia, and measuring the Qp:Qs have been the most common signs directing management. Various options are available for closing the fistula and include coil or balloon embolization, vascular plugs, venous ligation or a covered stent. Redoing the surgery is also an option. Spontaneous closure of the fistula has also been reported. Lastly, if redo surgery is not performed then regardless of fistula closure, coronary intervention for the native diseased artery may be pursued to relieve symptoms. References Boden et al; COURAGE Trial Research Group. Optimal medical therapy with or without PCI for stable coronary disease. N Engl J Med. 2007 Apr 12;356(15):1503-16. doi: 10.1056/NEJMoa070829. Epub 2007 Mar 26. PMID: 17387127.Maron et al; ISCHEMIA Research Group. Initial Invasive or Conservative Strategy for Stable Coronary Disease. N Engl J Med. 2020 Apr 9;382(15):1395-1407. doi: 10.1056/NEJMoa1915922. Epub 2020 Mar 30. PMID: 32227755; PMCID: PMC7263833.Klocke et al; ACC/AHA/ASNC guidelines for the clinical use of cardiac radionuclide imaging--executive summary: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (ACC/AHA/ASNC Committee to Revise the 1995 Guidelines for the Clinical Use of Cardiac Radionuclide Imaging). J Am Coll Cardiol. 2003 Oct 1;42(7):1318-33. doi: 10.1016/j.jacc.2003.08.011. PMID: 14522503.Chow et al; Diagnostic accuracy and impact of computed tomographic coronary angiography on utilization of invasive coronary angiography. Circ Cardiovasc Imaging. 2009 Jan;2(1):16-23. doi: 10.1161/CIRCIMAGING.108.792572. PMID: 19808560.Sheiban et al; Iatrogenic left internal mammary artery-coronary vein anastomosis treated with covered stent deployment via retrograde percutaneous coronary sinus approach. Catheter Cardiovasc Interv. 2006 Nov;68(5):704-7. doi: 10.1002/ccd.20842. PMID: 17039511.Lumley et al; Inadvertent left internal mammary artery (LIMA): great cardiac vein anastomosis. BMJ Case Rep. 2013 Feb 15;2013:bcr2012007450. doi: 10.1136/bcr-2012-007450. PMID: 23417930; PMCID: PMC3618535.Stout et al; AHA/ACC Guideline for the Management of Adults With Congenital Heart Disease: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines. J Am Coll Cardiol. 2019 Apr 2;73(12):e81-e192. doi: 10.1016/j.jacc.2018.08.1029. Epub 2018 Aug 16. Erratum in: J Am Coll Cardiol. 2019 May 14;73(18):2361-2362. PMID: 30121239.Olshansky B. Placebo and nocebo in cardiovascular health: implications for healthcare, research, and the doctor-patient relationship. J Am Coll Cardiol. 2007 Jan 30;49(4):415-21. doi: 10.1016/j.jacc.2006.09.036. Epub 2007 Jan 16. PMID: 17258086.Ido et al; Coronary sinus occlusion enhances coronary collateral flow and reduces subendocardial ischemia. Am J Physiol Heart Circ Physiol. 2001 Mar;280(3):H1361-7. doi: 10.1152/ajpheart.2001.280.3.H1361. PMID: 11179085.Banai et al; Coronary sinus reducer stent for the treatment of chronic refractory angina pectoris: a prospective, open-label, multicenter, safety feasibility first-in-man study. J Am Coll Cardiol. 2007 May 1;49(17):1783-9. doi: 10.1016/j.jacc.2007.01.061. PMID: 17466229.Gaudino et al; ATLANTIC (Arterial Grafting International Consortium) Alliance members. Arterial Grafts for Coronary Bypass: A Critical Review After the Publication of ART and RADIAL. Circulation. 2019 Oct 8;140(15):1273-1284. doi: 10.1161/CIRCULATIONAHA.119.041096. Epub 2019 Oct 7. PMID: 31934782. CardioNerds Case Report Production Team Karan Desai, MD Amit Goyal, MD Daniel Ambinder, MD

Mar 16, 2022

CardioNerds (Daniel Ambinder), ACHD series co-chair, Dr. Josh Saef (ACHD fellow at University of Pennsylvania), and ACHD FIT lead Dr. Charlie Jain (Mayo Clinic) join ACHD expert Dr. George Lui (Medical Director of The Adult Congenital Heart Program at Stanford and Program Director for the ACGME adult congenital heart disease fellowship at Stanford) to discuss Tetrology of Fallot. Audio editing by CardioNerds Academy Intern, Dr. Leticia Helms. Tetralogy of Fallot (ToF) is the most common cyanotic heart disease and one of the most common congenital heart diseases that we see in adults overall. The anatomy includes a ventricular septal defect (VSD), an overriding aorta, and infundibular hypertrophy with subpulmonic +/- pulmonic valvular +/- supravalvular stenosis, which causes severe RV outflow obstruction and subsequent RV hypertrophy. Patients require surgery during childhood, which includes patching the VSD and relieving RV outflow obstruction. This results in pulmonic regurgitation (usually severe) and patients can live with this for decades. Adults with ToF commonly will require pulmonic valve replacement, potential relief of subvalvular or supravalvular stenoses, and tricuspid valve repair (for functional tricuspid regurgitation caused by RV dilation). These patients are at increased risk of atrial and ventricular arrhythmias and may warrant prophylactic ICDs. The CardioNerds Adult Congenital Heart Disease (ACHD) series provides a comprehensive curriculum to dive deep into the labyrinthine world of congenital heart disease with the aim of empowering every CardioNerd to help improve the lives of people living with congenital heart disease. This series is multi-institutional collaborative project made possible by contributions of stellar fellow leads and expert faculty from several programs, led by series co-chairs, Dr. Josh Saef, Dr. Agnes Koczo, and Dr. Dan Clark. The CardioNerds Adult Congenital Heart Disease Series is developed in collaboration with the Adult Congenital Heart Association, The CHiP Network, and Heart University. See more Disclosures: None Pearls • Notes • References • Guest Profiles • Production Team CardioNerds Adult Congenital Heart Disease PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls - Tetralogy of Fallot Tetralogy of Fallot is the most common cyanotic heart disease and the 4 anatomic features are: VSD, infundibular hypertrophy (with RVOT obstruction), overriding aorta, and RV hypertrophy. The most common lesion you will see in adults with repaired Tetralogy of Fallot is pulmonic regurgitation.Pulmonic regurgitation (PR) can be easy to miss on exam as the murmur is brief and even shorter when the PR is severe. In patients with PR and aortic regurgitation, remember PR is clearest when laying supine, in comparison to aortic regurgitation which is loudest while leaning forward.Patients with ToF may also have coronary anomalies (e.g. LAD off RCA), right-sided aortic arches, and also left-sided heart disease (LV diastolic or systolic dysfunction).Patients with ToF are at risk for atrial and ventricular arrhythmias, and clinicians should consider prophylactic ICD for those with multiple risk factors for sudden death (e.g. QRS >180ms, scar on MRI).In all patients with congenital heart disease, inspection is a key part of the physical exam (e.g. right thoracotomy could clue you into a prior BTT shunt) and in patients with prior BTT shunts and/or prior brachial cut-downs (look in the antecubital fossa for scars), radial arterial access is discouraged. Show notes - Tetralogy of Fallot LesionTTETEECardiac MRICardiac CTTetralogy of Fallot(1) Routine assessment of RV and LV size and function (2) Routine semiquantitative assessment of pulmonic valve regurgitation (3) Evaluation of PVR/conduit gradients, and RV pressure via tricuspid regurgitation gradient (4) Evaluation of proximal aortic dilation, proximal pulmonary artery branch stenosis (5) Identification of residual intracardiac shunts(1) Intraoperative management (pre- and post- bypass imaging). (2) Comprehensive echocardiographic evaluation when transthoracic windows are limited, and advanced imaging modalities are unavailable. (1) Quantitative evaluation of PR severity (phase contrast MRI) when echo-derived severity is inconclusive (2) Serial quantitative assessment of RV volume and ejection fraction to evaluate indications for PVR or conduit replacement in patients with pulmonary insufficiency. (3) MR angiography of aorta and pulmonary artery/branches to assess for dilation or stenosis. (4) Quantitative flow assessment of differential pulmonary arterial blood flow in the setting of branch PA stenosis (phase contrast MRI). (5) Late gadolinium enhancement imaging to assess for RV fibrosis in arrhythmia risk stratification. (1) Can be used for quantitative RV volume and ejection fraction assessment when CMR is contraindicated at expense of ionizing radiation. (2) Detailed evaluation of aortic and pulmonary arterial anatomy. (3) Detailed evaluation of coronary artery anatomy (e.g., relation of coronary artery to RV to PPA conduit prior to percutaneous valve implantation) (4) Evaluation of aortopulmonary collaterals. 1. What is the embryologic origin of Tetrology of Fallot (i.e. anterocephalad deviation of spiral septum)? With Tetralogy of Fallot, the most important considerations are in the embryology of the primitive outflow tract. In normal anatomy, early in gestation, the outflow tract starts as a hollow tube termed the conotruncus. Neural crest tissue migrates into the tube and forms two major collections of endocardial cushion tissue. The collections develop opposite each other, rotating in a counterclockwise spiral through the entire conotruncus. These cushions then grow into balanced left and right ventricular outflow tracts and fuse with the interventricular septum inferiorly.In ToF, there is 1) anterocephalad deviation of the muscular outlet septum which causes a large interventricular communication (i.e. VSD) to form underneath the aortic valve, and 2) abnormal arrangement of the septoparietal trabeculations. These 2 abnormalities cause RV outflow obstruction and subsequent RV hypertrophy.1 There can be a wide spectrum of disease from isolated subpulmonic obstruction with a relatively small VSD to a large VSD with near pulmonary valve atresia.Most patients with Tetralogy do not have an identifiable genetic mutation. However, up to 15% may have some type of genetic syndrome, most commonly 22q11 microdeletion (Velocardiofacial, or DiGeorge syndrome).2 This is clinically relevant because 22q11 microdeletion is an autosomal dominant mutation thus impacts pre-conception counseling in patients considering pregnancy. 2. What are the key features of ToF anatomy (e.g. VSD, RVOT obstruction, overriding aorta, RVH)? The classic 4 abnormalities originally described by Dr. Fallot in 1888 are 1) RVOT obstruction (always subvalvular +/- valvular/supravalvular), 2) interventricular communication/VSD, 3) aortic override, 4) RV hypertrophy which occurs secondary to the obstruction.This is repaired by closure of the VSD, relief of obstructive RVOT muscle, and relief of any potential pulmonic valve or supravalvular stenosis. Commonly the pulmonic annulus is hypoplastic, and traditionally was treated with enlargement with a transannular patch. This causes severe pulmonic regurgitation.Associated anomalies include right aortic arch, atrial septal defect, and less commonly AV canal defects.Coronary anomalies are common and one of the most common is an anomalous LAD off of the RCA. This is particularly relevant as its course over the RVOT complicates the surgical approach. 3. What are the hemodynamic consequences of the above structural abnormalities (e.g. RVOT obstruction, VSD shunting)? Prior to any repair, the RVOT obstruction is dynamic and in ways comparable to hypertrophic cardiomyopathy, but with the twist that is the VSD. “Blue Tets,” or patients who had cyanosis, had significantly decreased pulmonary blood flow from severe RV outflow obstruction and would have worsened symptoms from hypoxemia and low flow by anything that worsened pulmonary blood flow. This would be worsened in situations which caused stress (faster HR, smaller ventricle, more obstruction), hyperventilation and /or hypoxemia (higher pulmonary vascular resistance), or exercise (faster HR and also SVR drops more than PVR). These so called “Tet Spells” could be improved by increasing venous return to the right heart and/or increasing systemic vascular resistance. These can both be achieved by squatting, thus children with unrepaired Tetralogy will do this almost instinctively and in babies with cyanosis during crying the parents will be instructed to bring the babies legs toward the chest.3“Pink Tets” on the other hand have relatively mild obstruction to RV outflow and therefore have a lot of VSD flow from LV to the pulmonary vascular tree. This can cause left heart volume overload and CHF early on in life. If this goes uncorrected for a long time, it can predispose to pulmonary vascular disease. “Pink Tets” over time may develop worsened RV outflow obstruction and subsequently become “Blue Tets.” 4. How would an adult with corrected ToF anatomy present (e.g., VT, RV failure, PV endocarditis)? As above, the most common lesion in adults with repaired Tetralogy is severe pulmonic regurgitation. While this may be tolerated for decades, pulmonic valve replacement is indicated when the patient has:4≥ moderate PR with symptoms (commonly fatigue,

Mar 14, 2022

CardioNerds Rounds Co-Chairs, Dr. Karan Desai and Dr. Natalie Stokes and CardioNerds Academy Fellow, Dr. Najah Khan, join Dr. Martha Gulati – President-Elect of the American Society for Preventive Cardiology (ASPC) and prior Chief of Cardiology and Professor of Medicine at the University of Arizona – to discuss challenging cases in cardiac prevention. As an author on numerous papers regarding cardiac prevention and women’s health, Dr. Gulati provides many prevention pearls to help guide patient care. Come round with us today by listening to the episodes now and joining future sessions of #CardsRounds! This episode is supported with unrestricted funding from Zoll LifeVest. A special thank you to Mitzy Applegate and Ivan Chevere for their production skills that help make CardioNerds Rounds such an amazing success. All CardioNerds content is planned, produced, and reviewed solely by CardioNerds. Case details are altered to protect patient health information. CardioNerds Rounds is co-chaired by Dr. Karan Desai and Dr. Natalie Stokes. Speaker disclosures: None Cases discussed and Show Notes • References • Production Team CardioNerds Rounds PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Show notes - CardioNerds Rounds: Challenging Cases of Cardiovascular Prevention with Dr. Martha Gulati Case #1 Synopsis: A 55-year-old South Asian woman presents to prevention clinic for an evaluation of an elevated LDL-C. Her prior history includes hyperlipidemia, hypertension, obesity, and pre-eclampsia. She was told she had “high cholesterol” a few years prior and would need medication. She started exercising regularly and cut out sweets from her diet. Before clinic, labs showed: Total Cholesterol (mg/dL) of 320, HDL 45, Triglycerides 175, and (directly measured) LCL-C 180. Her Lipoprotein(a) is 90 mg/dL (ULN being ~ 30 mg/dL). Her HbA1C is 5.2% and her 10-year ASCVD Risk (by the Pooled Cohorts Equation) is 5.4%. Her recent CAC score was 110. She prefers not to be on medication and seeks a second opinion. Takeaways from Case #1 As Dr. Gulati notes, in the 2019 ACC/AHA Guideline on the Primary Prevention of Cardiovascular Disease, South Asian ethnicity is considered a “risk enhancing factor.” The pooled cohort equations (PCE) may underestimate risk in South Asians. Furthermore, risk varies within different South Asian populations, with the risk for cardiovascular events seemingly higher in those individuals of Bangladeshi versus Pakistani or Indian origin. There are multiple hypotheses for why this may be the case including cultural aspects, such as diet, physical activity, and tobacco use. A better understanding of these factors could inform targeted preventive measures.In the same 2019 ACC/AHA Guideline on the Primary Prevention of Cardiovascular Disease mentioned above, history of an adverse pregnancy outcome (APO) increases later ASCVD risk (e.g., preeclampsia) and is also included as a “risk-enhancing factor.” Studies have shown that preeclampsia is an independent risk factor for developing early onset coronary artery calcification. Recent data has shown that the risk for developing preeclampsia is not the same across race and ethnicity, with Black women more likely to develop preeclampsia. Black women also had the highest rates of peripartum cardiomyopathy, heart failure, and acute renal failure. After adjustment for socioeconomic factors and co-morbidities, preeclampsia was associated with increased risk of CVD events in all women, the risk was highest among Asian and Pacific Islander women. Listen to Episode #174. Black Maternal Health with Dr. Rachel Bond to learn more about race-based disparities in cardio-obstetric care and outcomes.Our patient thus has multiple risk-enhancing factors to help in shared decision making and personalize her decision for statin use. Another risk-enhancing factor for her is an elevated Lp(a), which is considered elevated when ≥ 50 mg/dL or ≥ 125 nmol/L. One other aspect that Dr. Gulati briefly covered was how CAC score may inform Aspirin use for primary prevention. There continues to be debate over when to prescribe aspirin when there is demonstrable calcium on imaging. In the MESA study, for individuals with CAC ≥ 100, the NNT (for 5 years to prevent an ASCVD event) was a 140 and NNH was 518. Case #2 Synopsis: A 58-year-old woman presents to establish care at a general cardiology clinic for shortness of breath. Her history includes hypertension, cutaneous lupus, and ongoing tobacco use. A year ago, she started having nausea, more common with stress or on exertion. She saw her PCP who obtained an EKG and GI evaluation. Endoscopy was unrevealing and EKG showed non-specific ST-T changes inferiorly. She was treated for GERD and then 6 months prior she developed dyspnea on exertion while exercising on her stationary bike after 10 minutes; she previously could go 30 minutes. She suffered a left knee meniscal tear shortly thereafter. She sees a cardiologist and obtains a cardiac PET-Stress which showed a small area of reversible ischemia in the basal to mid inferior wall and borderline reduced coronary flow reserve. Her symptoms continued and she was referred for LHC which showed non-obstructive CAD. No intracoronary physiologic testing was done. She is started on aspirin but still having symptoms. She seeks your opinion on how to prevent cardiovascular events. Takeaways Case #2 In the VIRGO study, investigators interviewed 2009 women and 976 men aged 18 to 55 years hospitalized for acute myocardial infarction (AMI) at 103 United States hospitals. Approximately 29.5% of women and 22.1% of men sought medical care for similar chest pain symptoms before their hospitalization; however, 53% of women reported that their provider did not think these symptoms were heart-related in comparison with 37% of men (p < 0.001).As Dr. Gulati noted, angiographically obstructive CAD is just the tip of the iceberg when it comes to ischemic heart disease. There are several important phenotypes including diffuse non-obstructive CAD and coronary microvascular dysfunction. Dr. Gulati shared the following image to demonstrate how ischemic heart disease is a unifying term for different syndromes. Academy Fellow, Dr. Najah Khan, has created the following infographic that provides a distinction between INOCA (ischemia and no obstructive coronary artery disease) and MINOCA (myocardial infarction with non-obstructive coronary arteries). Case #3 Synopsis: A 50-year-old man presents to cardiology clinic after a STEMI. His history includes hypertension, diabetes, obesity, and prior tobacco use. Four months ago, the patient suffered an inferior STEMI complicated by VF arrest treated with PCI to the proximal RCA. There was significant residual CAD and tentative plan for staged CABG. The patient was discharged on Aspirin, Prasugrel, Metoprolol Succinate, Lisinopril, Metformin and Atorvastatin. However, he started having muscle aches and so he stopped his Atorvastatin. He sees his PCP and before clinic gets a Lipid Panel (mg/dL) with Total Ch at 230, TG 237, HDL at 36 and LDL-C at 140. The patient starts ezetimibe and then comes to see you a month later to discuss best secondary prevention measures. Case #3 Takeaways: There are multiple opportunities for secondary prevention following acute coronary syndrome, with many patients undertreated. This includes but not limited to LDL-lowering medications, smoking cessation, cardiac rehabilitation, blood pressure control, diabetes management, weight loss, and targeting non-LDL particles when appropriate.Dr. Gulati points out that we need to make sure we categorize a patient’s risk appropriately, including patients at “very high risk” of ASCVD. This requires multiple ASCVD events (recent ACS, history of MI, history of ischemic stroke, symptomatic PAD) or an ASCVD event with multiple high-risk conditions (e.g., Age ≥ 65, heterozygous familial hypercholesterolemia, history of prior CABG or PCI outside of major ASCVD events, diabetes, hypertension, CKD, current tobacco use, persistently elevated LDL-C despite max statin therapy and ezetimibe, and/or history of congestive heart failure).Patients at very high risk of ASCVD should be on a high intensity statin or maximally tolerated statin (Class I). If PCSK9 inhibitors are considered, it is Class I to add ezetimibe to maximal statin therapy before initiating PCSK9i. If a patient is deemed to be on the maximal LDL-C lowering therapy that s/he is able to tolerate but LDL-C remains ≥ 70 mg/dL or non-HDL-C ≥ 100 mg/dL, adding PCSK9i is reasonable (Class IIa).A take home message from Dr. Gulati is that after more than a quarter century of treating LDL-C, generally the lower we can drive LDL-C levels the better for patient outcomes. References Arnett DK, Blumenthal RS, Albert MA, et al. 2019 ACC/AHA Guideline on the Primary Prevention of Cardiovascular Disease: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines. Circulation. 2019 Sep 10;140(11):e596-e646. doi: 10.1161/CIR.0000000000000678. Epub 2019 Mar 17. Erratum in: Circulation. 2019 Sep 10;140(11):e649-e650. Erratum in: Circulation. 2020 Jan 28;141(4):e60. Erratum in: Circulation. 2020 Apr 21;141(16):e774. PMID: 30879355; PMCID: PMC7734661.Benschop L, Brouwers L, Zoet GA, et al. Early Onset of Coronary Artery Calcification in Women With Previous Preeclampsia. Circ Cardiovasc Imaging. 2020 Nov;13(11):e010340. doi: 10.1161/CIRCIMAGING.119.010340. Epub 2020 Nov 16. PMID: 33190533.Cainzos-Achirica M, Miedema MD, McEvoy JW, et al. Coronary Artery Calcium for Personalized Allocation of Aspirin in Primary Prevention of Cardiovascular Disease in 2019: The MESA Study (Multi-Ethnic Study of Atherosclerosis).

Mar 6, 2022

CardioNerds (Amit Goyal), Dr. Natalie Stokes (Cardiology Fellow at UPMC and Co-Chair of the Cardionerds Cardio-Ob series), and episode lead Dr. Priya Freaney (Northwestern University cardiology fellow) discuss “The Fourth Trimester” with Dr. Malamo Countouris and Dr. Alisse Hauspurg, from the University of Pittsburgh Departments of Cardiology and Obstetrics and Gynecology, respectively. We discuss the cardiovascular considerations after adverse pregnancy outcomes in the postpartum and long-term follow-up periods. The discussion is focused mainly on hypertensive disorders of pregnancy (HDP), guided by a series of clinical vignettes. We cover a wide range of topics from cardiovascular complications and management considerations in the immediate postpartum period after a HDP, postpartum outpatient follow-up, long term cardiovascular morbidity related to HDP and related preventive strategies, contraceptive considerations for the cardiologist, and interdisciplinary care management pearls for cardiologists working in a cardio-obstetrics team. Notes • References • Guest Profiles • Production Team CardioNerds Cardio-Obstetrics Series PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls - The Fourth Trimester Blood pressures >160/110 should be treated like a true emergency during pregnancy and the postpartum period, as the cerebrovascular circulation is more sensitive to hypertension, due to hormonal changes related to pregnancy.Women with pre-eclampsia are at higher risk for peripartum cardiomyopathy. Have a low threshold to do a clinical heart failure evaluation (i.e., natriuretic peptides, echocardiogram), and administer diuretics as appropriate to improve volume status and blood pressure.Women with HDP should have their blood pressures monitored closely after discharge, ideally with a home BP monitoring program, as they can have exacerbations of their HTN for up to 2 weeks postpartum.The American Rescue Plan Act of 2021 included a landmark policy to extend postpartum Medicaid coverage up to a year postpartum (from 60 days).Remember to take a reproductive history for every woman you see in cardiology clinic! This can be done in one minute. At a minimum, include obstetric history [number of pregnancies, outcome of each pregnancy, gestational age and weight at delivery, pregnancy complications (HDP, GDM, etc), and delivery method] and menopausal history (age at menarche, age at menopause).The Pooled Cohort Equations may underestimate ASCVD risk for a woman who has had pregnancy complications or premature menopause – consider obtaining a CAC score to aid in risk-stratification in middle-aged women who may have underestimated risk.Low dose aspirin during pregnancy in women who have risk factors for pre-eclampsia reduces the risk of development of HDP by 15-20%. Quotables - The Fourth Trimester “Some of our traditional approaches to caring for women in the postpartum period just aren’t realistic…we need to think about how we can improve care from a policy standpoint to ensure women have access to care and think about how we deliver care.” – Dr. Alisse Hauspurg “Silos are never good. Cardio-obstetrics is a space where you really want to have open communications, be truly collaborative – taking into consideration the expertise of multiple disciplines…because it’s really hard to do it alone.” – Dr. Malamo Countouris Show notes - The Fourth Trimester For more on hypertensive disorders of pregnancy enjoy: Episode #128: Cardio-Obstetrics: Hypertensive Disorders of Pregnancy with Dr. Jennifer LeweyEpisode #66: Case Report: Severe Pre-eclampsia & Cardio-Obstetrics – UPMC Hypertensive Disorders of Pregnancy 1. What are some of the immediate postpartum cardiovascular risks and complications following a hypertensive disorder of pregnancy (HDP) and how do you manage these? Persistent hypertension: there can be a spike in BP in the days following delivery, and clinicians should remember that preeclampsia may develop de novo intra- or early postpartum. BPs >160/110 are considered severe HTN and should be treated urgently with an aggressive rapid-acting anti-HTN regimen to prevent stroke. BPs should be monitored at least every 4 to 6 hours for at least 3 days postpartum.1 A return visit for BP monitoring should be arranged at 1 week following discharge; alternatively, a home BP monitoring program may be consideredPulmonary edema: Women with preeclampsia should be delivered if they develop pulmonary edema. This is more likely to occur in women who have more severe preeclampsia features. Clinical practice guidelines suggest limiting intrapartum fluid intake/replacement to 60-80mL/h to avoid risks of pulmonary edema, with a goal euvolemic fluid balance.1Peripartum cardiomyopathy: Preeclampsia, gestational hypertension, and chronic hypertension all strongly predispose women to peripartum cardiomyopathy (PPCM). PPCM is defined as cardiomyopathy with reduced EF, usually EF 160/110) in the intra- and post-partum periods are associated with increased risk for stroke. BPs should be aggressively managed (see above) in the postpartum period to avoid this complication. 2. How should women who have had a HDP be followed in the postpartum period? What are the healthcare coverage considerations in the postpartum period? Blood pressures should be monitored closely in the postpartum period, especially in the 2 weeks following delivery – either via return in-person visits or a home BP monitoring program with remote visitsDepending on the location of care, specialized postpartum cardio-obstetrics clinics may or may not exist. Regardless, women with HDP history should be counseled (whether by OB, cardiology, PCP, etc.) regarding their long-term risk for cardiovascular diseaseThey should be counseled on the importance of optimizing their cardiovascular health (with maintenance of optimal weight and regular aerobic exercise).In addition to regular BP monitoring, these women should have periodic monitoring of their fasting lipids and blood sugars1Until recently, Medicaid coverage for pregnant women extended only 60 days postpartum, leaving many women uninsured just 2 months after delivery. In March 2021, the American Rescue Plan Act of 2021 was passed and calls for extension of Medicaid coverage from 60 days to 12-months postpartum. 3. What are the long-term cardiovascular complications related to HDPs? A history of HDP increases a woman’s risk of a diverse range of long-term cardiovascular risk factors and cardiovascular diseases (including HTN, CAD, Stroke, HF, and CV Mortality) (see figure below)6 Heart failure: A wide spectrum of changes in LV structure and function have been described in association with HDP. This includes increased LV wall thickness, adverse LV remodeling, and diastolic dysfunction (see below).7 Women with HDP also have been shown to have lower global longitudinal strain without overt systolic dysfunction8, PPCM (as described above) and later life cardiomyopathy.9 ASCVD: Women with pre-eclampsia are more likely to have atherosclerotic cardiovascular disease (CAD, CVA) than women without pre-eclampsia, independent of other traditional risk factors.6Despite significant independent association of HDP with long-term ASCVD, there was no incremental benefit in 10-year ASCVD risk prediction when added to the Pooled Cohort Equations (see below)10 4. How do you take a reproductive history in cardiology clinic? An optimal well-woman preventive cardiovascular visit should include a thorough reproductive history to identify adverse pregnancy outcomes and menstrual risk factors, amongst other sex-specific cardiovascular disease risk factors11Obstetric history: ask about pregnancies complicated by HDP (eclampsia, pre-eclampsia, gestational hypertension), low birth weight (<2500 grams), preterm delivery (<37 weeks gestation), or gestational diabetesMenstrual history: ask about age at menarche and presence of premature menopause (defined by most as menopause <40years and others as menopause <45 years). If premature menopause present, ask about natural versus surgical menopause (removal of both ovaries) 5. What methods of contraception are optimal for women with a history of cardiovascular risk factors or cardiovascular disease? It is important to discuss contraceptive options in women with history of HDP, cardiovascular RFs, and cardiovascular diseaseOften, in these women, long-acting reversible contraception (LARC) such as IUDs and implants are best. Permanent sterilization procedures can also be considered if a woman has completed desired childbearing.Dr. Hauspurg highly recommends the following app from the CDC for those interested in medical eligibility criteria for various contraceptive methods, sorted by specific medical conditions:https://www.cdc.gov/reproductivehealth/contraception/mmwr/mec/summary.

Feb 27, 2022

CardioNerds (Amit Goyal & Karan Desai) join Dr. Matthew Delfiner (Cardiology fellow, Temple University Hospital) and Dr. Katie Vanchiere (Internal medicine resident, Temple University Hospital) in the beautiful Fairmount Park in Philadelphia. They discuss a case of a 53-year-old man with an LVAD who presents with progressive dyspnea since LVAD implant due to right-to-left shunting due to a PFO. Dr. Val Rakita (Assistant professor of medicine and advanced heart failure and transplant specialist at Temple University Hospital) provides the E-CPR for this episode. Episode introduction by CardioNerds Clinical Trialist Dr. Anthony Peters (Duke Heart Center). This case has been published by Circulation: Heart failure. See Invasive Hemodynamic Study Unmasks Intracardiac Shunt With Ventricular Assist Device. Claim free CME just for enjoying this episode! Disclosures: NoneJump to: Pearls - Notes - References CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Case Summary - Dyspnea with an LVAD: A Tale of Hypoxia and Hemodynamics A 53-year-old man with an LVAD placed 3 months prior presents with progressive dyspnea since LVAD implant, though it has acutely worsened over the past 2 weeks. Two weeks ago, he had a hemodynamic and echocardiographic ramp study, where the LVAD speed was increased. By increasing the speed, his LV was more adequately decongested, and flow improved. In the Emergency Department, he was hypoxic on room air, and remained so with escalation ultimately with intubation. Even then he remained severely hypoxic requiring cannulation to veno-venous ECMO. Chest imaging was normal, and LVAD parameters were normal without any alarms. An astute clinician noticed that when the patient became hypertensive, his oxygen saturation improved. A subsequent echocardiogram revealed a patent foramen ovale, with right to left shunting. The patient then went to the cath lab, where simultaneous right atrial and left atrial pressures and oxygen pressures were measured, along with trans-esophageal echocardiography, while adjusting LVAD speed. It became evident that right-to-left shunting occurred only when there was high LVAD speed and low peripheral blood pressure. Essentially, faster LVAD speeds (sucking blood from the LV) and low systemic blood pressure (reducing LV afterload) increased right to left shunting by decreasing the left atrial pressure relative to the right atrial pressure. The PFO was closed at that time, drastically improving oxygenation. He was decannulated and extubated the following day. Invasive Hemodynamic Study Unmasks Intracardiac Shunt With Ventricular Assist Device | Circulation: Heart Failure (ahajournals.org) Episode Teaching -Dyspnea with an LVAD: A Tale of Hypoxia and Hemodynamics Pearls PFOs are present in up to 25% of individuals, including those with LVADs.LV unloading, and therefore LA decompression, depends on both LVAD speed and systemic vascular resistance.Blood pressure dependent hypoxia may be suggestive of a right-to-left intracardiac shunt.Hypoxia refractory to mechanical ventilation should raise suspicion for intracardiac shunt.Patients with LVADs can suffer from the same diseases that anyone can. Notes - Dyspnea with an LVAD: A Tale of Hypoxia and Hemodynamics 1. What factors influence LVAD flow? Factors that influence LVAD flow include pump speed, blood pressure, volume status, RV function, cardiac rhythm, and some other variables. The faster the pump is spinning, the more flow you should provide (to an extent). However, if your LV is underfilled, either from systemic hypovolemia or an RV not providing the needed LV preload, then you have no blood to flow! If you have high systemic vascular resistance, then you will have less forward flow, just as a native heart would. We must always think about the interaction between a patient and the LVAD, not just the machine settings. 2. What can cause dyspnea and hypoxia in LVAD patients? The same things that cause dyspnea in any other patient! But also… inadequate unloading of the LV due to the above factors in addition to possible suction events. Aortic regurgitation can cause an endless loop of flow from: LV > LVAD > aorta > AV > LV. Pump malfunction must always be considered, including inflow/outflow obstruction and pump thrombosis. Anemia may also contribute, as patients with LVAD are prone to both bleeding and hemolysis. 3. What are the ideal LVAD settings? There are no standard settings for LVADs, especially because there are different manufacturers. But most importantly, every patient is different, and therefore the patient-LVAD interaction is different. Overall, the ideal LVAD speed would decongest the heart while preserving RV function, maintaining the interventricular septum midline, and having intermittent aortic valve opening. 4. Explain how PFOs can result in hypoxemia. PFOs, or any septal defect, allow intra-cardiac flow from one side of the heart to the other. Flow will follow a pressure gradient. Usually, the left heart will have higher pressures than the right heart, but if the right heart pressure exceeds the left, then de-oxygenated venous blood can bypass the pulmonary circulation and enter the left heart and systemic circulation, causing hypoxemia. 5. List the methods that are used to diagnose and evaluate the severity of intra-cardiac shunts. Doppler color flow and bubble study with TTE or TEE. Blood gas measurement across various chambers can be used as well. For an in-depth review of LVADs, enjoy Ep #15. LVAD 101 with Dr. Steve Hsu​. References Uriel, Nir, et al. "Clinical hemodynamic evaluation of patients implanted with a fully magnetically levitated left ventricular assist device (HeartMate 3)." The Journal of Heart and Lung Transplantation 36.1 (2017): 28-35. Adamson, R. M., et al. "Single center, 23 year experience with PFO management during HeartMate LVAD implants." The Journal of Heart and Lung Transplantation 34.4 (2015): S219. Bacich, Daniela, et al. "Patent foramen ovale-related complications in left ventricular assist device patients: A reappraisal for cardiovascular professionals." Journal of Artificial Organs 23.2 (2020): 98-104. Burkhoff, Daniel, et al. "Hemodynamics of mechanical circulatory support." Journal of the American College of Cardiology 66.23 (2015): 2663-2674. Jaski, Brian E., et al. "Assessment of recurrent heart failure associated with left ventricular assist device dysfunction." The Journal of heart and lung transplantation 24.12 (2005): 2060-2067. Stainback, Raymond F., et al. "Echocardiography in the management of patients with left ventricular assist devices: recommendations from the American Society of Echocardiography." Journal of the American Society of Echocardiography 28.8 (2015): 853-909. CardioNerds Case Report Production Team Karan Desai, MD Amit Goyal, MD Daniel Ambinder, MD

Feb 21, 2022

CardioNerds, Daniel Ambinder and CardioNerds Academy Program Director, Dr. Tommy Das (Cardiology fellow, Cleveland Clinic), Dr. Jacqueline Latina (Structural heart fellow, Johns Hopkins) discuss aortic stenosis and the story of TAVR from both the historical perspective and in terms of future directions with Dr. Jon Resar, Professor of Medicine and Director of the Adult Catheterization Laboratory and Interventional Cardiology at the Johns Hopkins Hospital. This episode is brought to you for Heart Valve Disease Awareness Day. Audio editing by CardioNerds Academy Intern, Shivani Reddy. As many as 11 million Americans have heart valve disease (HVD)—a potentially disabling and deadly disease—yet 3 out of 4 Americans know little to nothing about heart valve disease. Learn more about valve disease. Pearls • Notes • References • Guest Profiles • Production Team CardioNerds Aortic Stenosis SeriesCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls and Quotes - Aortic Stenosis and the Story of TAVR In the previous century, patients with severe aortic stenosis who were treated “medically” had 50% mortality over 2 years after developing symptoms. Balloon aortic valvuloplasty was initially touted as extremely “efficacious” for aortic stenosis but follow-up studies showed that the improvement in symptoms were not durable, and long-term prognosis was dismal. The PARTNER Trial started enrolling in 2007 in extreme risk patients – patients who were not surgical candidates. In 2010, the PARTNER trial was published and TAVR blew away the “standard of care” in inoperable patients at the time, cutting outcomes in half (composite of death and repeat hospitalization). The PARTNER trial studied balloon expandable intra-annular valve implantation. The CoreValve trial studied self-expanding supra-annular valve implantation and was published in 2014. The “Heart Team” approach entails collaborative decision making between cardiologists and cardiac surgeons to personalize management for patients. Both intra-annular and supra-annular valves show non-inferior outcomes to surgery in intermediate and low risk patients. Revascularization prior to TAVR is an evolving arena; the trend has been interventionalists performing fewer PCIs prior to TAVR given the benefit is not clear if angina is not a prominent symptom. Show notes - Aortic Stenosis and the Story of TAVR (TAVR/TAVI are using interchangeably) CardioNerds Aortic Stenosis, updated 1.20.21 1. In the 1990s, patients with severe aortic stenosis (AS) who were deemed to be at high surgical risk would weigh the risks of surgery and prolonged recovery. Balloon Aortic Valvuloplasty (BAV) was first performed by Dr. Alain Cribier in 1986. The technique was based on the foundation of pulmonary valvuloplasty performed initially in 1982 by Drs. Jean Kan and Bob White, and mitral valvuloplasty in 1984. BAV was initially touted as an efficacious cure for aortic stenosis, but unfortunately it had a high restenosis rate as well as high risks for stroke and vascular complications (no closure devices at that time) with an overall poor long-term prognosis. Balloon aortic valvuloplasty was primarily used for decompensated Class IV heart failure in non-surgical candidates. 2. Transcatheter aortic valve replacement (TAVR/TAVI) was developed and first performed in human in 2002.(1) This was performed by Dr. Alain Cribier in France in 2002, initially by trans-septal approach and then by retroaortic approach. Here is a representative diagram of the procedure. Figure: Transcatheter Aortic-Valve Replacement. The transcatheter valve is positioned at the level of the native aortic valve during the final step of valve replacement, when the balloon is inflated within the native valve during a brief period of rapid ventricular pacing. The delivery system is shown after it has traversed the aorta retrograde over a guidewire from its point of insertion in the femoral artery (transfemoral placement). Before balloon inflation, the valve and balloon are collapsed on the catheter (dark blue) and fit within the sheath (blue). After balloon inflation, the calcified native valve (upper panel) is replaced by the expanded transcatheter valve (lower panel, shown in short-axis view from the aortic side of the valve). Smith CR et al. N Engl J Med 2011;364:2187-2198. 3. The PARTNER trial was first published in a landmark NEJM article in extreme surgical risk patients comparing TAVR (with a balloon-expandable aortic valve implant) versus stndard “medical” therapy of aortic stenosis. TAVR markedly reduced the composite outcome of all-cause mortality and repeat hospitalization in these patients.(2) PARTNER then compared TAVR to aortic valve surgery in high risk patients, and TAVR performed quite well, though there were more strokes and vascular complications in the TAVR group compared to surgery.(3) Figure: PARTNER Trial Time-to-Event Curves for the Primary End Point and Other Selected End Points. Leon MB et al. N Engl J Med 2010;363:1597-1607. 4. CoreValve/Medtronic then published their results for their self-expanding valve, enrolling over 1400 participants.(4) The rate of death in the TAVR group was non-inferior to the SAVR group, and a subsequent test for superiority actually showed TAVR was superior to surgery in these high risk patients. Figure: Kaplan–Meier Cumulative Frequency of Death from Any Cause. The rate of death from any cause in the TAVR group was noninferior to that in the surgical group (P<0.001). A subsequent test for superiority at 1 year showed that TAVR was superior to surgical replacement (P=0.04). The inset shows the same data on an enlarged y axis. Adams DH et al. N Engl J Med 2014;370:1790-1798. 5. Both balloon expandable (PARTNER 3) and self-expanding valves (Evolut Low Risk) have since been studied in intermediate and low surgical risk patients.(5-8) In low risk patients, the balloon expandable valve showed the rate of the composite of death, stroke, or rehospitalization at 1 year was significantly lower with TAVR than with surgery. In low risk patients, TAVR with a self-expanding supraannular bioprosthesis was noninferior to surgery with respect to the composite end point of death or disabling stroke at 24 months. 6. Coronary artery disease in TAVR patients: the decision for coronary revascularization prior to TAVR is complex and practice is evolving. Initially, most patients were being revascularized for obstructive coronary artery stenosis electively prior to TAVR. More recently, if the disease is not proximal (or a small area of myocardium at risk) and if angina is not a prominent symptom, we have moved towards deferring coronary revascularization. References - Aortic Stenosis and the Story of TAVR 1. Cribier A, Eltchaninoff H, Tron C et al. Early experience with percutaneous transcatheter implantation of heart valve prosthesis for the treatment of end-stage inoperable patients with calcific aortic stenosis. J Am Coll Cardiol 2004;43:698-703. 2. Leon MB, Smith CR, Mack M et al. Transcatheter Aortic-Valve Implantation for Aortic Stenosis in Patients Who Cannot Undergo Surgery. New England Journal of Medicine 2010;363:1597-1607. 3. Smith CR, Leon MB, Mack MJ et al. Transcatheter versus Surgical Aortic-Valve Replacement in High-Risk Patients. New England Journal of Medicine 2011;364:2187-2198. 4. Adams DH, Popma JJ, Reardon MJ et al. Transcatheter Aortic-Valve Replacement with a Self-Expanding Prosthesis. New England Journal of Medicine 2014;370:1790-1798. 5. Leon MB, Smith CR, Mack MJ et al. Transcatheter or Surgical Aortic-Valve Replacement in Intermediate-Risk Patients. N Engl J Med 2016;374:1609-20. 6. Reardon MJ, Van Mieghem NM, Popma JJ et al. Surgical or Transcatheter Aortic-Valve Replacement in Intermediate-Risk Patients. N Engl J Med 2017;376:1321-1331. 7. Popma JJ, Deeb GM, Yakubov SJ et al. Transcatheter Aortic-Valve Replacement with a Self-Expanding Valve in Low-Risk Patients. N Engl J Med 2019;380:1706-1715. 8. Mack MJ, Leon MB, Thourani VH et al. Transcatheter Aortic-Valve Replacement with a Balloon-Expandable Valve in Low-Risk Patients. N Engl J Med 2019;380:1695-1705. Guest Profiles Dr. Jon Resar received his medical degree from the Medical College of Wisconsin and completed fellowships in cardiovascular medicine and interventional cardiology at The Johns Hopkins Hospital where he serves as the director of the adult cardiac catheterization and serves as Professor of Medicine. He has been a pioneer in percutaneous management of coronary artery disease and structural heart disease. Dr. Jackie Latina Dr. Jacqueline Latina is currently a Structural Heart Fellow at Johns Hopkins. She was born and raised in the suburbs of Boston, MA, but fortunately escaped without a Boston accent. She is a graduate of Princeton University with an A.B. in chemistry. She earned her M.D. at Tufts University School of Medicine. Her internship and internal medicine residency were completed at Mount Sinai Hospital in New York City, where she stayed on for an American Heart Association postdoctoral research fellowship. She completed an M.S. in clinical research methods at the Columbia Mailman School of Public Health during that time. She completed general and interventional cardiology fellowships at Johns Hopkins.

Feb 17, 2022

CardioNerds (Amit Goyal and Daniel Ambinder), Dr. Leticia Helms (Internal medicine resident at Columbia University), Dr. Silia DeFilippis (AHFT FIT at Columbia University), and Dr. Anu Lala (AHFT faculty and program director at Mount Sinai Hospital) to discuss diversity and inclusion in academic cardiology and more in this installment of the Narratives in Cardiology Series. The President of the New York ACC Chapter Dr. Hima Vidula discusses D&I initiatives at her chapter. Episode introduction and audio editing by CardioNerds Academy Intern, Shivani Reddy. Although women compose 50% of medical students in the United States, cardiology remains a male dominated field. Gender disparity is even more prominent when we look at leadership positions. In this episode we discuss why and how cardiology (and advanced heart failure) can be such a rewarding field for women. The episode reflects on the significant contributions women have made to the field in the past and how they continue to move the field with respect to clinical care and research. The PA-ACC & CardioNerds Narratives in Cardiology is a multimedia educational series jointly developed by the Pennsylvania Chapter ACC, the ACC Fellows in Training Section, and the CardioNerds Platform with the goal to promote diversity, equity, and inclusion in cardiology. In this series, we host inspiring faculty and fellows from various ACC chapters to discuss their areas of expertise and their individual narratives. Join us for these captivating conversations as we celebrate our differences and share our joy for practicing cardiovascular medicine. We thank our project mentors Dr. Katie Berlacher and Dr. Nosheen Reza. Video Version • Notes • Production Team Claim free CME just for enjoying this episode! There are no relevant disclosures for this episode. The PA-ACC & CardioNerds Narratives in Cardiology PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Tweetorial - Raising Women Leaders in Academic Cardiology with Dr. Anu Lala https://twitter.com/Gurleen_Kaur96/status/1509286469051031556?s=20&t=9BFDUXbSnWLcAc5-daXK2A Video version - Raising Women Leaders in Academic Cardiology with Dr. Anu Lala https://youtu.be/vVuhUCbqwYk Quotables - Raising Women Leaders in Academic Cardiology with Dr. Anu Lala “We all have multiple roles – and those roles don’t always have to be completely distinct and separate from one another. You know, our ability in one role, maybe it makes us better at another.”“I felt like being there was like in medical Disneyland for research.” - Anu Lala“Heart failure is unique in that it truly requires that cross disciplinary collaboration at the precipice of what is often life and death.” - Anu Lala“It points to the importance of seeing people do things before you who look like you.” - Anu Lala“All human beings want to feel heard. They want to feel seen and they want to feel like their voice matters.” - Anu Lala“consciously deliberately disruptive”“I like the idea of calling it work-life harmony.” Show notes - Raising Women Leaders in Academic Cardiology with Dr. Anu Lala How do women compare to men in cardiology in 2022?Although nearly 50% of US medical graduates and more than 40% of internal medicine graduates are women, the field of cardiology remains male dominated.Approximately 20% of general cardiology fellows are women, which is comparable to women in surgical subspecialties like neurosurgery (17%), thoracic surgery (21%), and orthopedic surgery (15%) (Reza 2021).Additionally, women hold significantly fewer leadership positions and are less likely to be promoted to senior academic ranks.Out of LBCT presented at ACC 2021, zero had a female first author and zero were presented by women (Kaur 2021).What may make heart failure unique with respect to the recruitment of women?Heart failure is the only subspecialty of cardiology that was founded by a woman. Dr. Sharon Hunt is often described as the founder of the subspecialty.She posited a few reasons why heart failure may attract a higher proportion of women including presence of models and mentors for women, women have been included since the inception of the field, and one that requires collaboration (Hunt 2019).The number of women in HF training programs ranges between 26 to 36% which is much higher than that of women in other subspecialties like EP and interventional cardiology (Reza 2021).How can we increase diversity in clinical trial leadership?Women only represent 1 in 10 authors of cardiovascular trials in high impact journals (Van Spall 2021).Build diverse research team.Hold stakeholders accountable including academic institutions, professional societies, industry sponsors, funding agencies, and scientific journals (Van Spall 2021).Be deliberate about editorial authorship as well as equal representation of women on manuscripts.How can we increase the diversity of participants in clinical trials?We know that increasing the diversity of women investigators in clinical trials is associated with increased enrollment of women participants (Reza 2020).Increased enrollment of diverse populations is key to increasing the generalizability of findings (Van Spall 2021).Build partnerships with the community and community-level providers.Meet social and cultural needs such as family and child care responsibilities; socioeconomic and financial barriers; as well as absenteeism from work (Reza 2022).Provide sex-specific materials to encourage enrollment.For a related discussion, enjoy Ep #135. Underrepresentation in Clinical Trials & Guidelines with Dr. Clyde Yancy.How has the COVID-19 pandemic affected women in academic medicine?Women often bear disproportionate demands of personal life including schooling and caregiving duties and affected by school closures (Reza 2021).Data have suggested that female academic productivity has been affected as measured by decreased publication authorship which may translate into decreased research support (DeFilippis 2021).The decreased submission of manuscripts has been particularly pronounced among junior cohorts of women in academics (Squazzoni 2021). Production Team Dr. Gurleen Kaur Amit Goyal, MD Daniel Ambinder, MD

Feb 16, 2022

CardioNerds Tommy Das (Program Director of the CardioNerds Academy and cardiology fellow at Cleveland Clinic), Rick Ferraro (Director of CardioNerds Journal Club and cardiology fellow at the Johns Hopkins Hospital), and CardioNerds Healy Honor Roll Ambassador Dr. Justice Oranefo (UConn cardiology fellow) discuss omega-3 fatty acids acid with Dr. Ty Gluckman, preventive cardiologist and medical director of the Center for Cardiovascular Analytics, Research, and Data Science (CARDS) at the Providence St. Joseph Heart Institute in Portland, Oregon. Audio editing by CardioNerds Academy Intern, Christian Faaborg-Andersen. In the recent years, purified omega 3 fatty acids and its esters have emerged as a potential new tool in our arsenal for management of hypertriglyceridemia and atherosclerotic coronary artery disease. In this episode we review the sources and basic structure of these compounds, as well as their metabolic effects as it pertains to cardiovascular disease. Using hypothetical patient cases, we also discuss scenarios in which these therapies can be useful. This episode is part of the CardioNerds Lipids Series which is a comprehensive series lead by co-chairs Dr. Rick Ferraro and Dr. Tommy Das and is developed in collaboration with the American Society For Preventive Cardiology (ASPC). Relevant disclosures: None Pearls • Notes • References • Guest Profiles • Production Team CardioNerds Lipid Series PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls Omega 3 (n-3) fatty acids are a class of polyunsaturated fatty acids [PUFA]. The most studied n-3 fatty acids include eicosapentaenoic acid [EPA], docosahexaenoic acid [DHA] and alpha linoleic acid [ALA]. ALA is found in certain vegetable oils while EPA and DHA are abundant in fish sources.Cardiovascular benefits of n-3 fatty acids include blood pressure reduction, enhanced diastolic function, triglyceride reduction, and immunomodulatory properties.Inflammation plays a major role in the atherogenic process and plaque rupture. Inflammatory marker hs-CRP is a risk enhancing factor for predicting future ASCVD risk. Ongoing trials are investigating therapy that target the inflammatory process in treatment of atherosclerotic heart disease.Prevention and management of ASCVD require aggressive lifestyle modifications and medical therapy addressing risk factors and underlying inflammatory conditions.Purified forms of n-3 fatty acids are approved for the treatment of severe hypertriglyceridemia and as an adjunct therapy to statins for reduction of coronary events in high-risk individuals. Show notes 1. What are omega 3 (n-3) fatty acids? What are the natural sources of n-3 fatty acids? n-3 fatty acids are class of polyunsaturated fatty acids [PUFA]. PUFA are types of unsaturated fats that have more than one double bond in their backbone. PUFAs are important constituents of the phospholipids of all cell membranes.The most studied n-3 fatty acids include eicosapentaenoic acid [EPA], docosahexaenoic acid [DHA] and alpha linoleic acid [ALA].ALA is found in certain vegetable oils including walnuts, flaxseeds, chia seeds. EPA and DHA are abundant in cold water fish oils such as salmon, mackerel, tuna sardines. Interestingly, farm raised fish usually have higher levels of EPA and DHA than wild caught fish; however, this depends on what the fish are fed. Another important class of PUFAs are omega 6 (n-6) fatty acids, found in vegetable oils (1,2). 2. What are the metabolic effects of omega 3 fatty acids? Multiple early studies have demonstrated the anti-inflammatory properties of n-3 fatty acids.The typical Western diet with a high arachidonic acid (an n-6 fatty acid) content promotes atherogenesis leading to the high incidence of CAD in this population.Supplementation with diets rich in DHA and EPA has been associated with reduced arachidonic acid content as well as reduced markers of inflammation. The relative dietary ratios of n-6:n-3 fatty acids have major implications for cardiovascular health.Anti-inflammatory mechanism of n-3 fatty acids include cell membrane stabilization, anti-oxidant properties, reduced leukocyte chemotaxis. (1-3).Other studied cardiovascular benefits of n-3 fatty acids include triglyceride lowering properties (11, 12), blood pressure and heart rate reduction (13, 14), improved endothelial function and antithrombotic properties (15, 16).Importantly, EPA and DHA are distinct molecules (different hydrocarbon length and number of double bonds) with different biologic effects. EPA assumes an extended conformation in cellular membranes, allowing it to neutralize reactive oxygen species, facilitate membrane stabilization, and limit oxidation of LDL cholesterol more easily. In contrast, DHA has a longer carbon chain and has one additional double bond, resulting in less membrane stabilization. DHA also inhibits formation of Dihomo-γ-linolenic acid (DGLA), which is important for production of anti-inflammatory eicosanoids and thus can also increase levels of LDL cholesterol. 3. What role does inflammation play in coronary artery disease? The impact of inflammation in the pathogenesis of atherosclerosis and plaque rupture has been well studied. Inflammatory mediators such CRP, IL-6, and myeloperoxidase have been found to be associated with increased cardiovascular risk.The JUPITER trial demonstrated the benefit of statin therapy in patients with elevated hsCRP. Subsequent trials targeting inflammation in the management of CAD have shown promise. Examples include the LoDoCo which investigated colchicine therapy and the CANTOS trial with investigated the IL-1 beta inhibitor canakinumab.The pathogenic role of inflammation and potential therapeutic role of anti-inflammatory therapy remain key areas of interest and multiple pharmacologic agents are undergoing investigation. (6, 7, 8, 17, 18).Check out the #CardsJC on the LoDoCo 2 trial for more on Colchicine in the management of CAD. Table 1 below summarizes notable trials of anti-inflammatory therapies for ASCVD. 4. What is the role for n-3 fatty acids in management of coronary artery disease? While a diet rich in n-3 fatty acids is associated with a lower risk of cardiovascular events, supplementation with over-the-counter fish oil containing supplements have not demonstrated significant cardiovascular benefits.Purified forms of high dose n-3 fatty acid esters consisting of EPA and/or DHA have shown mixed results as therapies for ASCVD.In the JELIS trial, patients with hypercholesterolemia treated with high dose icosapent ethyl (an EPA ester) in addition to pravastatin 10mg/day or simvastatin 5mg/day experienced reduced incidence of cardiac events and reduced LDL with greater benefit seen in patients with impaired glucose metabolism.The REDUCE-IT trial showed similar results in patients with atherosclerotic disease and high risk patients with elevated fasting triglycerides.Interestingly, the STRENGTH trial, in which patients were treated with combination EPA+DHA, did not show a benefit in the treatment arm.Icosapent ethyl is currently indicated as an adjunct therapy in addition to maximally tolerated statin therapy in patients with triglyceride levels ≥150 mg/dL and either established cardiovascular disease or type 2 diabetes mellitus plus ≥2 risk factors for cardiovascular disease to reduce incidence of cardiac events. (19 – 21).Check out the #CardsJC on the STRENGTH trial for an overview of relevant trial data. Table 2 below summarizes notable trials of omega-3 fatty acids for ASCVD. 5. What is the role of n-3 fatty acids in management of hypertriglyceridemia? In the approach to hypertriglyceridemia, be sure to identify and treat secondary causes (alcoholism, hypothyroidism, uncontrolled diabetes, etc) before instituting pharmacotherapy. Enjoy the CardioNerds “Causes of Hypertriglyceridemia” infographic developed by Dr. Teodora Donisan.The 2021 ACC expert consensus decision pathway on the management of ASCVD in patients with hypertriglyceridemia provides guidelines and algorithmic strategies to management of hypertriglyceridemia in several patient populations (22).The triglyceride reducing properties of n-3 fatty acids have been demonstrated on several trials including the EVOLVE trial (11). One should note that while several therapies reduce triglycerides, the potential benefits from n-3 fatty acids likely extend beyond triglyceride reduction. Table 1. Previous randomized controlled trials investigating colchicine and other anti-inflammatory therapies in the treatment of atherosclerotic ischemic heart disease Table 2. Review of relevant randomized control trials on Omega-3 fatty acids. CAD, coronary artery disease; CV, cardiovascular; DHA, docosahexaenoic acid; EPA, eicosapentaenoic acid; MACE, major adverse cardiovascular events. Infographic. Causes of Hypertriglyceridemia by Dr. Teodora Donisan. References - Triglycerides MOZAFFARIAN, D. & WU, J.H.Y., 2011. Omega-3 Fatty Acids and Cardiovascular Disease: Effects on Risk Factors, Molecular Pathways, and Clinical Events. Journal of the American College of Cardiology, 58(20), pp.2047–2067.Calder, Philip C, 2010. Omega-3 fatty acids and inflammatory processes. Nutrients, 2(3), pp.355–374.Raphael, William & Sordillo, Lorraine M, 2013. Dietary polyunsaturated fatty acids and inflammation: The role of phospholipid biosynthesis. International journal of molecular sciences, 14(10), pp.21167–21188.Schwalfenberg, G., 2006. Omega-3 fatty acids: their beneficial role in cardiovascular health. Canadian family physician, 52(6), pp.734–740.Hansson, Göran K, 2005. Mechanisms of disease: Inflammation, atherosclerosis, and coronary artery disease. The New England journal of medicine, 352(16), pp.1626–1695.Ridker, Paul M et al., 2008.

Feb 10, 2022

CardioNerds (Amit Goyal and Daniel Ambinder) join Dr. Loie Farina (Northwestern University CardioNerds Ambassador), Dr. Josh Cheema, and Dr. Graham Peigh from Northwestern University for drinks along the shores of Lake Michigan at North Avenue Beach. They discuss a case of a 52-year-old woman with limited cutaneous systemic sclerosis who presents with progressive symptoms of heart failure and is found to have a severe, non-ischemic cardiomyopathy. The etiology of her cardiomyopathy is not clear until her untimely death. She is ultimately diagnosed with cardiac AL amyloidosis with isolated vascular involvement a real occam’s razor or hickam’s dictum conundrum. We discuss the work-up and management of her condition including a detailed discussion of the differential diagnosis, the underlying features of systemic sclerosis with cardiac involvement as well as cardiac amyloidosis, the role of a shock team in managing cardiogenic shock, and how to identify those with advanced or stage D heart failure. Advanced heart failure expert Dr. Yasmin Raza (Northwestern University) provides the ECPR segment. Episode introduction by CardioNerds Clinical Trialist Dr. Liane Arcinas. Audio editing by CardioNerds Academy Intern, Christian Faaborg-Andersen. Claim free CME just for enjoying this episode! Disclosures: NoneJump to: Pearls - Notes - References CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Case Summary - Occam’s Razor or Hickam’s Dictum? This is a case of a 52-year-old woman with limited cutaneous systemic sclerosis who presented with progressive dyspnea on exertion and weight loss over the course of 1 year. Her initial work-up was notable for abnormal PFTs and finding of interstitial pneumonia on high-resolution CT, an ECG with frequent PVCs and normal voltage, a transthoracic echocardiogram with a mildly reduced ejection fraction of 40%, and a right/left heart catheterization with normal coronary arteries, filling pressures, and cardiac output. Scleroderma-related cardiac involvement is suspected. She is placed on GDMT, but her condition worsens over the next several months, and repeat echocardiogram shows severely reduced biventricular function, reduced LV global longitudinal strain (GLS) with apical preservation of strain, severely reduced mitral annular tissue Doppler velocities, and a normal left ventricular wall thickness. Scleroderma-related cardiac involvement remains highest on the differential, but because of some findings on the echo that are concerning for cardiac amyloidosis, an endomyocardial biopsy was obtained. It showed vascular amyloid deposition without interstitial involvement. The diagnosis of cardiac amyloid was discussed but deemed unlikely due to lack of interstitial involvement. However, a serologic work-up soon revealed a monoclonal serum lambda light chain and a follow-up bone marrow biopsy showed 20% plasma cells. She was discharged with very near-term follow-up in oncology clinic with a presumptive diagnosis of AL amyloidosis, but she unfortunately returned in shock and suffered a cardiac arrest. She initially survived and underwent emergent veno-arterial extracorporeal membrane oxygenation (VA ECMO) cannulation with subsequent left ventricular assist device placement (LVAD). However, she passed away due to post-operative hemorrhage. Autopsy was consistent with a final diagnosis of cardiac AL amyloidosis with isolated vascular involvement. Case Media - Occam’s Razor or Hickam’s Dictum? EKG CXR TTE Pathology CMR Episode Teaching -Occam’s Razor or Hickam’s Dictum? Pearls Scleroderma causes repeated focal ischemia-reperfusion injuries which result in patchy myocardial fibrosis. Cardiac involvement in scleroderma is frequent but often not clinically evident; when symptomatic, it is associated with a poor prognosis. Myocardial dysfunction in cardiac AL amyloidosis can result from myocardial infiltration, vascular deposition causing microvascular dysfunction and ischemia, and direct cardiotoxicity from circulating light chains. While isolated vascular amyloid is very rare, it can occur and can be seen without key characteristics of interstitial amyloid deposition, namely left ventricular hypertrophy and low voltage on an ECG. Cardiogenic shock outcomes are improved by multi-disciplinary discussions, commonly referred to as a “shock team call.” Heart failure is a progressive, morbid, and potentially fatal condition. LVADs and heart transplantation improve life expectancy and decrease morbidity among patients with stage D heart failure. Identification of patients with advanced heart failure can be challenging – a helpful mnemonic is “I NEED HELP Notes - Occam’s Razor or Hickam’s Dictum? 1. How does scleroderma affect the heart? Scleroderma is a connective tissue disorder characterized by extracellular matrix deposition, with widespread fibrosis of the skin and visceral organs, microvascular injury, and evidence of immune system activation. Cardiac involvement is common, although likely underestimated as it is often subclinical, and the estimated prevalence varies widely. Myocardial involvement is identified in up to 80% of patients in histological studies and clinical myocardial dysfunction is recognized in 15-25%. When clinically evident, cardiac involvement portends a poor prognosis, with up to a 70% mortality at 5 years. Approximately 25% of scleroderma-related deaths are due to cardiac causes. Primary involvement is thought to be mediated by repeated focal ischemic-reperfusion injury, impaired microcirculation, inflammation, and eventual focal irreversible fibrosis leading to heart failure and arrhythmias. Cardiac involvement can also occur secondary to lung or renal disease, pulmonary arterial hypertension, or other cardiovascular risk factors. Cardiac manifestations: Myocardial failure: diastolic dysfunction is frequently reported but less commonly associated with diastolic heart failure. Systolic dysfunction can also occur, but severe systolic dysfunction is rare. Electrical failure: arrhythmias and conduction disorders Pericardial failure: pericarditis and pericardial effusion Coronary failure: coronary microvascular dysfunction Valvular failure: valvular involvement (uncommon) 2. What is cardiac amyloidosis (CA) and what is the pathophysiology? For an in-depth review of Cardiac Amyloidosis, enjoy the CardioNerds Cardiac Amyloid Series! Amyloidosis is a process in which proteins misfold, aggregate, and form amyloid fibrils that deposit in various organs, thereby causing tissue injury and organ malfunction. The most common types of cardiac amyloidosis are AL (light chain) and TTR (transthyretin). AL amyloidosis is a hematologic disorder of clonal plasma cells that overproduce light chains, which may deposit in any organ sparing the central nervous system, and commonly deposit in the heart and kidneys. Delayed diagnoses are common, with an estimated one-third of patients visiting five or more physicians before receiving the diagnosis. Cardiac involvement with heart failure portends a particularly poor prognosis, with a median survival from onset of heart failure of less than six months without treatment. Stem cell transplantation has been shown to improve survival if performed prior to the diagnosis of advanced heart failure. Unfortunately, about 80% of patients are not candidates for aggressive therapy due to advanced stage of disease. In CA, amyloid deposits infiltrate and expand the extracellular space which results in increased ventricular wall thickness and classically manifests as a restrictive cardiomyopathy with relatively preserved EF; however, a subset of patients may present with reduced LVEF and minimal or no ventricular wall thickening. Patients with AL cardiac amyloidosis tend to have greater severity of heart failure than TTR despite less morphological involvement (in terms of LV wall thickness), felt due to the toxic effect of light chain amyloid fibrils on the tissue resulting in a toxic-infiltrative cardiomyopathy. Additional mechanisms thought to play a major contributing role in cardiac AL amyloidosis: Circulating light chains cause direct cardiotoxicity through cardiomyocyte oxidant stress and abnormal vascular reactivity, impairing vasodilation Vascular amyloid deposition in the small intramural coronary vessels results in microvascular dysfunction and global myocardial ischemia. Vascular involvement is common in AL cardiac amyloidosis (much more common than in TTR cardiac amyloid). A pathology study demonstrated obstructive intramural coronary amyloidosis in 63 of 96 patients (66%) and 86% of these patients had microscopic evidence of myocardial ischemia. Isolated vascular involvement, however, is rare - 97% of patients in this study had interstitial involvement. Coronary microvascular dysfunction occurs via 3 major mechanisms: Structural - with amyloid deposition in the vessel wall causing wall thickening and luminal stenosis Extravascular - through extrinsic compression of the microvasculature from perivascular and interstitial amyloid deposits and decreased diastolic perfusion Functional - through autonomic and endothelial dysfunction 3. What are common cardiac MRI (CMR) findings in scleroderma heart disease and cardiac amyloidosis? First, a review of a few key concepts in CMR (also, enjoy Episode #33. Cardiac MRI with Dr. Deborah Kwon): Native T1 signals are increased by edema (e.g. acute infarction) and an increase in interstitial space (e.g. fibrosis, amyloidosis). T1 signals are decreased by lipid and iron overload.

Feb 7, 2022

Approximately 350,000 adults per year in the US experienced out-of-hospital cardiac arrest (OHCA). Only about 10% of such patients survive their initial hospitalization. The key drivers of successful resuscitation from OHCA are bystander cardiopulmonary resuscitation (CPR) and public use of an automated external defibrillator (AED). Survival rates from OHCA vary dramatically between US regions. For instance, the extracorporeal CPR (eCPR) program at the University of Minnesota has over a 40% survival rate in patients with OHCA and refractory ventricular fibrillation (VF) based on data published in the ARREST trial. In this episode, we are joined by experts from the University of Minnesota, including Dr. Jason Bartos (Interventional and Critical Care Faculty) and Dr. Julie Power (Chief Fellow at University of Minnesota and CardioNerds Academy Fellow), along with Dr. Yoav Karpenshif (Co-Chair Critical Care Series, University of Pennsylvania) and CardioNerds Co-Founders (Amit Goyal and Dan Ambinder) to discuss cardiac arrest, E-CPR, & post-arrest care. This includes targeted temperature management, coronary angiography and revascularization, as well as the growing field of eCPR and VA ECMO. Episode introduction by CardioNerds Clinical Trialist Dr. Jason Feinman. Audio editing by CardioNerds Academy Intern, Shivani Reddy. The CardioNerds Cardiac Critical Care Series is a multi-institutional collaboration made possible by contributions of stellar fellow leads and expert faculty from several programs, led by series co-chairs, Dr. Mark Belkin, Dr. Eunice Dugan, Dr. Karan Desai, and Dr. Yoav Karpenshif. Claim free CME for enjoying this episode! Disclosures: None Pearls • Notes • References • Guest Profiles • Production Team CardioNerds Cardiac Critical Care PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Abbreviations - Cardiac Arrest, E-CPR, & Post-Arrest Care eCPR- extracorporeal cardiopulmonary resuscitation VA ECMO- veno-arterial extracorporeal membrane oxygenation VT/VF- ventricular tachycardia/ventricular fibrillation ACLS- advanced cardiovascular life support ROSC- return of spontaneous circulation- OHCA- out-of-hospital cardiac arrest IHCA- in-hospital cardiac arrest TTM- targeted temperature management Pearls and Quotes - Cardiac Arrest, E-CPR, & Post-Arrest Care The ARREST trial showed early VA ECMO-facilitated resuscitation for patients with OHCA and refractory VF significantly improved survival to hospital discharge when compared to standard ACLS treatment.Coronary artery disease is common in the setting of cardiac arrest, with up to 96% of patients with STEMI on post resuscitation EKG and up to 85% of refractory out-of-hospital VT/VF arrests.Guidelines recommend emergent coronary angiography for patients with ST-segment elevation on the post-ROSC ECG.The role of timing of revascularization after ROSC in patients without STEMI or shock is unknown.The role of coronary angiography in cardiac arrest with nonshockable rhythms is also unclear.The current AHA guidelines recommend initiation of targeted temperature management between 32°C and 36°C for at least 24 hours for all patients who do not follow commands after ROSC in both OHCA and IHCA. Show notes - Cardiac Arrest, E-CPR, & Post-Arrest Care 1. What are early post arrest management considerations? The key drivers of successful resuscitations from OHCA: CPR and public use of AEDs in the field. After initial stabilization, care of the critically ill post-arrest patient hinges on hemodynamic support, mechanical ventilation, temperature management, attending to adverse sequelae of arrest, and diagnosis and treatment of underlying causes of arrest. Coronary artery disease is common in the setting of VT/VF cardiac arrest, with up to 96% of patients with STEMI on post resuscitation EKG and up to 85% of refractory out-of-hospital VT/VF arrests.In the early post-arrest state, it is also important to diagnose and treat infections and any neurologic injury. Neurologic compromise is a common cause of mortality in patients who achieve ROSC. Over 50%, and in some cohorts around 75%, of patients with death after resuscitated OHCA die of neurologic injury. 2. What is the current evidence for targeted temperature management (TTM)? “[This is] the most hotly debated topic right now in the field of cardiac arrest.” - Dr. Jason BartosCurrent AHA guidelines recommend initiation of targeted temperature management between 32°C and 36°C for at least 24 hours for all patients who do not follow commands after ROSC in both OHCA and IHCA. TTM is a relatively safe and effective strategy that can improve neurological outcomes in patients who remain comatose after achieving ROSC from cardiac arrest. Current evidence supports a broad range of TTM from 33°C to 36°C and should be maintained for 24 hours. Although TTM should be initiated as early as possible, prehospital initiation of cooling has not been shown to improve survival outcomes.The TTM2 trial showed that in patient with coma following OHCA, targeted hypothermia versus normothermia (i.e., fever control) was not associated with improved survival or functional outcomes compared to normothermia. It should be noted that patients on VA ECMO were not included in this trial. 3. What are some possible complications from TTM? Arrhythmias: Hypothermia slows cardiac conduction leading to bradycardia and QT prolongation which can exacerbate underlying arrhythmias such as VT/VF. Consideration can be given to actively rewarming the patient in the setting of VT/VF.Clotting: Core temperatures below 35°C impede the clotting cascade and platelet function. Because of this, if a patient develops significant non-compressible bleeding while undergoing TTM, consideration should be given to actively rewarm the patient.Shivering is a natural response to hypothermia. Suppression of this is crucial for TTM. First line strategies include propofol, fentanyl, or midazolam. Dexmedetomidine is effective, but side effects of bradycardia can limit its use. Buspirone (a 5-HT agonist), when used in conjunction with opiate analgesia or dexmedetomidine, has been shown to lower the shivering threshold. Neuromuscular blocking agents are highly effective at preventing shivering but confound the neurologic examination and may mask seizures. Patients need to be deeply sedated (typically RASS –4 or lower) and be followed with train-of-four assessments.Diuresis increases with hypothermia potentially leading to electrolyte loss of potassium, magnesium and phosphorous. Therefore, electrolytes need to be frequently monitored. Interestingly, total body potassium may not actually be low due to cellular shifts; thus, conservative replacement is recommended.Insulin resistance can develop as well. 4. How do we select appropriate patients to pursue revascularization and consider the timing of revascularization in patients with recent cardiac arrest? Guidelines recommend emergent coronary angiography for patients with ST-segment elevation on the post-ROSC ECG.However, the role and timing of revascularization after ROSC in patients without STEMI or shock is unknown.The role of coronary angiography in cardiac arrest with non-shockable rhythms is also unknown. 5. What is the physiologic basis for eCPR? The biggest predictor of post-arrest outcome is time.In the ALPS trial (2016), patients who underwent zero to nine minutes of CPR with ROSC had a survival of 65%. Survival dropped by 17% for every extra 10 minutes of CPR, such that there were no survivors in the amiodarone arm of the trial after 40 minutes.The results of this study were replicated at the University of Minnesota: OHCA brought to University of Minnesota Cath lab within 30 minutes of their cardiac arrest had a >90% survival rate. Survival rate drops over elapsed time: for every additional 10 minutes of ACLS, there is 25% additional mortality. If VA ECMO is initiated >90 minutes after arrest, survival is poor (10-15%). The study showed eCPR was associated with improved neurologically favorable survival at all CPR durations 3 shocks or >15-20 min of ongoing CPR without recovery of a perfusing rhythm, VA ECMO should be considered. References - Cardiac Arrest, E-CPR, & Post-Arrest Care Bartos JA, Grunau B, Carlson C, et al. Improved Survival With Extracorporeal Cardiopulmonary Resuscitation Despite Progressive Metabolic Derangement Associated With Prolonged Resuscitation. Circulation.

Feb 4, 2022

CardioNerd (Amit Goyal), Dr. Zarina Sharalaya (Interventional cardiology fellow at the Cleveland Clinic), Dr. Ashley Mohadjer (Interventional cardiology fellow, Vanderbuilt Heart and Vascular Institute), and Dr. Laurie Mbuntum (Cardiology fellow, UTSW) join Dr. Ki Park (Associate professor of medicine and an interventional cardiologist at the University of Florida and Malcom Randall VA Medical Center in Gainesville, FL.) for a a well-rounded discussion on all things ‘Women-in-Cardiology' #WIC . Dr. Ki Park discusses how she nurtured her interest in interventional cardiology, and further shares her thoughts and passion for cardio-obsetrics. She shares her advice for trainees thinking about interventional or cardioobetrics and anecdotes from her training as a successful woman in the field. We discuss the need for education on pregnancy outcomes and long-term cardiovascular risk, ideas to lower maternal mortality, how to start a women’s cardiovascular clinic, and her thoughts on how the field may look in the future. Special message by Florida ACC State Chapter Governor, Dr. David Perloff. Episode introduction and audio editing by CardioNerds Academy Intern, Shivani Reddy. The PA-ACC & CardioNerds Narratives in Cardiology is a multimedia educational series jointly developed by the Pennsylvania Chapter ACC, the ACC Fellows in Training Section, and the CardioNerds Platform with the goal to promote diversity, equity, and inclusion in cardiology. In this series, we host inspiring faculty and fellows from various ACC chapters to discuss their areas of expertise and their individual narratives. Join us for these captivating conversations as we celebrate our differences and share our joy for practicing cardiovascular medicine. We thank our project mentors Dr. Katie Berlacher and Dr. Nosheen Reza. Video Version • Notes • Production Team Claim free CME just for enjoying this episode! There are no relevant disclosures for this episode. The PA-ACC & CardioNerds Narratives in Cardiology PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Video version - Interventional Cardiology, Cardioobstetrics, & Work Life Integration with Dr. Ki Park https://youtu.be/_oYUc-_sdfU Tweetorial - Interventional Cardiology, Cardioobstetrics, & Work Life Integration with Dr. Ki Park https://twitter.com/gurleen_kaur96/status/1495921275545563136?s=21 Quotables - Interventional Cardiology, Cardioobstetrics, & Work Life Integration with Dr. Ki Park “I like the work life integration as opposed to work life balance. Balance just implies that you always have everything aligned perfectly at all times and that is just not doable.”Dr. Ki Park Show notes - Interventional Cardiology, Cardioobstetrics, & Work Life Integration with Dr. Ki Park Why is screening for OB-GYN history for cardiovascular risk is important, and who should be responsible? Pregnancy is nature’s stress test and in some women can unmask someone’s predisposition to cardiac diseaseYearly screening for diabetes, hypertension, dyslipidemiaBig interdisciplinary effort in attempt to try to capture all women at risk, as many will not present with manifestation of disease initially How did you nurture your interest in cardioobsetrics? In interventional cardiology? Meetings and societiesConnect with those who work in the field, social mediaRegarding interventional cardiology – having interest in procedures, do as many cases “hands on” as possible, learning from mistakes What advise do you have to achieve work and life balance? It's important to understand the various occupational hazards of radiation exposure which include but are not limited to brain tumors, cataracts, thyroid disease, cardiovascular diseases, musculosketal problems and reproductive side effects. Have grace, one can’t be 100% at every single thing all the timeIts more work life integration as opposed to a balancePrioritize different things on different days, be honest with children and explain why you do what you do in age appropriate terms Maternal mortality is high in this country with cardiovascular disease as a leading cause. What are important factors to improve maternal mortality? EducationImproving access to care in the peripartum stage for mothers, particularly since the focus in that period is on babyLegislature to improve insurance coverage Where do you see cardioobsetrics field going in the next few years? Make the knowledge more mainstreamEducation of subspecialty fellows within cardiovascular educationCollaboration with ACOG and maternal fetal medicine societiesMore registries of patients to continue to learn more about these women What was involved to create the women’s heart clinic in your institution? Start small – there are plenty of women who want to seek specialized careHaving an MFM and congenital faculty at the same institution was helpfulSeek advice from those at expert centers What advise do you have for trainees looking to pursue a career in interventional cardiology who are worried about work-life integration? Understand what you’re getting into, particularly for that year Don’t be afraid to ask for help from friends or family at home to allow for more quality time with significant others, kids, friends, etc -- this isn’t a sign of weaknessYou don’t have to be perfect Physicians have been found to delay childbearing compared to peers in other professions. What are your thoughts on this? Progress has been made and overall there is increased awareness and supportLeave for trainees should be more flexible More societal and institutional support Production Team Dr. Gurleen Kaur Amit Goyal, MD Daniel Ambinder, MD

Jan 27, 2022

CardioNerds (Amit Goyal and Daniel Ambinder), ACHD series co-chair Dr. Daniel Clark (Vanderbilt University), and ACHD FIT lead Dr. Danielle Massarella (Toronto University Health Network) join ACHD expert Dr. Yuli Kim (Associated Professor of Medicine & Pediatrics at the University of Pennsylvania), to discuss single ventricular heart disease and Fontan palliation. They cover the varied anatomical conditions that can require 3-step surgical palliation culminating in the Fontan circulation, which is characterized by passive pulmonary blood flow, high venous pressures, and low cardiac output. Audio editing by Dr. Gurleen Kaur (Director of the CardioNerds Internship and CardioNerds Academy Fellow). The CardioNerds Adult Congenital Heart Disease (ACHD) series provides a comprehensive curriculum to dive deep into the labyrinthine world of congenital heart disease with the aim of empowering every CardioNerd to help improve the lives of people living with congenital heart disease. This series is multi-institutional collaborative project made possible by contributions of stellar fellow leads and expert faculty from several programs, led by series co-chairs, Dr. Josh Saef, Dr. Agnes Koczo, and Dr. Dan Clark. The CardioNerds Adult Congenital Heart Disease Series is developed in collaboration with the Adult Congenital Heart Association, The CHiP Network, and Heart University. See more Claim free CME for enjoying this episode! Disclosures: None Pearls • Notes • References • Guest Profiles • Production Team CardioNerds Adult Congenital Heart Disease PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls There are various forms of unpalliated ‘single ventricle’ congenital heart disease. The three main hemodynamic issues that need to be addressed in any form are unbalanced flow, pulmonary over-circulation, and blood mixing. The Fontan palliation is a series of operations for congenital heart disease patients in whom biventricular repair is not feasible. In the completed Fontan circulation, systemic venous blood is surgically routed directly to the lungs, effectively bypassing the heart, and creating passive pulmonary blood flow. The hallmarks of the Fontan circulation (and Fontan failure) are elevated central venous pressure and low cardiac output. Patients with Fontan circulation may experience significant morbidity in the long term from both cardiac and non-cardiac sequelae, and require lifelong specialist care. Show notes 1. Why do some patients require Fontan palliation? Many different types of anatomies may ultimately require single ventricular palliation via the Fontan procedure due to inadequate biventricular function to support both pulmonary and systemic circulations. Some examples include Tricuspid Atresia (hypoplastic RV), Double Inlet Left Ventricle (DILV; hypoplastic RV), Hypoplastic Left Heart Syndrome (HLHS; hypoplastic LV), and atrioventricular septal defects (AVSD; either RV or LV may be inadequate based on “commitment” of the common AV valve). The Fontan procedure was first described in 1971; at this time, mortality of single ventricular patients exceeded 90% in the first year of life. 2. What are the stages of Fontan palliation? Effective pulmonary blood flow/balancing flow to the pulmonary and systemic circulations: for many conditions, this involves retrograde pulmonary blood flow from a systemic -> PA shunt (i.e. Blalock-Taussig-Thomas “BTT” shunt in which the subclavian artery is turned down and anastomosed to the pulmonary artery). In infants, the pulmonary vascular resistance (PVR) is high perinatally and gradually lowers over the first 3 months of life to adult levels with exposure to the atmosphere’s natural pulmonary vasodilator: oxygen. Thus, in the first 3 months of life babies have an intrinsic PVR that is too high to directly connect the venous system to the lung arteries and thereby require staged surgeries. Protect the pulmonary vasculature from overcirculation: ultimately, the goal of single ventricular palliation is rerouting systemic venous drainage directly to the pulmonary vasculature passively, without a cardiac pumping chamber. This volume unloads the common ventricle and allows it a better chance to function over the lifespan by pumping only to a single circuit: the systemic vascular bed. Thus, steps 2 and 3 of Fontan palliation are passive head/neck venous connection to the pulmonary arteries (now typically accomplished with the modified bidirectional Glenn operation that anastomoses the SVC to the RPA typically) and finally total cavopulmonary connection by the Fontan conduit connecting the lower body’s venous return from the IVC to the Fontan tunnel and up to the RPA. 3. What is the ultimate “plumbing” of Fontan circulation? Venous blood from the head/neck is connected directly from the SVC to the right pulmonary artery (RPA; typically, via a Glenn operation).Venous blood from the legs, abdomen/pelvis and lower body is connected directly to the RPA via the Fontan tunnel.In sum, the pulmonary blood flow enters passively, without a pump to send venous blood to the lungs. http://pted.org/?id=fontan3 4. What are the types of Fontan? The classic Fontan operation involved a direct venous connection to the right atrium with an atriopulmonary connection to the RPA.Contemporary era Fontan operations typically involve the lateral tunnel (LT) or extracardiac conduit. The LT incorporates pericardium in the creation of the Fontan conduit along the surface of the heart, while the extracardiac conduit is entirely prosthetic material (typically GoreTex). https://www.ahajournals.org/doi/epub/10.1161/CIR.0000000000000696 5. What are the common complications of Fontan circulation? CardiacArrhythmias: both atrial and ventricular arrhythmias can be common, especially owing to surgical scar lines, residual valvular disease, and hemodynamic sequelae of the Fontan palliationVentricular dysfunction: this may take the form of both systolic and/or diastolic dysfunctionValvular disease: atrioventricular valvular insufficiency, etc.Thromboembolic complications: venous stasis, endothelial damage, and exposure of von Willebrand factor contribute to a risk of thrombosis and risk of paradoxical emboli into the systemic circulation for patients with residual venous-arterial system connections (such as Fontan fenestration/baffle leak) ExtracardiacNeurocognitive: mental health disorders (including PTSD, depression, and anxiety) are common, as are executive function limitations that can be identified as early as childhoodFontan-associated liver disease (FALD): including risk of developing hepatocellular carcinomaRenal disease: chronic kidney disease/renal venous hypertensionLymphatic: protein-losing enteropathy (PLE) and plastic bronchitis 6. When is it time to refer a patient with Fontan palliation for heart transplantation evaluation? This is a very challenging, multidisciplinary decision that must weigh operative risk, HT candidacy, allosensitization, need for multi-organ transplantation (heart-liver, heart-lung, etc.), and patient-centered discussion about their goals of care.The team must way high near-term per-transplantation risk with improved long-term outcomes. References 1. Cetta F, Dearani J, O'Leary P and Driscoll D.Tricuspid Valve Disorders: Atresia, Dysplasia and Ebstein Anomaly. In: H. Allen, R. Shaddy, D. Penny, T. Feltes and F. Cetta, eds. Moss and Adams' Heart Disease in Infants, Children and Adolescents Philadelphia: Wolters Kluwer; 2016. 2. Book WM, Gerardin J, Saraf A, Valente AM, Rodriquez III F. Clinical phenotypes of fontan failure: implications for management. Congenit Heart Dis. 2016;11:296–308. https://pubmed.ncbi.nlm.nih.gov/27226033/ 3. Rychlik J, Atz AM, Celermajer DS, Deal BJ, Gatzoulis MA, Gewillig MH et al. American Heart Association Council on Cardiovascular Disease in the Young and Council on Cardiovascular and Stroke Nursing. Evaluation and Management of the Child and Adult With Fontan Circulation: A Scientific Statement From the American Heart Association. Circulation. 2019 Jul 1. https://www.ahajournals.org/doi/10.1161/CIR.0000000000000696 Meet Our Collaborators! Adult Congenital Heart AssociationFounded in 1998, the Adult Congenital Heart Association is an organization begun by and dedicated to supporting individuals and families living with congenital heart disease and advancing the care and treatment available to our community. Our mission is to empower the congenital heart disease community by advancing access to resources and specialized care that improve patient-centered outcomes. Visit their website (https://www.achaheart.org/) for information on their patient advocacy efforts, educational material, and membership for patients and providers CHiP Network The CHiP network is a non-profit organization aiming to connect congenital heart professionals around the world. Visit their website (thechipnetwork.org) and become a member to access free high-quality educational material, upcoming news and events, and the fantastic monthly Journal Watch, keeping you up to date with congenital scientific releases. Visit their website (https://thechipnetwork.org/) for more information. Heart UniversityHeart University aims to be “the go-to online resource” for e-learning in CHD and paediatric-acquired heart disease. It is a carefully curated open access library of educational material for all providers of care to children and adults with CHD or children with acquired heart disease, whether a trainee or a practicing provider. The site provides free content to a global audience in two broad domains: 1. A comprehensive curriculum of training modules and associated testing for trainees.

Jan 21, 2022

CardioNerds (Amit Goyal), Dr. Natalie Stokes (Cardiology Fellow at UPMC and Co-Chair of the Cardionerds Cardio-Ob series), fellow lead Dr. Victoria Thomas (Cardionerds Ambassador, Vanderbilt University Medical Center), join Dr. Rachel Bond (Women's Heart Health Systems Director at Dignity Health, Arizona) for a cardio-obstetrics discussion about Black maternal health. Episode introduction by CardioNerds Clinical Trialist Dr. Chistabel Nyange. Audio editing by CardioNerds Academy Intern, Christian Faaborg-Andersen. This episode was developed in collaboration with the Association of Black Cardiologists. ABC is a 501(c)3 nonprofit organization whose mission is to promote the prevention and treatment of cardiovascular disease, including stroke, in Black persons and other minority populations, and to achieve health equity for all through the elimination of disparities. Learn more at https://abcardio.org/. Notes • References • Guest Profiles • Production Team CardioNerds Cardio-Obstetrics Series PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Show notes 1. Why does Black Maternal Health need to be deliberately highlighted episode on CardioNerds? Black women are three-four times more likely to die during their pregnancy. The deaths are primarily tied to cardiomyopathy and cardiovascular conditions such as coronary artery disease, pulmonary hypertension, chronic hypertension, preeclampsia, and eclampsia.63-68% of this cardiovascular mortality is preventable depending on one’s racial identity. As CardioNerds, we must educate ourselves on why this occurs and identifying diseases that may place patients at increased risk.Studies have shown the Black maternal mortality crisis exist irrespective of one’s education or socioeconomic status.We must recognize and admit that some patients are being treated differently because of their race and ethnicity alone. 2. When we consider or acknowledge a patient’s race, what should CardioNerds think about? Race is an important factor to think about, but we must remember that it is an imperfect variable. We should not focus on biology or genetic make-up. We should think about social determinants of health. 60% of the time social and personal aspects dictate one’s health.Unconscious biases and structural racism are likely playing a major role in race-based health inequities. 3. What are other vulnerable groups that have increased mortality rates related to cardioobstetric care? Native American women have similar maternal mortality rates to Black populations.Women who are veterans, live in rural communities, and/or are currently incarcerated have increased risk of mortality 4. What are some of the social determinants of health that should be considered for these patients? Food deserts or having poor access to nutrient rich/quality foods make these vulnerable patients have increased risk factors for high cholesterol, high blood pressure, obesity, and diabetes which increase the risk for pregnancy complications and infertility.The above vulnerable populations can have less access to higher levels of care for high-risk pregnancies. 5. What are some of the preventable causes of maternal mortality? Clinicians should actively listen to their patients' concerns. There have been several media stories in the news and on CardioNerds episodes where women’s concerns were not acknowledged or taken seriously.Preconception counseling is important to provide to all patients. 50% of women have one risk factor for cardiovascular disease when entering pregnancy. We should have discussions with patients regarding their lifestyles, with an emphasis on exercise and diet. 6. What are some of the psychosocial or health related differences we see in black mothers when compared to other races? The effect of stress is affecting not just black mothers but black women in general by predisposing them to increased cardiovascular disease and cognitive impairment. The stress effects on black women are being called superwoman schema.Superwoman schema is a combination/phenomenon of gender and racial oppression’s effect on the allostatic load (cumulative biological stress). Studies have shown that black women’s chronic stress levels affect their sympathetic nervous system with an inability to fight off or perhaps produce too much inflammatory response. This increases the risk of a variety worsening chronic morbidities in particular worsening cardiovascular health.One in eight women will struggle with infertility. Black women are two times more likely to suffer from infertility compared to their White counterparts. This is largely due to increased uterine fibroids. Black women are also less likely to be referred to a reproductive endocrinology specialist. 7. What pre-counseling assessments or work-up should be considered for women trying to conceive? Consider getting a baseline ECG as that would give a nice idea of structurally of what is going on within the heart. If there are several risk factors, there can be consideration for a baseline echocardiogram.There should be a specific focus on lifestyle. As cardiologists, we should try to have our patients monitor their weight and follow a well-balanced diet with exercise. They should monitor their blood pressure.Also try to have a birthing plan with OBGYN team as there is data to support that a birthing plan can lead to better outcomes for high-risk pregnancy. 8. What are some of the tools that have been recently used to help reduce black maternal mortality? Patients that are likely to have higher pregnancy complications should be considered to follow not only with a maternal fetal medicine doctor, but there should be consideration for extra help with a doula or a midwife if possible.We should promote home blood pressure monitoring during pregnancy and post-partum as there have been trials supporting the fact that blood pressure control was more successful using texting/ambulatory monitoring strategies vs office visits alone.Digital platforms such as MAHMEE are closing gaps in care to connect patients in their pregnancy and postpartum care to help with all patients but especially underserved populations. References 1. Bond RM, Gaither K, Nasser SA, et al. Working Agenda for Black Mothers: A Position Paper from the Association of Black Cardiologists on Solutions to Improving Black Maternal Health. Circ Cardiovasc Qual Outcomes. 2021;14(2):e007643. doi:10.1161/CIRCOUTCOMES.120.007643 2. Havranek EP, Mujahid MS, Barr DA, et al. Social Determinants of Risk and Outcomes for Cardiovascular Disease: A Scientific Statement From the American Heart Association. Circulation. 2015;132(9):873-898. doi:10.1161/CIR.0000000000000228 3. Chandra A, Copen CE, Stephen EH. Infertility and impaired fecundity in the United States, 1982-2010: data from the National Survey of Family Growth. Natl Health Stat Report. 2013;(67):1-19. 4. Woods-Giscombé CL. Superwoman schema: African American women's views on stress, strength, and health. Qual Health Res. 2010;20(5):668-683. doi:10.1177/1049732310361892 5. Allen AM, Wang Y, Chae DH, et al. Racial discrimination, the superwoman schema, and allostatic load: exploring an integrative stress-coping model among African American women. Ann N Y Acad Sci. 2019;1457(1):104-127. doi:10.1111/nyas.14188 6. Ofili EO, Schanberg LE, Hutchinson B, et al. The Association of Black Cardiologists (ABC) Cardiovascular Implementation Study (CVIS): A Research Registry Integrating Social Determinants to Support Care for Underserved Patients. Int J Environ Res Public Health. 2019;16(9):1631. Published 2019 May 10. doi:10.3390/ijerph16091631 7. Lantz PM, Low LK, Varkey S, Watson RL. Doulas as childbirth paraprofessionals: results from a national survey. Womens Health Issues. 2005;15(3):109-116. doi:10.1016/j.whi.2005.01.002 8. Pregnancy mortality surveillance system. Centers for Disease Control and Prevention. https://www.cdc.gov/reproductivehealth/maternal-mortality/pregnancy-mortality-surveillance-system.htm. Published November 25, 2020. Accessed December 18, 2021. 9. Cairns AE, Tucker KL, Leeson P, et al. Self-Management of Postnatal Hypertension: The SNAP-HT Trial. Hypertension. 2018;72(2):425-432. doi:10.1161/HYPERTENSIONAHA.118.10911 10. Hirshberg A, Sammel MD, Srinivas SK. Text message remote monitoring reduced racial disparities in postpartum blood pressure ascertainment. Am J Obstet Gynecol. 2019;221(3):283-285. doi:10.1016/j.ajog.2019.05.011 11. Vedam S, Stoll K, MacDorman M, et al. Mapping integration of midwives across the United States: Impact on access, equity, and outcomes. PLoS One. 2018;13(2):e0192523. Published 2018 Feb 21. doi:10.1371/journal.pone.0192523 Guest Profiles Dr. Rachel Bond Rachel M Bond, MD, FACC, Women's Heart Health & Prevention Specialist is devoted to expert diagnosis and treatment for improved patient outcomes. Her expertise is in cardiovascular disease with special interest in women's heart health, prevention, lipid disorders, pregnancy-related heart disease, cardio-oncology and autoimmune-related heart disease.Dr. Bond is a board-certified attending cardiologist and the System Director of the Women's Heart Health Program at Dignity Health in Arizona. She is affiliated with Chandler Regional Medical Center & Mercy Gilbert Medical Center. She is board certificated in cardiovascular disease, internal medicine, echocardiography and nuclear cardiology and is a registered physician in vascular interpretation. Dr. Bond is a well-known spokesperson for the American Heart Association, Go Red for Women Campaign. Dr. Victoria Thomas Dr.

Jan 17, 2022

CardioNerds (Amit Goyal and Daniel Ambinder) join Dr. Jaya Kanduri, Dr. Dan Lu, and Dr. Joe Wang from Weill Cornell Cardiology for Levain cookies in Central Park. The ECPR is provided by Dr. Harsimran Singh (Cardiology Program Director and Interventional Cardiologist with expertise in ACHD). Episode introduction by CardioNerds Clinical Trialist Dr. Jeremy Brooksbank. We discuss a case of a 24-year-old female with a history of unicuspid aortic valve with associated aortopathy status post mechanical aortic valve replacement and Bentall procedure at age 16 presents with acute onset substernal chest pain and shortness of breath. She was found to have mechanical aortic valve obstruction and severe aortic regurgitation resulting in cardiogenic shock. Unfortunately, the shock quickly progressed to refractory cardiac arrest requiring mechanical support with VA-ECMO before valve debridement was performed in the operating room. The differential for mechanical prosthetic valve stenosis includes pannus, thrombus, or vegetation. She was eventually found to have thrombus obstructing the outflow tract and holding the mechanical leaflets open leading to torrential regurgitation. She underwent successful surgical debridement. We discuss unicuspid aortic valve and associated aortopathy, surgical considerations regarding AVR, diagnosis and management of prosthetic valve dysfunction, approach to cardiogenic shock and considerations around activating and managing VA-ECMO. With this episode, the CardioNerds family warmly welcomes Weill Cornell Cardiology to the CardioNerds Healy Honor Roll. The CardioNerds Healy Honor Roll programs support and foster the the CardioNerds spirit and mission of democratizing cardiovascular education. Healy Honor Roll programs nominate fellows from their program who are highly motivated and are passionate about medical education. The Weill Cornell fellowship program director, Dr. Harsimran Singh has nominated Dr. Jaya Kanduri for this position. Claim free CME just for enjoying this episode! Disclosures: NoneJump to: Pearls - Notes - References CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Case Media ECGCXREchoRHC PSL AP3 Color LHC - LCA LHC - LCA RCA Aortogram TEE TEE 2 Episode Teaching Pearls - Mechanical Valve Thrombosis (1) Unicuspid aortic valves present with aortic stenosis earlier in life. There can be concurrent aortic regurgitation and, like bicuspid aortic valves, unicuspids can be associated with aortopathy as well as other congenital anomalies. (2) Prosthetic valve stenosis is assessed with different echocardiographic parameters than what we use for native valves. The differential for mechanical valve stenosis includes pannus, thrombus, or vegetation. Patient prosthesis mismatch may also lead to elevated gradients. (3) VA-ECMO provides robust flow in the setting of cardiogenic shock as well as gas exchange. While this flow may improve end-organ perfusion, it also increases left ventricular afterload, thereby potentially worsening LV ischemia and impeding LV recovery. Elevated afterload may also decrease innate contractility and prevent aortic valve leaflets from opening. Therefore, if a patient with a mechanical valve is on VA-ECMO, ensuring valve opening to prevent valve (or ventricular) thrombosis is paramount. (4) Venting is sometimes necessary to decrease the left ventricular end diastolic pressure from the high afterload imposed by VA-ECMO. A microaxial temporary LVAD (example – Impella device) directly unloads the left ventricle, but cannot be used in the setting of a mechanical aortic valve. TandemHeart is also a consideration (inflow cannula placed across the interatrial septum in the left atrium) to unload the LV, but does not improve flow across the aortic valve so can lead to thrombus if a mechanical valve is present. Intra-aortic balloon counterpulsation using an IABP can be used to decrease afterload on the native heart and increase coronary perfusion, but does not directly unload the left ventricle. (5) Acute mechanical valve thrombosis can be managed with emergency surgery or with low dose fibrinolytic therapy. Surgery is preferable when operative risk is low and if there are contraindications to fibrinolytic therapy such as prior intracranial hemorrhage or active bleeding. (6) VA-ECMO can be weaned by slowly decreasing flow rates and assessing native cardiac function, hemodynamic response, and end-organ perfusion with assessments including echocardiography and pulmonary artery catheterization. Notes - Mechanical Valve Thrombosis 1. What is a unicuspid aortic valve? Unicuspid aortic valves (UAVs) are rare with an incidence of only 0.02%.There are two types of UAVs. Acommisural UAVs have a single cusp with a stenotic central orifice and rudimentary commissures that do not divide the valve (pin-hole shaped), and are usually complicated by severe stenosis in early childhood. Unicommisural UAVs are composed of a single cusp with a single commissural attachment to the aortic wall and an elongated orifice (slit-like orifice), which has a less aggressive course and is generally discovered in adulthood.Aortic stenosis is almost universal among UAVs, present with or without aortic regurgitation in 92% of cases. Some series have shown 14% of cases with concurrent aortopathy.UAVs may be associated with congenital abnormalities likes anomalous coronaries, PDA, VSD and coarctation. 2. How do we assess for aortic prosthetic valve stenosis? Assessment for mechanical valve stenosis involves different echocardiographic parameters than when evaluating a native valve. Doppler velocity index (DVI) is the dimensionless index with LVOT VTI/AV VTI, with severe stenosis suggested by a ratio of 100msec (it takes longer to gush through a more stenotic valve). Effective orifice area (EOA) 0.8cm2), presence of LA thrombus or concomitant CAD in need of revascularization, presence of other valve disease, and presence of possible pannus (which would not respond to fibrinolysis). 6. What is the approach to weaning VA-ECMO? Assessment of echocardiographic features, hemodynamics, and end-organ perfusion is essential for a successful VA-ECMO wean. First a turndown of the circuit is performed where the ECMO flow is decreased in a protocolized fashion. This should reduce afterload and therefore increase LV contractile reserve, as well as increase preload with return of flow through the ventricles. With these changes, successful hemodynamic parameters to look for are stable cardiac index, central venous pressure, pulmonary arterial pressures, and systemic blood pressures. Successful echocardiographic parameters include an increase in LVEF >20-25%, aortic VTI ≥10 cm, lateral mitral annulus peak systolic velocity ≥6 cm/s,

Jan 11, 2022

The hemodynamic evaluation of cardiogenic shock obtained via a Swan-Ganz catheter plays an essential role in the characterization of cardiogenic shock patients. Join Dr. Nosheen Reza, (Assistant Professor of Medicine and Advanced Heart Failure and Transplant cardiologist at the Hospital of the University of Pennsylvania), episode fellow lead Dr. Brian McCauley (Interventional and Critical Care Fellow at the Hospital of the University of Pennsylvania), Dr. Mark Belkin (Cardiac Critical Care Series Co-Chair and AHFT fellow at University of Chicago), and CardioNerds Co-Founders, Amit Goyal and Dan Ambinder, for this tour through the heart aboard the Swan-Ganz catheter. In this episode, we evaluate three separate admissions for a single patient to highlight pearls regarding waveform assessment, evaluating cardiac output, phenotyping hemodynamic profiles, targeted therapies based on hemodynamics and so much more. Episode introduction and audio editing by Dr. Gurleen Kaur (Director of the CardioNerds Internship). Claim free CME for enjoying this episode! Disclosures: None Pearls • Notes • References • Guest Profiles • Production Team CardioNerds Cardiac Critical Care PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls and Quotes - Hemodynamic Evaluation of Cardiogenic Shock Swan-Ganz catheters are not dead #ReviveTheSwan! They remain a useful tool to characterize cardiac patients & to help direct therapy, especially in Cardiogenic Shock.When looking at Swan-Ganz catheter data, it is important to always interpret your own tracings, to know what values are acquired directly, and which values are derived.It is important to understand the strengths and weakness of hemodynamic characterization by Swan-Ganz cathetersAdvanced metrics such as cardiac power output, pulmonary artery pulsatility index, and aortic pulsatility index are extremely useful in further phenotyping patients as well as guiding mechanical support platforms“The data will be wrong if the preparation is not right” Show notes - Hemodynamic Evaluation of Cardiogenic Shock 1. Swan-Ganz catheters are a useful tool to characterize cardiac patients and to direct therapy. With the ESCAPE trial in 2004, Swan-Ganz catheter utilization dropped drastically outside transplant centers across the United States (2). While the ESCAPE trial did demonstrate the possibility of harm when using a Swan-Ganz catheter, many of the truly ill cardiac patients we care for would have been excluded from the trial. For instance, patients on dobutamine at doses above 3 µg/kg/min or any dose of milrinone during the hospitalization were excluded from the trial.This is a classic example of “throwing the baby out with the bath water.”In a recent large, multicenter cardiogenic shock registry, complete hemodynamic assessment using pulmonary artery catheters prior to MCS is associated with lower in-hospital mortality compared with incomplete or no assessment (3). 2. When looking at Swan-Ganz catheter data, it is important to always interpret your own tracings, to know what values are acquired directly, and which values are derived. Incomplete or incorrect data can lead to mischaracterization of our patients. Therefore, it is essential to review all of the tracings, calculations, and data acquired for each individual patient before any clinical adjustments are made (1). An incomplete pulmonary capillary wedge tracing is an example from clinical practice (causing the PCWP, and therefore the left-sided filling pressures to be overestimated). It is equally important to know the limitations of cardiac output equations, and that no one measurement is perfect.Foibles of the Fick equation include assumed rather than measured oxygen consumption and variations in hemoglobin concentration. Traditionally, thermodilution has been thought to be likely less accurate in presence of tricuspid regurgitation, which could lead to blending of the cold dilutant, but recent data suggests even in these circumstances it remains the preferred method for estimating cardiac output over indirect Fick. 3. What are some tips of measuring a PCWP correctly? To ensure that we get the wedge pressure correctly, we must first make sure we understand the wedge pressure in relation to the respiratory cycle. For the majority of patients, the end expiratory intrathoracic pressure will be close to 0, and it will have the least influence on our readings. Thus, for most patients, that is why we measure the wedge pressure at end expiration.However, in patients with severe lung disease or significant obesity, the intrathoracic pressure may not be close to 0 at end expiration or there may be wide swings in intrathoracic pressure. For these patients, it is a reminder to look at the tracings yourself, and we may need to average the PCWP over the respiratory cycle.When we are measuring the PCWP, we have to remember that we are using it as a surrogate of the LV end-diastolic pressure. The point of the cardiac cycle when the pressure in the pulmonary veins, left atrium and LV are closest to equal is end-diastole. Thus, we typically want to measure the PCWP in end-diastole, which would specifically be measuring the mean of the A-wave.Now, for patients with severe mitral regurgitation and/or significant atrial myopathy leading to large V-waves, the wedge pressure estimated at end-diastole will not necessarily reflect the mean wedge (averaged throughout the cardiac cycle) that the pulmonary circulation “sees” throughout the cardiac cycle. As has been a theme in this episode, we have to make sure our inputs are accurate to appropriately help our patients. In this circumstance of large V-waves, if we were calculating the pulmonary vascular resistance (Mean PA Pressure – PCWP / CO), but used the end-diastolic PCWP instead of the PCWP averaged through the cardiac cycle we may end up with an inaccurate estimation of PVR. 4.Advanced metrics such as cardiac power output, pulmonary artery pulsatility index, and aortic pulsatility index are extremely useful in further characterizing hemodynamics. Over the past several years individual indices of ventricular performance have been developed and studied, these include CPO, PAPi, API, and LVSWI (4,5,10-12). These values can further flesh out our hemodynamic profiles, and help guide decision-making for choosing the proper mechanical circulatory support platform (7,8,9).See the infographic developed by CardioNerds Academy Fellow Ahmed Ghoneem for more information on different thresholds for these parameters.The API is a novel hemodynamic parameter that was recently applied to ESCAPE trial patients by series Co-Chair, Mark Belkin. 5. “The data will be wrong if the preparation is not right.” Dr. Reza’s point on the episode is apt and high-yield.Incorrect data acquisition and/or interpretation will not benefit our patients. We need to know what values are measured directly (chamber pressures, SvO2) and which are derived (cardiac output/index, SVR/PVR, CPO/PAPi/API, and so forth). As cardiologists and intensivists, we need to be critical of the tracings themselves, avoid anchoring to a single value, and be observant of the overall hemodynamic trajectory our patient is taking. Only through thoughtful intervention in coordination with careful and consistent monitoring will we bring to bear the benefits bestowed by Swan-Ganz catheter supplemented-care (1). Schematics and Graphics - Hemodynamic Evaluation of Cardiogenic Shock RHC Tracings Discussed in the Episode References - Hemodynamic Evaluation of Cardiogenic Shock 1.Ragosta M. Textbook of Clinical Hemodynamics. Elsevier; 2017. 2.Binanay C, Califf RM, Hasselblad V, et al. Evaluation study of congestive heart failure and pulmonary artery catheterization effectiveness: the ESCAPE trial. JAMA. 2005;294(13):1625-33. https://jamanetwork.com/journals/jama/fullarticle/201634 3. Garan AR, Kanwar M, Thayer KL, et al. Complete hemodynamic profiling with pulmonary artery catheters in cardiogenic shock is associated with lower in-hospital mortality. JACC Heart Fail. 2020;8(11):903-913. https://pubmed.ncbi.nlm.nih.gov/33121702/ 4.Korabathina R., Heffernan K.S., Paruchuri V., Patel A.R., Mudd J.O., Prutkin J.M., et al: The pulmonary artery pulsatility index identifies severe right ventricular dysfunction in acute inferior myocardial infarction. Catheter Cardiovasc Interv 2012; 80: pp. 593-600. https://pubmed.ncbi.nlm.nih.gov/21954053/ 5.Fincke R, Hochman JS, Lowe AM, et al. Cardiac power is the strongest hemodynamic correlate of mortality in cardiogenic shock: a report from the SHOCK trial registry. J Am Coll Cardiol. 2004;44(2):340-8. https://pubmed.ncbi.nlm.nih.gov/15261929/ 6.Kochav SM, Flores RJ, Truby LK, Topkara VK. Prognostic impact of pulmonary artery pulsatility index (Papi) in patients with advanced heart failure: insights from the escape trial. J Card Fail. 2018;24(7):453-459. https://pubmed.ncbi.nlm.nih.gov/29597051/ 7.Feldman D, Naidu SS. Percutaneous Mechanical Circulatory Support Devices. Cardiac Interventions Today. 2016; 10 (1): 26-33. https://citoday.com/articles/2016-jan-feb/cover-stories 8.Briceno N, Kapur NK, Perera D. Percutaneous mechanical circulatory support: current concepts and future directions. Heart. 2016;102(18):1494-507. https://pubmed.ncbi.nlm.nih.gov/27503999/ 9.Baran DA, Grines CL, Bailey S, et al. Scai clinical expert consensus statement on the classification of cardiogenic shock: this document was endorsed by the american college of cardiology (Acc), the american heart association (Aha), the society of critical care medicine (Sccm), and the society of thoracic surgeons (Sts) in april 2019. Catheter Cardiovasc Interv. Published online May 19, 2019:ccd.28329. https://pubmed.

Jan 7, 2022

CardioNerds (Amit Goyal and Daniel Ambinder), Dr. Zarina Sharalaya (Interventional Cardiology Fellow at the Cleveland Clinic), and Dr. Simrat Kaur (General Cardiology Fellow at the Cleveland Clinic) join Dr. Samir Kapadia, the Chair of the Robert and Suzanne Tomsich Department of Cardiovascular Medicine, Sydell and Arnold Miller Family Heart, Vascular & Thoracic Institute at Cleveland Clinic. They discuss future advancements in the field of structural interventional cardiology. Dr. Kapadia sheds light on his journey starting as an international medical graduate from India and speaks about his mentors that helped shape his career and his life. We later delve into several advancements in the field of structural and interventional cardiology, along with the amalgamation of different sub-specialities with intervention such as heart failure and critical care cardiology. We also discuss the measures being taken to reduce the occupational hazards associated with interventional cardiology and how to make this field more appealing to women in cardiology. Special message by Ohio ACC State Chapter Governor, Dr. Kanny Grewal. The PA-ACC & CardioNerds Narratives in Cardiology is a multimedia educational series jointly developed by the Pennsylvania Chapter ACC, the ACC Fellows in Training Section, and the CardioNerds Platform with the goal to promote diversity, equity, and inclusion in cardiology. In this series, we host inspiring faculty and fellows from various ACC chapters to discuss their areas of expertise and their individual narratives. Join us for these captivating conversations as we celebrate our differences and share our joy for practicing cardiovascular medicine. We thank our project mentors Dr. Katie Berlacher and Dr. Nosheen Reza. Video Version • Notes • References • Production Team Claim free CME just for enjoying this episode! There are no relevant disclosures for this episode. The PA-ACC & CardioNerds Narratives in Cardiology PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Tweetorial on Innovation, Excellence and Leadership in Interventional Cardiology with by Dr. Gurleen Kaur https://twitter.com/gurleen_kaur96/status/1484205728663576590?s=21 Video version - Innovation, Excellence and Leadership in Interventional Cardiology with Dr. Samir Kapadia https://youtu.be/BfqnRkaVGkk Quotables - Innovation, Excellence and Leadership in Interventional Cardiology with Dr. Samir Kapadia “A very important thing for all international medical graduates and for everybody, for that matter - it is important to recognize that the opportunities are what you perceive and not what others perceive.”Dr. Samir Kapadia Show notes - Innovation, Excellence and Leadership in Interventional Cardiology with Dr. Samir Kapadia How do international medical graduates contribute to the work force in medicine across the United States of America? International medical graduates account for 25% of the physician work force, with over 85% being involved in direct patient care.IMGs are usually accomplished, consummate and highly motivated physicians who often have to overcome challenges such as language proficiency, acculturation and difficulties with obtaining a visa status in the United States.IMGs also help fill gaps in health care by working in geographical areas that are otherwise not desirable by US or Canadian medical graduates.IMGs contribute to diversity of the field which provides a richer training environment, improved access to health care for underrepresented minorities, as well as better patient outcomes. What are key qualities of a good mentor? A good mentor is responsible for enhancing the education of his or her mentees along with motivating them to challenge their limits.Qualities of a good mentor extend beyond mere mentorship to sponsorship, where the mentor opens up his or her network for the mentee allowing them to pursue a path of success.A mentor serves as an advisor and a counselor, helping his or her mentees navigate difficult paths teaching them to become resilient physicians.A mentor also serves as a confidante for the trainee with whom mentees can share their dreams, aspirations and vulnerabilities knowing not only will this be kept in confidence but will also provide a catalyst for their growth. What are the recent advancements in minimizing radiation exposures for structural cardiologists? It's important to understand the various occupational hazards of radiation exposure which include but are not limited to brain tumors, cataracts, thyroid disease, cardiovascular diseases, musculosketal problems and reproductive side effects.When dealing with possible occupational radiation exposure, we should strive for the ALARA (as low as reasonably achievable) principle of radioprotection.The RADPAD (RADPAD 5100A-O; Worldwide Innovations & Technologies, Inc, Lenexa, KS) is a new development that is a lead field shield that is placed between the patient and the operator to reduce scatter radiation and significantly reduce operator radiation exposure.The use of Zero gravity lead is a novel suspension shield which has also been shown to significantly reduce the operator radiation exposure and potentially decrease orthopedic injuries particularly spinal injuries secondary to the protective lead garments. What are the future directions for structural interventions and how is the field of structural cardiology going to evolve in the next few years? The future of structural cardiology provides great promise. After the success of transcatheter aortic valve replacement (TAVR) and transcatheter mitral valve edge to edge repair (TEER), there has been increasing development in tricuspid interventions as well as interventions for severe mitral stenosis due to mitral annular calcification.The amalgamation of structural interventional cardiology and heart failure as well as with critical care are also exciting fields that is still developing. Advancements in left ventricular restoration devices such as the Revivant TC system may help several patients with end stage congestive heart failure due to ischemic heart disease. References Steward DE. The internal medicine workforce, international medical graduates, and medical school departments of medicine. Am J Med 2003;115(1):80–4. Doi: 10.1016/s0002-9343(03)00307-3.Kostis JB., Ahmad B. International medical graduates and the cardiology workforce. J Am Coll Cardiol 2004;44(6):1172–4. Doi: 10.1016/j.jacc.2004.05.081.Al Hussein Al Awamlh B. Alien J-1 Physicians in a Pandemic. JAMA Intern Med 2021;181(6):743–4. Doi: 10.1001/jamainternmed.2021.0730.David YN., Issaka RB. Advancing diversity: the role of international medical graduates. Lancet Gastroenterol Hepatol 2021;6(12):980–1. Doi: 10.1016/S2468-1253(21)00376-9.Shikhar A. Mentorship During Fellowship. J Am Coll Cardiol 2014;64(15):1637–8. Doi: 10.1016/j.jacc.2014.08.017.Tobin MJ. Mentoring: seven roles and some specifics. Am J Respir Crit Care Med 2004;170(2):114–7. Doi: 10.1164/rccm.2405004.Picano E., Vano E. The Radiation Issue in Cardiology: the time for action is now. Cardiovasc Ultrasound 2011;9(1):35. Doi: 10.1186/1476-7120-9-35.Vlastra W., Delewi R., Sjauw KD., et al. Efficacy of the RADPAD Protection Drape in Reducing Operators’ Radiation Exposure in the Catheterization Laboratory: A Sham-Controlled Randomized Trial. Circ Cardiovasc Interv 2017;10(11). Doi: 10.1161/CIRCINTERVENTIONS.117.006058.Zanca F., Dabin J., Collard C., et al. Evaluation of a suspended radiation protection system to reduce operator exposure in cardiology interventional procedures. Catheter Cardiovasc Interv Off J Soc Card Angiogr Interv 2021;98(5):E687–94. Doi: 10.1002/ccd.29894.GP., Y.S. C. Continuing Advances and Challenges of Structural Heart Imaging. JACC Cardiovasc Imaging 2021;14(1):128–30. Doi: 10.1016/j.jcmg.2020.12.002.Klein P., Anker SD., Wechsler A., et al. Less invasive ventricular reconstruction for ischaemic heart failure. Eur J Heart Fail 2019;21(12):1638–50. Doi: 10.1002/ejhf.1669. Production Team Dr. Gurleen Kaur Amit Goyal, MD Daniel Ambinder, MD

Jan 3, 2022

In this episode, CardioNerds (Amit Goyal), ACHD series co-chair, Dr. Josh Saef (ACHD fellow at University of Pennsylvania) and episode lead fellow, Dr. Brynn Connor (Pediatric Cardiology fellow at Lucile Packard Children's Hospital at Stanford) are joined by Dr. Maan Jokhadar (Advanced heart failure and adult congenital heart disease specialist at Emory University) to discuss transposition of the great arteries. Audio editing by CardioNerds Academy Intern, Dr. Maryam Barkhordarian. For a brief review of the basic anatomy and physiology of D-TGA, check-out this great video by Dr. Maan Jokhadar! The CardioNerds Adult Congenital Heart Disease (ACHD) series provides a comprehensive curriculum to dive deep into the labyrinthine world of congenital heart disease with the aim of empowering every CardioNerd to help improve the lives of people living with congenital heart disease. This series is multi-institutional collaborative project made possible by contributions of stellar fellow leads and expert faculty from several programs, led by series co-chairs, Dr. Josh Saef, Dr. Agnes Koczo, and Dr. Dan Clark. The CardioNerds Adult Congenital Heart Disease Series is developed in collaboration with the Adult Congenital Heart Association, The CHiP Network, and Heart University. See more Claim free CME for enjoying this episode! Disclosures: None Pearls • Notes • References • Guest Profiles • Production Team CardioNerds Adult Congenital Heart Disease PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! https://www.youtube.com/watch?v=Ifu8nVtXT_c Pearls (1) In D-TGA following an atrial switch operation, the right ventricle IS the systemic ventricle! (2) Evaluation of systemic right ventricular function often requires use of both transthoracic echocardiography and cardiac MRI. (3) Use of medical heart failure therapies should be individualized, without any proven long-term mortality benefit and potential unique complications in this patient population (i.e. SA node dysfunction). Show notes D-transposition of the great arteries (D-TGA) is one of the most common forms of cyanotic congenital heart disease presenting in the newborn period. Anatomically, d-transposition of the great arteries is characterized by atrioventricular concordance and ventriculoarterial discordance, such that the aorta arises from the morphologic right ventricle and pulmonary artery arises from the morphologic left ventricle. The resultant physiology is that of a parallel circulation, with deoxygenated blood recirculating in the systemic circulation (via the RA-RV) and oxygenated blood recirculating in the pulmonary circulation (via the LA-LV). At birth, this invariably results in cyanosis, with survival dependent upon adequate mixing of the two circulations via an atrial or ventricular level defect. Prior to surgical advances in the late 1950s, this lesion was uniformly fatal, with most infants dying before their first birthday. The subsequent development of the Senning and Mustard atrial-level repairs led to good immediate outcomes and improved long-term survival. However, following these “physiologic” types of repair, patients are far from cured, with several long-term established complications, including (1) dysfunction of the systemic right ventricle, (2) tricuspid regurgitation (the systemic atrioventricular valve), (3) atrial and ventricular arrhythmias, and (4) systemic and pulmonary venous baffles leaks and obstruction. These complications ultimately lead to substantial morbidity and premature mortality, with ACHD providers facing unique challenges in the medical and surgical management of this heterogenous patient population. 1. What are the basic anatomic features of d-transposition of the great arteries (d-TGA)? D-transposition of the great arteries is defined by the origin of the arterial trunks from the morphologically inappropriate ventricle, specifically with the aorta arising from the morphologic right ventricle (now the systemic ventricle) and the pulmonary trunk arising from the morphologic left ventricle.This is termed “ventriculoarterial discordance”, and importantly, does not define the spatial relationship of the great arteries. Rather, the “d” terminology refers to the looping of the ventricles and distinguishes d-TGA from l-TGA (or congenitally corrected transposition), where there is additional atrioventricular discordance. The resultant physiology is that of a parallel circulation, with deoxygenated blood recirculating in the systemic circulation and oxygenated blood recirculating in the pulmonary circulation. At birth, this invariably results in cyanosis, with survival dependent upon adequate mixing of the two circulations via an atrial or ventricular level defect.There are three major anatomic variations in dTGA, including dTGA with an intact ventricular septum (most common), dTGA with a ventricular septal defect, and dTGA with LVOT obstruction. These anatomic subtypes can lead to variable presentations in the neonatal period, as well as pose unique challenges to surgical repair, and are therefore important diagnostic considerations.The arrangement of the coronary arteries and their spatial course can additionally be highly variable, posing added complications when performing the arterial switch operation (which requires reimplantation of the coronary arteries into the neo-aortic root). The most common, “usual,” arrangement is the left coronary artery originating off the anterior facing sinus, and the right coronary artery originating off the posterior facing sinus. 2. What surgical approaches have been utilized in the management of D-TGA?What are the key features of aortic coarctation anatomy? Prior to surgical advances in the late 1950s, this lesion was uniformly fatal, with most infants dying before the age of 1 year.Infants were initially palliated with an atrial septostomy, which allowed for mixing at the atrial level and improved survival in the immediate newborn period. However, these infants were still left with profound cyanosis, with inevitable mortality in the first year of life.In the mid-1950s, the Senning (1958) and Mustard (1964) atrial-level repairs were first performed, with good short-term outcomes and improved long-term survival.In the Senning procedure, a baffle is created within the atria that redirects the deoxygenated caval blood to the mitral valve and the oxygenated pulmonary venous blood to the tricuspid valve with use of native atrial tissue.Mustard subsequently described a simpler technique with creation of an atrial baffle using synthetic patch material. By the late 1980s, late complications of these repairs became well recognized, with the ultimate adoption of the neonatal arterial switch operation, which remains the gold standard for surgical management of transposition. 3. What are the long-term complications of the Mustard and Senning procedures? Systemic Right Ventricular Dysfunction:Clinical Features - Systemic RV dysfunction is an evitable consequence of the atrial switch operation, with 50% of patients developing right ventricular systolic dysfunction by 30 years of age.While right ventricular dysfunction is often mild and clinically asymptomatic for several years, patients ultimately develop related symptomatology over the subsequent 10-20 years.Most commonly, patients present to care with diminished exercise tolerance, with symptomatic arrhythmias being an additional common reason for patients to seek care. DiagnosisAccurate assessment of RV size and function in this population is critical for adequate surveillance and management planning. However, quantitative right ventricular assessment remains challenging, with no model for comparison and no clear criteria for abnormalities.Volumetric assessments are the gold standard, although made difficult by the complex geometry of the right ventricle.Cardiac MRI is most commonly utilized to assess RV size and systolic function, and additionally permits simultaneous evaluation of the systemic and pulmonary venous baffles and quantitative assessment of the degree of tricuspid regurgitation (the systemic AV valve).Transthoracic echocardiography is still routinely employed for serial evaluation of systemic right ventricular function. However, providers should have a low threshold to obtain further advanced imaging with any significant change in symptomatology or qualitative decrement in right ventricular systolic function on serial echocardiographic assessment.ManagementMedical Therapy: In contrast to ischemic cardiomyopathy, there are no long-term, randomized, placebo-controlled drug trials evaluating the efficacy of ACEI/ARB/ARNI or beta-blockers on systemic RV function. Small studies performed to date have not shown any appreciable benefit of ACEI/ARB on improving right ventricular ejection fraction or exercise capacity, which may reflect minimal baseline activation of the renin-angiotensin-aldosterone system in this form of heart failure. Use of beta-blocker therapy pathophysiologically makes sense, specifically reducing myocardial oxygen demand and allowing for improved ventricular filling; however, prior studies have produced mixed results, with evidence of improved right ventricular remodelingalthough no appreciable improvement in right ventricular ejection fraction, functional class, or long-term survival. Use of beta-blockers should also be cautioned in patients with established SA node dysfunction.Left Ventricular Re-Training: Conversion to an arterial switch operation often requires a staged approach to ensure that the left ventricle is adequately “trained” to handle systemic pressures.

Dec 26, 2021

CardioNerds (Amit Goyal and Daniel Ambinder) join Dr. Patrick Azcarate and Dr. Antoinette Birs from the University of California San Diego along with a guest host Dr. Christine Shen from Scripps Health for a hike along Torrey Pines. They discuss a case of a 30-year-old man with a history of malignant thymoma status post two partial lung resections and radiation for pleural/pulmonary metastasis, as well as a history of myasthenia gravis on rituximab, and Ig deficiency on IVIG presents with progressive exertional chest pain. We focus on the differential diagnosis of patients with a history of chest radiation exposure and dive into the complex management and surveillance for patients with radiation associated cardiac disease (RACD). The E-CPR is provided by Dr. Milind Desai (multimodality cardiovascular imaging expert, Director of Clinical Operations, Director of Center for HCM, Medical Director for Center for Aortic Diseases, and Medical Director for Center for Radiation Heart Disease at the Cleveland Clinic). Claim free CME just for enjoying this episode! Disclosures: NoneJump to: Pearls - Notes - References CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Case Media TTE TTE TTE TTE AP Cranial Pre PCI LAO Caudal Pre PCI RAO Caudal Pre PCI RAO Cranial Pre PCI AP cranial Post PCI Episode Teaching Pearls - radiation associated cardiac disease Radiation-associated cardiac disease (RACD) is a heterogeneous disease that can manifest several years, or decades following radiation exposure to the chest and is associated with high morbidity and mortality. Given the non-specific or vague symptoms, one of the greatest challenges for this patient population may be diagnosing RACD which requires high clinical suspicion. In patients with a history of chest radiation, we should remember to ask three important questions: 1. What was the total dose of radiation given? 2. How long ago was radiation therapy administered? 3. Was the heart exposed?A cumulative dose of >30 Gray (Gy) chest radiation significantly increases the risk of RACD long-term, but cardiac damage can occur at even lower doses. Effects from chest radiation can take years to become clinically detectable. Screening for radiation induced coronary artery disease with stress testing should start 5 years following XRT and in low-risk patients (without risk factors for typical coronary artery disease) and continue at 5-year intervals, and 2-year intervals in high-risk patients. Valvular heart disease surveillance should begin 10 years post XRT and can be accomplished with echocardiogram. Regarding revascularization planning, a Heart Team approach is recommended. However, percutaneous intervention is preferred over bypass surgery in most cases. Notes - radiation associated cardiac disease 1. What is Radiation-Associated Cardiac disease (RACD)? A spectrum of disease that can affect any part of the heart and typically develops anywhere from 5 to 20 years after radiation. It may present with non-specific or vague symptoms. Manifestations include myocarditis, pericarditis (typically early in the course) and well as long term sequela such as myocardial fibrosis, valvular heart disease (regurgitation or stenosis), pericardial disease, vasculopathy (CAD), conduction system disease. Radiation may impact any tissue of the heart: Vascular: microvascular, coronary artery disease, macrovascular (ascending aorta) Valvular: has a longer latency ~10-20 years with the left sided valves being more commonly affected; Aorto-mitral curtain thickening/calcification is a hallmark of previous heart radiation and associated with higher mortality Conduction: Sick sinus syndrome, AV nodal block, atrial fibrillaiton; infra-nodal conduction disease and RBBB are common. Myocardial: fibrosis in the myocardium leading to HFpEF, or HFrEF; XRT + anthracycline is thought to be synergistic. Pericardial: chronic pericardial inflammation, scarring, calcification, restrictive physiology. Constrictive pericarditis from radiation has a particularly poor prognosis given often concurrent myocardial involvement. 2. What is the Pathophysiology of RACD? The severity of disease is related to total radiation dose, fraction size and volume of the heart in the radiotherapy field. The resulting cell damage leads to activation of the acute inflammatory cascade and pro-fibrotic milieu. 3. What are the additional risk factors for RACD? Therapy-related risk factors:Net dosage (dependent on cancer type and tumor site) > 30Gy received by the heart.Proximity to heart to the radiation field.Concomitant chemotherapy – anthracyclines may particularly have a radiation sensitizing effect, thereby increasing the risk of RACD.Patient-related risk factors:Life expectancy – younger age at the time of radiation and a good cancer prognosis, as these patients may have more time to manifest the longer-term sequelae of RACD.Presence of traditional cardiovascular risk factors 4. How common is RACD? RACD is most often seen in those receiving chest radiation for breast cancer (particularly left sided), Hodgkin Lymphoma, lung cancer and esophageal cancers.There is a distinct population presenting with latent symptoms from treatment with wide-field radiation of Hodgkin lymphoma that was more commonly practiced 20-40 years ago.Prevalence of radiation associated cardiomyopathy is ~10% based on population studies although difficult to determine given the heterogeneity of presentation and under-recognition. Valvular abnormalities in 7-39% at 10 years, 12-60% at 20 years Mitral and aortic valves are most affected; symptoms arise 1-2 decades after radiation and later than CAD; AR in 60% vs 4% at 20 years vs 10 years post treatment. Aorto-mitral curtain thickening/calcification is a hallmark of previous heart irradiation, and its extent is strongly associated with mortality in subjects undergoing cardiac surgery. Radiation induced coronary vasculopathy has a prevalence of 85%. 5. What is Radiation induced coronary artery disease (RICAD)? Pathophysiology: inflammatory plaque, with accumulation of myofibroblasts, resulting in intimal proliferation with aggregation of lipid-rich macrophages; high collagen and fibrin content like accelerated atherosclerosis; doses of > 0.50 Gy can initiate atherosclerosis and affects micro and macro vasculature.Angiographically: Ostial or proximal epicardial coronary lesions of the anterior and central vessels are most common (left main trunk, proximal LAD, mid diagonal, or RCA) given the location of the heart in the chest.Lesions are often severe, proximal, and diffuse. They are typically long, smooth, concentric, and tubular and may require intravascular ultrasound (IVUS) for diagnosis as they can appear normal on coronary angiography (lumenography). 6. What are different types of radiation? 3D vs Intensity modulated radiation therapy (IMRT): both are x-ray-based radiationProton therapy: Unlike x-rays which go all the way through the body, protons are charged and can go to a specified depth causing less scatter radiation 7. What techniques may be used to reduce cardiac exposure to the radiotherapy field? ABC device, breathing techniques such as deep inspiratory breath hold (DIBH) which pulls the heart more inferiorly in the chest and allows treatment of the upper mediastinum with less cardiac exposure, shielding 8. What are the surveillance recommendations? The risk of RACD is 7.5% per Grey Unit (Gy) and is constant, beginning several years after exposure and persists for at least 2-3 decades (>50% of excess ischemic events occurring >10 years after RT). Those who will receive >30 Gy may warrant cardiology consultation prior to treatmentScreening for CAD: 5 years after radiation exposureScreening for valvular disease: 10 years after exposure with 5-year surveillance intervals 9. What is the recommended approach for revascularization for RICAD? PCI is generally preferred if feasible over bypass given chest radiation as this patient group has increased risk of complications from bypass surgery related to severely calcified aorta, possible radiation injury to the IMAs, restrictive lung disease, difficulty weaning patient from a ventilator, and lack of intra-thoracic lymphatics References Desai MY, Jellis CL, Kotecha R, Johnston DR, Griffin BP. Radiation-Associated Cardiac Disease: A Practical Approach to Diagnosis and Management. JACC Cardiovasc Imaging. 2018 Aug;11(8):1132-1149. doi: 10.1016/j.jcmg.2018.04.028. PMID: 30092970. https://www.jacc.org/doi/abs/10.1016/j.jcmg.2018.04.028 Desai MY, Windecker S, Lancellotti P, Bax JJ, Griffin BP, Cahlon O, Johnston DR. Prevention, Diagnosis, and Management of Radiation-Associated Cardiac Disease: JACC Scientific Expert Panel. J Am Coll Cardiol. 2019 Aug 20;74(7):905-927. doi: 10.1016/j.jacc.2019.07.006. https://www.jacc.org/doi/full/10.1016/j.jacc.2019.07.006 Cuomo JR, Javaheri SP, Sharma GK, Kapoor D, Berman AE, Weintraub NL. How to prevent and manage radiation-induced coronary artery disease. Heart. 2018 Oct;104(20):1647-1653. doi: 10.1136/heartjnl-2017-312123. Epub 2018 May 15. PMID: 29764968; PMCID: PMC6381836. https://heart.bmj.com/content/104/20/1647.long Wu W., Masri A., Popovic Z.B.et al. : "Long-term survival of patients with radiation heart disease undergoing cardiac surgery: a cohort study". Circulation 2013; 127: 1476. https://www.ahajournals.org/doi/epub/10.1161/CIRCULATIONAHA.113.001435 CardioNerds Case Report Production Team Karan Desai, MDAmit Goyal, MDDaniel Ambinder, MD

Dec 21, 2021

Cardiogenic shock is a state of cardiac dysfunction leading to hemodynamic instability and end-organ hypoperfusion. At the bedside, clinicians take various data points – from history to physical exam to labs/imaging and invasive hemodynamics – to make an assessment of the etiology, severity and management of cardiogenic shock. Health systems have developed “Shock Teams” to collectively interpret this data to deliver the optimal care for each patient. In this episode, Dr. Mark Dela Cruz (Advanced Heart Failure and Transplant Fellow at University of Chicago), CardioNerds Critical Care Series Co-Chairs Dr. Mark Belkin (Advanced Heart Failure and Transplant Fellow at University of Chicago) and Dr. Karan Desai (General Cardiology Fellow at University of Maryland), and CardioNerds Co-Founder Dr. Daniel Ambinder (Structural Fellow at Johns Hopkins Hospital) join Dr. Anu Lala (Director of the AHFT Fellowship, Associate Professor of Medicine and Cardiology at Mount Sinai Hospital and Deputy Editor of the Journal of Cardiac Failure) on a Shock Team Call! Dr. Lala leads us in a discussion of the systematic bedside evaluation of cardiogenic shock, from understanding a patient’s physiology and their humanity, to manage their illness and make a rapid but thorough evaluation when on the Shock Call. Audio editing and episode introduction by CardioNerds Academy Intern, Hirsh Elhence. Claim free CME for enjoying this episode! Disclosures: None Pearls • Notes • References • Guest Profiles • Production Team CardioNerds Cardiac Critical Care PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls and Quotes - Shock Team Call The classic definition of cardiogenic shock was derived from studies of left ventricular dysfunction in the setting of acute myocardial infarction. With the advent of early primary percutaneous coronary intervention (PCI) and trends in cardiovascular disease risk factors, the prevalence of non-ischemic etiologies of cardiogenic shock (e.g., progression/exacerbation of chronic heart failure) has increased significantly. The diagnosis of cardiogenic shock should be made by integrating key clinical features such as physical exam findings and objective laboratory and imaging data in an iterative fashion. Focused transthoracic echocardiography and invasive hemodynamics are helpful in further characterizing the type of shock and the etiology of cardiogenic shock. Early evaluation of right ventricular function is an important aspect of cardiogenic shock evaluation. Significant RV dysfunction portends poor prognosis, can necessitate more aggressive interventions, and defines the types of mechanical circulatory support necessary. Classification systems for cardiogenic shock help to further characterize a patient’s illness severity. The INTERMACS and SCAI classification systems are particularly designed to allow for early identification of patients who would most benefit from more advanced interventions such as vasoactive medications or mechanical circulatory support. Shock Team Calls improve mortality for patients in cardiogenic shock. By rapidly bringing together heart failure specialists, interventional cardiologists, cardiothoracic surgeons, and critical care physicians, appropriate interventions and contingencies can be discussed and quickly implemented without adding delays to patient care. Importantly, these calls should attempt to integrate patient goals of care in order to best serve our patients. Show notes - Shock Team Call 1. What is the classic definition of cardiogenic shock? The classic definition of cardiogenic shock was initially derived from the Shock Trial published in 1999 (1). In this trial, cardiogenic shock was defined as shock due to left ventricular dysfunction occurring in the setting of acute myocardial infarction in the setting of acute MI as confirmed by specific criteria: Clinical criteria: SBP 90mmHgEnd-organ hypoperfusion as defined by cool extremities, UOP 60bpmHemodynamic criteria: CI ≤ 2.2 L/min/m2 BSAPCWP ≥ 15mmHgWith the advent of primary percutaneous coronary intervention, non-ischemic etiologies have become more prevalent as the etiology of cardiogenic shock such as decompensation of chronic heart failure, valvular heart disease, etc.As discussed on the episode, cardiogenic shock occurs on a spectrum from a “pre-shock” state to “extremis.” To facilitate early recognition of cardiogenic shock, appropriate phenotyping (e.g., LV-predominant, RV-predominant, biventricular, pericardial, valvular, pulmonary vascular, etc), timely interventions, and allocation of advanced therapies (e.g., mechanical circulatory support), a more granular approach to the classification is needed (see below regarding SCAI classification). 2. What are some of the clinical features of cardiogenic shock? Physical Exam Findings - A careful head-to-toe assessment should be conducted during the initial patient encounter. Important markers include (but are not limited to):Signs of hypervolemiaPatient positioning as a sign of orthopneaElevated JVPTachypneaPresence of pulmonary ralesLower extremity edemaHepatomegalyAscitesSigns of poor organ perfusionCool extremitiesPoor hourly urine output.Confusion or Altered Mental StatusSigns of poor cardiac outputPulse quality – is it fast, slow, thready?Pulsus alternans – alternation between strong and weak beats in sinus rhythm without change in cadence or cycle length (a marker of low output and ejection from the LV) (2).Narrow pulse pressureClues to help determine the etiology of the shockPoint of maximal impulse displacementRight ventricular heaveAuscultation of murmurs may indicate a valvular and/or congenital anomaliesAn accentuated P2 may indicate pulmonary hypertensionGallops may indicate filling pressures and/or underlying cardiomyopathyA pericardial knock may indicate constrictive pericarditisAn irregular pulse may indicate an arrhythmia causing or contributing to shockLaboratory studiesLaboratory markers of end organ hypoperfusion include markers of renal function such as creatinine and of hepatic injury (AST, ALT) and function (INR).Lactate has also been shown to display prognostic significance though clear correlations between objective thresholds to clinical outcomes have yet to be fully established.More important than individual values themselves are their temporal trends and the integration of multiple data points across numerous variables. Early Imaging studies EKG should be obtained and reviewed early after presentation to evaluate for acute coronary syndrome and need for urgent coronary angiography.Chest x-ray findings of pulmonary edema or effusions, assessment of heart size, and presence of cardiovascular hardware (sternal wires, implantable electrical devices, valvular interventions, etc). Focused transthoracic echocardiography, if available in the acute setting, can be helpful.Focused TTE should assess left and right ventricular morphology and function, the presence of a left ventricular thrombus, stenotic or regurgitant valvular lesions, or dynamic outflow tract obstructions.Echo surrogates of filling pressures may be supportive though may be limited by technique and image quality. Evaluation of RV function and illness severitySignificant RV dysfunction is a marker of illness severity and leads to worse clinical outcomes.RV dysfunction limits total cardiac output, worsens systemic venous congestion, and worsens end organ dysfunction.RV assessment is critical when evaluating for the need for mechanical circulatory support, and severe RV dysfunction may increase the likelihood that MCS will be necessary.Severe RV dysfunction may necessitate the use of specific MCS devices (e.g., RV assist devices). It may also impact decision-making regarding what types of temporary or, even more importantly, durable MCS devices the patient may qualify for. Enjoy the upcoming RV-Predominant Shock Episode with Dr. Ryan Tedford for a more in-depth discussion!Invasive hemodynamic assessment Invasive hemodynamic evaluation with a pulmonary arterial catheter (PAC) is particularly useful for confirming and profiling cardiogenic shock as well as tailoring initial and subsequent management.An accurate assessment of filling pressures, cardiac output (by Thermodilution or Indirect Fick), right ventricular function, systemic vascular resistance, and specific calculated indices (e.g., CPO, PAPi, RA/PCWP) provide a more nuanced evaluation of a patient’s shock.Specifically, a PAC can assist in early identification of an under-recognized form of cardiogenic shock, under the classic Stevenson paradigm, a “wet and warm” picture. These patients have a systemic inflammatory response in addition to or as a result of their cardiac pathology, with a reduced cardiac index, low to normal SVR, and elevated pulmonary capillary pressures.Enjoy the upcoming Invasive Hemodynamics episode with Dr. Nosheen Reza and the following infographic from CardioNerds Academy Fellow, Dr. Ahmed Ghoneem, for more details! 3. How is cardiogenic shock classified and how are these classifications useful in the management of cardiogenic shock? Differentiating cardiogenic shock from other types of shock and the severity of shock can often be challenging. Constructs such as Dr. Lynne Warner Stevenson’s physical exam-based shock classifications are helpful in broadly phenotyping cardiogenic shock at the bedside (3). However, these classification systems may have their limitations. Determining the underlying etiology relies heavily on integrating various pieces of clinical information ranging from the physical exam as well as laboratory and imaging information. In clinical practice,

Dec 16, 2021

In this episode, CardioNerds (Amit Goyal), Cardio-OB series co-chair and UT Southwestern cardiology fellow, Dr. Sonia Shah, and episode lead fellow, Dr. Laurie Femnou (UT Southwestern) are joined by Dr. Michael Luna (UT Southwestern) to discuss cardiovascular interventions during pregnancy. We discuss practical considerations for performing coronary angiography and valvular interventions in the pregnant patient, the timing and indication of procedures, and ways to minimize radiation exposure to both mom and baby. Audio editing by CardioNerds Academy Intern, Hirsh Elhence. This episode is made possible with support from Panacea Financial. Panacea Financial is a national digital bank built for doctors by doctors. Visit panaceafinancial.com today to open your free account and join the growing community of physicians nationwide who expect more from their bank. Panacea Financial is a division of Primis, member FDIC. Pearls • Notes • References • Guest Profiles • Production Team CardioNerds Cardio-Obstetrics Series PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls- Cardiac Interventions during Pregnancy Attempt should be made to manage pregnant patients with valvular disease with medical therapy, and cardiac interventions during pregnancy should be considered a last resort.Ideally, procedures in the gravid patient should be performed after 20 weeks gestation to minimize fetal risk. Specific ways to minimize radiation to the pregnant patient and fetus in the catheterization lab include: using an abdominal shield, radial access for coronary procedures, proper positioning of the C-arm to avoid extreme angulation, using collimation, and minimizing fluoroscopic time, frame rate, and use of cine-acquisition. When appropriate, intracoronary imaging modalities (ie. IVUS or OCT) should also be considered.Fetal monitoring should be performed during any cardiac intervention in the pregnant patientMultidisciplinary involvement and contingency planning are critical for the success of any high-risk cardiac intervention in the pregnant patient. Quatables - Cardiac Interventions during Pregnancy “Meetings including all providers— our cardiac surgical colleagues, cardiac anesthesiologists, and our obstetrics team—in the care of [pregnant] patients has to be had well ahead of a cardiac procedure to plan every detail.” Show notes - Cardiac Interventions during Pregnancy 1. What are special considerations for performing a balloon valvuloplasty in a pregnant patient with mitral stenosis? In pregnant patients with severe mitral stenosis who cannot be adequately managed with medical therapy, percutaneous balloon mitral valvuloplasty (PMBV) is the treatment of choice given the high risk of morbidity and fetal loss with cardiac surgery.Ideally, procedures in the gravid patient should be performed after 20 weeks gestation to minimize risk to the fetus. Assessment of valve anatomy and consideration of the Wilkin’s score are especially important in pregnant patients to minimize the risk of peri-procedural complications.PBMV should performed at experienced centers with cardiac surgery and MFM available.Complications of PBMV are rare but include atrial perforation, cardiac tamponade, arrhythmias, emboli, mitral regurgitation, hypotension and maternal death. Mechanical support should be readily available and a delivery strategy in place in case there is sudden maternal or fetal deterioration. 2. What are ways to minimize radiation exposure in the catheterization lab to the pregnant patient and fetus? The general principle for imaging during pregnancy is similar to imaging for the general population, with the goal of radiation exposure being as low as reasonably achievable (ALARA). The mean radiation exposure to the unshielded abdomen is 1.5 mGy, and <20% of this reaches the fetus. Specific ways to minimize radiation to the pregnant patient and fetus in the catheterization lab include the following: using an abdominal shield, radial access for coronary procedures, proper positioning of the C-arm to avoid extreme angulation, using collimation, and minimizing fluoroscopic time, frame rate, and use of cine-acquisition. When appropriate, intracoronary imaging modalities (ie IVUS or OCT) should also be considered. 3. What should we know about coronary angiography and revascularization in the pregnant woman? According to a large US-based study of 859 patients presenting with acute myocardial infarction during pregnancy and the postpartum period, less than half of patients undergo cardiac catheterization. In stable, low-risk NSTEMI, a non-invasive approach should be considered per ESC guidelines. In pregnant patients who present with STEMI, PCI is the preferred revascularization strategy.Radial access should be used if possible, as femoral artery access involves direct pelvic radiation.In pregnancy-associated SCAD, enhanced vascular vulnerability should be considered when performing angiography, from obtaining access to engaging the coronary ostia.Fetal monitoring should be performed during any cardiac intervention in the pregnant patient 4. What is the role of mechanical support in the management of peripartum patients with cardiogenic shock? Urgent intervention with mechanical assist support, including intra-aortic balloon pump, impella, and VA-ECMO, may be necessary in rare circumstances. Prompt assessment of hemodynamics can be helpful to determine the level of support needed. Axillary access may be considered in patients with favorable anatomy. References Patel C, Akhtar H, Gupta S, Harky A. Pregnancy and cardiac interventions: What are the optimal management options? Journal of Cardiac Surgery, 2020. 35(7): 1589-1596. Regitz-Zagrosek V, Lundqvist CB, Borghi C, et al. ESC Guidelines on the management of cardiovascular diseases during pregnancy The Task Force on the Management of Cardiovascular Diseases during Pregnancy of the European Society of Cardiology (ESC). European Heart Journal, 2011. 32, 3147–3197 doi:10.1093/eurheartj/ehr218 Guest Profiles Dr. Michael Luna Dr. Michael Luna is an associate professor of cardiology at UT Soutwestern trained in interventional cardiology, with additional focused training in congenital heart disease. He specializes in adult congenital heart defects, heart valve disorders, and complex coronary artery disorders. Dr. Luna also serves as one of the supervising attendings in the Parkland Congenital Heart Disease Fellow’s Clinic. Dr. Laurie Femnou Dr. Laurie Femnou Mbuntum is currently a general cardiology fellow at The University of Texas Southwestern. She completed her undergraduate degree at The University of Maryland Baltimore County. She then moved down South to complete residency at The University of Texas Southwestern where she stayed for cardiology fellowship where she is planning to stay for advanced training in interventional cardiology. She has a special interest in cardio obstetrics and figuring out ways to reduce cardiovascular maternal death. When not in the hospital, she loves spending time with her two boys and learning more about makeup artistry. CardioNerds Cardioobstetrics Production Team Natalie Stokes, MD Sonia Shah, MD Amit Goyal, MD Daniel Ambinder, MD

Dec 9, 2021

CardioNerds Rounds Co-Chair, Dr. Karan Desai, joins Dr. Michelle Kittleson (Director of Postgraduate Education in Heart Failure and Transplantation, Director of Heart Failure Research, and Professor of Medicine at the Smidt Heart Institute at Cedars-Sinai) to discuss challenging cases of hypertrophic cardiomyopathy. As a guideline author on the 2020 ACC/AHA Hypertrophic Cardiomyopathy Guidelines, Dr. Kittleson shows us how the latest evidence informs our management of HCM patients, while sharing many #Kittlesonrules and pearls on clinical care. Come round with us today by listening to the episodes now and joining future sessions of #CardsRounds! This episode is supported with unrestricted funding from Zoll LifeVest. A special thank you to Mitzy Applegate and Ivan Chevere for their production skills that help make CardioNerds Rounds such an amazing success. All CardioNerds content is planned, produced, and reviewed solely by CardioNerds. Case details are altered to protect patient health information. CardioNerds Rounds is co-chaired by Dr. Karan Desai and Dr. Natalie Stokes. Speaker disclosures: None Cases discussed and Show Notes • References • Production Team CardioNerds Rounds PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Show notes - Hypertrophic Cardiomyopaty Cases Case #1 Synopsis: Two non-white brothers in their early 20s come to clinic to establish care. They have no cardiopulmonary symptoms, normal EKGs and normal echos, but there was a possible family history of HCM. Their mother had LV hypertrophy and underwent septal myectomy, but she could not afford genetic testing and was no longer in the patients’ lives. The path report suggested “myocyte hypertrophy without disarray or bundles of myocytes.” How would you advise these patients regarding screening and surveillance? Listen to #CardsRounds for the full details! Quotes from Case #1: “Let’s take a walk down memory lane and let’s get to our evolution of understanding hypertrophic cardiomyopathy… [our understanding] follows the parable of the six blind men and the elephant. Each of the six blind man approached it from different angles, its tusk, its ear, its tail, and they all try to convince each other what an elephant is … because none of them can see the big picture.” Dr. Kittleson on the history of HCM and coming to a unifying diagnosis “The next time you are sitting there mashing your teeth because you have to memorize what the HCM murmur does squat to stand, Valsalva, or handgrip … remember you are standing on the shoulder of Giants. They [Drs. Braunwald and Morrow] pioneered surgical myectomy based on physical exam and cath lab findings” Dr. Kittleson on the physical exam guiding HCM management Takeaways from Case #1 Before we round, we think it is important to get on the same page regarding the nomenclature around HCM. Since the original characterization of hypertrophic cardiomyopathy (HCM) more than 60 years ago (see the Braunwald Chronicles for the origin stories!), different terms have been used to describe the disease. These include idiopathic hypertrophic subaortic stenosis, hypertrophic obstructive cardiomyopathy (HoCM), and “burnt out HCM” when heart failure develops.The 2020 guideline committee recommended a common language to avoid confusion: since left ventricular (LV) outflow tract obstruction (LVOTO) occurs in >60% of patients over time, but one-third remain non-obstructive, the recommendation is t0 call the disease state HCM with or without outflow tract obstruction.Dr. Kittleson added that when heart failure develops we should characterize the pathology as HCM with heart failure rather than “burnt out HCM.” Do we use HCM to describe any LV that has thick walls? Some clinicians will use HCM to describe all disease states that can lead to increased LV wall thickness, including those associated with systemic disorders such as RASopathies, mitochondrial myopathies, glycogen/lysosomal storage diseases, Fabry’s disease, hemochromatosis, Danon disease, and amyloidosis (especially in adults).However, the pathophysiologic mechanisms, genetic underpinnings, and treatment of these diseases are different. Secondary causes of left ventricular hypertrophy (LVH) – such as athlete’s heart and hypertensive disorders – can also cause confusion with identifying the correct terminology and diagnosis.As Dr. Kittleson (and the guidelines) made clear, the clinical definition of HCM is a disease state in which (1) the morphologic expression is restricted to the heart, characterized primarily by LVH in the absence of another systemic; (2) a metabolic or cardiac cause; (3) and for which a disease-causing sarcomere (or sarcomere-related) variant is identified or genetic etiology remains undetermined.See some of our original CardioNerds episodes to review the clinical manifestations, diagnosis and treatment of HCM! Ok. We are with you on the terminology! But as you mentioned there are many disease states that can look like HCM. What are phenocopies? As alluded to above, there are multiple genes that can lead to the phenotypic appearance of HCM, but rather these are “phenocopies” masquerading as HCM.Dr. Kittleson noted that many of these phenocopies are diagnosed in childhood (e.g., glycogen storage diseases, Friedrich ataxia, Danon disease); however, for adult cardiologists, particular attention should be given to recognizing amyloidosis (see our Amyloidosis page).We should remain alert for “LVH+” states: when we see left ventricular hypertrophy but also systemic signs including peripheral neuropathy, renal dysfunction, and skin changes, which could clue us into a systemic pathology like Amyloidosis. After all, Imitation is the sincerest form of flattery!The classic pathologic findings of HCM include myocyte disarray (where individual cardiomyocytes vary in size, shape and form), abnormal intercellular connections, expansion of the interstitial compartment and areas of replacement fibrosis, and small vessel disease (in which intramural vessels are narrowed by medial hypertrophy). So back to this case. It is possible the patients’ mother had a HCM phenocopy. And the pathology was not classic for HCM. What do the guidelines say regarding genetic screening in general? It was not until the 1990s when DNA sequencing of HCM pedigrees led to the discovery of variants in genes coding for sarcomere proteins were co-inherited in patients with LVH. Thus, HCM since has been regarded as a monogenic cardiac disease.The two most common genes with damaging variants are beta myosin heavy chain (MYH7) and myosin-binding protein C3 (MYBPC3).70% of variant-positive patients have gene variants in these genes; however, it is important to recognize that many patients with HCM are currently without any identifiable pathogenic genetic etiology to their disease (40 to 60% of patients depending on the study).Thus, genetic testing is crucial to the diagnosis and management of HCM, especially to inform cascade testing in family member and preconception and prenatal genetic counseling. As has been discussed previously on the CardioNerds podcast, appropriate pre- and post-test genetic counseling is necessary to ensure patients and their families understand the medical, social, psychological, ethical and professional implications of having a genetic disease, underscoring the value of multidisciplinary HCM centers. How do we apply the guidelines regarding genetic screening to our patients? As was done in this case, a detailed family history of at least three generations regarding HCM and SCD events should be taken. Typically, genetic testing for HCM is first done in the family member with clear phenotypic evidence of HCM – the index case. The 2020 ACC/AHA HCM guidelines nicely outline subsequent testing based on whether a variant is pathologic (Figure 1) Please remember to review the Guidelines yourself as it is a comprehensive text that provides key details not covered here!However, the index case could not afford genetic testing and the pathology available to us was not definitive for HCM. Postmortem testing for HCM-associated variants using blood or tissue samples collected at autopsy is possible, but access to a molecular autopsy and insurance coverage can vary significantly based on jurisdiction.Our patients (the brothers in their 20s) were arriving without genetics to inform their screening. In this circumstance we utilize Figure 2 (below) from the guidelines and would consider the index patient (the mother) phenotype negative. And since no variant was identified in the index patient, we would likely offer screening ECG/Echo (or cardiac MRI) to the brothers and follow up with clinical surveillance with imaging/ECG every 3-5 years. How do we decide if a variant is pathogenic? The pathogenicity of variants is based on American College of Medical Genetics and Genomics criteria and can actually change over time. As Dr. Kittleson noted, there are fewer quality genetic data in non-white HCM populations.The five highest frequency variants for HCM in the Human Gene Mutation Database of the NHLBI Exome sequencing Project were more frequent in Black Americans vs. White Americans which could lead to false positive diagnoses of HCM in Blacks. Furthermore, a lack of diverse racial/ethnic control populations could lead to a misclassification of benign variantsAs Dr. Kittleson noted on #CardsRounds, this again highlights the importance of multidisciplinary HCM clinics that have the expertise to periodically re-evaluate the pathogenicity of variants. If they a particular variant has been reclassified (either upgraded or downgraded), it would affect cascade testing and clinical surveillance in families. Case #2 Synopsis:

Dec 2, 2021

CardioNerds (Amit Goyal and Daniel Ambinder) join CardioNerds Ambassadors Dr. Pablo Sanchez (FIT, Stanford University) and Dr. Christine Shen (FIT, Scripps Clinic) for a discussion with Dr. Bob Harrington (Interventional Cardiologist, Professor of Medicine, and Chair of the Department of Medicine at Stanford University) about diversity and inclusion in the field of cardiology. This episode discusses Dr. Harrington’s broader approach to mentorship, sponsorship, and allyship; and particularly how (and why) he used his position as the president of the American Heart Association to advocate against all-male panels, or “manels.” Listen to the episode to learn the background and motivations behind his evidence-based efforts to make Cardiology a more inclusive field. Special message by California ACC State Chapter President, Dr. Jamal Rana. The PA-ACC & CardioNerds Narratives in Cardiology is a multimedia educational series jointly developed by the Pennsylvania Chapter ACC, the ACC Fellows in Training Section, and the CardioNerds Platform with the goal to promote diversity, equity, and inclusion in cardiology. In this series, we host inspiring faculty and fellows from various ACC chapters to discuss their areas of expertise and their individual narratives. Join us for these captivating conversations as we celebrate our differences and share our joy for practicing cardiovascular medicine. We thank our project mentors Dr. Katie Berlacher and Dr. Nosheen Reza. Video Version • Notes • References • Production Team Claim free CME just for enjoying this episode! There are no relevant disclosures for this episode. The PA-ACC & CardioNerds Narratives in Cardiology PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Video version - Diversity and Inclusion https://youtu.be/SnUadVRhH70 Quotables - Diversity and Inclusion “If senior men don’t change the field, it’s not going to change. We have the senior positions. We have to change it.”“You’re missing talent. You’re missing talent of the women who have decided not to go into Cardiology. I say to a lot of my male colleagues...don’t you care about the health of our specialty? Don’t you want the very best people going into it?”“How great is that--to open up an artery in the middle of the night?... What could be better than that?...Why would you not want to be a cardiologist? Frankly, maybe the field is not so friendly to women...And that bothers me greatly because I love the specialty.”“To those who have been given much, much is expected. That’s what people like me should do.”Dr. Bob Harrington Show notes - Diversity and Inclusion What are the gender disparities in the field of Cardiology? 45.8% of residents and fellows in ACGME-accredited programs are women. 14.9% of cardiologists are women. 8% of interventional cardiologists are women [1]. 30.6% of male faculty were full professors, while 15.9% of female faculty are full professors [2].Men are more likely to be influenced by positive attributes of a field, while women are more likely to be influenced by negative attributes [3].3% of percutaneous coronary interventions in the United States are performed by female operators [4]. What is mentorship, sponsorship, and allyship? A mentor provides advice and helps someone develop a skill.A sponsor is an advocate who helps someone secure career advancement opportunities.An ally partners with people, utilizing their power and influence to champion the rights of others [5].According to some studies, women report less sponsorship experiences than men. Additionally, in women it seems to translate less frequently into experiences that further their career (speaking engagements, serving on editorial boards, etc) [6].“I’m a mentor to a few people, I'm a sponsor to many, and I’m an ally to all.” - Dr. Bob Harrington Why is a diverse cardiovascular workforce so important? Teams that are diverse pursue innovative and creative solutions.Medicine requires meaningful connections and having a physician with a common background enhances the patient-doctor interaction by a spectrum of constructive effects.Minority groups are less likely to be treated with effective cardiac medications [7].There continue to be barriers in clinical trials to include diverse and underrepresented patients [8].A diverse workforce of clinical scientists is crucial to promoting diversity in clinical trials, including understanding the problem, asking the right questions, and proposing solutions [9]. References AAMC 2019. Physician Specialty Data Report. Accessed November 18, 2021.Blumenthal DM, Olenski AR, Yeh RW, et al. Sex Differences in Faculty Rank Among Academic Cardiologists in the United States. Circulation. 2017;135(6):506-517. doi:10.1161/CIRCULATIONAHA.116.023520Yong CM, Abnousi F, Rzeszut AK, et al. Sex Differences in the Pursuit of Interventional Cardiology as a Subspecialty Among Cardiovascular Fellows-in-Training [published correction appears in JACC Cardiovasc Interv. 2019 Apr 8;12(7):695]. JACC Cardiovasc Interv. 2019;12(3):219-228. doi:10.1016/j.jcin.2018.09.036Wang TY, Grines C, Ortega R, et al. Women in interventional cardiology: Update in percutaneous coronary intervention practice patterns and outcomes of female operators from the National Cardiovascular Data Registry®. Catheter Cardiovasc Interv. 2016;87(4):663-668. doi:10.1002/ccd.26118Sharma G, Narula N, Ansari-Ramandi MM, Mouyis K. The Importance of Mentorship and Sponsorship: Tips for Fellows-in-Training and Early Career Cardiologists. JACC Case Rep. 2019;1(2):232-234. Published 2019 Aug 21. doi:10.1016/j.jaccas.2019.06.007Patton EW, Griffith KA, Jones RD, Stewart A, Ubel PA, Jagsi R. Differences in Mentor-Mentee Sponsorship in Male vs Female Recipients of National Institutes of Health Grants. JAMA Intern Med. 2017;177(4):580-582. doi:10.1001/jamainternmed.2016.9391Tran HV, Waring ME, McManus DD, et al. Underuse of Effective Cardiac Medications Among Women, Middle-Aged Adults, and Racial/Ethnic Minorities With Coronary Artery Disease (from the National Health and Nutrition Examination Survey 2005 to 2014). Am J Cardiol. 2017;120(8):1223-1229. doi:10.1016/j.amjcard.2017.07.004Clark LT, Watkins L, Piña IL, et al. Increasing Diversity in Clinical Trials: Overcoming Critical Barriers [published correction appears in Curr Probl Cardiol. 2021 Mar;46(3):100647]. Curr Probl Cardiol. 2019;44(5):148-172. doi:10.1016/j.cpcardiol.2018.11.002Poppas A, Albert MA, Douglas PS, Capers Q 4th. Diversity and Inclusion: Central to ACC's Mission, Vision, and Values. J Am Coll Cardiol. 2020;76(12):1494-1497. doi:10.1016/j.jacc.2020.08.019 Production Team Dr. Gurleen KaurAmit Goyal, MDDaniel Ambinder, MD

Nov 30, 2021

CardioNerds (Amit Goyal and Daniel Ambinder), are joined by guest host Dr. Alex Pipilas (CardioNerds Ambassader, Boston University), and Cleveland Clinic fellows, Dr. Gary Parizher, Dr. Ambreen Ali, and Dr. Tiffany Dong. They discuss a case of an 18-year-old man with Autism Spectrum Disorder presented with advanced nonischemic dilated cardiomyopathy. Due to anxiety, he was unable to tolerate right heart catheterization, and the initial evaluation for advanced heart failure therapies was deferred. With assistance from a multidisciplinary team, catheterization was successful, and he underwent cardiac transplantation. Faculty experts, Dr. Richard Dane Meredith (Cardiovascular Imaging, Mission healthcare), Dr. Julie Niezgoda (Congenital Cardiac Anesthesiologist, CCF), and Dr. Ran Lee (Critical Care Cardiology and Advanced HF/Transplant Cardiologist, CCF) provide the E-CPR for this episode. Audio editing by CardioNerds Academy Intern, Dr. Leticia Helms. Claim free CME just for enjoying this episode! Disclosures: NoneJump to: Pearls - Notes - References CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Case Media Episode Teaching Pearls - Heart Failure with Autism Spectrum Disorder Autism spectrum disorder should not be regarded as a contraindication to organ transplantation.Respect for patient discomfort with procedures, and efforts to mitigate that discomfort, are essential.A multidisciplinary team approach, especially one utilizing allied health support services, is important to provide care to adolescent patients with advanced organ dysfunction, particularly those with developmental disabilities. Notes - Heart Failure with Autism Spectrum Disorder Autism spectrum disorder (ASD) is a developmental disability characterized by impairments in social interaction and the presence of restricted, repetitive patterns of behaviors, interests, or activities (2). In 2016 the CDC estimated one in 54 children age 8 had ASD (3). Despite ASD’s prevalence, studies of organ transplantation in children and adolescents with developmental disabilities are lacking. Guidelines from the International Society for Heart Lung Transplantation indicate that heart transplantation cannot be recommended in patients suffering from severe cognitive-behavioral disabilities (4). However, the definition of “severe” is not clear, so the assessment of severity of a cognitive impairment, as well as whether the impairment constitutes a contraindication to organ transplantation, falls to healthcare providers on a case-by-case basis. Cardiac transplantation in a patient with ASD has been documented previously (5). Nonetheless our case represents an important example of advocacy for lifesaving care in patients with developmental disability. Without any one component of the team taking care of our patient, including physicians and allied healthcare providers, he would have died of refractory cardiogenic shock. However, with individualized care and a multidisciplinary combined effort, his providers were able to overcome the obstacles posed by his ASD and deliver indicated interventions. References - Heart Failure with Autism Spectrum Disorder 1. Baran, David A., et al. "SCAI clinical expert consensus statement on the classification of cardiogenic shock" Catheterization and Cardiovascular Interventions 94.1 (2019): 29-37. 2. American Psychiatric Association: Diagnostic and Statistical Manual of Mental Disorders. 5th edition. Arlington, VA: American Psychiatric Association, 2013. 3. Baio J, Wiggins L, Christensen D, et al. Prevalence of Autism Spectrum Disorder among children aged 8 years - Autism and Developmental Disabilities Monitoring Network, 11 Sites, United States, 2014. MMWR Surveillance Summaries 2018; 67:1-23. 4. Mehra M, Canter C, Hannan M, et al. The 2016 International Society for Heart Lung Transplantation listing criteria for heart transplantation: a 10-year update. J Heart Lung Transplant 2016; 35:1-23. 5. Bailey D, Schneider L, Maeda K, et al. Orthotopic heart transplant in a child with nonverbal autism. Austin J Autism & Relat Disabil 2016;2:1017. 6. Chen Y, Shlofmitz E, Khalid N, et al. Right Heart Catheterization-Related Complications: A review of the literature and best practices. Cardiol Rev 2020;28:36-41. CardioNerds Case Report Production Team Karan Desai, MDAmit Goyal, MDDaniel Ambinder, MD

Nov 25, 2021

Pregnancy is a hypercoagulable state associated with increased risk of thromboembolism. Managing anticoagulation during pregnancy has implications for both the mother and the fetus. CardioNerd Amit Goyal joins Dr. Akanksha Agrawal (Cardiology Fellow at Emory University), Dr. Natalie Stokes (Cardiology Fellow at UPMC and Co-Chair of the Cardionerds Cardio-Ob series), and Dr. Katie Berlacher (Program Director of the Cardiovascular Disease Fellowship and Director of the Women’s Heart Program at UPMC) as they discuss the common indications for anticoagulation and their management before, during, and after pregnancy. In this episode, we focus on management of pregnant patients with mechanical valves and venous thromboembolism. Audio editing by CardioNerds Academy Intern, Dr. Maryam Barkhordarian. Pearls • Notes • References • Guest Profiles • Production Team CardioNerds Cardio-Obstetrics Series PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls- Pregnancy and Anticoagulation Pregnancy is a hypercoagulable state. Pregnancy-associated VTE is a leading cause of maternal morbidity and mortality.The use of anticoagulation requires a balance between the risks and benefits to the mother and her fetus.The agent of choice for anticoagulation during pregnancy depends on the indication, pre-pregnancy dose of vitamin K antagonist (VKA), and the trimester of pregnancy. For instance, patients with mechanical heart valves, warfarin is generally recommended in the first trimester if the daily dose is less than 5 mg and as the first option for all patients with mechanical valves in the 2nd and 3rd trimester. Use of direct oral anticoagulants (DOACs) has not been systematically studied, they do cross the placenta and their safety remains untested.Warfarin crosses the placenta but is not found in breast milk. LMWH does not cross the placenta and is not found in breast milk. Thus, both these agents can be used by a lactating mother. Quatables - Pregnancy and Anticoagulation “[We] can’t highlight enough that good communication and documentation is vital in such situations” says Dr. Berlacher while discussing the role of a multidisciplinary team including cardiologists, obstetricians and fetal medicine physicians in taking care of a pregnant patient on anticoagulation. “What I love about cardio-obstetrics is that we really can help women in a time that is so important in their life…this is one of the most memorable times in their life..” says Dr. Berlacher when asked what makes your heart flutter about cardio-obstetrics. “Knowledge is power...not just for providers, but also for the patients” says Dr. Berlacher emphasizing the importance of clear communication between physicians and patients. Show notes - Pregnancy and Anticoagulation 1. What makes pregnancy a hypercoagulable state? Pregnancy is a hypercoagulable state associated with higher risk of thromboembolic phenomenon. The three components of Virchow’s triad: hypercoagulability, stasis, and endothelial injury are all present during pregnancy. This leads to a 5-fold increased risk of venous thromboembolism (VTE) during pregnancy that persists for 12 weeks postpartum. The risk for VTE seems to be highest in the first 6 weeks postpartum, with a higher prevalence of clot in the left lower extremity.There are additional risk factors for developing VTE in the postpartum period besides pregnancy itself, and this includes but is not limited to preeclampsia, emergent c-section, hypertension, smoking, and postpartum infection.Choosing anticoagulant therapies during pregnancy involves a fine balance between the risks and benefits to both the mother and fetus. A multidisciplinary team involving the obstetrician, cardiologist, and maternal-fetal medicine team is critical to guide anticoagulation in pregnancy. 2. What are some of the common indications for anticoagulation during pregnancy? One of the most common indications for anticoagulation in pregnancy is valvular disease, and specifically mitral valve stenosis with atrial fibrillation or a prior embolic event.Patients with a mechanical heart valve will require anticoagulation during pregnancy. Patients with a bioprosthetic valve (surgical or transcatheter) are generally continued on low dose Aspirin; in the uncommon scenario of pregnancy in the first 3-6 months following implantation of a bioprosthetic valve, the decision to pursue anticoagulation is individualized.Other indications include acute VTE, atrial fibrillation, antiphospholipid syndrome, and inherited thrombophilias that may predispose a patient to developing VTE during pregnancy. 3. For mechanical heart valves, how do anticoagulation recommendations vary based on trimester? The European Society of Cardiology has divided various valvular heart diseases into 4 classes as per the modified World Health Organization classification of maternal cardiovascular risk, and having a mechanical valve falls under Class III where the maternal cardiac event rate varies between 19-27%. Such patients should get their care at expert centers for pregnancy and cardiac disease.Anticoagulation for mechanical valve during pregnancy varies with each trimester to balance the risks and benefits. During the first trimester, the period of organogenesis, the decision of whether to continue warfarin (a potential teratogenic) depends on the dose of warfarin. If a patient has been taking 5 mg/day of warfarin, the American Heart Association (AHA) recommends stopping warfarin and using alternate agents like LMWH/UFH (Class IIa).During the second and third trimesters, it is typically advised to continue warfarin until prior to the vaginal delivery when continuous infusion of UFH should be used as the anticoagulant agent of choice. Expert multidisciplinary teams are needed not only to guide these general recommendations, but to individualize the treatment based on patient preferences and specific factors (e.g., previous prosthetic valve thromboembolic complication).For a mechanical mitral valve replacement, 2014 AHA/CC guidelines recommend a goal INR of 3.0. For a mechanical aortic valve replaceent, the goal depends on the presence or absence of risk factors. In a patient with high-risk conditions like atrial fibrillation, previous thromboembolism, LV dysfunction, hypercoagulable condition, and older-generation mechanical valve, a goal INR of 3.0 (2.5 to 3.5), similar to MVR is recommended. However, if no high-risk features exist, then an INR goal of 2.5 (2.0 to 3.0) is recommended. Additionally, no additional bridging is required in the latter group of patients if their VKA therapy is interrupted for non-cardiac procedures. With certain AVR valves and no other risk factors (e.g. ON-X), a lower INR goal may be pursued. 4. What are the major differences between Warfarin, Heparin products, and DOACs in pregnancy and lactation? Warfarin crosses the placenta and has a dose-dependent relationship with adverse fetal outcomes (e.g., miscarriage, stillbirth, embryopathy). Warfarin’s teratogenic effects are also trimester-dependent with fetal bone and cartilage abnormalities occurring in the 1st trimester and CNS abnormalities (e.g., microencephaly, spasticity, hypotonia, optic atrophy) if teratogenic levels are reached in the 2nd and 3rd trimester. When compared with LMWH and UFH, warfarin has the least maternal risk for those with mechanical heart valves, but lowest rates of livebirths. [4] LMWH does not cross the placenta and is associated with the highest number of livebirths. However, the challenges of using LMWH include its monitoring. Weight-based LMWH should be accompanied by peak anti-Xa levels drawn 4-6 hours post-dose to achieve a goal level of 1.0-1.2 U/ml.UFH is the preferred agent of choice at the time of delivery, since this is the highest period of bleeding for a pregnant woman. It is usually stopped 4-6 hours before delivery and restarted 4-6 hours after delivery if there is no bleeding.DOACs have not been studied in pregnant patients on a large scale. And the limited data present revealed a high miscarriage rate and possible embryopathy. There use is not recommended in pregnant women.Anticoagulants such as UFH, LMWH, warfarin, fondaparinux, or danaparoid are all recommended as safe options for breastfeeding women with indication for anticoagulation. DOACs are not recommended for lactating women. 5. What are the recommendations for VTE management during pregnancy? Venous thromboembolism (VTE) complicates ∼1.2 of every 1000 deliveries. Despite these low absolute risks, pregnancy associated VTE is a leading cause of maternal morbidity and mortality.Women with VTE on chronic anticoagulation are recommended to continue anticoagulation during (and after) pregnancy. Weight-based LMWH guided by Xa levels (to achieve a goal level of 1.0-1.2 U/ml) is the preferred agent, but warfarin (daily dose ≤5 mg) is an alternative.In patients with recent pulmonary embolism (PE), postpartum heparin treatment should be restarted 6 hours after a vaginal birth and 12 hours after a caesarean delivery if no significant bleeding has occurred. There should be subsequent overlap with VKAs for at least 5 days.In the absence of significant bleeding, VKAs may be started on the second day after delivery and continued for at least 3 months, or for 6 months if PE occurred late in pregnancy. The goal INR should be between 2 and 3.Anticoagulation decisions are complex and should be determined in collaboration with a multidisciplinary cardio-obstetrics team. References Alshawabkeh L, Economy KE, Valente AM .

Nov 22, 2021

The CardioNerds are thrilled to launch The Cardiac Critical Care Series! The series Co-Chairs – Dr. Mark Belkin (Advanced Heart Failure FIT, U Chicago), Dr. Yoav Karpenshif (FIT, U Penn), Dr. Eunice Dugan (CardioNerds Academy Chief Fellow and FIT, Cleveland Clinic), and Dr. Karan Desai (CardioNerds Academy Editor and FIT, U Maryland) - join CardioNerds Co-Founders, Amit Goyal and Daniel Ambinder to delve into high-yield topics in critical care cardiology. We kickstart this series with one of the early pioneers and national leaders in cardiac critical care – Dr. Jason Katz, Director of Cardiovascular Critical Care and Co-Director of Mechanical Circulatory Support and the CICU at Duke University Medical Center. In this episode, we learn about Dr. Katz’s career path and what motivated him to train in Critical Care Cardiology. He shares early struggles, notable changes in this field’s nascent period, and ongoing challenges in training and practice. We discuss collaboration with other cardiac and non-cardiac specialties and their importance in comprehensive care. Furthermore, we discuss how to advance critical care research, including the Critical Care Cardiology Trials Network and future randomized controlled trials to inform our practice and develop standardized protocols. In this small but rapidly growing field, we learn there is much to discover together. Audio editing by CardioNerds Academy Intern, Hirsh Elhence. Claim free CME for enjoying this episode! Disclosures: None Pearls • Notes • References • Guest Profiles • Production Team CardioNerds Cardiac Critical Care PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls and Quotes “I think it's really important not to be afraid of change in order to potentially succeed [...] it's okay to not entirely know what you want to do.” - Dr. Katz when sharing his non-direct career path in a novel field.“There is no greater team sport in cardiology than Cardiac Critical Care” and “I oftentimes think of the Critical Care Cardiologist as sort of the conductor that helps to orchestrate [the team]...” - Dr. Katz when discussing the importance of multidisciplinary teams and need to collaborate with other cardiac and non-cardiac sub-specialties.Many general surgical or medical residency/fellowship graduates are not comfortable caring for patients in the critical care setting. There is a need to revamp critical care training without significantly prolonging training time in order to complement and enhance our current workforce to care for complex, critically ill cardiac patients.“I don't think there's necessarily a one size fits all model, and I think we should be malleable or adaptable to the needs of our trainees and the needs of our patients.” - Dr. Katz when discussing training pathways in Critical Care Cardiology or combining Critical Care with other subspecialties like Interventional Cardiology or Advanced Heart Failure.Dr. Katz suggests that when choosing a Critical Care Cardiology training program: “consider geography, the flexibility of the curriculum, the overall fellowship and social experience, and the clinical setting. Everything that's really important to choosing a cardiology fellowship is more important in my mind than if they actually have a standardized, cardiac critical care pathway.” Show notes 1. What are some recent changes in the field of Critical Care Cardiology? Compared to even just a decade ago, there is a growing interest from medical students to young faculty in pursuing a career in critical care cardiology.At the same time there is evidence that the patient demographics in our CICUs are changing, including more multi-organ dysfunction and many non-cardiac diagnoses. In a recent paper from the Critical Care Cardiology Trials Network (CCCTN), the proportion of patients with a primary diagnosis of acute coronary syndrome was only approximately 32%. Following overall trends in heart failure, a greater proportion of CICU patients have heart failure and/or heart failure phenotype cardiogenic shock requiring clinicians to be facile with the spectrum of mechanical support devices.These demographic and workforce trends are requiring cardiologists to re-think how to best meet the needs of the modern CICU. 2. What continue to be some challenges in practicing Critical Care Cardiology? CICU patients are a heterogenous group with varying baseline characteristics, comorbidities, illness severity, and treatment responses. Since distinct pathophysiologic targets are lacking, challenges exist when devising strategies to improve outcomes. Similarly, these challenges extend to developing and executing research protocols to inform management.As Dr. Katz discussed on the episode, the lack of standardization, consistent terminology, and even who belongs in the CICU, remains a barrier to devising who should staff the CICU and how we train physicians to care for CICU patients.Dr. Katz described the cardiac intensivist as akin to the conductor of an orchestra working with multiple cardiac and non-cardiac subspecialists, and other professionals such as RNs, dieticians, physical therapy, social work, chaplaincy etc. Understanding the roles of multidisciplinary members can help inform resource utilization and allocate costs. 3. What are some challenges in Critical Care Cardiology training? There continues to be a supply-demand mismatch when it comes to the growing clinical need and the availability of trained cardiac critical care clinicians.Many surgical or medical residency/fellowship graduating trainees do not feel comfortable caring for critically ill patients. Thus, Dr. Katz advocates for outside the box thinking to find novel ways to supplement current cardiovascular training – whether it be in general fellowship, advanced heart failure or interventional training – with adequate critical care training for interested trainees.Accomplishing this goal without excessive increases in numbers of years in training – and assuring competency and exposure to aspects of critical care medicine not seen in general cardiology training – may require creating more blended pathwaysFurthermore, the optimal timing of when to obtain critical care training remains unclear. As few integrated options currently exist, trainees most commonly pursue critical care training after general cardiology or subspecialty cardiology fellowship training. Without integrated options, however, there is concern that trainees may not maintain their cardiac clinical skills or competency in areas such as echocardiography during dedicated critical care medicine years. 4. What about combining critical care with other cardiac-subspecialities like Interventional Cardiology or Advanced Heart Failure? There isn’t a “one size fits all” model. Training pathways should be flexible to accommodate the needs and interests of trainees. Recent opinion pieces have suggested blending Advanced Heart Failure training with Critical Care Training in a preferably 5-year pathway.Regardless of who is staffing the CICU, optimal care requires continued collaboration – not just during admission but frequent revisitation of management plans with cardiac subspecialists to direct patient care. 5. What can we learn from our cardiac intensivist colleagues in Europe? Europe has a more established training pathway for cardiac critical care with a dedicated scientific symposium, credentialing pathway, and journal.Although we have different regulatory authorities and settings for care of delivery, with colleagues in Europe having been through the process of establishing this new field, we can learn from their struggles and successes.Furthermore, there are opportunities for multinational collaboration in research, training, and education. References Il'Giovine ZJ, Menon V. The Intersection of Heart Failure and Critical Care: The Contemporary Cardiac Intensive Care Unit and the Opportunity for a Unique Training Pathway. J Card Fail. 2021 Oct;27(10):1152-1155. doi: 10.1016/j.cardfail.2021.03.014. PMID: 34625134. Katz J, Turer A, Becker R. Cardiology and the critical care crisis: a perspective. Journal of the American College of Cardiology. Published online 2007. doi:10.1016/J.JACC.2006.11.036 Bhatt AS, Berg DD, Bohula EA, et al. De Novo vs Acute-on-Chronic Presentations of Heart Failure-Related Cardiogenic Shock: Insights from the Critical Care Cardiology Trials Network Registry. J Card Fail. 2021 Oct;27(10):1073-1081. doi: 10.1016/j.cardfail.2021.08.014. PMID: 34625127; PMCID: PMC8514080. Guest Profiles Dr. Jason Katz Dr. Jason Katz is the Director of the Cardiac ICU, Mechanical Circulatory Support, and LVAD programs at Duke University. After completing his Internal Medicine residency at UT-Southwestern, he went on to complete a Cardiology Fellowship at Duke University, a Clinical Research Fellowship with the DCRI, and a finally Critical Care Fellowship at Duke. He has published over 100 articles across a range of topics within Cardiac Critical Care, including multiple reviews and statements addressing the role of, and training options for, Cardiac Intensivists. He is considered an early pioneer, and continues to be a leader, in this growing field, currently serving as the immediate past-President of the AHA Acute Cardiac Care Committee. CardioNerds Cardiac Critical Care Production Team Karan Desai, MDDr. Mark BelkinAmit Goyal, MDDaniel Ambinder, MD

Nov 19, 2021

CardioNerds Tommy Das (Program Director of the CardioNerds Academy and cardiology fellow at Cleveland Clinic) and Rick Ferraro (Director of CardioNerds Journal Club and cardiology fellow at the Johns Hopkins Hospital) join Dr. Erin Michos (Associate Professor of Cardiology at the Johns Hopkins Hospital and Editor-In-Chief of the American Journal of Preventative Cardiology) for a discussion about the effect of DHA and EPA on triglycerides and why DHA/EPA combinations may have exhibited limited benefits in trials. This episode is part of the CardioNerds Lipids Series which is a comprehensive series lead by co-chairs Dr. Rick Ferraro and Dr. Tommy Das and is developed in collaboration with the American Society For Preventive Cardiology (ASPC). Relevant disclosures: None Pearls • Notes • References • Guest Profiles • Production Team CardioNerds Lipid Series PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls The best intervention for heart disease is prevention! The InterHeart trial showed that 9 modifiable risk factors (dyslipidemia, smoking, hypertension, diabetes, abdominal obesity, dietary patterns, physical activity, consumption of alcohol, and psychosocial factors) predict 90% of acute myocardial infarction. So many acute events can be prevented1.Atherosclerotic vascular disease events increase across a range of triglyceride levels, even from 50-200mg/dL. So even in a relatively normal range, lower triglycerides seem to be better. Over ¼ of US adults have triglycerides over 150.While 8% of US adults take fish oil supplements, multiple meta-analyses have failed to show any benefit to the use of dietary omega-3 supplementation2. Dietary supplements these are not meant for medical use and are not studied or regulated as such! Show notes 1. What are DHA and EPA? DHA, or docosahexaenoic acid, and EPA, or eicosapentaenoic acid, are n-3 polyunsaturated fatty acids, also known as omega-3 fatty acids. These compounds have been of considerable interest for over two decades given observed association of high dietary omega-3 fatty acid intake with reduced cardiovascular events3. As both are important omega-3 fatty acids, trials on the benefits of DHA and EPA have often focused on the two compounds in combination. 2. What was the GISSI-Prevenzione Trial and why was it Important? GISSI-Prevenzione trial (Lancet 1999), was one of the earliest trials to study DHA and EPA4. In this trial, the authors evaluated the effect of omega-3 supplementation as a combination pill of DHA and EPA on cardiovascular events and death in patients with recent myocardial infarction (the last three months). Over a 3.5-year follow-up period, participants treated with DHA/EPA combination experienced a significant reduction in death, nonfatal MI, and stroke.As this was an early trial, patients were largely not on statins, as these were not supported at the time of study initiation (Only 5% were on cholesterol-lowering medications at baseline, and only 45% were on cholesterol-lowering therapy at study completion). The benefits seen in this trial may not extend to modern practice with patients on contemporary background therapy.The trial participants were also not representative of our modern patients for a variety of other reasons. 85% of participants in the trial were men. 42.2% of patients in EPA/DHA arm were current smokers, and 35.4% were prior smokers. Only 14.2% of patients had diabetes and 14.7% with BMI >30.Notably, the decrease in triglycerides in this trial was only 3%, implying that triglyceride lowering did not entirely explain the benefit in cardiovascular events seen. 3. What about the data after the GISSI-Prevensione Trial? After this positive trial for DHA/EPA in combination, subsequent trial data in support of DHA/EPA has been less robust.The Alpha Omega trial in 2010, ORIGIN in 2012, ASCEND in 2018, and VITAL in 2019 were all trials of DHA/EPA combinations versus placebo, and all exhibited no significant differences in cardiovascular events with DHA/EPA use5–8.The recent STRENGTH trial, published in 2020, also showed no reduction in cardiovascular events when taking DHA/EPA in combination (and as discussed in CardioNerds episode 136!)9. This remained the case upon sub-analysis of patients from the STRENGTH trial with the highest levels of serum EPA, who again exhibited no cardiovascular benefit. 4. Why then don’t DHA and EPA seem to work in combination? In short, we do not know.It seems that the beneficial effects of EPA – which as monotherapy has shown benefit across numerous trials (namely JELIS and REDUCE-IT) – are somehow offset by the combination with DHA, via a mitigation of anti-inflammatory processes or otherwise – this remains theoretical10,11.The EVAPORATE trial of purified EPA showed lower total plaque in participants taking EPA, suggesting a possible mechanism of effect12. 5. What About Dietary Omega-3 Supplements? 8% of US adults take fish oil supplements.Multiple meta-analyses have failed to show any benefit to the use of dietary omega-3 supplementation2.Note that the term “over the counter” is not correct when referring to these supplements! Over the counter refers to medications that are FDA regulated, just not prescription. Omega-3 supplements have minimal FDA oversight, which is perhaps another reason to avoid them. References - Triglycerides 1. Yusuf S, Hawken S, Ôunpuu S, et al. Effect of potentially modifiable risk factors associated with myocardial infarction in 52 countries (the INTERHEART study): case-control study. The Lancet. 2004;364(9438):937-952. doi:10.1016/S0140-6736(04)17018-9 2. Abbasi J. Another Nail in the Coffin for Fish Oil Supplements. JAMA. 2018;319(18):1851-1852. doi:10.1001/jama.2018.2498 3. Bang HO, Dyerberg J, Hjørne N. The Composition of Food Consumed by Greenland Eskimos. Acta Medica Scandinavica. 1976;200(1-6):69-73. doi:10.1111/j.0954-6820.1976.tb08198.x 4. GISSI-Prevenzione, Investigators. Dietary supplementation with n-3 polyunsaturated fatty acids and vitamin E after myocardial infarction: results of the GISSI-Prevenzione trial. The Lancet. 1999;354(9177):447-455. doi:10.1016/S0140-6736(99)07072-5 5. Kromhout D, Giltay EJ, Geleijnse JM. n–3 Fatty Acids and Cardiovascular Events after Myocardial Infarction. N Engl J Med. 2010;363(21):2015-2026. doi:10.1056/NEJMoa1003603 6. The ORIGIN Trial Investigators. n–3 Fatty Acids and Cardiovascular Outcomes in Patients with Dysglycemia. N Engl J Med. 2012;367(4):309-318. doi:10.1056/NEJMoa1203859 7. The ASCEND Study Collaborative Group. Effects of n−3 Fatty Acid Supplements in Diabetes Mellitus. N Engl J Med. 2018;379(16):1540-1550. doi:10.1056/NEJMoa1804989 8. Manson JE, Cook NR, Lee IM, et al. Vitamin D Supplements and Prevention of Cancer and Cardiovascular Disease. N Engl J Med. 2018;380(1):33-44. doi:10.1056/NEJMoa1809944 9. Nicholls SJ, Lincoff AM, Garcia M, et al. Effect of High-Dose Omega-3 Fatty Acids vs Corn Oil on Major Adverse Cardiovascular Events in Patients at High Cardiovascular Risk: The STRENGTH Randomized Clinical Trial. JAMA. 2020;324(22):2268-2280. doi:10.1001/jama.2020.22258 10. Bhatt DL, Steg PG, Miller M, et al. Cardiovascular Risk Reduction with Icosapent Ethyl for Hypertriglyceridemia. N Engl J Med. 2019;380(1):11-22. doi:10.1056/NEJMoa1812792 11. Yokoyama M, Origasa H, Matsuzaki M, et al. Effects of eicosapentaenoic acid on major coronary events in hypercholesterolaemic patients (JELIS): a randomised open-label, blinded endpoint analysis. The Lancet. 2007;369(9567):1090-1098. doi:10.1016/S0140-6736(07)60527-3 12. Budoff MJ, Bhatt DL, Kinninger A, et al. Effect of icosapent ethyl on progression of coronary atherosclerosis in patients with elevated triglycerides on statin therapy: final results of the EVAPORATE trial. European Heart Journal. 2020;41(40):3925-3932. doi:10.1093/eurheartj/ehaa652 Guest Profiles Dr. Erin Donnelly Michos Dr. Erin Donnelly Michos is an Associate Professor of Medicine at Johns Hopkins School of Medicine, with joint appointment in the Department of Epidemiology at the Johns Hopkins Bloomberg School of Public Health. She is the Director of Women’s Cardiovascular Health and the Associate Director of Preventive Cardiology with the Johns Hopkins Ciccarone Center for the Prevention of Cardiovascular Disease. Dr. Michos completed medical school at Northwestern University in Chicago, IL, and then completed both her Internal Medicine residency and Cardiology fellowship at the Johns Hopkins Hospital in Baltimore, MD. She also completed her MHS in Cardiovascular Epidemiology at the Johns Hopkins Bloomberg School of Public Health. She has authored or co-authored over 300 manuscripts in peer reviewed journals and is an internationally known leader in preventive cardiology and women’s health. CardioNerds Lipids Production Team Tommy Das, MD Dr. Rick Ferraro Amit Goyal, MD Daniel Ambinder, MD

Nov 16, 2021

CardioNerds (Amit Goyal and Daniel Ambinder), join CardioNerds FIT Ambassador, Dr. Natasha Cuk and her co-fellows, Dr. Lily Stern, and Dr. Paul Marano from the Cedars-Sinai Cardiology Fellowship for some late afternoon smoothies on the beach. They discuss the case of a 46-year-old woman who presented with sudden cardiac arrest and was ultimately found to have a mobile intraluminal aortic thrombus adherent to a penetrating ulcer in the ascending aorta. This mobile thrombus was ultimately thought to be the cause of transient ischemia and the patient’s cardiac arrest. We discuss a differential for sudden cardiac arrest, initial management after resuscitated cardiac arrest, a differential for arterial thrombus, and review an illness script for penetrating atherosclerotic ulcers. Dr. Dominick Megna provides the provides the E-CPR for this episode. Audio editing by Dr. Gurleen Kaur (Director of the CardioNerds Internship). This Case Report has been published in JACC Case Reports! Claim free CME just for enjoying this episode! Disclosures: NoneJump to: Pearls - Notes - References CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Episode Teaching https://twitter.com/LilySternMD/status/1460811173113184263?s=20 Pearls - Cardiac Arrest due to Aortic Thrombus After cardiac arrest, the initial ECG obtained after the return of spontaneous circulation can provide important information on the etiology of the arrest. The ECG can narrow our structured differential, for which one approach would be the following breakdown: acute ischemic events, structural heart disease, arrhythmogenic syndromes with no structural abnormality, and then non-cardiac causes such as drugs, toxins, trauma, metabolic arrangementsThe risk vs benefit of emergent angiography after sudden cardiac arrest depends on balancing the potential benefit from revascularization in an acute ischemic event vs bleeding risks and potential delays in other aspects of care, particularly given that a large percentage of mortality is related to neurologic injury from the arrest, which would not be impacted by immediate angiography. The available randomized controlled trial evidence has not demonstrated a survival or neurologic outcome benefit to immediate angiography, and the decision depends on weighing the risk/benefit for each patient.Due to high flow, a thrombus in the aorta should prompt an investigation for causes focused on the other two ‘points’ of Virchow’s triad (aside from stasis): endothelial injury and hypercoagulability.A penetrating atherosclerotic ulcer (PAU) is a deep atherosclerotic lesion where there is a focal ulceration of the elastic lamina that extends through the medial layer of the aortic wall. These lesions are most commonly associated with extensive atherosclerosis, but can also occur related to inflammatory, infectious, or traumatic causes.A PAU is a type of acute aortic syndrome and accounts for up to 8% of total acute aortic syndromes. It may present with a spectrum of symptoms, including as an incidental finding on cardiothoracic imaging or a severe chest and back pain, like an aortic dissection. While it is a subtype of aortic syndrome, PAU can also progress to become aortic dissection and rupture. Notes - Cardiac Arrest due to Aortic Thrombus 1. How might a post-ROSC ECG help determine the etiology of a sudden cardiac arrest? During our case, we discussed a systematic approach to the differential diagnosis for sudden cardiac arrest. We broke down the causes into the buckets of: Acute ischemic eventsStructural heart diseaseArrhythmogenic syndromes with no structural heart diseaseNon-cardiac causes such as drugs, toxins, trauma, and metabolic arrangements The post-ROSC ECG can provide immediate information to help narrow our differential. Evidence of acute ischemia (e.g. STEMI) would provide a likely etiology and would direct immediate next steps. We can look at ECG features such as axis and conduction abnormalities to look for evidence of an underlying structural abnormality. We can also see features of arrhythmogenic syndromes without underlying structural defects, such a short or long QT or a Brugada pattern. 2. Should all patients who present with sudden cardiac arrest and for whom ROSC is achieved undergo immediate coronary angiography? In considering the timing of coronary angiography after sudden cardiac arrest, clinical experience and the available evidence indicate a tension between: The high pre-test probability for acute ischemic events as the etiology for VT/VF arrest, and possible improvement in post-ROSC outcomes from immediate coronary angiography (and revascularization).A large portion of the morbidity and mortality associated with sudden cardiac arrest is driven by neurologic injury. Immediate angiography may expose patients to additional risk (delays in targeted temperature management, bleeding risk), without benefit to a patient’s ultimate outcome due to neurologic injury. Observational data has suggested a benefit for immediate angiography after resuscitated sudden cardiac arrest, though there was concern for selection bias. Recently, there have been two randomized controlled trials that have investigated the role for immediate angiography after sudden cardiac arrest. These trials are the COACT and PEARL trials, published in 2019 and 2020, respectively. These trials each have their own limitations, though they did not demonstrate a benefit for immediate angiography on outcomes such as mortality or neurologic outcomes. There are multiple ongoing trials to provide further guidance.The most recent AHA/ACC guideline on the topic recommends immediate coronary angiography for patients with STEMI on the post-ROSC ECG (Class I), and give a Class IIa recommendation that emergency coronary angiography is reasonable for selected patients (e.g. hemodynamically or electrically unstable) with sudden cardiac arrest of suspected cardiac origin without STEMI. 3. What is an illness script for penetrating atherosclerotic ulcers? Definitions: A penetrating atherosclerotic ulcer (PAU) is a deep atherosclerotic lesion where there is a focal ulceration of the elastic lamina that extends through the medial layer of the aortic wall. PAU is a type of acute aortic syndrome (along with other disease processes such as aortic dissection, intramural hematoma). While a distinct entity, PAU can also progress and lead to intramural hematoma, dissection, and even aortic rupture.Epidemiology: PAU accounts for 8% of total acute aortic syndromes. It is typically associated with extensive atherosclerosis in older adults (age > 65) and is most commonly found in the descending thoracic aorta. It is less commonly associated with infectious, inflammatory, or traumatic etiologies.Clinical Presentation: PAU may present with a spectrum of symptoms, including as an incidental finding on cardiothoracic imaging or a severe chest and back pain, like an aortic dissection.Diagnosis: PAU can be diagnosed by multiple imaging modalities, including computed tomography angiography, magnetic resonance imaging, and transesophageal echocardiography. 4. How are penetrating aortic ulcers treated? Management of symptomatic penetrating aortic ulcers is similar to management of aortic dissection with indications for surgery including recurrent pain despite medical treatment, hemodynamic instability, aortic diameter enlargement to >55 mm, and significant periaortic hemorrhage. In asymptomatic patients who are hemodynamically stable, management is controversial--some centers support aggressive early surgical intervention while others opt for conservative medical management along with serial surveillance for aortic enlargement. References Lemkes JS, Janssens GN, van der Hoeven NW, Jewbali LSD, Dubois EA, Meuwissen M, Rijpstra TA, Bosker HA, Blans MJ, Bleeker GB, Baak R, Vlachojannis GJ, Eikemans BJW, van der Harst P, van der Horst ICC, Voskuil M, van der Heijden JJ, Beishuizen A, Stoel M, Camaro C, van der Hoeven H, Henriques JP, Vlaar APJ, Vink MA, van den Bogaard B, Heestermans TACM, de Ruijter W, Delnoij TSR, Crijns HJGM, Jessurun GAJ, Oemrawsingh PV, Gosselink MTM, Plomp K, Magro M, Elbers PWG, van de Ven PM, Oudemans-van Straaten HM and van Royen N. Coronary Angiography after Cardiac Arrest without ST-Segment Elevation. New England Journal of Medicine. 2019;380:1397-1407.Kern KB, Radsel P, Jentzer JC, Seder DB, Lee KS, Lotun K, Janardhanan R, Stub D, Hsu CH and Noc M. Randomized Pilot Clinical Trial of Early Coronary Angiography Versus No Early Coronary Angiography After Cardiac Arrest Without ST-Segment Elevation: The PEARL Study. Circulation. 2020;142:2002-2012.Callaway CW, Donnino MW, Fink EL, Geocadin RG, Golan E, Kern KB, Leary M, Meurer WJ, Peberdy MA, Thompson TM and Zimmerman JL. Part 8: Post–Cardiac Arrest Care. Circulation. 2015;132:S465-S482.Hiratzka LF, Bakris GL, Beckman JA, Bersin RM, Carr VF, Casey DE, Eagle KA, Hermann LK, Isselbacher EM, Kazerooni EA, Kouchoukos NT, Lytle BW, Milewicz DM, Reich DL, Sen S, Shinn JA, Svensson LG and Williams DM. 2010 ACCF/AHA/AATS/ACR/ASA/SCA/SCAI/SIR/STS/SVM Guidelines for the Diagnosis and Management of Patients With Thoracic Aortic Disease. Circulation. 2010;121:e266-e369. CardioNerds Case Report Production Team Karan Desai, MDAmit Goyal, MDDaniel Ambinder, MD

Nov 10, 2021

CardioNerds (Amit Goyal and Daniel Ambinder), ACHD series co-chair Dr. Agnes Koczo (UPMC), and episode FIT lead, Dr. Natasha Wolfe (Washington University) join Dr. Ari Cedars (Director of the Adult Congenital Heart Disease Program at Johns Hopkins) for a discussion about coarctation of the aorta. In this episode we discuss the presentation and management of unrepaired and repaired coarctation of the aorta in adults. We discuss the unique underlying congenital anatomy of coarctation and how that impacts physiology, clinical presentation, and diagnostic findings. We discuss the importance of long-term routine follow-up and screening of patients (including those who have been “repaired”) for common complications such as hypertension, re-coarctation, and aneurysm development. We end with a discussion of treatment options for coarctation and its complications. Audio editing by CardioNerds Academy Intern, Dr. Maryam Barkhordarian. The CardioNerds Adult Congenital Heart Disease (ACHD) series provides a comprehensive curriculum to dive deep into the labyrinthine world of congenital heart disease with the aim of empowering every CardioNerd to help improve the lives of people living with congenital heart disease. This series is multi-institutional collaborative project made possible by contributions of stellar fellow leads and expert faculty from several programs, led by series co-chairs, Dr. Josh Saef, Dr. Agnes Koczo, and Dr. Dan Clark. The CardioNerds Adult Congenital Heart Disease Series is developed in collaboration with the Adult Congenital Heart Association, The CHiP Network, and Heart University. See more Claim free CME for enjoying this episode! Disclosures: None Pearls • Notes • References • Guest Profiles • Production Team CardioNerds Adult Congenital Heart Disease PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls Coarctation of the aorta can occur as a discrete stenosis or as a long and hypoplastic hypoplastic aortic arch segment. Most commonly it is a discrete stenosis located at the insertion site of the ductus arteriosus just distal to the left subclavian artery.Three quarters of patients with coarctation of the aorta also have a bicuspid aortic valve.Hypertension is the most common long-term complication of coarctation of the aorta, whether repaired or unrepaired. Unrepaired coarctation is a rare cause of secondary hypertension in young adults with a difference in upper extremity and lower extremity BP by ≥ 20 mmHg. Systemic hypertension may not be consistently identifiable at rest in those with repaired coarctation, thus guidelines recommend ambulatory blood pressure monitoring or stress testing to identify hypertension with exertion.Chest and brain imaging via CT or MRI should be done every 5-10 years to screen for other long-term complications including re-coarctation (rate ~11%), aortic aneurysm development (higher risk in those with concurrent bicuspid aortic valve), pseudoaneurysm, aortic dissection, and cerebral aneurysms.Repair of coarctation or re-coarctation is indicated for patients who are hypertensive with a BP gradient ≥ 20 mmHg (Class I recommendation). Catheter-based stenting is the preferred approach when technically feasible. Show notes 1. What is the proposed embryologic origin of coarctation of the aorta? The aortic arch and its branches develop at 6-8 weeks fetal gestation. We all start with six aortic arches that go on to become the great arteries of the head and neck. The 4th arch forms the thoracic aortic arch and isthmus. The 6th arch persists as the proximal pulmonary arteries and ductus arteriosus. Thoracic aortic coarctation is therefore a manifestation of abnormal embryologic development of the 4th and 6th arches.There are two main theories regarding how aortic coarctation occurs.The first is the “ductus tissue theory”, which proposes that coarctation develops as the result of migration of ductal smooth muscles cells in the periductal aorta, with subsequent constriction and narrowing of the aortic lumen.The “hemodynamic theory” proposes that coarctation develops because of hemodynamic disturbances from other left sided congenital lesions that reduce the volume of blood flow through the fetal aortic arch – recall the “no flow, no grow” tenet.In all likelihood, both are true and play a role in aortic coarctation embryologic development. 2. What are the key features of aortic coarctation anatomy? Coarctation is, strictly speaking, a congenital narrowing of the aorta.Most commonly, this occurs at the insertion of the ductus arteriosus just distal to the left subclavian artery and is more of an isolated ridge or shelf that causes obstruction and narrowing.There are several other variants, however and include discrete thoracic lesions, long-segmental defects, tubular hypoplasia, and more rarely, coarctation located in the abdominal aorta.Other common congenital anomalies found in patients with aortic coarctation include supra- or subaortic stenosis, Shone complex (a series of left-sided obstructive lesions), and hypoplastic left heart syndrome. Enjoy Episode #121 for more on Shone Complex.Patients with Turner Syndrome and Williams Syndrome have high rates of aortic coarctation. 3. What are the hemodynamic consequences of aortic coarctation? While coarctation can be severe, it is often well tolerated in utero given ~2/3 of cardiac output flows through the ductus arteriosus into the descending thoracic aorta, bypassing the area of narrowing.After birth, however, increasing amounts of cardiac output must bypass the area of constriction. The severity of narrowing correlates with the amount of added afterload beyond what we would expect to see in normal hemodynamics. The consequences thus vary depending on this severity, from asymptomatic to mild hypertension to heart failure and overt cardiogenic shock.Compensatory mechanisms the heart can use to counteract this extra afterload are 1) hypertrophy and 2) increasing LV dimensions – neither of which are ideal for a young patient!The systemic circulation may compensate for the coarctation by developing collateral blood flow involving the intercostal, internal mammary, and scapular vessels.Upper extremity systemic arterial hypertension with a 20-mmHg gradient between the upper and lower extremitiesDelayed and diminished femoral arterial pulses, rarely with symptoms of claudicationSystolic murmur at left sternal border with radiation to the back and possible thrill in suprasternal notch reflective of high flows through the coarctPossible continuous murmur from development of arterial collaterals 4. How might an adult with a history of repaired coarctation of the aorta present? 10-20% of those with repaired coarctation go on to develop hypertension in adulthood. This is an important risk factor in these patients for premature coronary artery disease, stroke, cardiomyopathy, and aneurysm (aortic and cerebral) rupture.Even in those with normal blood pressure at rest, many have hypertension that can be unmasked with exercise.~11% of patients develop re-coarctation.Patients are at risk of developing aneurysm, aortic dissection, or pseudoaneurysms at the site of prior repair (risk is higher in those with concurrent bicuspid aortic valve).~10% of patients with coarctation of the aorta develop cerebral aneurysms and in 5% of coarctation patients, the cause of death is ruptured cerebral aneurysm. 5. What are long-term considerations for coarctation of the aorta? In patients with unrepaired coarctation or re-coarctation with a BP gradient ≥ 20 mmHg (Class I recommendation) and hypertension, repair is indicated with transcatheter stenting preferred when technically feasible.In patients with repaired coarctation and normal BP at rest, guidelines recommend consideration of ambulatory blood pressure monitoring or exercise stress test to diagnose hypertension with exertion. If this is found, treatment with low dose anti-hypertensive is indicated.Routine chest and brain imaging via CT or MRI every 5-10 years is indicated to screen for long-term complications at the site of prior repair and for cerebral aneurysm development.Surgical management is indicated for ascending aorta aneurysm >50mm in diameter or those with rapid progression due to high risk of rupture or dissection. References Stout KK, Daniels CJ, Aboulhosn JA, Bozkurt B, Broberg CS, Colman JM, Crumb SR, Dearani JA, Fuller S, Gurvitz M, Khairy P, Landzberg MJ, Saidi A, Valente AM, Van Hare GF. 2018 AHA/ACC Guideline for the Management of Adults With Congenital Heart Disease: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines. J Am Coll Cardiol. 2019 Apr 2;73(12):e81-e192. doi: 10.1016/j.jacc.2018.08.1029. Epub 2018 Aug 16. Erratum in: J Am Coll Cardiol. 2019 May 14;73(18):2361-2362. PMID: 30121239.Baumgartner H, De Backer J, Babu-Narayan SV, Budts W, Chessa M, Diller GP, Lung B, Kluin J, Lang IM, Meijboom F, Moons P, Mulder BJM, Oechslin E, Roos-Hesselink JW, Schwerzmann M, Sondergaard L, Zeppenfeld K; ESC Scientific Document Group. 2020 ESC Guidelines for the management of adult congenital heart disease. Eur Heart J. 2021 Feb 11;42(6):563-645. doi: 10.1093/eurheartj/ehaa554. PMID: 32860028.Kenny D, Hijazi ZM. Coarctation of the aorta: from fetal life to adulthood. Cardiol J. 2011;18(5):487-95. doi: 10.5603/cj.2011.0003. PMID: 21947983.Nguyen L, Cook SC. Coarctation of the Aorta: Strategies for Improving Outcomes. Cardiol Clin. 2015 Nov;33(4):521-30, vii. doi: 10.1016/j.ccl.2015.07.011. Epub 2015 Aug 29. PMID: 26471817.Horlick EM, McLaughlin PR, Benson LN. The adult with repaired coarctation of the aorta. Curr Cardiol Rep. 2007 Jul;9(4):323-30. doi: 10.1007/BF02938381. PMID: 17601399.

Nov 4, 2021

CardioNerds (Amit Goyal and Daniel Ambinder), Cardio-OB series co-chair and University of Texas Southwestern Cardiology Fellow, Dr. Sonia Shah, and episode FIT lead and UT Southwestern Cardiology Fellow Dr. Laurie Femnou discuss valvular heart disease in pregnancy with cardio-obstetrics expert Dr. Uri Elkayam, Professor of Medicine and OB Gyn at the University of Southern California. In this pearl-packed episode, we discuss the diagnosis, acute management, and long-term considerations of valvular heart disease in pregnancy. Through a series of cases, we review the physiologic changes in pregnancy that make certain valvular lesions well-tolerated, while others are associated with a much higher risk of peripartum complications. We also discuss which patients to consider referring for valvular intervention, the ideal timing, and which valvular interventions are safest in the peripartum period. We promise, you won’t want to miss this clinically high-yield episode with Dr. Elkayam, the father of cardio-obstetrics and an absolute legend in the field! Audio editing by CardioNerds Academy Intern, Adriana Mares. Pearls • Notes • References • Guest Profiles • Production Team CardioNerds Cardio-Obstetrics Series PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls Most women with severe valvular heart disease can be managed medically throughout pregnancy.Right sided valvular lesions are generally better tolerated than left-sides lesions, and regurgitant lesions are generally better tolerated than stenotic lesions. However, the context and etiology of the valve dysfunction must be taken into consideration. Severe tricuspid valve regurgitation, for example, can be associated with a failing right ventricle and undiagnosed pulmonary hypertension. Changes in BNP, severity of symptoms, and right ventricular systolic pressure (RVSP) assessed by echocardiography can be helpful in differentiating normal pregnancy-related symptoms from symptoms due to hemodynamically significant valvular lesions.Valvular interventions during pregnancy are safe when well-planned and performed by experienced operators, and they can significantly improve morbidity and mortality in women who remain symptomatic despite medical management.A multidisciplinary team-based approach is important when managing patients with valvular heart disease during pregnancy. Quatables “We do not need to perform prophylactic valvular intervention in women prior to pregnancy if they do not meet criteria for intervention otherwise. A patient with regurgitant lesion will tolerate pregnancy well, provided that they are not candidates for surgery already.” “Valvuloplasty during pregnancy is a great and effective procedure, but restenosis occurs. For women who desire future pregnancies, preconception evaluation is important to determine if valve intervention is indicated prior to conceiving.” Show notes What is the epidemiology of valvular heart disease in pregnancy?Cardiovascular conditions affect up to 4% of pregnancies, with valvular heart disease being the most common cardiac pathology encountered during pregnancy worldwide.In the developing world, rheumatic valve disease is still the most common etiology, with mitral valve most commonly affected, followed by the aortic valve.In the developed world, congenital aortic valve pathology is most common. What are the hemodynamic effects of stenotic vs. regurgitant lesions during pregnancy?In normal pregnancy, there is a significant drop in systemic vascular resistance as early as 5 weeks gestational age. This drop leads to a transient decrease in perfusion to the kidneys, causing an increase in fluid retention and expansion of plasma volume. At the same time, there is an increase in heart rate which becomes more pronounced later in the second trimester.These changes ultimately lead to an increase in cardiac output. Patients with stenotic lesions have a fixed obstruction, and therefore can have a difficult time adjusting to these physiologic changes of pregnancy. In mitral stenosis for example, the increase in heart rate leads to less atrial emptying time in diastole, which leads to an underfilled left ventricle and increase in left atrial preload.In contrast, regurgitation lesions are often better tolerated than stenotic lesions during pregnancy because of the ability of the cardiac chambers to dilate and accommodate the increase in plasma volume.These rules are generally true, provided that the ventricular systolic function is preserved. A patient with functional mitral regurgitation secondary to a failing left ventricle may not tolerate the hemodynamic changes of pregnancy well. What is involved with preconception evaluation and valvular heart disease?Preconception evaluation and counseling is recommended for all women with a history of heart disease to assess risk and modify them if indicated. If already pregnant, a complete risk assessment should be performed as soon as possible by the cardio-obstetrics team.Women with a known or suspected valvular lesion should have a complete echocardiogram performed as part of their assessment. It is important to also assess functional status, as poor baseline functional status is associated with worse outcome during pregnancy. For women with severe valvular lesions and no symptoms at baseline, stress testing can be helpful in assessing functional capacity.Modified WHO, CARPREG and ZAHARA are risk assessment tools that can be used during pregnancy to counsel patients. (See below)Preconception evaluation is a good opportunity to review medications and stop potential teratogenic medications depending on the risks and benefits. What are the guidelines for the management of valve disease during pregnancy: medical vs invasive management?Women who otherwise qualify for valve repair or replacement should be strongly considered for valve intervention prior to pregnancy. RecommendationCORIntervention before pregnancy in asymptomatic MS with VA <1.5 cm2IAortic valve intervention in severe AS prior to pregnancy if asymptomaticIIaPMBC should be considered during pregnancy refractory symptoms despite medical managementIIaBAV should be considered during pregnancy with severe symptoms despite medical managementIIaValve operation should not be performed during pregnancy in the absence of severe refractory HFIII Shared decision-making is important when it comes to evaluating therapeutic and interventional options for women who want to become pregnant with valve disease. Mechanical valve replacement, for example, is typically the most durable option for a young patient, but the need for systemic anticoagulation during pregnancy often makes it an unattractive option for some patients. Bioprosthetic valve is an alternative if trying to avoid systemic anticoagulation during pregnancy, with the understanding that patient will likely need reoperation in the future. For women with aortic valve dysfunction, a Ross procedure is another option. In this procedure, a patient’s own pulmonic valve is placed in the aortic position, and the pulmonic valve is replaced using a donor valve. The advantage of this is that no anticoagulation is necessary. It is a more complex surgery, but outcomes are good when performed by experienced operators. Balloon valvuloplasty can also be performed with good result, although restenosis can occur within months of initial procedure; women who undergo valvuloplasty should have repeat assessment immediately prior to conception to ensure that the valve is not re-stenosed. For women who are already pregnant with persistent symptoms despite medical therapy, balloon valvuloplasty should be considered. How should be monitor women with valvular heart disease during pregnancy?The frequency of monitoring during pregnancy depends on the severity of disease and symptoms. Serial echocardiograms in the absence of symptoms are usually not required.Echocardiograms can be helpful in estimating pulmonary pressures and left atrial pressures. Gradients across the valves in stenotic lesions are expected to increase due to the increase flow and management should not be guided based on this alone.Obtaining cardiac biomarkers such as BNP early in pregnancy can help differentiate between normal symptoms of pregnancy versus hemodynamic compromise from valve disease.Right heart catheterization can be helpful in cases where the symptoms are discordant with the objective data (echo and BNP) especially when result can affect major decision like cesarian section versus vaginal delivery. However, this should be done in expert hands given the increased risk of vascular complications during pregnancy. What is the morbidity and mortality associated with severe left sided valvular obstruction during pregnancy?Women with severe left-sided valvular obstruction have the highest risk of morbidity and mortality during pregnancy. A recent meta-analysis of studies published between 1985 and 2019 of women treated in specialized centers in developed countries showed a mortality rate of 3% and 2% in severe mitral and aortic stenosis respectively. Heart failure was more common in mitral stenosis 37% as compared to 9% in AS. New or recurrent arrhythmia were reported in 16% of women with severe MS and 4% in women with severe AS.Fetal outcomes were similarly worse than in the general population.Women who remain symptomatic after initiation of adequate medical therapy should be considered for intervention, as they are in the highest risk group.Valvuloplasty, if valve anatomy allows, to relieve the obstruction is preferred over surgery given high risk of morbidity and fetal loss with cardiac surgery.

Oct 31, 2021

CardioNerds (Amit Goyal and Daniel Ambinder), join CardioNerds FIT Ambassador, Dr. Pablo Sanchez, and his co-fellows, Dr. Jimmy Tooley and Dr. Maggie Ning from Stanford University for an important case discussion about an An otherwise healthy young adult presented with fatigue and was found to be in complete heart block due to sarcoidosis. Dr. Ronald Witteles, (Stanford University Program Director for the Stanford Internal Medicine residency program and advanced heart failure specialist who's particular expertise focuses in the treatment of amyloidosis, sarcoidosis, and cardio-oncology) provides the E-CPR for this episode. Claim free CME just for enjoying this episode! Disclosures: Dr. Witteles reports that he has served as an advisor for Pfizer, Alnylam, Eidos, Regerenon Pharmaceuticals, Janssen, and IonisJump to: Patient summary - Case teaching - References CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Patient Summary - Notes - Complete Heart Block due to Sarcoidosis An otherwise healthy young adult presented with fatigue and was found to be in complete heart block. Imaging studies were suspicious for cardiac and pulmonary sarcoidosis. Sarcoidosis was confirmed on biopsy. Given the high risk of future cardiac events our patient underwent a dual chamber ICD implantation. He was started on prednisone and methotrexate for immunosuppression. Case Media - Click to enlarge Episode Teaching - Notes - Complete Heart Block due to Sarcoidosis Pearls - Complete Notes - Complete Heart Block due to Sarcoidosis Cardiac sarcoidosis is a disease characterized by noncaseating granulomas involving the heart that can exist alone or together with other organ system involvementDepending on the sites of cardiac involvement it can present as conduction system disease, ventricular arrhythmia, or heart failureCardiac sarcoidosis should be considered in patients with history of sarcoidosis involving other organ systems who develop left ventricular dysfunction, wall motion abnormalities, or arrhythmiasCardiac sarcoidosis should be considered in patients who present with otherwise unexplained heart block or ventricular tachycardia (VT) It is generally recommended that patients with cardiac sarcoidosis with an indication for pacemaker receive an ICD at time of implantation regardless of history of VT Notes - Complete Heart Block due to Sarcoidosis 1. What is Sarcoidosis? Sarcoidosis is a rare disorder of inflammation characterized by the formation of noncaseating granulomas in affected tissues. It most commonly involves the pulmonary system, but other organ systems can be involved including the heart. Sarcoidosis typically affects young adults, and its etiology is still uncertain. 2. What is Cardiac Sarcoidosis and how is it diagnosed? Cardiac sarcoidosis (CS) can occur alone or with systemic disease and depending on the cardiac sites of involvement, can present as conduction system disease, ventricular arrhythmia, heart failure, or sudden cardiac death. 3. How is Cardiac Sarcoidosis diagnosed? Diagnosis of CS is challenging as the gold standard is endomyocardial biopsy (EMB), though sensitivity of EMB is low given the often-patchy tissue involvement. Societal guidelines on the diagnosis of CS require either a positive EMB or biopsy-confirmed extracardiac sarcoidosis with evidence of secondary criteria to suggest cardiac involvement - unexplained VT, high grade AV block, third degree AV block, LVEF 50% of CS patients who presented with AV block experienced a fatal cardiac event at 34 months follow up. Societal recommendations reflect this increased cardiac risk in CS patients and give a Class IIa recommendation for ICD implantation in CS patients with indication for permanent pacing, unexplained syncope, or inducible VT/VF. References Barra, Sérgio Nuno Craveiro, Rui Providência, Luís Paiva, José Nascimento, and António Leitão Marques. “A Review on Advanced Atrioventricular Block in Young or Middle-Aged Adults: ATRIOVENTRICULAR BLOCK IN YOUNG ADULTS.” Pacing and Clinical Electrophysiology 35, no. 11 (November 2012): 1395–1405. https://doi.org/10.1111/j.1540-8159.2012.03489.x.Birnie, David H., William H. Sauer, Frank Bogun, Joshua M. Cooper, Daniel A. Culver, Claire S. Duvernoy, Marc A. Judson, et al. “HRS Expert Consensus Statement on the Diagnosis and Management of Arrhythmias Associated With Cardiac Sarcoidosis.” Heart Rhythm 11, no. 7 (July 2014): 1304–23. https://doi.org/10.1016/j.hrthm.2014.03.043.Kandolin, Riina, Jukka Lehtonen, and Markku Kupari. “Cardiac Sarcoidosis and Giant Cell Myocarditis as Causes of Atrioventricular Block in Young and Middle-Aged Adults.” Circulation: Arrhythmia and Electrophysiology 4, no. 3 (June 2011): 303–9. https://doi.org/10.1161/CIRCEP.110.959254.Nery, Pablo B., Rob S. Beanlands, Girish M. Nair, Martin Green, Jim Yang, Brian A. Mcardle, Darryl Davis, et al. “Atrioventricular Block as the Initial Manifestation of Cardiac Sarcoidosis in Middle-Aged Adults: Cardiac Sarcoidosis Presenting as Atrioventricular Block.” Journal of Cardiovascular Electrophysiology 25, no. 8 (August 2014): 875–81. https://doi.org/10.1111/jce.12401.Takaya, Yoichi, Kengo Fukushima Kusano, Kazufumi Nakamura, and Hiroshi Ito. “Outcomes in Patients With High-Degree Atrioventricular Block as the Initial Manifestation of Cardiac Sarcoidosis.” The American Journal of Cardiology 115, no. 4 (February 2015): 505–9. https://doi.org/10.1016/j.amjcard.2014.11.028.Terasaki, Fumio, Arata Azuma, Toshihisa Anzai, Nobukazu Ishizaka, Yoshio Ishida, Mitsuaki Isobe, Takayuki Inomata, et al. “JCS 2016 Guideline on Diagnosis and Treatment of Cardiac Sarcoidosis ― Digest Version ―.” Circulation Journal 83, no. 11 (October 25, 2019): 2329–88. https://doi.org/10.1253/circj.CJ-19-0508.Uemura, A., S. Morimoto, S. Hiramitsu, Y. Kato, T. Ito, and H. Hishida. “Histologic Diagnostic Rate of Cardiac Sarcoidosis: Evaluation of Endomyocardial Biopsies.” American Heart Journal 138, no. 2 Pt 1 (August 1999): 299–302. https://doi.org/10.1016/s0002-8703(99)70115-8. CardioNerds Case Report Production Team Karan Desai, MDAmit Goyal, MDDaniel Ambinder, MD

Oct 18, 2021

CardioNerds Dan Ambinder, Dr. Tommy Das (Program Director of the CardioNerds Academy and cardiology fellow at Cleveland Clinic), and episode lead, Dr. Teodora Donisan (CardioNerds Academy fellow and incoming Chief fellow and Beaumont Health Internal Medicine resident) join Dr. Matthew Budoff (professor of medicine at David Geffen School of Medicine at UCLA and the Endowed Chair of Preventive Cardiology at Harbor-UCLA Medical Center) for a discussion about triglycerides from pathophysiology to clinical outcomes. This episode is part of the CardioNerds Lipids Series which is a comprehensive series lead by co-chairs Dr. Rick Ferraro and Dr. Tommy Das and is developed in collaboration with the American Society For Preventive Cardiology (ASPC). Triglyceride (TG) metabolism can produce a by-product called remnant lipoproteins, which can be atherogenic. Most guidelines consider hypertriglyceridemia to start at values ≥ 150 mg/dl. It is the most common dyslipidemia, as it can occur in 30% of the general population. Although fasting levels are usually obtained per the current US protocol, there is evidence that non-fasting TG levels might be a better indicator of cardiovascular (CV) risk as these levels may better reflect the usual levels that the body is exposed to. There are multiple primary (genetic) causes of elevated TG, but these are rarer than lifestyle factors, medical conditions, or medications. Genetic association studies are helping better define the level of CV risk stemming from elevated TG-levels, which will impact how we target lifestyle and treatment interventions in the future. #CardsJC STRENGTH Trial Journal Club Relevant disclosures: Dr. Matthew Budoff has funding from General Electric. Pearls • Notes • References • Guest Profiles • Production Team CardioNerds Lipid Series PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls - Triglycerides - Pathophysiology to Clinical Outcomes In the process of metabolizing TG, remnant lipoproteins are formed, which have been shown to promote atherogenesis. TG themselves have not been directly linked to this process and have not been studied in large population studies, and so are considered risk enhancing factors, and not risk factors per se. Elevated triglyceride levels measured on our traditional lipid panels act as a proxy for the Apo-B rich lipoproteins, such as VLDL, which directly cause atherogenesis.Hypertriglyceridemia is defined as TG values of ≥150 mg/dl, although there is emerging evidence that even high-normal values (100-140 mg/dl) can still be associated with increased CV risk. You can think of TG in a similar fashion to glucose values (patients with prediabetes are still at higher CV risk than those with normal glycemic level). These are continuous and not binary variables!Fasting lipid levels are not necessarily a better predictor of CV events than non-fasting lipid levels. A non-fasting TG level can potentially provide information on the body’s metabolism similarly to how we interpret glucose tolerance tests, although there isn’t such a standardized approach in the lipid world yet.Before testing for genetic causes, make sure you review secondary causes of elevated TG. Don’t forget to evaluate for lifestyle factors and medical causes (diabetes, alcohol abuse, hypothyroidism, pregnancy) and to review the medication list (pay attention to thiazides, non-selective beta blockers, antipsychotics and others).TG values of ≥ 175 mg/dl are considered a risk enhancing factor and can aid in the decision to be more aggressive with lifestyle changes or starting treatment.Although treatment will be reviewed in depth in future episodes, Dr. Budoff suggests we “back away from using fibrates for CV event protection.” Even though they are efficient at lowering TG levels, they haven’t been shown to have a beneficial impact on ASCVD. New trials are exploring the role of pemafibrate for CV outcomes (1). Furthermore, EPA treatment can be considered for TG < 500 mg/dl with the goal of CV risk reduction. We should remember that omega-3 dietary supplements are impure, may be stored in improper conditions, and may be unsafe, even though more affordable to patients. Show notes - Triglycerides - Pathophysiology to Clinical Outcomes 1. What is the basic biochemical structure of triglycerides (TG), and how are they metabolized by the body? TG are hydrophobic substances packed into the core of lipoproteins. Lipoproteins are made up of a lipid rich core bound to proteins called apolipoproteins and can travel freely through the extracellular environments inside the body. The main way to transport dietary and endogenous TG to the tissues is through 2 types of TG-rich lipoproteins secreted by the intestine and the liver: chylomicrons and very low-density lipoproteins (VLDL). In order to unpack these TG-rich lipoproteins, the body produces lipoprotein lipase, which releases free fatty acids (FFA) and remnant lipoproteins. The main places in the body where this process occurs is in adipose tissue, where FFA are used for storage, and in the muscle tissue, where FFA are used for energy production. Both skeletal muscle and cardiac muscle use FFA as an energy source for contraction. Remnant chylomicrons and VLDL are then mostly taken up by the liver using low-density lipoproteins (LDL) receptors and they are then used to produce VLDL or LDL which return to the circulation. Some of the remnant lipoproteins can be taken up by the vessel wall, thereby leading to endothelial dysfunction, vascular inflammation, and atherogenesis (2-4). 2. What is the epidemiology of hypertriglyceridemia? How prevalent is hypertriglyceridemia in the general population? The normal TG levels in American men and women are 128 mg/dl and 110 mg/dl respectively (5). Hypertriglyceridemia is defined as fasting TG levels of ≥ 150 mg/dl by most guidelines and expert committees (6-9). Emerging evidence indicates that high-normal TG values (100-149 mg/dl) may still be associated with increased risk of cardiovascular events (10). Similar to how we regard glucose values and the increased risk people can have even as prediabetics, so too are TG a continuous variable. Hypertriglyceridemia is the most common form of dyslipidemia in the general population. An estimated 53% of American adults have dyslipidemia, 27% have elevated LDL levels, 23% have low HDL levels, and 30% have elevated TG levels (12). Of these, men have a higher prevalence of hypertriglyceridemia than women (28.7% and 21.5% respectively). The age distribution is different between the genders as well (highest prevalence in men ages 40-59 years old and women over 60 years old) (13). Some of these differences mainly stem from lifestyle – dietary habits and exercise levels. 3. What is the best way to measure TG values in the blood and what is the clinical significance of fasting vs non-fasting values? Fasting lipid levels are not necessarily a better predictor of cardiovascular events than non-fasting lipid levels. To the contrary, there is evidence that non-fasting TG levels might actually be a better indicator of increased cardiovascular risk (14,15). The European guidelines recommend obtaining a fasting sample when non-fasting TG levels are greater that 440mg/dL (16). The convention in the US is to obtain fasting lipid panels and TG levels, as the fasting TG value can be used to calculate LDL through the Friedewald equation. To continue building on the analogy with glucose values above, a non-fasting TG level can potentially provide information on the body’s metabolism similarly to how we interpret glucose tolerance tests, although there isn’t such a standardized approach in the lipid world yet. 4. What are some of the main causes of elevated TG? Causes that we more frequently encounter in our clinical practice include lifestyle factors (i.e., diet, alcohol, decreased physical activity, and smoking) or medical conditions (i.e., obesity, metabolic syndrome, uncontrolled diabetes, pregnancy, Cushing’s, hypothyroidism, or nephrotic syndrome) (11). We must not forget that there are medications which can cause mild to moderate elevations (e.g., thiazides, non-selective BB, atypical antipsychotics, glucocorticoids), or ones that can cause severe TG elevations (e.g., estrogen and estrogen receptor blockers, propofol, interferon, and various cancer therapies such as isotretinoin, ciclosporin, sirolimus, capecitabine, and protease inhibitors) (11). We can consider primary genetic abnormalities if secondary causes have been excluded. Primary genetic causes more frequently encountered include familial hypertriglyceridemia and familial combined hyperlipidemia (which are polygenic with environmental influences), followed by familial dysbetalipoproteinemia (which is usually autosomal recessive, but can be autosomal dominant), and familial chylomicronemia syndrome (which is AR and extremely rare) (11). Genetic screening would be considered if TG levels are ≥ 500 mg/dl or even ≥ 1000 mg/dl, for family risk stratification. 5. What is the clinical significance of hypertriglyceridemia? What is the difference between “risk factors” and “risk enhancing factors?” The consequences associated with hypertriglyceridemia include acute pancreatitis and increased CV risk. As discussed above, the biochemical components that contribute to atherosclerosis formation are remnant lipoproteins that are able to enter the arterial intima and lead to atherogenesis. Because of this, hypertriglyceridemia is considered a “risk enhancing factor,” as it is not a direct causal agent for CV morbidity and mortality. Furthermore, original risk factor studies focused mostly on LDL and HDL and did not include TG. Of note,

Oct 15, 2021

CardioNerds (Amit Goyal and Josh Saef) join ACHD fellow Dr. Prashanth Venkatesh and ACHD program director Dr. Jeannette Lin, both from the University of California, Los Angeles, for a deep dive into the complex disease entity that is Ebstein anomaly. They discuss the anatomic features of the dysplastic tricuspid valve as well as the right ventricle in patients with Ebstein anomaly, and how these structural features affect cardiovascular physiology and clinical presentation. This is followed by an in-depth discussion into associated entities including arrhythmias and atrial-level shunts as well as the appropriate multimodality evaluation. Finally, they tackle the difficult question of when and how to intervene, delving into the various interventional treatments and exploring their outcomes using illustrative case-based examples. Audio editing CardioNerds Academy Intern, Pace Wetstein. The CardioNerds Adult Congenital Heart Disease (ACHD) series provides a comprehensive curriculum to dive deep into the labyrinthine world of congenital heart disease with the aim of empowering every CardioNerd to help improve the lives of people living with congenital heart disease. This series is multi-institutional collaborative project made possible by contributions of stellar fellow leads and expert faculty from several programs, led by series co-chairs, Dr. Josh Saef, Dr. Agnes Koczo, and Dr. Dan Clark. The CardioNerds Adult Congenital Heart Disease Series is developed in collaboration with the Adult Congenital Heart Association, The CHiP Network, and Heart University. See more Claim free CME for enjoying this episode! Disclosures: None Pearls • Notes • References • Guest Profiles • Production Team CardioNerds Adult Congenital Heart Disease PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls Ebstein anomaly is characterized by an inherent myopathy which is often more clinically consequential than the more obvious tricuspid valvulopathy. This can affect not only the right ventricle due to ‘atrialization’ and severe tricuspid regurgitation (TR) but also the left ventricle that is often small due to chronic preload deprivation from reduced RV outflow (no flow, no grow)!Diagnosing severe TR on echocardiography in patients with Ebstein anomaly is challenging, due to the frequent absence of a clearly defined vena contracta and lack of hepatic vein systolic flow reversal. Be on the lookout for severe low gradient TR, which may manifest as a triangular doppler signal rather than the normal parabolic profile.If an electrocardiogram of a patient with Ebstein anomaly suggests prior inferior myocardial infarction, be very suspicious for a right-sided accessory pathway! These are seen in nearly a third of patients with Ebstein anomaly, and manifest as negative delta waves in the inferior leads, leading to a pseudo-infarct pattern. NOTE: infarction, aberrancy, and ventricular hypertrophy should not be coded in the presence of an accessory pathway (i.e., WPW pattern).Patients with Ebstein anomaly who are planned for tricuspid valve replacement should undergo an electrophysiology study preoperatively, since the cavo-tricuspid isthmus responsible for atrial flutter that plagues a large number (>20%) of these patients will be covered by a tricuspid prosthetic valve ring and be inaccessible for future catheter ablation.Certain patients with Ebstein anomaly with significant baseline RV dysfunction who require tricuspid valve surgery may benefit from a concomitant Glenn shunt, which is a surgical anastomosis of the superior vena cava to the right pulmonary artery. This relieves the dysfunctional RV of a third of its baseline preload, potentially enabling it to recover effectively from the stress of cardiopulmonary bypass. Show notes 1. What is Ebstein anomaly and why does it occur? Ebstein anomaly is a rare congenital heart defect of the tricuspid valve (TV) and the myocardium. It occurs in approximately 1 in 200,000 live births.Ebstein anomaly occurs because of defective delamination of the TV. Delamination is the process by which the TV leaflets form from tissue that peels away from the endocardium and myocardium of the right ventricle.Specifically, the septal and posterior leaflets of the TV are inadequately delaminated in Ebstein anomaly. Since they didn’t peel away sufficiently from the myocardium to form the TV at the valve annulus, these leaflets are small, dysplastic and attach significantly more apical to the true tricuspid valve annulus.The anterior TV leaflet is attached to the true TV annulus, but is long, redundant, and floppy, hence often described as ‘sail-like’. It may have fenestrations and can have fibrous attachments to the free wall of the RV. It may also be non-restricted and prolapse into the RV outflow tract, causing outflow obstruction. 2. How is the myocardium affected in Ebstein anomaly and what are the hemodynamic sequelae? Ebstein anomaly is characterized by an inherent ventricular myopathy which often is more clinically important than the tricuspid valve dysfunction.The apically displaced tricuspid valve resulting from inadequate delamination causes the RV to be partitioned into a ‘functional RV’ which is responsible for generating RV outflow and an ‘atrialized RV’ which is a redundant chamber anterior to the true TV annulus but posterior to the septal and posterior leaflets.The atrialized RV is redundant since it does not contribute to RV output, and hence takes out a lot of the RV contractile reserve, especially in cases of severe apical displacement of the TV. In these cases, the functional RV chamber generating the output may be small and can get dysfunctional due to the superimposed severe TR.Also, since the RV output is reduced, the left ventricle (LV) is chronically deprived of preload and is often smaller than normal (remember – no flow, no grow). The LV may also have features of noncompaction cardiomyopathy, further contributing to myocardial dysfunction. 3. What are the major clinical findings in Ebstein anomaly? Look for clubbing, cyanosis, and hypoxemia at rest or on exertion, which may occur due to interatrial shunting.Extra heart sounds are common in Ebstein anomaly, due to flow across the abnormal TV. It has been memorably described as sounding like someone falling down the stairs.A TR murmur may or may not be heard and may be suppressed due to the presence of laminar rather than turbulent flow, through a very wide regurgitant valve orifice.A CV wave, usually seen in patients with acquired severe TR, are usually absent in patients with Ebstein anomaly despite having severe TR, since the severely dilated RA typically absorbs the regurgitant flow and blunts the transmission of pressure into the internal jugular vein during systole.Manifestations of RV failure including ascites, leg edema, and exertional dyspnea are often seen in cases of severe RV dysfunction. 4. What are some of the key echocardiographic features of Ebstein anomaly? The key finding that you need to identify immediately on an apical 4 chamber view is the abnormal apical position of the septal attachment of the TV. NOTE that the tricuspid valve normally attaches more apically than the mitral valve. To meet echocardiographic criteria for Ebstein anomaly, the attachment of the septal leaflet of the TV should be >8mm/m2 (normalized for body surface area) apical from the septal attachment of the anterior mitral valve leaflet.The right atrium is usually severely dilated and comprises both the anatomic right atrium (posterior to the true TV annulus) and the ‘atrialized RV’.Tricuspid regurgitation is seen in essentially all cases of Ebstein anomaly and is commonly severe or torrential. However, this may not be obvious because the malcoaptation of the leaflets is often so severe that a vena contracta may not be seen.Hepatic vein flow reversal in systole from severe TR is usually absent because the extra flow of the TR is absorbed by the severely dilated RA and does not cause high pressure in the hepatic vein.A sharp, triangular profile of the TR jet on continuous wave doppler rather than its usual parabolic form may be the only indication of severe low gradient TR seen in Ebstein anomaly.RV myopathy can lead to interventricular dyssynchrony that can manifest as abnormal motion of the interventricular septum. 5. What conditions are associated with Ebstein anomaly and how are they best diagnosed? Up to 90% of Patients with Ebstein anomaly have an atrial level shunt, which is either an atrial septal defect or patent foramen ovale, best seen on transesophageal echocardiography. Right-to-left interatrial shunting can cause exertional hypoxia that is detected on cardiopulmonary exercise testing. These defects may also predispose to paradoxical emboli.One-third of Patients with Ebstein anomaly have associated Wolff-Parkinson-White syndrome from accessory pathways. Two-thirds of these are right-sided pathways and can be diagnosed on electrocardiography, where they manifest as negative delta waves in the inferior limb leads, often mimicking a Q-wave myocardial infarction. These can be definitively diagnosed with an electrophysiology study.Additional arrhythmias include AV nodal re-entrant tachycardia and focal atrial tachycardia in up to 20% of patients, as well as atrial flutter in approximately 20% of patients.Markedly tall P-waves with amplitude > 2.5 mm are seen in nearly all Ebstein’s patients, due to severe (often massive) right atrial enlargement. The P-waves are classically known as ‘Himalayan’ P-waves due to their markedly peaked morphology. Most Patients with Ebstein anomaly have right bundle branch block on ECG.

Oct 11, 2021

CardioNerds, Amit Goyal and Daniel Ambinder, join Duke University CardioNerds Ambassador and Correspondent, Dr. Kelly Arps for the diuretic showdown of a lifetime. Join us for this Cardiology vs. Nephrology discussion and respective approach to volume overload and diuretic strategies with Dr. Michael Felker (Professor of Medicine with tenure in the Division of Cardiology at Duke University School of Medicine), and Dr. Matt Sparks (Founding member of the Nephrology Social Medial Collective and #NephJC and Associate Professor of Medicine and Program Director for the Nephrology Fellowship Program at Duke University School of Medicine). Episode introduction, audio editing and Approach to Diuretic Resistance infographic by Dr. Gurleen Kaur (Director of the CardioNerds Internship). Volume overload is a common indication for hospitalization in patients with heart failure. Loop diuretics are first line therapy for volume overload in heart failure, with assessment for adequate response within 3-6 hours after administration. Elevation in creatinine is common with venous congestion as well as during decongestion. While other causes of renal injury should be considered, an elevated creatinine in this context should not automatically trigger avoidance or cessation of diuresis. Diuretic resistance is an exaggerated form of natural safety mechanisms in the face of diuresis. Strategies for addressing diuretic resistance include optimizing dose and frequency of loop diuretic administration, adding adjunctive medication for sequential nephron blockade (i.e., thiazide diuretic, potassium sparing diuretic, acetazolamide, tolvaptan, SGLT2 inhibitor), and, in refractory cases, hemodialysis with ultrafiltration. In the outpatient setting, transition to a more potent loop diuretic (i.e., torsemide or bumetanide from furosemide), addition of a mineralocorticoid antagonist, or intermittent dosing of thiazide diuretic may augment maintenance diuretic therapy for patients with diminished response to loop diuretics. Check out the CardioNerds Failure Heart Success Series Page for more heart success episodes and content! Relevant disclosures: None Pearls • Notes • References • Guest Profiles • Production Team CardioNerds Heart Success Series PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! The CardioNerds Heart Success Series is developed in collaboration with the Heart Failure Society of America. The Heart Failure Society of America is a multidisciplinary organization working to improve and expand heart failure care through collaboration, education, research, innovation, and advocacy. Its members include physicians, scientists, nurses, nurse practitioners, and pharmacists. Learn more at hfsa.org. Pearls - Cardiology vs Nephrology: A Diuretic Showdown Elevation in creatinine is expected in both congested states and during diuresis. Do not avoid or stop diuresis in a patient who is clearly volume overloaded based on an elevated creatinine. There may be a role for right heart catheterization if the fluid and/or hemodynamic status is unclear. Alkalosis in the setting of loop diuretic administration and diuretic resistance may represent a natural response to loop diuretics and not volume depletion. Ensure adequate potassium repletion and try using a mineralocorticoid antagonist to correct this alkalosis. Acetazolamide is rarely necessary but may be of use.Currently available evidence does not support extreme fluid or salt restriction in hospitalized patients with volume overload. Consider permissive restrictions and focus on choosing appropriate diuretic dosing for each individual patient. Diuretic resistance is an exaggerated form of diuretic braking, the kidney’s natural response to prevent dangerous degrees of sodium loss from the NKCC2-blocking effects of loop diuretics. Torsemide has improved bioavailability and duration of action compared to furosemide and may be a good choice for outpatient therapy in patients with limited diuretic response. Quotable - Cardiology vs Nephrology: A Diuretic Showdown Permissive hypercreatinemia Eventually the…body recognizes that, Hey, if we're going to live without this very important, cotransporter in KCC2, we're going to have to kick on things in the distal nephron to basically have a steady state. - Dr. Sparks I would rather the patient feel good with a creatinine of 2 than terrible with creatinine of 1 and a half. - Dr. Felker I think it's pretty clear that in the long run, if they're accompanied by effective decongestion, [minor elevations in creatinine] are actually if anything, a favorable prognostic indicator in terms of heart failure, prognosis, as opposed to an adverse one. - Dr. Felker I think we hit a record for that. The most number of times a cardiologist has mentioned urine and measuring something in the urine. - Dr. Sparks I can tell you my experience and it's biased because I take care of people with pretty bad heart failure, but nine times out of 10, if we do a right-heart cath, because we're not sure if the patient is still volume overloaded, they still are. - Dr. Felker The more, when you look at the data, the more high quality, the study design, so randomized versus non-randomized, uh, the worst sodium and fluid restriction look. The one thing we are guaranteed to do though, is create unhappy patients. - Dr. Felker Show notes - Cardiology vs Nephrology: A Diuretic Showdown 1. Approach to diuretic therapy for inpatients with volume overload Evaluate for non-cardiac sources of edema (nephrotic syndrome, hepatic dysfunction, VTE, etc).Choose a starting dose of loop diuretic. The effective home dose is a helpful guide.Evaluate diuretic response within 2-3 hours of each dose. If inadequate response, double the next dose of loop diureticIf inadequate or diminishing response to high-dose loop diuretic, consider additional pharmacotherapies (discussed below) Consider right heart catheterization whenConcerned for low output state Exam is unclear for volume status 2. Initial dose of diuretic therapy for hospitalized patients The kidney alters its compensatory mechanisms to avoid being poisoned by too much blockade of important transporters like NKCC-2 (loop diuretic) and NCC (thiazide diuretics). Start with at least double the patient’s maintenance dose of diuretic Patients on chronic high-dose diuretics need higher initial IV dosesPatients with CKD need higher doses of diuretic 3. Evaluating for adequate response to diuretic in a hospitalized patient 2-3 hours after the dose: Urine output: should be >150 mL / hour in the 2-3 hours after an adequate diuretic dose. Spot urine sodium: should be >50-70 mmol/L after an adequate diuretic dose Daily: assess for improvement in jugular venous distension, lower extremity edema, weight, calculated ratio of fluid intake to output, and symptoms (orthopnea, dyspnea on exertion). 4. Approach to elevated creatinine in a volume overloaded patient Evaluate for alternative causes of hypercreatinemia: urinary obstruction, nephrotoxic agents (i.e. IV contrast, antibiotics, NSAIDs). If exam and/or invasive hemodynamic data are consistent with volume overload, renal vascular congestion may be contributing to elevated creatinine, and is expected to improve with euvolemia. 5. Approach to ‘contraction alkalosis’ in a patient undergoing diuresis Alkalosis in the setting of loop diuretic administration and diuretic resistance may not indicate volume depletion. Diuretics increase delivery of sodium to the distal nephron, which accelerates potassium and proton secretion and results in bicarbonate reclamation, resulting in hypokalemic metabolic alkalosis. Diuresis triggers activation of the renin-angiotensin system, which increases apical ATPase activity, increasing hydrogen ion secretion into the urine. Repleting potassium (with potassium chloride, not potassium citrate) can correct metabolic alkalosis. Use of mineralocorticoid receptor antagonists can improve this metabolic alkalosis.Acetazolamide may be used in refractory cases with severe metabolic alkalosis. 6. Approach to hyponatremia in heart failure Consider reasonable degree of fluid restriction (available evidence does not support extreme fluid restriction. Pharmacotherapy options for extreme hyponatremia includes urea and tolvaptan. 7. Causes of diuretic resistance Processes outside the nephron: venous congestion, low-output heart failure, hypoalbuminemia, increased intraabdominal pressureIntra-renal causes (response to sodium loss, caused by NKCC2 blockade by loop diuretics): reflexive upregulation of sodium intake in the proximal tubule, increased expression of sodium reabsorption channels (e.g., ENAC, NCC, pendrin) 8. Treatment options for diuretic resistance Increase dose +/- frequency of loop diureticThiazide diuretic (and monitor electrolytes closely)Potassium sparing diuretic (i.e., spironolactone, amiloride)Tolvaptan SGLT2 inhibitor (“a diuretic enabler”) Oral loop diuretics FurosemideBumetanideTorsemidePO: IV conversion~2:11:11:1Dose ratio (to furosemide)---1:401:2Bioavailability in oral dosingWidely variableNearly 100%Nearly 100% References - Cardiology vs Nephrology: A Diuretic Showdown Reviews Ellison DH, Felker GM. Diuretic Treatment in Heart Failure [published correction appears in N Engl J Med. 2018 Feb 1;378(5):492]. N Engl J Med. 2017;377(20):1964-1975. doi:10.1056/NEJMra1703100 Felker GM, Ellison DH, Mullens W, Cox ZL, Testani JM. Diuretic Therapy for Patients With Heart Failure: JACC State-of-the-Art Review. J Am Coll Cardiol. 2020;75(10):1178-1195. doi:10.1016/j.jacc.2019.12.059 Trials 3T trial: Cox ZL, Hung R, Lenihan DJ, Testani JM.

Oct 8, 2021

CardioNerds (Amit Goyal and Daniel Ambinder), join Dr. Anjali Wagle (Internal medicine resident, Johns Hopkins Hospital) and Dr. Nick Smith (Cardiology fellow, Johns Hopkins Hospital) for an important discussion involving a patient with non-ischemic dilated cardiomyopathy and biventricular heart failure who had developed diuretic resistance. They discuss the role for invasive hemodynamic assessment of volume overload, initial strategies in managing a patient with volume overload, the role of guideline directed therapy in the management of patients with recurrent volume overload, and advanced strategies for diuretic resistance. Dr. Nisha Gilotra (Director of the Cardiac Sarcoidosis Program and assistant professor of medicine, Johns Hopkins Hospital) provides the E-CPR for this episode. Audio editing and Approach to Diuretic Resistance infographic by Dr. Gurleen Kaur (Director of the CardioNerds Internship). This episode is made possible with support from Panacea Financial. Panacea Financial is a national digital bank built for doctors by doctors. Visit panaceafinancial.com today to open your free account and join the growing community of physicians nationwide who expect more from their bank. Panacea Financial is a division of Primis, member FDIC. Claim free CME just for enjoying this episode! Disclosures: NoneJump to: Patient summary - Case teaching - References CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Patient Summary - Diuretic Resistance A young woman in her 20s with non-ischemic dilated cardiomyopathy and NYHA class IV ACC stage D biventricular heart failure with an LV ejection fraction of 30-35% on palliative inotropic therapy complicated by cardiogenic cirrhosis and stage IIIb chronic kidney disease presented with acute decompensated heart failure with volume overload. During her hospitalization she exhibited profound signs of diuretic resistance with minimal improvement after increasing inotropes, increasing IV loop diuretics, adding IV thiazides, and trialing continuous IV furosemide. She was given high dose mineralocorticoids, IV acetazolamide, and hypertonic saline paired with IV furosemide and had a durable treatment response. Episode Teaching - Diuretic Resistance Pearls - Diuretic Resistance Diuretic resistance is a complex clinical problem defined as inadequate natriuresis despite an adequate diuretic regimen. However, the practitioner cannot overlook low output heart failure and/or insufficient renal perfusion as the causes for inadequate diuretic response. In cases of inadequate urine output due to low cardiac output, increased inotropic or mechanical support would be the first objective.Confirming adequate cardiac output to support renal perfusion and/or confirming high filling pressures may require invasive hemodynamic assessment.Sodium avidity is most effectively blunted by treating the patient with maximally tolerated guideline directed therapy. This includes but is not limited to a backbone of ARNI (or ACE or ARB), mineralocorticoid receptor antagonists, beta-blockers, and SGLT-2 inhibitors.In cases of advanced diuretic resistance, hypertonic saline paired with high dose IV furosemide can be an effective strategy.In cases of diuretic resistance combined with cirrhosis and heart failure there is a synergistic hyperaldosteronism that can be targeted with higher doses of mineralocorticoid receptors as is seen in the treatment of cirrhosis with ascites. Notes - Diuretic Resistance 1. What is the role for invasive hemodynamic assessment in acute decompensated heart failure? Cases where intracardiac filling pressures are in question: right heart catheterization (RHC) can give insight into the presence and degree of right versus left sided filling pressures. We discussed the concepts of “RV equalizer” vs “RV compensated” groups in Episode 142 with Dr. Mark Drazner.Cases where cardiac output is in question, especially to guide vasoactive infusions during low flow states: RHC can assess cardiac output and cardiac power output.Cases with rising creatinine during diuresis despite a clinical exam suggesting volume overload.Cases where body habitus prevents optimal evaluation. 2. What are the initial strategies in managing a patient with volume overload? Initial furosemide dosing: The patient’s home dose, renal function, and reason for decompensation all help decide the initial IV diuretic dosing. However, in general if a patient has an outpatient furosemide regimen, the initial diuretic dose should 2.5 times the oral dosing for intermittent IV doses. For example, if a patient is taking 40 mg PO daily as an outpatient, a starting dose of 100 mg IV as a starting dose is appropriate.Furosemide escalationIV dosing: constantly assess the appropriateness of each furosemide dose by monitoring hourly urine output and daily standing weight changes. Post-dose urine sodium is another option. If the patient has not made 300 cc/hr after their last furosemide dose, you may need to escalate the dose. Due to the furosemide threshold effect, the patient may need to double the prior dose for every uptitration. Additionally, even though furosemide lasts for 6 hours, if the diuretic effect is minimal, immediately prescribe double the last dose of furosemide.Continuous infusion vs bolus: The DOSE trial, or Diuretic Optimization Strategies Evaluation, randomized 308 patients to either IV furosemide q12 or an equivalent dose as a continuous infusion and found no difference in secondary endpoints of change in weight or net fluid loses. There may be a role for continuous infusion furosemide in patients who are sensitive to large fluid shifts, such as patients with right heart failure.Adjunctive diureticsThiazide diuretics: when high dose IV furosemide is failing, thiazide diuretics are commonly the first adjunct use. When given in combination with loop diuretics, they allow blockade of both the sodium-potassium-chloride channels in the loop as well as the sodium chloride channels distally to allow increased blockade of the ability to reabsorb sodium and potassium.Potassium sparing diuretics: the addition of potassium-sparing diuretics (i.e., mineralocorticoid receptor antagonists or ENaC inhibitors like amiloride or triamterene) may be especially helpful for hypokalemia caused by loop +/- thiazide diuretics.Acetazolamide: is a carbonic anhydrase inhibitor and acts in the proximal convoluted tubule. It aids in the excretion of sodium and bicarbonate. It is commonly, but not always, used in situations where serum bicarbonates become elevated. 3. What is the role of guideline directed therapy in the management of patients with recurrent volume overload? In short, maximally tolerated guideline directed therapy blunts sodium retention through multiple mechanisms, but none more so than blockers of the renin-angiotensin-aldosterone-system. By blocking aspects of this pathway, the kidneys’ propensity to reabsorb sodium is blunted upstream of the nephron, preventing some of the need for high dose diuretics. Individual GDMT therapies and some of their effects on diuretic dosing are explained below.ARNI (angiotensin receptor neprilysin inhibitor): post-hoc analysis of the PARADIGM trial demonstrated that patients were more likely to decrease diuretic dosing on ARNI compared to placebo. Other single center studies have demonstrated similar effects, finding that loop diuretic dosing decrease was achieved in 1/3 of patients with a mean reduction of 10±38 mg furosemide equivalent across the entire population. Conversely, be cautious of diuretic dosing when initiating a patient on an ARNI agent. Enjoy Episode 148 with Dr. Milton Packer discussing the history of ARNI!MRA: Post-hoc analysis of EPHESUS demonstrated that the mineralocorticoid receptor antagonist Eplerenone led to a mean furosemide equivalent dose reduction of −2.2 mg/day (−2.9 to −1.6) throughout the follow-upMADIT-CRT: A post-hoc analysis of the MADIT-CRT trial showed that CRT implant led to diuretic cessation in 9.7% of patients. In a subsequent retrospective study of 352 subjects on baseline diuretics, 36% of patients tolerated a down-titration of loop diuretic dose following CRT-implant. These effects appeared sustained and were associated with both an improved hemodynamic performance and decreased probability of HF or death.SGLT-2 inhibitors: SGLT-2 inhibitors have a modest diuretic effect through glycosuria. Post-hoc analysis of the DAPA-HF trial did not show reduction in diuretic requirements over the 18-month trial, however SGLT-2 inhibitors have been shown to lead to reduction in diuretic requirements when used in combination when used in combination with MRA, BB, and ARNI therapy as part of a GDMT regimen. 4. What are some advanced strategies for diuretic resistance? Dopamine: The ROPA-DOP trial was a small single center trial performed in hospitalized patients with acute decompensated heart failure with preserved ejection fraction. It showed that continuous low dose dopamine infusion had no significant impact on renal function or decongestion.High Dose Spironolactone: Post-hoc analyses of trials involving spironolactone have not demonstrated reductions in diuretic dosing. However, in patients with a combination of cirrhosis and heart failure the hyperaldosteronism that results can be profound. For these patients, natriuretic doses of aldosterone antagonists (spironolactone >50 mg/day) may be a potential option and have been studied in small proof-of-principle studies. The competitive natriuretic response of aldosterone antagonists is related to activity of the renin-angiotensin-aldosterone system: the higher the renin-angiotensin-aldosterone system activity,

Oct 4, 2021

CardioNerds (Amit Goyal and Daniel Ambinder), Cardio-OB series co-chair and University of Texas Southwestern Cardiology Fellow, Dr. Sonia Shah, episode lead fellow, Dr. Kaitlyn Ibrahim (Temple University now practicing with Lankenau Heart Group), join Dr. Afshan Hameed (Maternal-Fetal Medicine, Obstetrics & Gynecology, UC Irvine), Dr. Paul Forfia (Co-Director, Pulmonary Hypertension, Right Heart Failure & CTEPH Program, Temple University Hospital), and Dr. Marie-Louise Meng (Obstetric and Cardiothoracic Anesthesiology, Duke University) to discuss pregnancy and multidisciplinary critical care. Three experts from varied subspecialties including Cardiology, Pulmonary Hypertension, Maternal Fetal Medicine, Cardiac Anesthesia and Obstetrical Anesthesia guide listeners through a case of a patient with a congenital conotruncal ventricular septal defect, Eisenmenger physiology, and pulmonary hypertension who becomes pregnant. The discussion touches on pre-conception risk assessment, pulmonary hypertension medical therapy in pregnancy, maternal monitoring during pregnancy, development of detailed multidisciplinary delivery plans and accessibility of such plans, and peri- and post-partum multidisciplinary management of high-risk patients. Audio editing and episode introduction by CardioNerds Academy Intern, Christian Faaborg-Andersen. Pearls • Notes • References • Guest Profiles • Production Team CardioNerds Cardio-Obstetrics Series PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls Cyanotic congenital heart disease presents multiple risks to the fetus, the most significant being intrauterine growth restriction. In a patient with Eisenmenger physiology, maternal oxygenation should be monitored closely throughout pregnancy, as hypoxia is often a marker of increased right to left shunting in these patients.In patients with pulmonary hypertension, the RV-PA coupling relationship is the best indicator of maternal cardiovascular reserve through the pregnancy and post-partum period. The goal of therapy is to get the pulmonary vascular resistance down to a point where the right heart can adapt to that load and function either at a normal or a near-normal level.When a high-risk patient meets with Anesthesia, it is important to consider the A’s: 1. Airway (anticipating any potential difficulties); 2. Access (whether this may present a challenge at the time of delivery); 3. Anxiety (specifically differentiating true hemodynamic changes in high-risk patients versus physiologic changes from anxiety); 4. Anticoagulation (knowledge of what agent the patient is on to determine safety of neuraxial anesthesia); 5. Availability (determining who else needs to be in the room, i.e. CT surgery, cardiothoracic anesthesia, ECMO team); 6. Arena (where is the safest place for this patient to deliver).In patients with a shunt who undergo a Cesarean section, the uterus should not be exteriorized due to risk of venous micro air emboli.As Dr. Forfia says, “panic is more dangerous sometimes than pulmonary hypertension!” Meaning, it is important to meet as a multidisciplinary team to develop a clear, easily accessible delivery plan for the patient. It is also prudent to have “everyone functioning in the environment they function best” like delivering the baby on the labor and delivery floor where all the necessary equipment and team members are available and bringing in other experts if needed rather than a cardiac operating room. For a deep dive into Pregnancy & Pulmonary Hypertension, enjoy: Episode #124 with Dr. Candice Silversides.Episode #144 – Case Report: A Mother with Shortness of Breath Show notes 1. How does a multidisciplinary team play a role in the care for a high risk cardio-obstetrics patient, particularly one with congenital heart disease and pulmonary hypertension? According to the 2018 ESC guidelines, a multidisciplinary team is required to care for the pregnant patient with PH. This should include a PH expert at an experienced center for pregnancy and cardiac disease. Maternal outcomes in patients with PH have improved with targeted therapies as well as a multidisciplinary, team-based approach.A multidisciplinary team for a high-risk cardio-obstetrics patient should have representation from several subspecialties, typically including Cardiology (and in patients with PH, a PH expert should be included), Maternal Fetal Medicine, and Anesthesiology. Additional subspecialities can be added depending on the underlying diagnosis of the patient and any potential challenges anticipated at the time of delivery. (i.e. CT Surgery if ECMO may be needed).The key is consistent membership within the group for optimal team dynamics, working relationships, and continuity of patient care. Familiarity among group members helps to facilitate improved communication.Team members should be experienced in the care of high-risk cardio-obstetrics patients. As Dr. Forfia mentions during the podcast, panic can be the downfall of a well-functioning team in a high stake setting and is often dangerous to the patient.Frequent meetings should happen amongst group members to discuss patients and to form individualized, multidisciplinary delivery plans. The delivery plan should detail each aspect of labor and delivery, include the names and contact information of providers involved in the patient’s care, and should be easily accessible (ideally in a prominent location in the patient’s electronic medical record).If possible, providers should be allowed to work in their usual environment. For example, a high-risk patient should deliver on the L&D floor/L&D OR with OB/MFM and other members of the multidisciplinary team should come to that area. This ensures all necessary equipment and experienced staff will be present during the delivery. 2. What are the important considerations during the Anesthesia evaluation of a high-risk pregnant patient? When a high-risk patient meets with Anesthesia during pregnancy, the A’s should be considered, listed below:Airway: It is important to perform an assessment of the patient’s airway prior to delivery to anticipate any potential difficulties and to ensure that the appropriate equipment is available at the time of delivery if a difficult airway is anticipated.Access: Potential intravenous access sites should be assessed prior to delivery to determine whether access may present a challenge at the time of delivery.Anxiety: An Anesthesiologist for a high-risk patient should be adept at differentiating true hemodynamic alterations versus physiologic changes from anxiety to provide appropriate therapy and counseling.Anticoagulation: A subset of high-risk cardiac patients will be on chronic anticoagulation therapy during pregnancy. Knowledge of a patient’s anticoagulant is critical in determining the safety of neuraxial anesthesia. It is also important to highlight that Eisenmenger’s can lead to thrombocytopenia, which (if severe enough) can be a contraindication to neuraxial anesthesia.Availability: It is vital to determine who will need to be available for a high-risk patient’s delivery, particularly which specialists, but also which subspecialists (i.e. cardiac anesthesia, cardiologists with expertise in pulmonary hypertension, ECMO team etc.). This allows adequate planning and staffing at the time of delivery.Arena: The multidisciplinary team should discuss the best place for the patient to deliver (i.e. the L&D floor, L&D OR, cardiac OR) depending on the expected course of delivery. Often, it is best to have the patient delivery on a dedicated obstetrical floor and bring any necessary consultants there to ensure all necessary equipment for the delivery and experienced obstetrical staff are present. 3. What are some pearls for the multidisciplinary management of high-risk cardio-obstetrics patients and specifically those with pulmonary hypertension and a shunt lesion during delivery? As mentioned previously, a detailed delivery plan should be created in advance of delivery with input from the multidisciplinary team caring for the patient. This should be easily accessible by all team members at the time of delivery.Most of these patients should deliver by 37 weeks gestation at a center with cardiology and intensive care unit support if needed.Patients with pulmonary hypertension should avoid Valsalva/pushing as much as possible. This is accomplished by an assisted second stage of labor.Patients with uncorrected cyanotic congenital heart disease should be considered for antibiotic prophylaxis for endocarditis at the time of delivery.In patients with an intracardiac shunt, all intravenous lines should have filters to prevent paradoxical air embolism. Additionally, the OB team should avoid “exteriorizing” the uterus during a C-section due to risk of paradoxical air embolism. This is particularly important in right-to-left shunt lesions.Fetal heart rate can serve as the “5th vital sign” of the mother during the time of delivery and can add to the overall assessment of the mother and fetus.Specialized Anesthesia care may involve the insertion of a central line and/or arterial line for close hemodynamic monitoring during delivery and in the immediate post-partum period. 4. What are the interdisciplinary critical care considerations in the post-partum period for high-risk patients, and specifically those with pulmonary hypertension and shunt lesions? According to the 2018 ESC guidelines, the highest risk period is during puerperium and early post-partum where fluid shifts and hemodynamic changes are the greatest. As part of the delivery plan, immediate post-partum care should also be specified.

Sep 30, 2021

CardioNerds (Amit Goyal, Daniel Ambinder) and Dr. Mark Belkin, (CardioNerds Correspondent) and Dr. Shirlene Obuobi (CardioNerds Ambassador) from University of Chicago are honored to bring to you the Dr. Milton Packer perspective on the evolution of the neurohormonal hypothesis as part of The CardioNerds Heart Success Series. In part 6 Dr. Packer reflects on a conversation he had with Dr. Eugene Braunwald about mentorship and its role in immortality. This episode is particularly meaningful to the CardioNerds team as mentorship and sponsorship is such an important part of the CardioNerds mission. Check out the CardioNerds Heart Failure Success Series Page for more heart success episodes and content! This is a non CME episode. Disclosures: Milton Packer reports receiving consulting fees from Abbvie, Actavis, Amgen, Amarin, AstraZeneca, Boehringer Ingelheim, Bristol Myers Squibb, Casana, CSL Behring, Cytokinetics, Johnson & Johnson Health Care Systems Inc., Eli Lilly and Company, Moderna, Novartis, ParatusRx, Pfizer, Relypsa, Salamandra, Synthetic Biologics, Teva Pharmaceuticals USA Inc. and Theravance Biopharma Inc. CardioNerds Heart Failure Success Series PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! This CardioNerds Heart Failure Success Series was created in memory of Dr. David Taylor. We thank our partners at the Heart Failure Society of America which is a multidisciplinary organization working to improve and expand heart failure care through collaboration, education, research, innovation, and advocacy. Its members include physicians, scientists, nurses, nurse practitioners, and pharmacists. Learn more at hfsa.org.

Sep 27, 2021

CardioNerds (Amit Goyal, Daniel Ambinder) and Dr. Mark Belkin, (CardioNerds Correspondent) and Dr. Shirlene Obuobi (CardioNerds Ambassador) from University of Chicago are honored to bring to you the Dr. Milton Packer perspective on the evolution of the neurohormonal hypothesis as part of The CardioNerds Heart Success Series. In part 5, Dr. Packer shares his thoughts on the term “guideline directed medical therapy,” guidelines in general, and the challenges of using the ejection fraction to measure systolic function. Check out the CardioNerds Heart Failure Success Series Page for more heart success episodes and content! This is a non CME episode. Disclosures: Milton Packer reports receiving consulting fees from Abbvie, Actavis, Amgen, Amarin, AstraZeneca, Boehringer Ingelheim, Bristol Myers Squibb, Casana, CSL Behring, Cytokinetics, Johnson & Johnson Health Care Systems Inc., Eli Lilly and Company, Moderna, Novartis, ParatusRx, Pfizer, Relypsa, Salamandra, Synthetic Biologics, Teva Pharmaceuticals USA Inc. and Theravance Biopharma Inc. CardioNerds Heart Failure Success Series PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! This CardioNerds Heart Failure Success Series was created in memory of Dr. David Taylor. We thank our partners at the Heart Failure Society of America which is a multidisciplinary organization working to improve and expand heart failure care through collaboration, education, research, innovation, and advocacy. Its members include physicians, scientists, nurses, nurse practitioners, and pharmacists. Learn more at hfsa.org.

Sep 27, 2021

CardioNerds (Amit Goyal, Daniel Ambinder) and Dr. Mark Belkin, (CardioNerds Correspondent) and Dr. Shirlene Obuobi (CardioNerds Ambassador) from University of Chicago are honored to bring to you the Dr. Milton Packer perspective on the evolution of the neurohormonal hypothesis as part of The CardioNerds Heart Success Series. In part 4, Dr. Packer shares his perspective on the revolutionary SGLT2 inhibors. We discuss the mechanisms of action and the data regarding their role in the care of heart failure patients. This episode is particularly historic in that Dr. Packer shares his thoughts about the EMPEROR-PRESERVED trial well before the data was available. Also see Dr. Mark Belkin's DocWire News article EMPEROR’s New Groove? Empagliflozin Provides Long-Awaited Treatment for HFpEF where Dr. Packer is quoted as saying “we are pleased to have the first trial in patients with HFpEF that shows an unequivocally positive and clinically important result. We are looking forward to many secondary papers that will provide detailed information about what we have found, and what it means for patients.” Check out the CardioNerds Heart Failure Success Series Page for more heart success episodes and content! This is a non CME episode. Disclosures: Milton Packer reports receiving consulting fees from Abbvie, Actavis, Amgen, Amarin, AstraZeneca, Boehringer Ingelheim, Bristol Myers Squibb, Casana, CSL Behring, Cytokinetics, Johnson & Johnson Health Care Systems Inc., Eli Lilly and Company, Moderna, Novartis, ParatusRx, Pfizer, Relypsa, Salamandra, Synthetic Biologics, Teva Pharmaceuticals USA Inc. and Theravance Biopharma Inc. CardioNerds Heart Failure Success Series PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! This CardioNerds Heart Failure Success Series was created in memory of Dr. David Taylor. We thank our partners at the Heart Failure Society of America which is a multidisciplinary organization working to improve and expand heart failure care through collaboration, education, research, innovation, and advocacy. Its members include physicians, scientists, nurses, nurse practitioners, and pharmacists. Learn more at hfsa.org.

Sep 20, 2021

CardioNerds (Amit Goyal, Daniel Ambinder) and Dr. Mark Belkin, (CardioNerds Correspondent) and Dr. Shirlene Obuobi (CardioNerds Ambassador) from University of Chicago are honored to bring to you the Dr. Milton Packer perspective on the evolution of the neurohormonal hypothesis as part of The CardioNerds Heart Success Series. In part 3 Dr. Packer reflects on the value of neutral trials and recounts the journey that led to the PARADIGM Trial Check out the CardioNerds Heart Failure Success Series Page for more heart success episodes and content! This is a non CME episode. Disclosures: Milton Packer reports receiving consulting fees from Abbvie, Actavis, Amgen, Amarin, AstraZeneca, Boehringer Ingelheim, Bristol Myers Squibb, Casana, CSL Behring, Cytokinetics, Johnson & Johnson Health Care Systems Inc., Eli Lilly and Company, Moderna, Novartis, ParatusRx, Pfizer, Relypsa, Salamandra, Synthetic Biologics, Teva Pharmaceuticals USA Inc. and Theravance Biopharma Inc. CardioNerds Heart Failure Success Series PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! This CardioNerds Heart Failure Success Series was created in memory of Dr. David Taylor. We thank our partners at the Heart Failure Society of America which is a multidisciplinary organization working to improve and expand heart failure care through collaboration, education, research, innovation, and advocacy. Its members include physicians, scientists, nurses, nurse practitioners, and pharmacists. Learn more at hfsa.org.

Sep 20, 2021

CardioNerds (Amit Goyal, Daniel Ambinder) and Dr. Mark Belkin, (CardioNerds Correspondent) and Dr. Shirlene Obuobi (CardioNerds Ambassador) from University of Chicago are honored to bring to you the Dr. Milton Packer perspective on the evolution of the neurohormonal hypothesis as part of The CardioNerds Heart Success Series. In part 2 Dr. Packer shares his journey as the trailing spouse and tells the story of how the neurohormonal hypothesis was developed. Check out the CardioNerds Heart Failure Success Series Page for more heart success episodes and content! This is a non CME episode. Disclosures: Milton Packer reports receiving consulting fees from Abbvie, Actavis, Amgen, Amarin, AstraZeneca, Boehringer Ingelheim, Bristol Myers Squibb, Casana, CSL Behring, Cytokinetics, Johnson & Johnson Health Care Systems Inc., Eli Lilly and Company, Moderna, Novartis, ParatusRx, Pfizer, Relypsa, Salamandra, Synthetic Biologics, Teva Pharmaceuticals USA Inc. and Theravance Biopharma Inc. CardioNerds Heart Failure Success Series PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! This CardioNerds Heart Failure Success Series was created in memory of Dr. David Taylor. We thank our partners at the Heart Failure Society of America which is a multidisciplinary organization working to improve and expand heart failure care through collaboration, education, research, innovation, and advocacy. Its members include physicians, scientists, nurses, nurse practitioners, and pharmacists. Learn more at hfsa.org.

Sep 19, 2021

CardioNerds (Amit Goyal, Daniel Ambinder) and Dr. Mark Belkin, (CardioNerds Correspondent) and Dr. Shirlene Obuobi (CardioNerds Ambassador) from University of Chicago are honored to bring to you the Dr. Milton Packer perspective on the evolution of the neurohormonal hypothesis as part of The CardioNerds Heart Success Series. In part 1 Dr. Packer discusses taking risks, upsetting people and the ridiculousness of humanity and how stand-up comedy helped contribute and shape his career in cardiovascular medicine. Dr. Packer also discusses how the study of afterload agents in heart failure and the discovery of tachyphylaxis with prazosin helped inspire a long and prosperous career in academic cardiology by changing the status quo. Check out the CardioNerds Heart Failure Success Series Page for more heart success episodes and content! This is a non CME episode. Disclosures: Milton Packer reports receiving consulting fees from Abbvie, Actavis, Amgen, Amarin, AstraZeneca, Boehringer Ingelheim, Bristol Myers Squibb, Casana, CSL Behring, Cytokinetics, Johnson & Johnson Health Care Systems Inc., Eli Lilly and Company, Moderna, Novartis, ParatusRx, Pfizer, Relypsa, Salamandra, Synthetic Biologics, Teva Pharmaceuticals USA Inc. and Theravance Biopharma Inc. CardioNerds Heart Failure Success Series PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! This CardioNerds Heart Failure Success Series was created in memory of Dr. David Taylor. We thank our partners at the Heart Failure Society of America which is a multidisciplinary organization working to improve and expand heart failure care through collaboration, education, research, innovation, and advocacy. Its members include physicians, scientists, nurses, nurse practitioners, and pharmacists. Learn more at hfsa.org.

Sep 14, 2021

CardioNerds (Amit Goyal and Daniel Ambinder), ACHD series co-chair Dr. Agnes Koczo (UPMC), and ACHD FIT lead Dr. Katia Bravo (UCLA) join ACHD expert Dr. Carole Warnes (Professor of Medicine and founder of the Adult Congenital Heart Disease Clinic at Mayo Clinic), to discuss adult congenial heart disease and pregnancy. They cover preconception counseling in women with congenital heart disease, appropriate risk stratification to estimate maternal and neonatal morbidity using existing tools and an individualized care approach and preparation for a multidisciplinary delivery plan. Audio editing by CardioNerds Academy Intern, Dr. Leticia Helms. The CardioNerds Adult Congenital Heart Disease (ACHD) series provides a comprehensive curriculum to dive deep into the labyrinthine world of congenital heart disease with the aim of empowering every CardioNerd to help improve the lives of people living with congenital heart disease. This series is multi-institutional collaborative project made possible by contributions of stellar fellow leads and expert faculty from several programs, led by series co-chairs, Dr. Josh Saef, Dr. Agnes Koczo, and Dr. Dan Clark. The CardioNerds Adult Congenital Heart Disease Series is developed in collaboration with the Adult Congenital Heart Association, The CHiP Network, and Heart University. See more Claim free CME for enjoying this episode! Disclosures: None Pearls • Notes • References • Guest Profiles • Production Team CardioNerds Adult Congenital Heart Disease PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls Women with congenital heart disease can safely carry a pregnancy if appropriate risk stratification and management is performed by an expert multidisciplinary cardio-obstetrics team.There are a myriad of hemodynamic and vascular changes which impact congenital cardiac physiology and evolve throughout the different stages of pregnancy. Therefore, planning is key. An evaluation of heart rate response to exercise and optimization of potential factors that could worsen during pregnancy, such as arrhythmias, are recommended.Maternal morbidity & mortality risk-stratification systems such as the modified WHO, CARPREG or ZAHARA criteria are helpful starting points. Ultimately, each patient requires individualization given the heterogeneity that exists among congenital heart defects.Vaginal delivery is generally preferred over C-section from a cardiac standpoint. An assisted second stage of labor during the period of greatest hemodynamics changes should also be considered if vaginal delivery is pursued. Show notes Pregnancy and Adult Congential Heart Disease: Created by Dr. Katia Bravo and Dr. Teodora Donisan and reviewed by Dr. Candice Silversides 1. Why is preconception counseling important in women with congenital heart disease and what does it entail? Ensuring women with congenital heart disease are optimized prior to conception decreases maternal and neonatal complications. For this reason, preconception counseling is paramount for these patients.In addition, counseling leads to patients making more informed decisions about family planning.The integral parts of preconception counseling include: (1) discussing the current anatomical and physiological status, (2) discussing possible complications during pregnancy specific to the patient's congenital heart defect (with genetic counseling referral if appropriate), (3) evaluating cardiac medications, taking into account benefits vs teratogenic potential, (4) discussing and planning for necessary pre-pregnancy tests or interventions (exercise stress testing is an important tool in evaluating how the patient will tolerate the stressors of pregnancy), (5) organizing antepartum care with high-risk obstetrics teams, (6) discussing location, timing and mode of delivery, (7) discussing alternative options to carrying a pregnancy in women who are at extreme risk (ie Fontan physiology, Eisenmenger syndrome) and (8) discussing postpartum contraception. 2. How do we risk stratify women with congenital heart disease who are contemplating pregnancy? An expert evaluation by an ACHD specialist is recommended using a thorough clinical and hemodynamic assessment centered around the individual patient and her values. Several risk prediction tools are available and should be used as a starting point. These include the modified World Health Organization (mWHO) classification, risk factors derived from CARPREG II (CARdiac disease in PREGnancy II), and ZAHARA (acronym based on Dutch translation for Pregnancy in congenital heart defects - Zwangerschap bij Aangeboren HARtAfwijkingen I) studies. The mWHO classification groups congenital hearts conditions into class I to IV, with higher classes indicating higher predicted risk of cardiovascular maternal morbidity and mortality.The CARPREG II risk prediction index assigns points based on a number of different predictors including prior cardiac events or arrhythmias, baseline New York Heart Association Class III-IV or cyanosis, presence of a mechanical valve, ventricular dysfunction, high risk left-sided valve disease or left ventricular outflow tract obstruction, pulmonary hypertension, and coronary artery disease or high-risk aortopathies.The ZAHARA risk score also considers sub-pulmonary atrioventricular valve regurgitation and cardiac medications before pregnancy as additional risk factors as well. 3. What are the potential fetal/neonatal risks associated with pregnancy in congenital heart conditions? Some of the risks include spontaneous abortion, premature birth, small for gestational age neonate, and congenital heart disease in the baby (which may be different than maternal CHD (see Table 1). Most of these are related to maternal heart failure; however other complications such as arrhythmias, endocarditis, thromboembolic events, and medication adverse effects predispose to neonatal complications. Specifically, women with uncorrected cyanotic heart disease and pulmonary hypertension with saturation levels ≤ 85% reach a live birth rate of only 12%. Table 1. Recurrence rate for congenital heart lesions in affected mothers. LesionRecurrence rateAtrial septal defect4-6%Ventricular septal defect6-10%Atrioventricular septal defect11.5-14%Coarctation of the aorta4-6.5%Left ventricular outflow tract obstruction8-18%Right ventricular outflow tract obstruction4-6.5%Tetralogy of Fallot2-2.5%Transposition of the great arteries2%Congenitally corrected transposition of the great arteries3-5%Univentricular hearts21% What should a multidisciplinary delivery plan include? Detailed delivery planning should be undertaken prior to expected delivery date to plan for obstetric anesthesia and analgesia, inpatient peripartum management (level of acuity, need for bubble filters in cases of shunts, avoidance of excessive volume load, infective endocarditis prophylaxis, mode of delivery), as well as postpartum care and discharge planning including post-partum contraception. Maternal and Neonatal Risk by Congenital Lesion AnatomyMaternal RiskFetal/ Neonatal riskPoints to considerRight ventricular outflow tract obstruction or regurgitation- Increased pregnancy-induced preload can promote RV dilatation and heart failure- Preterm labor - Small for gestational ageUsually well tolerated during pregnancyLeft-sided obstructive lesions- Heart failure in patients with severe symptomatic AS with volume expansion in pregnancy - Small for gestational ageBalloon valvuloplasty in severe, symptomatic casesSystemic right ventricle- Heart failure - Atrial arrhythmias - Worsening systemic tricuspid regurgitation- 25-50% prematurity - Small for gestational ageSystemic RV function may be impacted by repeat pregnanciesCoarctation of the aorta- Hypertensive disorders of pregnancy - Heart failure- Small for gestational age- Hormonal changes may impact aortic vasculature into the postpartum periodEbstein’s anomaly- Cyanosis - Arrhythmias can be triggered by increased preload - Related to maternal oxygen saturation- Use bubble filters to avoid paradoxical emboli (high coexistence of ASD)Fontan circulation- Atrial arrhythmias can be triggered by increased preload - Thromboembolism due to hormonal changes - Discuss termination of pregnancy in failing Fontan - 40-70% prematurity - Small for gestational ageBaseline oxygen saturation is the most important marker for fetal outcomes.Eisenmenger syndrome Also see Episode #124 – Pregnancy & Pulmonary Hypertension with Dr. Candice Silversides - Mortality 20-40%. - Discuss termination of pregnancy-Right ventricular failure from increased preload -Thromboembolism due to hormonal changesAortopathy Also see Episode #126 – Pregnancy & Aortic Disorders with Dr. Nupoor Narula- Hormonal changes impact aortic vasculature and can led to accelerated aortic enlargement - 10% risk aortic dissection risk (usually third trimester or postpartum) in Marfan syndrome with root diameter >40 mm, rapid dilation or previous dissection of the ascending aorta- 15% premature delivery due to premature rupture of membranes. - In cases of dissection, fetal demise can occur.Prophylactic aortic root replacement considered before pregnancy if diameter >40 mm, or smaller with rapid increase in dimensions, family history of dissection, or concomitant severe AI References Stout KK, Daniels CJ, Aboulhosn JA, et al. 2018 AHA/ACC Guideline for the Management of Adults With Congenital Heart Disease: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines. Circulation. Apr 2 2019;139(14):e698-e800. https://www.ahajournals.org/doi/10.1161/CIR.0000000000000603European Society of G, Association for European Paediatric C, German Society for Gender M,

Sep 5, 2021

CardioNerds (Amit Goyal and Daniel Ambinder) join Dr. Kushani Gajjar and Dr. Mitha Naik from the Allegheny Health Network for a walk along the Three Rivers Trail in Pittsburgh. They discuss a case of young woman in her third trimester of pregnancy with a known history of pulmonary arterial hypertension. The management of pulmonary hypertension in pregnancy and RV failure in the context of pregnancy is described. The E-CPR segment is provided by Dr. Nandita Scott, Co-Director Corrigan Women's Heart Health Program and Cardiovascular Disease and Pregnancy Service at Massachusetts General Hospital. Special cameo appearance by Dr. Dani Crousillat. If you’re a current internal medicine resident, interested in the intersection between medical education, cardiovascular disease and digital media, consider applying to the CardioNerds Academy using this link. The deadline for this application is October 15th 2021. Learn more by visiting the CardioNerds Academy page. Claim free CME just for enjoying this episode! Disclosures: None Jump to: Patient summary - Case media - Case teaching - References CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Patient Summary - Pulmonary Hypertension in Pregnancy A 33-year-old woman in the third trimester of pregnancy, with a known history of untreated PAH in the setting of TKI therapy, presents with shortness of breath. She is found to have PA pressure greater than systemic pressure with PASP >130. We describe the management of PH and RV failure in the context of a pregnancy. The patient was admitted to the ICU where a multidisciplinary team was mobilized, involving high risk ob-gyn, maternal fetal medicine, critical care, anesthesiology, and advanced heart failure. They began pulmonary vasodilators including treprostinil, tadalafil and inhaled nitric oxide. They also added inotropic and vasopressor support for right ventricular dysfunction with her severe PAH. Fetal heart monitoring was performed. PAH also led to worsening of known chronic thrombocytopenia in the setting of CML. HELLP syndrome was ruled out. The patient had preterm rupture of membranes at 32 weeks of gestation and the team pursued assisted vaginal delivery to prevent vagal response. Following successful delivery, the patient elected to undergo intra-uterine device placement. Post-delivery, vasopressors and inotropes were weaned, and she was discharged on treprostinil, ambrisentan and tadalafil. Thankfully both the mother and baby returned healthy and well at 1 month follow up. Case Media - Pulmonary Hypertension in Pregnancy CMRCXRTTETTEClick to Enlarge Episode Teaching - Pulmonary Hypertension in Pregnancy Pearls - Pulmonary Hypertension in Pregnancy Pulmonary Hypertension is defined as a mean pulmonary arterial pressure (mPAP) of >20mmHg. There are 5 major types of pulmonary hypertension. Risk modifiers include symptom burden, exercise capacity, presence of pericardial effusion, RV function and hemodynamics.Multidisciplinary care teams are the key to achieving optimal pregnancy outcomes in patients with PH. It is critical to create a team of experts with experience in pulmonary hypertension and plan for constant communication before, during, and after pregnancy.Pregnant women who are already on PAH therapy outpatient should continue them during pregnancy (under the direction of PH experts) except for endothelin receptor blockers which fall in pregnancy category X.PH during pregnancy is associated with up to 38% maternal mortality rate as the right ventricle (RV) is often unable to handle the volume shifts and hemodynamic changes that occur during pregnancy, labor, and delivery.Patients with RV failure leading to low cardiac output and hypotension, like in this case, may benefit from vasopressors with the goal to maintain systemic blood pressure above pulmonary arterial pressures, preserving right coronary blood flow and preventing intracardiac shunting. Swan-guided management may be useful - to titrate inotropes and vasopressors, optimize pulmonary vasodilators and ensure that the patient is being adequately fluid-optimized to maintain a CVP of around 8-10. Notes - Pulmonary Hypertension in Pregnancy 1. What are the different types of pulmonary hypertension (PH)?The WHO separates PH into 5 groups: Group 1Pulmonary arterial hypertension (e.g., idiopathic, heritable [BMPR2], anorexigen associated, drug or toxin-associated, HIV, connective tissue disease associated, schistosomiasis, portal hypertension, congenital heart disease, etc) Group 2Pulmonary hypertension due to left sided heart disease (e.g., HFrEF, HFpEF, left-side valvular heart disease) Group 3Pulmonary hypertension due to lung disease or hypoxia: (e.g., COPD, ILD, OSA, hypoxia without lung disease such as high altitude, developmental lung disorders) Group 4PH due to pulmonary artery obstructions most commonly Chronic Thromboembolic Pulmonary Hypertension (CTEPH)Group 5Multifactorial causes such as hematologic disorders (chronic hemolytic anemia, as with myeloproliferative disorders), metabolic disorders (e.g., Gaucher disease, glycogen storage diseases, CKD), and systemic disorders (e.g., pulmonary Langerhans cell histiocytosis, neurofibromatosis, sarcoidosis) 2. What is the role of TTE and RHC in the workup of PH? Tyrosine kinase inhibitors are known to cause PAH and there should be a low threshold to do screening TTEs in these patients when there is concern for the development of PAH.Echocardiogram is essential in the evaluation of PH –for positing the presence of PH, evaluating the left heart and congenital defects for clues to PH etiology, and assessing the structural consequences of PH on the right heart. In addition to estimating the pulmonary artery systolic pressure (PASP) by measuring the tricuspid regurgitant jet, we can characterize RV and RA size, RV function, and RV wall thickness, which may help both support the diagnosis and gauge prognosis for PH. Further, we can evaluate for left-sided heart disease contributing to PH. The presence of a pericardial effusion is a poor prognostic sign in those with pulmonary hypertension. Notably, the PASP is not of prognostic value due both to inaccuracies in measurement and falling values in the context of severe PH with failing RV function; a such PASP should not be used to surveil patients with PH or monitor response to PH therapies. McLaughlin et al suggest using a checklist in the echocardiographic assessment of PH which includes the following1: ChecklistSalient pointsEstimated PASPTo calculate mean PAP, usually PA diastolic pressure needs to be assessed which often requires a PR jet which is both difficult to obtain and not often present.Evaluate RV size and functionSize: abnormal RV basal diameter >4.2 cm, wall thickness in subcostal view >5 mm Function: TAPSE (abnormal 20≤ 15≥ 31, 3, 4, 5Post-capillary> 20> 15 20> 15≥ 32, 5, multifactorial Furthermore, we can determine if a patient is “vasodilator responsive.” In the catheterization lab, a positive vasodilator response is defined as a decrease in mPAP ≥ 10 mmHg to an absolute value of ≤ 40 mmHg (without a decrease in cardiac output) with the use of inhaled nitric oxide or IV epoprostenol. If a patient has positive vasodilator test, calcium channel blockers can be initiated, however not all patients will be long term responders. We tend to do vasoreactivity testing in patients with PAH and not for other forms of PH (e.g., Pulmonary Veno-Occlusive Disease or Groups 2, 3, 4, or 5). 3. What are PAH-specific pharmacologic treatments? Remember that PAH is fundamentally a disease of increased pulmonary vascular resistance (PVR) causing elevated pulmonary pressures. The consequence of increased PVR includes increased RV afterload and hypoxemia and the subsequent clinical manifestations of PAH. Normally, the pulmonary vascular bed has a balance between vasodilators and vasoconstrictors that maintain a low-resistance, high-compliance state. This balance is disturbed in PAH and the goal of therapy is to “restore” balance between vasodilation and vasoconstriction.The management of PAH relies on 3 primary medication groups1:

Sep 1, 2021

CardioNerds Dr. Rick Ferraro, Director of the #CardsJC Journal Club and cardiology fellow at Johns Hopkins, and Dr. Tommy Das, Program Director of the CardioNerds Academy and cardiology fellow at Cleveland Clinic, learn all about the clinical application of the ASCVD primary and secondary prevention guidelines in terms of lifestyle modifications and lipid lowering strategies from Dr. Allison Bailey, Editor-in-Chief of the ACCEL Audio Journal and Advanced Heart Failure and Transplant Cardiologist at Centennial Heart. Dr. Baily was a co-author on the 2018 ACC/AHA Guideline on the Management of Blood Cholesterol. In this episode we will learn about the current guidelines for primary prevention of ASCVD, the evidence for specific dietary changes in improving cardiovascular outcomes, the current guidelines for secondary prevention of ASCVD, how successful are clinicians and patients in meeting LDL-C recommendations, and what the recent SAMSON trial teaches us about statin intolerance. If you're a current internal medicine resident, interested in the intersection between medical education, cardiovascular disease and digital media, consider applying to the CardioNerds Academy using this link. The deadline for this application is October 15th 2021. Learn more by visiting the CardioNerds Academy page. Relevant disclosure: None Pearls • Notes • References • Guest Profiles • Production Team CardioNerds Lipid Series PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Qoatables - Lipid Lowering with Dr. Alison Bailey “Lifestyle should be the first step and the last step of everything we do.” Pearls - Lipid Lowering with Dr. Alison Bailey In patients without established clinical ASCVD, the percent reduction in LDL-C is the strongest predictor of cardiovascular benefit. In patients with high LDL-C levels, a 50% reduction in LDL-C levels should be targeted.In high-risk patients with established clinical ASCVD, we should target a 50% reduction in LDL-C levels and an LDL-C level less of than <70mg/dL. Lower LDL-C levels are associated with better ASCVD outcomes, and European guidelines recommend targeting an LDL-C level of <55mg/dL.LDL-C lowering starts with promoting a health-lifestyle with emphasis on regular exercise and heart-healthy diet. Randomized trials support the efficacy of the Mediterranean diet in reducing cardiovascular events. Show notes - Lipid Lowering with Dr. Alison Bailey 1. What are the current guidelines for primary prevention of ASCVD? The 2019 ACC/AHA Guidelines on the primary prevention of Cardiovascular Disease provides the following guidance for clinicians (applicable to those without established clinical ASCVD):For all patients, a heart-healthy lifestyle focused on diet and exercise is the most important way to prevent atherosclerotic disease.For any patient with an LDL-C ≥ 190 mg/dL, a high intensity statin is recommended.Patients aged 40-75 years old who have diabetes mellitus warrant at least a moderate intensity statin, and may benefit from a high-intensity statin based on additional risk factorsFor patients aged 40-75 years old and with an LDL-C between 70-189 mg/dL without diabetes, the pooled cohort equation can determine 10-year ASCVD risk and guide a patient-centric risk discussion.Percent reduction in LDL-C is the strongest predictor of cardiovascular benefit; a 50% reduction in LDL-C should be targeted for most patients. 2. What evidence exists for specific dietary changes in improving cardiovascular outcomes? A diet emphasizing intake of vegetables, fruits, legumes, nuts, whole grains, and fish is recommended to decrease ASCVD risk factors. Additionally, minimizing intake of processed meats, refined carbohydrates, and sweetened beverages can reduce ASCVD risk.The PREDIMED trial showed that among patients with high cardiovascular risk, a Mediterranean diet supplemented with extra-virgin olive oil or nuts reduced the incidence of major cardiovascular events when compared to a control diet (with advice to reduce dietary fat).In a sub-study analysis of PREDIMED, a Mediterranean diet supplemented with nuts was associated with delayed progression of internal carotid intima-media thickness and plaque height by ultrasound, suggesting a mechanistic cause of the Mediterranean diet’s cardio-protective effect.The Adventist Health Study-2 cohort demonstrated a significant association between vegetarian diets and decreased all-cause mortality and cardiovascular mortality. 3. What are the current guidelines for secondary prevention of ASCVD? Secondary prevention of ASCVD is important for all patients with history of clinical ASCVD (e.g. prior history of ACS, MI, stable or unstable angina, stroke, TIA, or PAD including aortic aneurysm of atherosclerotic origin).In these patients, a healthy lifestyle should be emphasized as the first intervention.In addition, patients should be started on a high intensity statin. For all patients we should target a percent LDL-C reduction of at least 50%. In high-risk patients (those with a history of multiple major ASCVD events or one major ASCVD event and multiple high-risk conditions), we should target a LDL-C level of ≤70 as well.While American guidelines recommend targeting a goal of ≤70 mg/dL, European guidelines recommend a target of ≤55 mg/dL. Most data suggests that lower is better for LDL-C; to learn why, enjoy Episode #132 - LDL Physiology & Function with Dr. Peter Toth)!If LDL-C remains above goal (of 70 mg/dL), ezetimibe should be started for an anticipated extra 20% lipid lowering.If LDL-C remains above goal, a PCSK-9 inhibitor should be considered. Notably, the ACC’s prior authorization tool is designed to collect data on the approval of these medications. 4. How successful are clinicians and patients in meeting LDL-C recommendations? In a recent analysis of the PINNACLE registry (made up of over 2.5 million patients with known ASCVD), 52.7% had no history of being prescribed lipid lowering therapy, and 71.9% did not meet an LDL-C goal of ≤70.In the ISCHEMIA trial, only 41% patient patients were on optimal medical therapy by the end of the trial.Dr. Bailey suggests an approach to patient counseling wherein patients are aware of which medications actively improve their symptoms, and which medications improve longevity. Additionally, polypharmacy should be avoided through careful medication reconciliation. 5. What does the recent SAMSON trial teach us about statin intolerance? In this recent trial, 60 patients with a prior history of statin intolerance were randomized to either atorvastatin 20mg, a placebo, or no treatment. Each patient cycled through all three treatment options.When patients were taking either the statin or placebo, they reported significantly more side effects compared to when they were taking no treatment.Notably, after learning whether they were taking placebo or statin while experiencing symptoms at the completion of the trial, roughly 50% of patients were able to tolerate a statin. References - Lipid Lowering with Dr. Alison Bailey Arnett DK, Blumenthal RS, Albert MA, et al. 2019 ACC/AHA Guideline on the Primary Prevention of Cardiovascular Disease: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines [published correction appears in Circulation. 2019 Sep 10;140(11):e649-e650] [published correction appears in Circulation. 2020 Jan 28;141(4):e60] [published correction appears in Circulation. 2020 Apr 21;141(16):e774]. Circulation. 2019;140(11):e596-e646. doi:10.1161/CIR.0000000000000678Estruch R, Ros E, Salas-Salvadó J, et al. Primary Prevention of Cardiovascular Disease with a Mediterranean Diet Supplemented with Extra-Virgin Olive Oil or Nuts. N Engl J Med. 2018;378(25):e34. doi:10.1056/NEJMoa1800389Sala-Vila A, Romero-Mamani ES, Gilabert R, et al. Changes in ultrasound-assessed carotid intima-media thickness and plaque with a Mediterranean diet: a substudy of the PREDIMED trial. Arterioscler Thromb Vasc Biol. 2014;34(2):439-445. doi:10.1161/ATVBAHA.113.302327Orlich MJ, Singh PN, Sabaté J, et al. Vegetarian dietary patterns and mortality in Adventist Health Study 2. JAMA Intern Med. 2013;173(13):1230-1238. doi:10.1001/jamainternmed.2013.6473Grundy SM, Stone NJ, Bailey AL, et al. 2018 AHA/ACC/AACVPR/AAPA/ABC/ACPM/ADA/AGS/APhA/ASPC/NLA/PCNA Guideline on the Management of Blood Cholesterol: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines [published correction appears in Circulation. 2019 Jun 18;139(25):e1182-e1186]. Circulation. 2019;139(25):e1082-e1143. doi:10.1161/CIR.0000000000000625Authors/Task Force Members; ESC Committee for Practice Guidelines (CPG); ESC National Cardiac Societies. 2019 ESC/EAS guidelines for the management of dyslipidaemias: Lipid modification to reduce cardiovascular risk [published correction appears in Atherosclerosis. 2020 Jan;292:160-162] [published correction appears in Atherosclerosis. 2020 Feb;294:80-82]. Atherosclerosis. 2019;290:140-205. doi:10.1016/j.atherosclerosis.2019.08.014Wood FA, Howard JP, Finegold JA, et al. N-of-1 Trial of a Statin, Placebo, or No Treatment to Assess Side Effects. N Engl J Med. 2020;383(22):2182-2184. doi:10.1056/NEJMc2031173O'Keefe JH Jr, Cordain L, Harris WH, Moe RM, Vogel R. Optimal low-density lipoprotein is 50 to 70 mg/dl: lower is better and physiologically normal. J Am Coll Cardiol. 2004;43(11):2142-2146. doi:10.1016/j.jacc.2004.03.046 Guest Profiles Dr. Alison Bailey Alison L. Bailey @a_l_bailey is a General Cardiologist in Chattanooga, TN. She completed her medical training (all of it!) at the University of Kentucky and has been using what she learned there for the last 20 years.

Aug 24, 2021

CardioNerds Amit Goal, Daniel Ambinder, & Dr. Alex Pipilas (FIT, Boston University) discuss the clinical examination in patients with heart failure with Dr. Mark Drazner, professor of medicine, clinical chief of cardiology, and medical director of the LVAD and Cardiac Transplantation Program at UT Southwestern. In this pearl laden episode, they discuss how the exam can be used to non-invasively assess a patient's hemodynamic status, risk stratify and inform prognosis, and guide management. They also discuss ways to master the evaluation of the JVP and categorize patients based on their RA:PCWP ratio. Check out the CardioNerds Failure Heart Success Series Page for more heart success episodes and content! Relevant disclosures: None The CardioNerds Heart Success Series is developed in collaboration with the Heart Failure Society of America. The Heart Failure Society of America is a multidisciplinary organization working to improve and expand heart failure care through collaboration, education, research, innovation, and advocacy. Its members include physicians, scientists, nurses, nurse practitioners, and pharmacists. Learn more at hfsa.org. This episode is made possible with support from Panacea Financial. Panacea Financial is a national digital bank built for doctors by doctors. Visit panaceafinancial.com today to open your free account and join the growing community of physicians nationwide who expect more from their bank. Panacea Financial is a division of Primis, member FDIC. Pearls • Notes • References • Guest Profiles • Production Team CardioNerds Heart Success Series PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls - Clinical Examination in Heart Failure Begin hemodynamic assessment with the evaluation of congestion (“wet” vs “dry”) and perfusion (“cold” vs “warm”). In a 2x2 table, this breaks patients into 4 broad hemodynamic profilesThe most sensitive markers of congestion (PCWP > 30) are JVP >12 with an OR of 4.6 and the presence of orthopnea with an OR of 3.6“If you are cold, you are cold, if you are warm, you can still be cold”. Sensitivity for clinical markers of low cardiac index is very poor. Consider a low output state in patients with poor response to what are thought to be appropriate therapiesMost patients with acute on chronic heart failure have an RA:PCWP ratio of 1:2. These patients are the so called “concordant” phenotype. There are two other sub-phenotypes:The “RV equalizer group” have an elevated RA:PCWP ratioThe “RV compensated” group have a lower RA:PCWP ratioClinical congestion at the time of hospital admission as well as discharge portends a poor prognosis for patients with heart failure Show notes - Clinical Examination in Heart Failure Figure 1 1. What is the physical exam important in patients with heart failure? Important to view the physical exam as a diagnostic test with strengths and limitationsIt is a noninvasive way to assess hemodynamics and risk stratify patientsCan provide information on prognosisMay enhance the provider-patient relationship 2. How might we classify hemodynamics noninvasively? Framework begins with the “Stevenson” Classification, developed by Dr. Lynne StevensonClassifies patients along two axes: congestion and perfusionCongestion is the assessment of overall volume status and estimation of right and left sided filling pressures, broadly broken up into “wet” or “dry”:“Wet”, PCWP >15mmHg“Dry”, PCWP 2.2“Cold”, Cardiac index 12 predicts PCWP > 30 with an OR of 4.6 (Drazner, 2008).Rapidly developing ascites or edemaSquare wave test. The square wave test takes advantage of an abnormal response to Valsalva in patients with low systolic function and elevated filling pressures. In those with congestion, the MAP fails to fall with decrease in RV and LV preload from the Valsalva maneuver due to preexisting high filling pressures. This is likely the best evidence that the patient has elevated filling pressures and may help to identify patients with the discordant hemodynamic phenotypes.Symptoms:Orthopnea: one of the two most sensitive markers for congestion such that the presence of orthopnea predicts PCWP > 30 with an OR of 3.6 (Drazner, 2008).Bendopnea: the sensation of feeling breathless within 30 seconds of bending over. Bendopnea is associated with higher filling pressures and low cardiac index (Thibodeau JT T. A.-M., 2014), with increased risk of short term heart failure admission ( (Thibodeau JT J. B., 2017), and with elevated VE/VCO2 (more advanced HF marker from CPET) (Dominguez-Rodriguez A, 2016). Relief of bendopnea during hospitalization is associated with greater fall in median NT-proBNP.The following are less helpful for identifying patients with acute on chronic HFRales have a low sensitivity and specificity for acute on chronic decompensated heart failure. If rales are present in chronic HF patients, consider looking for pulmonary pathology. This doesn’t apply for patients with acute MI or flash pulmonary edema.Weight may be misleading as heart failure is a cachexia promoting illness such that variation in weight may not be referred to fluid status alone. Volume overload often leads to appetite changes and weight loss as well as fluid retention which together can lead to net negligible weight change. Additionally once patients are euvolemic and clinically improved, they might gain true caloric weight which makes tracking “dry weights” difficult. Weight may be helpful over the short term i.e with a report of 10lbs of weight gain within the past week + significant stigmata of overload. With these considerations, we must be cautious regarding targeting a fixed “dry” weight over long periods of time given true changes in body weight.Adjunctive data may help adjudicate the bedside assessment of congestion:Prognosis is better with down trending natriuretic peptides but no data clearly suggests benefit from tailoring therapy based on these levels.Echo parameters such as the PASP, mitral inflow pattern, and IVC size may be helpful in the right context.Implantable PA sensors (i.e. CardioMems) may be helpful. A large RCT looking at this, Guide-HF, trial is still enrolling. 4. What are some tips & tricks for measuring the JVP? We are not looking for venous structure, but rather referred pulsating waves, which are usually better seen than felt.Look on both sides of the neck!Carotid vs Jugular vein – if you compress BELOW the pulsation and it goes away then it is a VENOUS pulsation. If not, then it is likely carotid. Venous pulsation (not carotid pulsation) will change in height as you adjust the degree of patient’If unable to see the pulsation, sit the patient upright and assess. It may be too high to see when recumbentCan use the EJ if it is respirophasic. If it isn’t then the high level could be due to a valve in the vein in which case we need to be cautious with interpretation. 5. What is the connection of the JVP (i.e estimated RA pressure) to left sided filling pressures (i.e PCWP/LVEDP) (Drazner 2008)? The RAP:PCWP ratio is ~1:2 (“concordant”) in 70-75% of patients in acute on chronic heart failure from ESCAPE trial data. Importantly, this relationship does not hold in all groups of patients including those with acute MI or other conditions which may cause discordance between right- and left-sided filling pressures like primary pulmonary hypertension, significant valvular disease, etc.This relationship does not hold ~25-30% of the time, where the RAP and PCWP are “discordant.” The two sub-phenotypes to think about are: Right/left equalizers: high RAP:PCWP ratio (ratio ~≥ 2:3). Clinically, a high JVP may overestimate the overall fluid status. They may run into hypotension and worsening renal function because left sided pressures are lower than you would estimate by the JVP. These tend to be sicker patients with a generally worse prognosis (Grodin JL, 2015).Compensated RV group: low RAP:PCWP ratio (ratio ~≤ 1:3). In contrast to the right/left equalizers, those with a “compensated RV” may have a JVP which underestimates the overall fluid status since the RAP is lower for a given PCWP. Consider this phenotype in those with classic left sided HF symptoms despite a relatively low or normal JVP.There are no clear clinical makers to identify patients who are in the discordant phenotypes but if the clinical course is not what you expect, consider exploring if a patient’s hemodynamics fall within these discordant phenotypes.If a patient has had a RHC in the past, you can use their previous RA:PCWP ratio to estimate left sided filling pressures with JVP during subsequent encountersThere is some data to suggest that a given patient us unlikely to move from one extreme to another, at least over a short period of time (i.e move from right/left equalizers to compensated RV ect)More likely, a patient may move from extremes to the middle with either progression of disease or improvement 6. What is the role of the clinical exam in the assessment of perfusion: “Warm” or “Cold”? “If they are cold, they are cold. If they are warm, they still may be cold.” In other words, the sensitivity of the clinical evaluation is poor for the diagnosis of poor perfusion, but the specificity is high.

Aug 17, 2021

In the PA.ACC – CardioNerds Narratives in Cardiology episode, CardioNerd Amit Goyal joins Dr. Miranda Merrill (FIT, Oregon Health & Science University), Dr. Stephanie Fuentes Rojas (FIT, Houston Methodist Hospital), and Dr. Natasha Cuk (FIT, Cedars-Sinai Medical Center) for a discussion with Dr. Kamala Tamirisa (Clinical Cardiac Electrophysiologist, Texas Cardiac Arrhythmia, National ACC Women in Cardiology Leadership Council Member and Co-Chair for ACC Women in Cardiology Advocacy Work Group, and current co-chair of the Texas Chapter ACC EP section) about gender equity and women in cardiology and electrophysiology. This episode focuses on the experiences of women in cardiology across the spectrum of training, from medical school, fellowship, through the procedural field of electrophysiology, to local and national leadership and beyond. Listen to the episode to learn about the factors which have led to Dr. Tamirisa’s success as a private practice electrophysiologist incorporating leadership roles in medical education and national organizations. Closing remarks by Texas ACC chapter governor, Dr. Kenneth Shaffer. Episode script was developed by Dr. Miranda Merrill and episode notes were developed by Dr. Natasha Cuk. The PA-ACC & CardioNerds Narratives in Cardiology is a multimedia educational series jointly developed by the Pennsylvania Chapter ACC, the ACC Fellows in Training Section, and the CardioNerds Platform with the goal to promote diversity, equity, and inclusion in cardiology. In this series, we host inspiring faculty and fellows from various ACC chapters to discuss their areas of expertise and their individual narratives. Join us for these captivating conversations as we celebrate our differences and share our joy for practicing cardiovascular medicine. We thank our project mentors Dr. Katie Berlacher and Dr. Nosheen Reza. Video Version • Notes • References • Production Team Claim free CME just for enjoying this episode! There are no relevant disclosures for this episode. The PA-ACC & CardioNerds Narratives in Cardiology PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Video version - Women in EP https://youtu.be/e7Cjv4vPXqg Quotables - Women in EP “The exciting part today is to see three women who are interested in EP… like RBG said, when all EP physicians are women, that’s the day we’re going to celebrate” 07:15 “There's nothing (more) exciting… than EP, just that technology, the marriage between analytical thinking, tactile, touch, with a deductive logic.” 09:18 “Multiple studies have documented sex disparities in cardiovascular care… (Historically) women and minorities did not receive implantable cardioverter defibrillators or even BiV (biventricular) pacers… a potential driver for these disparities in cardiovascular disease is lack of diversity in the workforce. Very simple.” 19:28 “I still want to wear my lipstick. I still want to wear my heels. I want to do my hair. I still want to be a proceduralist and that's okay. Make room.” 28:00 Show notes - Women in EP While this episode and the following notes are specific to women in electrophysiology, these same basic principles apply to fostering a more inclusive and welcoming environment in other subspecialties for all persons regardless of sex, gender, race, ethnicity, IMG status, and the other factors which make us different from one another and which enrich our workforce. 1. Why choose electrophysiology? An EP career is unique – it combines the biology, physiology, and procedural skills learned in residency and fellowship training with engineering, mathematic, and imaging principles learned and refined in advanced EP fellowship.1EPs work in a spectrum of settings and with a spectrum of modalities: inpatient, outpatient clinic, EP lab and with fluoroscopy, echocardiography (including intracardiac echo), 3D mapping systems, intracardiac EGMs, surface EKGs. Bedside medicine is still key to this field.Curative procedures performed in EP have a meaningful impact on patients’ quality and quantity of life1 and life saving devices such as implantable cardioverter defibrillators have profound impacts on mortality with a number needed to treat to save one life between 3-27 for both primary and secondary prevention indications from multiple randomized controlled trials.2If you LOVE EKGs, find yourself dissecting telemetry strips, and bonding with your mentors over EKG analysis, then EP is the field for you!40% of the 130 clinical cardiac electrophysiology fellowship positions in the U.S. remain unfilled and there is a decline in the number of fellows choosing EP for advanced training over the last 5 years. Early exposure to internal medicine residents and first year cardiology fellows to the field will allow time for exploration and may help direct more trainees with an interest to this career.1 2. What are some opportunities for an electrophysiologist in private practice? Private practice can facilitate a certain level of independence and flexibility including directing choices both large and small such as which devices and tools are used, how the lab is set up, or even the ability to build an entirely new ablation program.Leadership is inherent to private practice, especially in EP - there are opportunities everywhere!Private practice facilitates close, longitudinal relationships with patients.Understanding the finances is important – take time to learn about this from mentors not just in EP but in other fields of medicine or even outside of medicine.Community initiatives can be a fulfilling aspect in addition to procedures, patient care, and leadership opportunities. Dr. Tamirisa earned a Healthcare Heroes Award for Northwest Ohio in 2017 for making an impact on community wellbeing, domestic violence/impact on cardiovascular disease, and health of minority women and was nominated for the Thomas Jefferson Award for the Northwest Ohio region in 2016 for her contribution to women's empowerment in the community. 3. Why and how should we promote diversity within electrophysiology? Women physicians across subspecialties are more likely to provide patient centered communication and may provide improved outcomes for certain patient populations.3,4Diversity drives innovation, which is why drawing more women and underrepresented minorities to EP will advance the field.5Women are “unicorns” in the procedural subspecialties of cardiology.6 Their representation is not growing at the same rate as in other parts of medicine; only 7-10% of EPs currently in practice are women and there remains limited visibility in leadership roles for women at the national level.1,7,8How can we address barriers to entry into the field? Dr. Tamirisa makes several suggestions in her EP lab digest article and in the podcast.1Adjust work and training environments so that they are more inclusive to women and URiM.Address sexual harassment and discrimination on the basis of sex, gender, race, ethnicity, and other factors which make us different and enrich our field.9Advocate for work-life integration for all, including flexible (full- and part-time) work schedules such as 4 day-a-week schedules.Acknowledge and respond to family planning concerns given that childbearing age may overlap with the training period: limit radiation exposure, protect research and family leave time, provide access to lactation areas, and consider reduced or flexible training schedules (such as 2.5 years/30 months of cardiology fellowship and 18 months of EP training). 4. Mentorship in Electrophysiology and Empowering Women to Succeed Mentorship in EP for women can and should be from both women and men! Initiatives such as social media hashtags #HeforShe and #TakeAWomanToTheCathLab and official speaking opportunities eliminating “manels” at national conferences are creating a more inclusive field.10Tips for mentors:Be kind always.Listen to your mentees – even without offering advice, just listening can lead to profound insights.Show your flaws – shattering the illusion of a perfect career or trajectory can help your foster confidence and the ability to tackle obstacles.Be open, vulnerable, and honest (both as a mentor and mentee!)Be inclusive with your projects.Understand the microaggressions that women and underrepresented minorities face in training and their careers. Help them with tools to address those issues including microresistance response strategies.11,12Engage and share your creative endeavors! Dr. Tamirisa writes poetry and journals as her outlet.13 References Tamirisa KP. The Importance of Choosing Cardiac Electrophysiology as a Career: Thoughts on the EP Fellow Shortage. EP Lab Digest. 2020;20(2). https://www.hmpgloballearningnetwork.com/site/eplab/importance-choosing-cardiac-electrophysiology-career-thoughts-ep-fellow-shortage 2. Al-Jefairi N, Burri H. Relevance of guideline-based ICD indications to clinical practice. Indian Heart J. 2014;66 Suppl 1:S82-87. https://www.ncbi.nlm.nih.gov/pubmed/24568834 3. Roter DL, Hall JA. Physician gender and patient-centered communication: a critical review of empirical research. Annu Rev Public Health. 2004;25:497-519. https://www.ncbi.nlm.nih.gov/pubmed/15015932 4. Tsugawa Y, Jena AB, Figueroa JF, Orav EJ, Blumenthal DM, Jha AK. Comparison of Hospital Mortality and Readmission Rates for Medicare Patients Treated by Male vs Female Physicians. JAMA Intern Med. 2017;177(2):206-213. https://www.ncbi.nlm.nih.gov/pubmed/27992617 5. Welson-Rossman T. Healthcare Needs More Diverse Experts To Guide Innovation. ForbesWomen. 2021. https://www.forbes.com/sites/traceywelsonrossman/2021/02/09/healthcare-needs-more-diverse-experts-to-guide-innovation/?sh=358d5b2769e6 6.

Jul 30, 2021

CardioNerds Dr. Rick Ferraro, Director of the #CardsJC Journal Club and cardiology fellow at Johns Hopkins and Dr. Tommy Das, Program Director of the CardioNerds Academy and cardiology fellow at Cleveland Clinic join Academy fellow and episode lead Dr. Julie Power, chief fellow at the University of Minnesota to learn all about the link between LDL-C and cardiovascular events and disparities in care from Dr. Keith Ferdinand, Professor of Medicine and Chair in Preventative Cardiology at Tulane University School of Medicine. As we’ve learned in prior episodes, LDL-C plays a key role in lipid pathophysiology. But how does it lead to cardiovascular events? LDL-C directly leads to plaque expansion and deposition in the arterial intima. Increasing levels of LDL-C are directly related to worsening plaque burden, a principle exhibited powerfully by the dose-dependent nature of coronary atherosclerosis in patients with underlying mutations leading to LDL-C elevation, such as familial hypercholesterolemia. Importantly, the treatment of atherosclerosis and implementation of lipid-lowering therapies are not uniform, with significant disparities throughout the community. The message is clear: Reducing LDL-C is of paramount significance in the prevention and treatment of coronary atherosclerosis and ensuring equitable access to care is critical to addressing the societal burden of cardiovascular disease and improving the health of our communities. There is no CME associated with this episode. To get free CME from other CardioNerds episodes, please visit VCU Health here. Relevant disclosure: Dr. Ferdinand reported severing as a consultant for Medtronic, Amgen, and Novartis. Pearls • Quotables • Notes • References • Guest Profiles • Production Team CardioNerds Lipid Series PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls - LDL, Cardiovascular Events, & Disparities in Care LDL-C is a major stimulant for the initiation and progression of atherosclerosis.The lower the LDL-C level, the greater the clinical benefit in both primary and secondary ASCVD prevention.Our healthcare systems continue to have major disparities in access to quality care and it is essential to reduce barriers to cardiovascular wellness for all communities.Lowering LDL-C in individuals at high cardiovascular risk, especially in those with familial hypercholesterolemia, prevents ASCVD events. Quotables - LDL, Cardiovascular Events, & Disparities in Care “Empower patients to be partners in their care” Dr. Keith Ferdinand Show notes - LDL, Cardiovascular Events, & Disparities in Care 1. What is the link between LDL-C and cardiovascular events? LDL-C is a major stimulant for the initiation and progression of atherosclerosis. The key events in the initiation of ASCVD are the retention and accumulation of cholesterol-rich lipoproteins within the arterial intima at sites with a predilection for plaque formation. As serum levels of LDL-C increase, the probability of intimal retention of LDL leading to the development of atherosclerotic plaque increases in a dose-dependent manner [4].The WOSCOPS trial demonstrated genes associated with lower LDL-C levels are also associated with a three-fold reduction in the risk of cardiovascular disease per unit reduction in LDL-C [4].The Emerging Risk Factors Collaboration (ERFC) and Prospective Studies Collaboration reported plasma LDL-C was associated with increased risk of non-fatal MI or CHD death [4].Statins uniformly reduce atherosclerotic risk across varying levels of baseline LDL-C and are first line therapy for primary and secondary prevention of ASCVD.In high-risk individuals and secondary prevention populations, AHA/ACC guidelines recommend 50% reductions in LDL-C, regardless of baseline, to 190. FH should be considered in adults with LDL-C levels > 190 mg/dL or total cholesterol levels > 310 mg/dL [5].Homozygous FH is a much rarer condition, with an extreme phenotype characterized by untreated plasma LDL-C levels above >400 from birth and almost universal development of ASCVD and xanthomas in childhood or early adolescence. Statins can be started as early as 8-10 years of age. PCSK-9 inhibitors may also be used. LDL apheresis is also a common treatment option [5].To learn more about personalized ASCVD risk assessment and FH, enjoy CardioNerds Episode #98: Personalized Risk Assessment for Cardiovascular Prevention with Dr. Amit Khera. 3. What is the interaction of LDL-C with other ASCVD risk factors? There are numerous risk factors for ASCVD: hypertension, diabetes mellitus, tobacco smoking, and more. Patients with more risk factors have a higher absolute rate of ASCVD in comparison with persons with fewer risk factors [4].However, reduction in LDL-C is associated with the same proportional risk reduction of ASCVD, regardless of the presence or absence of these other risk factors [4].Statin therapy reduces vascular event rates, including major coronary events, stroke, and coronary revascularization by 15-25% for each 1 mmol/L reduction in LDL-C [8]. 4. How do we best support the cholesterol management and cardiovascular health needs of underserved and low-resource communities? We must recognize and work together to address CV health disparities from both the individual and population levels.Reduced adherence to statin therapy among eligible patients is associated with increased mortality. Minority patients, those with low income, and those with barriers to health literacy have been found to be less likely to adhere to statins, signaling important disparities that must be addressed further. The reasons are likely multifactorial and require a multipronged approach to address.Team care delivered in nontraditional locations shows promise, but the cost-effectiveness and sustainability of these approaches need to be studied further [13].Barriers to treatment in low-resource communities exist at multiple levels: educational opportunities, environment, limited access to healthy food options, access to healthcare providers, transport to healthcare facility organization and practice settings where care occurs, and governmental health policy. Focus is needed on developing cross-sectional partnerships to target multiple barriers [13, 16]Programs need early-stage investigators committed to disparities research to bridge these findings to clinical practice and formulation of health policy.To learn about the use of community based participatory research to meaningfully engage and empower the community in addressing these barriers, enjoy CardioNerds Episode #131 with Dr. LaPrincess Brewer and Dr. Norrisa Haynes.To learn about strategies to engage minority patients in clinical trials, enjoy CardioNerds Episode #135 with Dr. Clyde Yancy. 5. What are some other benefits and consequences of lowering LDL-C? Intensive LDL-C lowering is associated with a greater reduction of all-cause mortality in addition to CV mortality [9].LDL-C lowering has exhibited protective effects against cerebrovascular events.The ODYSSEY trial in 2019 demonstrated that PCSK-9 therapy decreased the risk of stroke in patients with recent ACS and dyslipidemia; however, this was regardless of LDL-C levels achieved.There is no evidence for an increased risk of cognitive impairment (PROSPER trial) or hemorrhagic stroke with lower LDL-C levels. References - LDL, Cardiovascular Events, & Disparities in Care Baigent C, Blackwell L, Emberson J, et al. Efficacy and Safety of More Intensive Lowering of LDL Cholesterol: A Meta-Analysis of Data from 170,000 Participants in 26 Randomised Trials. Lancet. 2010; 376: 1670–81.Damask A, Steg PG, Schwartz GG et al. Patients With High Genome-Wide Polygenic Risk Scores for Coronary Artery Disease May Receive Greater Clinical Benefit From Alirocumab Treatment in the ODYSSEY OUTCOMES Trial. Circulation. 2020 Feb 25;141(8):624-636.Duran EK, Aday AW, Cook NR, et al. Triglyceride-Rich Lipoprotein Cholesterol, Small Dense LDL Cholesterol, and Incident Cardiovascular Disease. J Am Coll Cardiol. 2020 May 5; 75(17):2122-2135.Ference BA, Yoo W, Alesh I, et al. Effect of Long-Term Exposure to Lower Low-Density Lipoprotein Cholesterol Beginning Early in Life on the Risk of Coronary Heart Disease: a Mendelian Randomization Analysis. Journal of the American College of Cardiology. 2012; 60: 2631-9.Goldberg AC, Hopkins PN, Toth PP, et al. Familial Hypercholesterolemia: Screening,

Jul 26, 2021

CardioNerds (Amit Goyal and Daniel Ambinder) join fellow lead, Dr. Giselle A. Suero-Abreu (FIT, Massachusets General Hospital), Dr. Isadora Sande Mathias (FIT, Houston Methodist and CardioNerds Academy Fellow), and Dr. Victor Nauffal (FIT, Brigham and Women's Hospital) for a discussion with Dr. William Zoghbi (Chair, Department of Cardiology, Houston Methodist Hospital, Methodist DeBakey Heart & Vascular Center, Past President, the American College of Cardiology) about international medical graduates in the cardiology workforce. This episode focuses on the narratives of international medical graduates (IMGs) who make important contributions to the US medical workforce and scientific innovation. Listen to the episode to learn the state of IMGs in the US physician workforce and the field of Cardiology, an overview of factors that influence IMG selection when applying to residency and fellowship training programs in the US, the impact of recent changes in licensing exams and immigration restrictions, and how to address challenges and support IMGs throughout their medical careers. Audio editing by CardioNerds Academy Intern, Dr. Leticia Helms. Claim free CME just for enjoying this episode! Disclosures: None Cardionerds Narratives in Cardiology PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll Subscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Show notes 1. What is the definition of an international medical graduate (IMGs)? International medical graduates (IMGs) are physicians who who graduated from a medical school outside the United States, regardless of nationality. This group of foreign-trained physicians include US-IMGs (US citizens) and non-US IMGs (non-US citizens). Nearly 80% of IMGs are born abroad [1]. In a paper senior authored by Dr. Zoghbi, IMGs in the US physician workforce are described as “the multicultural, multiethnic, open-minded, and plural fabric that has defined American medicine and contributed to its success over the years” [2]. 2. Why are IMGs important? IMGs are an integral part of the U.S. healthcare system. They constitute about 25% of the physician workforce and, since 2010, the number of IMGs in practice has grown by nearly 18% [1, 3]. IMGs play a critical role in addressing healthcare inequities across the US, comprising a significant proportion of physicians in high-need rural and underserved urban areas [1, 3, 4]. IMGs contribute to the diversity and cultural competence in the US physician workforce with 98% of them speaking two or more languages fluently. They help patients overcome linguistic and cultural barriers that can interfere with their care [5]. Learn more about Diversity and inclusion (Episode 95) and Latinx representation in cardiology (Episode 129). Racial and ethnic concordance between physicians and their patients results in improved healthcare outcomes, and IMGs are essential in matching the needs of the increasingly diverse US population [6]. Many IMGs pursue the opportunity to train in the best academic programs in the US and return as leaders to serve their country. This becomes an avenue for international collaboration to help patients and contribute to research, innovation, and education. 3. What is the state of the IMG workforce in Cardiology? IMGs in cardiology serve as an important source of cardiac care in the United States. Data from the 2020 Physician Specialty Data Report from the Association of American Medical Colleges (AAMC) [7] showed that: Among active US physicians, IMGs comprise 31% of general cardiologists, 46% of interventional cardiologists, and 26% of pediatric cardiologists.Among ACGME trainees, IMGs constitute 38% of fellows in cardiovascular disease, 53% in interventional cardiology, and 20% in pediatric cardiology.Many IMGs have non-immigrant visas, including the J-1 Visitor Exchange visa, and pursue visa waivers at the end of their training. This provides an important source of care to patients in rural and underserved urban areas but can also pose restrictions that affect the career choices and post-training employment opportunities of these physicians [4, 8].For example, only a third of visa waiver positions can go to specialists, creating difficulty for highly trained cardiovascular subspecialists who are IMGs (such as interventionalists and electrophysiologists) who sometimes have limited options to find a job that matches their training when integrating into the US cardiology workforce [4]. 4. What are some challenges IMGs face? IMGs face a series of barriers when entering US residency programs, during their training experiences, and upon the transition into practice [2, 4, 8-11]. There are disparities and biases concerning IMGs during the residency and fellowship match process. For instance, data from the 2020 NRMP Program Director survey showed that 36% of program directors would “seldom” interview a non-US IMG and 18% would “never” do so. When ranking non-US IMGs, 37% of program directors would “seldom” and 21% would “never” do so [12]. These numbers have remained similar over recent years. Over the past few years, changes related to licensing exams, immigration policies, and the COVID-19 pandemic have impacted the recruitment and integration of IMGs into the US physician workforce [2, 8, 11] Nearly 15,000 IMGs in active clinical practice in the US are awaiting permanent residency status. This limits their ability to work to the fullest capacity and capability, especially during public health emergencies [13]. Understanding the challenges faced by IMGs can inform efforts to strengthen support and guidance for this resilient and hard-working group of physicians. 5. How can we support IMGs throughout their medical careers? There are many opportunities for addressing the professional and personal challenges faced by IMGs and supporting their integration throughout their medical careers (Table 1) [4, 5, 10, 11]. Discussion among program leadership at different institutions can help administrators learn from each other’s experiences regarding the recruitment and retention of IMGs and may help reduce barriers. Major medical organizations and the cardiology community can help address immigration and licensure policies affecting IMGs during training and when transitioning to the cardiology workforce in the US [2, 4, 13]. Incorporating diversity and inclusion efforts into the mission of organizations is paramount to ensuring professional satisfaction and success for IMGs as academic faculty. Advocacy, mentorship, and sponsorship enable IMGs to contribute to their highest potential in their medical careers in the US and internationally. Figure 1. Arjun et al [10]Table 1. (Zaidi, Z. et al) [5] CardioNerds Narratives in Cardiology The CardioNerds Narratives in Cardiology series features cardiovascular faculty representing diverse backgrounds, subspecialties, career stages, and career paths. Discussing why these faculty chose careers in cardiology and their passion for their work are essential components to inspiring interest in the field. Each talk will feature a cardiology faculty from an underrepresented group, within at least one of several domains: gender, race, ethnicity, religion, national origin, international graduate status, disadvantaged backgrounds, etc. Featured faculty will also represent a variety of practice settings, academic ranks, subspecialties (e.g. clinical cardiology, interventional cardiology, electrophysiology, etc), and career paths (e.g. division chief, journal editor, society leadership, industry consultant, etc). Faculty will be interviewed by fellows-in-training for a two-part discussion that will focus on: 1) Faculty's content area of expertise2) Faculty's personal and professional narrative As part of their narrative, faculty will discuss their unique path to cardiology and their current professional role with particular attention to challenges, successes, and advice for junior trainees. Specific topics will be guided by values relevant to trainees, including issues related to mentorship, work-life integration, and family planning. To help guide this important initiative, the CardioNerds Narratives Council was founded to provide mentorship and guidance in producing the Narratives series with regards to guests and content. The CardioNerds Narratives Council members include: Dr. Pamela Douglas, Dr. Nosheen Reza, Dr. Martha Gulati, Dr. Quinn Capers, IV, Dr. Ann Marie Navar, Dr. Ki Park, Dr. Bob Harrington, Dr. Sharonne Hayes, and Dr. Michelle Albert. The Narratives Council includes three FIT advisors who will lead the CardioNerds’ diversity and inclusion efforts, including the current project: Dr. Zarina Sharalaya, Dr. Norrisa Haynes, and Dr. Pablo Sanchez. Guest Profiles - Physician Scientists Women Electrophysiology Dr. William A. Zoghbi Dr. William A. Zoghbi, a renowned cardiology, echocardiography and cardiac imaging expert, has developed noninvasive heart function and valve disorder evaluation techniques. As a result, Dr. Zoghbi has overseen national and international heart valve evaluation guideline development.He built his reputation on his ischemic heart disease, myocardial function and hibernation research, as well as his development of echocardiographic techniques to evaluate valvular dynamics and measure valvular regurgitation. Dr. Zoghbi has authored more than 300 publications and lectured at every major cardiology conference worldwide. Dr. Giselle Alexandra Suero Abreu Dr. Giselle Alexandra Suero Abreu is a cardiology fellow at Massachusetts General Hospital. She was born and raised in Dominican Republic where she received her M.D. from the Instituto Tecnológico de Santo Domingo (INTEC). During medical school,

Jul 21, 2021

CardioNerds Cardio-OB series co-chairs University of Texas Southwestern Cardiology Fellow, Dr. Sonia Shah (FIT, University of Texas Southwestern) and Dr. Natalie Stokes, (FIT, University of Pittsburgh) join Dr. Nanette Wenger, Professor of Medicine in the Division of Cardiology at the Emory University School of Medicine and a consultant to the Emory Heart and Vascular Center and Dr. Sharonne Hayes, Professor of Internal Medicine and Cardiovascular Diseases and founder of the Women’s Heart Clinic at Mayo Clinic for an in depth discussion about lifelong advocacy for women's cardiovascular health. Audio editing by CardioNerds Academy Intern, Dr. Leticia Helms. CardioNerds Cardio-Obstetrics Series PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Guest Profiles - Advocacy for Women's Cardiovascular Health Dr. Nanette Wenger Dr. Nanette Wenger is Professor of Medicine in the Division of Cardiology at the Emory University School of Medicine. Dr. Wenger received her medical degree from Harvard Medical School in 1954 as one of their first female graduates followed by training at Mount Sinai Hospital where she was the first female to be chief resident in the cardiology department. She is among the first physicians to focus on heart disease in women with an expertise in cardiac rehabilitation and geriatric medicine.Dr. Wenger has received numerous awards including the Distinguished Achievement Award from the Scientific Councils of the American Heart Association and its Women in Cardiology Mentoring Award, the James D. Bruce Memorial Award of the American College of Physicians for distinguished contributions in preventive medicine, the Gold Heart Award, the highest award of the American Heart Association, a Lifetime Achievement Award in 2009 and the Inaugural Bernadine Healy Leadership in Women’s CV Disease Distinguished Award, American College of Cardiology. She chaired the U.S. National Heart, Lung, and Blood Institute Conference on Cardiovascular Health and Disease in Women, is a Past President of the Society of Geriatric Cardiology and is past Chair, Board of Directors of the Society for Women’s Health Research. Dr. Wenger serves on the editorial boards of numerous professional journals and is a sought-after lecturer for issues related to heart disease in women, heart disease in the elderly, cardiac rehabilitation, coronary prevention, and contemporary cardiac care. She is listed in Best Doctors in America. Dr. Sharonne N. Hayes Sharonne N. Hayes, M.D., studies cardiovascular disease and prevention, with a focus on sex and gender differences and conditions that uniquely or predominantly affect women. With a clinical base in the Women's Heart Clinic, Dr. Hayes and her research team utilize novel recruitment methods, social media and online communities, DNA profiling, and sex-specific evaluations to better understand several cardiovascular conditions. A major area of focus is spontaneous coronary artery dissection (SCAD), an uncommon and under-recognized cause of acute coronary syndrome (heart attack) that occurs predominantly in young women. Dr. Hayes also studies the diagnosis and treatment of nonobstructive (microvascular) coronary artery disease and chest pain syndromes and the subsequent risk of arrhythmias and other cardiac conditions in women who have had hypertension, diabetes or preeclampsia during a pregnancy. With the Pericardial Disease Study Group, Dr. Hayes is assessing the optimal management of pericarditis. Additionally, Dr. Hayes is involved in several research initiatives aimed at addressing health equity and reducing health disparities. Through partnerships with national professional women- and minority-serving organizations, Dr. Hayes assesses barriers faced by women and minorities that prevent or deter them from participating in research studies. Through surveys and national databases, Dr. Hayes is also studying the professional development of women and minorities in the health science professions, including the effects of pregnancy and childbearing during training, and evaluating disparities in academic promotion. CardioNerds Cardioobstetrics Production Team Natalie Stokes, MDSonia Shah, MDAmit Goyal, MDDaniel Ambinder, MD

Jul 19, 2021

In this special CardioOB series patient perspective episode, CardioNerds (Amit Goyal and Daniel Ambinder), join three incredible WomenHeart Champions, Ms. Porothea Dennis, Ms. Brandie Taylor, and Ms. Ellen Robin in the presence of two legendary leaders in cardiovascular medicine, Dr. Nanette Wenger and Dr. Sharonne Hayes. In addition to this episode being featured on our Cardio-Obstetrics topic page, you can also find this episode in our Patient and Family Perspective collection which features several moving and meaningful patient and family stories that remind us of why we do what we do. Special message by Ms. Celina Gorre, CEO of WomenHeart. Audio editing by CardioNerds Academy Intern, Dr. Leticia Helms. The CardioNerds Cardio-Obstetrics series is a comprehensive series led by series co-chairs Dr. Natalie Stokes CardioNerds ambassador from UPMC and Dr. Sonia Shah CardioNerds ambassador from UTSW, and produced in collaboration with WomenHeart. There is no CME for this episode. Relevant disclosures: None. CardioNerds Cardio-Obstetrics Series PageCardionerds Patient and Family Perspective PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Why Cardio-Obstetrics❓ Because it’s important, and relevant to anyone taking care of women who are, may become, or have been pregnant as cardiovascular disease is the #1 cause of pregnancy-related death. In order to raise awareness we’ve put together an fun, sometimes sobering, but comprehensive curriculum, so get ready, because this CardioNerds Cardio-Obstetrics cruise will dock at several ports along the way: ✔normal pregnancy physiology, ✔hypertensive disorders, ✔arrhythmia, ✔valvular heart disease, ✔anticoagulation, ✔pulmonary hypertension, ✔congestive heart failure, ✔aortopathies, ✔coronary artery disease, ✔critical care, ✔4th trimester, ✔Racial disparities in care, ✔interventional considerations, ✔patient perspectives including from womenheart champions, and more! CardioNerds Cardioobstetrics Production Team Natalie Stokes, MDSonia Shah, MDAmit Goyal, MDDaniel Ambinder, MD

Jul 16, 2021

Join CardioNerds for a great discussion about key ACC 2021 Prevention highlights featuring the ADAPTABLE and STRENGTH trials. This episode is produced in collaboration with the American College of Cardiology Prevention of Cardiovascular Disease Council with mentorship from the Council’s Chair Dr. Eugene Yang (University of Washington Medical Center) who provides a message at the end of the episode. First, Dr. Amit Goyal and Council Representative Dr. Mahmoud Al Rifai (FIT, Baylor College of Medicine) discuss the implications of the ADAPTABLE Trial with Dr. Gina Lundberg (Emory University School of Medicine). Then Dr. Tommy Das (FIT, Cleveland Clinic), Dr. Rick Ferraro (FIT, Johns Hopkins) and Council Representative Dr. Anum Saeed (FIT, University of Pittsburgh Medical Center) discuss the results of the STRENGTH trial’s secondary analysis with Dr. Steven Nissen (Cleveland Clinic). Disclosures: Dr Nissen reported grants from AstraZeneca during the conduct of the STRENGTH trial Cardionerds Cardiovascular Prevention PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll Subscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Show notes ADAPTABLE Trial The ADAPTABLE trial is a randomized open label pragmatic trial comparing two doses of aspirin (325 mg vs. 81 mg) for the secondary prevention of cardiovascular disease. The trial employed a range of innovative and low-cost methods to simplify the identification, recruitment, and follow-up of patients. The primary effectiveness outcome was a composite of death from any cause, hospitalization for myocardial infarction, or hospitalization for stroke. The primary safety outcome was hospitalization for major bleeding. A total of 15,076 patients were followed for a median of 26.2 months. The primary effectiveness and safety outcomes were not significantly different between the two groups. Together with Dr. Lundberg we discuss design and methodological issues related to the trial and applicability to clinical practice. ASA 81 mg is as effective as ASA 325 mg for reducing cardiovascular events ASA 325 mg does not cause more bleeding episodes than ASA 81 mg ASA dosing should be based on a clinician-patient risk discussion incorporating patients’ risk profile and their values and preferences Future trials should ensure adequate representation of women and race/ethnic minorities The results of the present trial suggest that either dose of ASA (81 mg or 325 mg) would be adequate to lower patients’ risk of death or atherosclerotic cardiovascular events with similar risk of bleeding. ASA dosing should be based on patient values and preferences and clinician judgement as the effectiveness and safety profile of these two regiments appears to be equivalent on the basis of the present trial. STRENGTH Trial, Secondary Analysis Whether omega-3 fatty acids eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) reduce cardiovascular risk has been long debated. Data have largely remained inconclusive with several previous trials, particularly the VITAL and ASCEND, showing no significant cardiovascular benefit DHA and EPA supplementation. However, the REDUCE-IT and the JELIS trials showed cardiovascular benefit with higher dose of purified EPA compared to placebo. Meanwhile, the STRENGTH trial did not show any difference in CVD outcomes in treatment groups using a combined EPA/DHA formulation. In this episode, we discuss a secondary anaylsis from the STRENGTH trial entitled “Association Between Achieved ω-3 Fatty Acid Levels and Major Adverse Cardiovascular Outcomes in Patients With High Cardiovascular Risk” presented at the ACC 2021 addressing the effects of carboxylic acid formulation of EPA/DHA (omega-3 CA) compared with placebo among patients with dyslipidemia and high cardiovascular risk. This analysis showed that there was no added clinical benefit or harm in those who achieved the highest tertiles of EPA and DHA. “It is very important to use a neutral comparator as a placebo and this is what we aimed to do in the STRENGTH trial by using corn oil as the placebo against EPA/DHA... you can only optimally interpret a clinical trial in the context of a neutral placebo.” The STRENGTH trial used carboxylic acid derivative which is better absorbed than other ester formulations used in other studies and its absorption is independent of food. The EPA concentration in the blood reached adequate levels (even up to 268% in the pooled analysis) in this study however, there was only a ~39% increase in DHA even though a formulation of both EPA and DHA was used. Reasons for this remain to be uncovered. Three most recent trials including REDUCE-IT, STRENGTH and OMEMI trial have all consistently showed an increase in atrial fibrillation with omega-3 FA use. The incidence is small but not trivial. Mechanistically, we do not know the reason for this. Opportunity to do further studies studying the effects of Omega-3FA on atherosclerotic disease itself and its progression or reduction remains wide open. Guest Profiles Dr. Eugene Yang Dr. Yang is medical director of the UW Medicine Eastside Specialty Center and a UW professor of medicine. He has particular expertise in the diagnosis and treatment of coronary artery disease, valvular heart disease, peripheral vascular disease, congestive heart failure, cardiac arrhythmias, hypertension and lipid disorders. He is especially interested in the primary and secondary prevention of heart disease through aggressive risk-factor modification and lifestyle change. He also conducts research on new cholesterol-lowering therapies and appropriate treatment options for patients with coronary artery disease. Dr. Yang received his bachelor’s and master’s degrees from Stanford University and his medical degree from the University of Pennsylvania School of Medicine. He completed his internal medicine residency and fellowships in cardiovascular disease and advanced cardiac imaging at Stanford University School of Medicine. Prior to joining the faculty at UW Medicine, he was a clinical instructor and physician-scientist at Stanford. Dr. Yang has been on the faculty at UW Medicine since 2007 and is actively involved with the teaching of medical students, residents and fellows. He is a fellow of the American College of Cardiology and is board certified in internal medicine and cardiovascular disease. Dr. Yang's personal interests include food, wine, golf, travel, and watching soccer. Dr. Gina Lundberg Gina Price Lundberg MD FACC FAHA is an Associate Professor of Medicine at Emory University School of Medicine and has served as the Clinical Director of the Emory Women’s Heart Center since it was founded in 2013. She is a Preventive Cardiologist and specializes in heart disease in women, lipid abnormalities and cardiovascular risk reduction. She founded the first women’s heart prevention program in the state of Georgia in 1998. Dr Lundberg’s service at Emory University includes improving outcomes for women with cardiovascular disease but also improving gender equity for women in cardiology and encouraging more women to choose cardiology for their careers. She attended the Medical College of Georgia at Augusta University and trained in Internal Medicine at Atlanta Medical Center. Her cardiology fellowship was at Rush University in Chicago. She is active with the ACC, AHA, and NLA. She is the Chair-elect for the ACC Women in Cardiology Leadership Council and is the co-chair for the WIC Communications and Social Media Committee. She is the Co-chair for the NLA Social Media and Communications committee and the co-Chair for NLA DE&I Committee. She serves on the AHA Clinical Cardiology Communications and Social Media committee and the AHA Familial Hypercholesterolemia and Hyperlipidemia working group. And she serves as the Social Media Supervisor for JACC Case Reports. Dr. Steven Nissen Steven Nissen, MD, is Chief Academic Officer, Sydell and Arnold Miller Family Heart, Vascular & Thoracic Institute, and holds the Lewis and Patricia Dickey Chair in Cardiovascular Medicine. Dr. Nissen has more than 35 years of experience as a physician. He is world-renowned for his work as a cardiologist, patient advocate and researcher. Equally as significant is his pioneering work in IVUS technology and its use in patients with atherosclerosis. Dr. Nissen has written more than 400 journal articles and 60 book chapters, including many published in the New England Journal of Medicine and the Journal of the American Medical Association. In recent years, he has also written on the subject of drug safety and was the author of manuscripts highlighting concerns about medications such as Vioxx™, Avandia™, and muraglitazar. He is heavily involved with the American College of Cardiology (ACC), serving as President from March 2006 to March 2007, a member of the ACC Executive Committee from 2004 to 2008, and spending 10 years as a member of the organization’s Board of Trustees. In addition, Dr. Nissen has served several terms on the Program Committee for the ACC Annual Scientific Sessions. In his leisure time, Dr. Nissen likes to bicycle whenever possible. He is also an advanced amateur photographer. Dr. Mahmoud Al Rifai Dr. Mahmoud Al Rifai earned his medical degree from American University of Beirutand M.P.H. from Johns Hopkins Bloomberg School of Public Health. He completed his internal medicine residency training at University of Kansas – Wichita where he also completed a chief residency year. His career interests include academic cardiology, imaging, risk prediction, cardiovascular disease prevention and his hobbies include tennis, healthy lifestyle, reading, and coffee making. Dr. Anum Saeed Dr.

Jul 12, 2021

CardioNerds (Amit Goyal and Daniel Ambinder), Dr. Victoria Thomas (Cardionerds Ambassador, Vanderbilt University Medical Center), and Dr. Quentin Youmans, cardiology fellow at Northwestern Medicine Bluhm Cardiovascular Institute, join Dr. Clyde Yancy, Vice Dean for Diversity and Inclusion and Chief of Cardiology in the Department of Medicine at Northwestern for an important discussion about underrepresentation in clinical trials and guidelines. This episode was recorded during a live event hosted by the ACC Illinois Chapter. Listen in to hear why diversity matters in clinical trials, how we can recruit more minorities in representation in CV trials and so much more! Stay tuned for a message by chapter Governor, Dr. Annabelle Volgman. The PA-ACC & CardioNerds Narratives in Cardiology is a multimedia educational series jointly developed by the Pennsylvania Chapter ACC, the ACC Fellows in Training Section, and the CardioNerds Platform with the goal to promote diversity, equity, and inclusion in cardiology. In this series, we host inspiring faculty and fellows from various ACC chapters to discuss their areas of expertise and their individual narratives. Join us for these captivating conversations as we celebrate our differences and share our joy for practicing cardiovascular medicine. We thank our project mentors Dr. Katie Berlacher and Dr. Nosheen Reza. Audio editing by CardioNerds Academy Intern, Dr. Gurleen Kaur. Video Version • Notes • References • Production Team Claim free CME just for enjoying this episode! There are no relevant disclosures for this episode. The PA-ACC & CardioNerds Narratives in Cardiology PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Video version https://youtu.be/5gGqWysdCT0 Show notes 1. Why does diversity matter in clinical trials? Having clinical trial enrollment being representative of the general population in which we practice is essential for the generalizability of the trial results.Representative populations matter so we can say to patients, “yes, there were patients that think like you and look like you in the trial.” We can confidently tell them how patients within the trial have done. This is important when we are trying to narrow health disparities to provide confidence and comfort to our patients.Advocacy for health equity is important but not enough. We need data or evidence to support why a change in our behaviors and clinical practice is needed. An evidence base that reflects and includes all our patients is key to bridging health disparities.In medicine, the case for diversity also includes to better serve diverse patients, to promote health equity, to provide diverse mentors at all levels, to bring different points of view to debates and problem solving, to better engage our communities, and to include investigators with a broad range of perspectives in their scholarly activities. (1) 2. How do we recruit more minorities in representation in cardiovascular trials? We need more advocates for diversity in trials in the room when the conversations about trial designs are being made. This is why diversity of leadership is important.There needs to be an intentional approach for every clinical trial to recruit people that are likely to be candidates for enrollment.Stop asking patients to come “downtown” but instead go to their town or their communities. Meet them where they are.Always make sure you are providing some additional advantage or opportunity for the patients you have recruited into your trials. Don’t make it a one-way street. Allow patients to feel that they are getting the best care and generate trust with them.To gain trust, try to get a sense of what is happening in your patient’s life. Find 2-3 minutes to ask them to give a mini biography of their lives. This goes for routine clinical care as well as conducting trials! 3. What advice do you share with people who are underrepresented in medicine, and who may potentially face racism or sexism? You have two choices when people promote division and hatred. You can choose to be angry, or you can choose to not let others’ poor decisions or thoughts define you.Your best tool as UIM is to control yourself and to be successful.Remember that your uniqueness can make a difference in the lives of so many others. It can help you execute making a large impact for so many more people. 4. How do we recruit more diversity in medicine or cardiology in general? One strategy is to establish new medical school(s) at Historically Black Colleges or Universities (HBCUs). HBCUs recognize broad talent, refine that talent, and propel that talent to success.The current 4 medical schools in part aligned with HBCUs and serving Black medical students represent 2.6% of total medical schools yet account for 15% of all Black medical students. (2)We must stop looking at diversity as a “representativeness” cause. We should all be striving for excellence. To achieve this, we need diversity of thought, diversity of ideas, and diversity of execution. This will not be accomplished if we continue all have the same “skin”.There must be intentionality for diverse leadership. There needs to be diversity in the C-suite of hospitals and the Dean’s executive committee of medical schools. Diversity in medicine will follow suit when there is a diverse thought process in those rooms that affect the future. 5. How has structural racism affected studies and guidelines? There has been a system in medicine early on in our country that intentionally separated people as a function of race such as the “Jim Crow experience”. This disabled many opportunities for certain groups of people.Physicians must recognize there are still residual consequences of the Jim Crow experience that have allowed for a “cultural set point” that continues to be operative today. (3)The “cultural set point” has allowed many generations to become acculturated subconsciously to believe there are distinct differences between people and then behave accordingly that leads to effect of how one may practice medicine. 6. How do we combat structural racism within cardiology or medicine? If you are trying to incite culture change, something abrupt likely will need to happen. You must embrace and enjoy the need for change.CardioNerds and the new generation of physicians have the license to be architects of the future in medicine. We have the power to change the culture as we practice and develop new studies and guidelines.Consider a positive disruptive change when making new ideas for the future in medicine to battle social injustices within medicine.We must fundamentally change the way we do things to change our already known processes. 7. Should there be race or gender-based guidelines or socioeconomic status guidelines? The first step is recognizing this is a complex issue and when one is developing a trial there needs to be a thoughtful conversation.We do need more data in the study of racial and gender differences.We still need race and gender-based research – not race/gender-based research looking for a different biology, but research trying to unravel where do we see these differences that are otherwise inexplicable, with the exception of bias. (4) 8. How to get your peers and patients to trust you to advocate and promote diversity, equity, and inclusion? Per Dr. Yancy you need 3 traits to become a strong and effective advocate: Competency: to strive to be best physician you can be and to give the best care you can. You need your voice to be respected.Civility: be able to stand in a room where there is a difference of opinions and hold yourself appropriate. Manage to have eye contact, manage your emotions, because remember if you allow people to make you angry and show it then they have won.Compassion: show people that you genuinely care. Remember you may have had opportunities that your patients or colleagues may never have had. Also remember to go back to evidence! The evidence is there to promote for more diversity within the physician workforce. This in turn leads to diversity of thought, ideation, and execution which help improve clinical trial subject representation.Remind people that in the 2019-2020 academic year, 21,863 first-year medical students were enrolled in the US, of whom 1,626 were Black—a number that has been stagnant since 1978. References Douglas, P. S., Williams, K. A., & Walsh, M. N. (2017). Diversity matters.Association of American Medical Colleges. Facts: Applicants, Matriculants, Enrollment, Graduates, MD-PhD, and Residency Applicants Data. Published 2020. Accessed December 3, 2020. https://www.aamc.org/data-reports/students-residents/report/factsYancy, C. W. (2020). COVID-19 and African Americans. Jama, 323(19), 1891-1892.Ioannidis, J. P., Powe, N. R., & Yancy, C. (2021). Recalibrating the use of race in medical research. JAMA, 325(7), 623-624.Steinecke A, Terrell C. Progress for whose future? the impact of the Flexner Report on medical education for racial and ethnic minority physicians in the United States. Acad Med. 2010;85(2):236-245. Production Team Dr. Gurleen KaurAmit Goyal, MDDaniel Ambinder, MD

Jul 5, 2021

CardioNerd Amit Goyal is joined by Dr. Erika Hutt (Cleveland Clinic general cardiology fellow), Dr. Aldo Schenone (Brigham and Women’s advanced cardiovascular imaging fellow), and Dr. Wael Jaber (Cleveland Clinic cardiovascular imaging staff and co-founder of Cardiac Imaging Agora) to discuss nuclear and complimentary multimodality cardiovascular imaging for the evaluation of cardiac sarcoidosis. Show notes created by Dr. Hussain Khalid (University of Florida general cardiology fellow and CardioNerds Academy fellow in House Thomas). To learn more about multimodality cardiovascular imaging, check out Cardiac Imaging Agora! Cardiac sarcoidosis is a leading cause of morbidity and mortality for patients with sarcoidosis. A high index of suspicion is needed for the diagnosis as it is often recognized late or unrecognized. It is difficult to diagnose given the focal nature of the cardiac involvement limiting the utility of biopsy and the available clinical criteria have limited diagnostic accuracy. Multimodality imaging plays a large role in the diagnosis and management of patients with cardiac sarcoidosis with the different imaging modalities offering complimentary information and functions. Collect free CME/MOC credit just for enjoying this episode! CardioNerds Multimodality Cardiovascular Imaging PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Quoatables “It’s not important for you to love the Soviet Union. It’s important for the Soviet Union to love you back [Stalin regarding the famous dissonant Russian poet Anna Akhmatova]. When we talk about PET, you love PET, but the PET has to love you back, and it has to love you back in a way where you have to know how to approach this test. With, first, some humility about its limitations: 1) inflammation is universal...and 2) the prep is extremely important.” -- 11:25 “A test without a good preparation is a preparation to fail.” --15:30 “Sarcoidosis is kind of the tuberculosis that we have in medicine—it can present as anything.” --36:40 Pearls Cardiac Magnetic Resonance Imaging (Cardiac MRI) and/or 18-Fluorodeoxyglucose Positron Emission Tomography (FDG-PET) are complimentary tests in the evaluation of cardiac sarcoidosis. Both tests look for scarring and inflammation. Cardiac MRI is a good initial test due to its high negative predictive value (i.e. absence of LGE makes cardiac sarcoidosis less likely) but not great for following a cardiac sarcoidosis patient’s response to therapy. Cardiac FDG-PET is great to follow a patient's response to therapy especially in patients with intracardiac devices such as a pacemaker. 18-fluorodeoxyglucose (FDG) is a glucose analog and just like glucose, is transported into the cell by transporters. Once in the cell, it is phosphorylated, like glucose is, by hexokinase in preparation for use in glycolysis. Unlike glucose, however, it does not proceed to be metabolized any further in the glycolysis pathway and remains trapped in the cell. In the inflammatory cells within sarcoid granulomas, glycolysis is significantly increased to fuel the large energy requirement. Thus, these inflammatory cells (i.e. macrophages) can take up large amounts of FDG. When planning to obtain a cardiac FDG-PET for evaluation of cardiac sarcoidosis, patient preparation is key! There are several available dietary protocols to accomplish the goal of switching the patient’s metabolism to be reliant on fatty acids instead of glucose as an energy source. One such protocol used by the discussants in the episode is prolonged fasting (10-12 hours) prior to the study preceded by two meals that are high in fat and proteins and low in carbohydrates—a ketogenic diet. By having the patient eat this diet, we are trying to switch the metabolism because there is no ability or no offer of glucose for the body to use as an energy source! After we have switched the body’s metabolism to purely fat, when we inject the patient with FDG, hopefully most of the myocardium not affected by inflammatory cells within a granuloma will not have any uptake! Why do we start with resting perfusion images in the imaging portion of the cardiac FDG-PET protocol for cardiac sarcoidosis? Resting perfusion images allow us to identify any perfusion defects at baseline. These images can be compared to the FDG images to see if there is match or mismatch in areas of abnormalities. Resting perfusion images also allow us to assess LV and RV function. Resting perfusion images in conjunction with FDG images can also allow us to monitor the patient’s response to treatment by demonstrating return to normal myocardium from active sarcoid granuloma after treatment or by showing the progression to development of scar. The hallmark for detecting cardiac sarcoidosis with cardiac MRI is late gadolinium enhancement (LGE) in the mid-wall and subepicardial regions. Gadolinium is an extracellular contrast agent that washes out slowly from areas of inflammation or scar (both processes with result in an expansion of the extracellular space). Because of this it is important to look at the distribution pattern of the LGE (i.e. a subendocardial enhancement in a coronary distribution is more suggestive of scar from a prior myocardial infarction in this area). Some features of LGE that favor the diagnosis of cardiac sarcoidosis include: 1) multifocal involvement and 2) involvement of the basal anteroseptum and inferoseptum with contiguous spread into the right ventricle. Show Notes 1. What is the typical patient population with cardiac sarcoidosis and how does it present? Sarcoidosis is a multisystem disorder of unclear etiology characterized by the formation of noncaseating granulomas in multiple organs with an annual incidence of 5 to 40 cases per 100 000 persons in the USA and Europe. It has a 3-fold higher risk in blacks than in whites and it is more common in females. In the USA most disease occurs between ages 25-45, however in Europe and Japan there is a second peak in women older than 70 years old. Around 5% of patients with pulmonary/systemic sarcoidosis have symptomatic cardiac involvement and autopsy studies have shown that there is cardiac involvement in 25% of patients. More recent advanced cardiac imaging studies in patients with known extracardiac sarcoidosis suggests asymptomatic cardiac involvement may be present in ~40% of patients. It is difficult to detect given its patchy focal distribution in the heart such that cardiac biopsy has a sensitivity of only 20-30% (this yield may improve with image guidance from cardiac MRI or FDG PET or guidance from electroanatomic voltage mapping). We may suspect cardiac sarcoidosis in patients presenting with new and unexplained atrioventricular (AV) block, atrial or ventricular arrhythmias, or left ventricular dysfunction—especially in patients with a history of prior non-cardiac sarcoidosis. Palpitations, presyncope, syncope or other nonspecific symptoms may also be the initial presentation.As with our patient in the episode, we should suspect cardiac sarcoidosis and infra-hisian disease in a young previously healthy and active patient who is presenting with evidence of cardiac conduction system disease (i.e. AV block, bundle branch block [BBB], etc.)! 2. Using the patient from the episode as an example (previously healthy presenting with syncope, BBB, frequent non-sustained tachycardia on telemetry monitoring, and intermittent complete heart block, with bilateral hilar fullness on chest x-ray), how should we proceed with evaluation for patients with suspected cardiac sarcoidosis? To continue our evaluation, we could obtain an echocardiogram to look for wall motion abnormalities and myocardial thinning in the basal areas—findings that can be seen with cardiac sarcoidosis. Even if this is evident, we should still rule out coronary artery disease (CAD) in these patients. In a patient with low risk factors for CAD, we can pursue a coronary computed tomography angiogram (CCTA) and if there is no evidence of obstructive CAD, then we start thinking about an inflammatory process with resultant scar causing the patient’s echocardiography findings. If we have an elderly patient or a patient with significant risk factors for obstructive CAD, then we can obtain a coronary angiogram for evaluation. The bottom line is: common things being common—we don’t want to miss obstructive CAD!Abnormal findings on echocardiography in patients with cardiac sarcoidosis include wall motion abnormalities, diastolic dysfunction, and changes in the left ventricular geometry including: 1) abnormal myocardial wall thickness in a noncoronary distribution (possibly caused by sarcoid granulomas), 2) myocardial wall thinning as a result of a later stage of the same process, 3) left ventricular dilation, and 4) left ventricular systolic dysfunction.Sensitivity, specificity, and negative predictive value of echocardiography for diagnosis of cardiac sarcoidosis are low.There are recent studies that have been published about the value of strain imaging with echocardiography in the diagnosis and assessment of response to therapy of patients with cardiac sarcoidosis, however this is still an evolving area or research.After ruling out obstructive CAD we can proceed to Advanced Cardiac Imaging modalities for further evaluation: Cardiac Magnetic Resonance Imaging (Cardiac MRI) and/or 18-Fluorodeoxyglucose Positron Emission Tomography (FDG-PET). These are complimentary tests. Both tests look for scarring and inflammation. Cardiac MRI is a good initial test but not great for following a cardiac sarcoidosis patient’s response to therapy. Cardiac FDG-PET is great to follow a patient's response to therapy especially in patients with intracardiac devices such as pacemaker or ICD.

Jun 30, 2021

CardioNerds (Amit Goyal and Daniel Ambinder), join cardiology fellows from the University of Chicago, (Dr. Mark Belkin, Dr. Ian Hackett, and Dr. Shirlene Obuobi) for an important discussion about case of a woman presenting with implantable cardioverter-defibrillator (ICD) discharges found to be in ventricular tachycardia (VT) storm and work through the differential of ventricular arrhythmias, etiologies of heart failure, and indications for permanent pacemaker and ICD placement. Advanced imaging modalities that aid in the diagnosis of cardiac sarcoidosis, manifestations and management of cardiac sarcoidosis are also discussed. Dr. Nitasha Sarswat and Dr. Amit Patel provide the E-CPR for this episode. Audio editing by CardioNerds Academy Intern, Leticia Helms. Claim free CME just for enjoying this episode! Disclosures: Dr. Amit Patel disclosed ownership of small stocks in GE Healthcare Bio-Sciences. Jump to: Case media - Case schematic & teaching - References CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Case Media Click to Enlarge Episode Teaching Pearls The etiology of wide-complex tachycardias (WCT) of ventricular origin can be broken down by structurally normal versus structurally abnormal hearts. WCT in structurally normal hearts can be further broken down into idiopathic or primary arrhythmia syndromes. WCT in structurally abnormal hearts can be broken down into ischemic and non-ischemic etiologies.In patients with an unexplained non-ischemic cardiomyopathy, conduction abnormalities and/or ventricular arrhythmias should raise suspicion for cardiac sarcoidosis. Additional manifestations include atrial arrhythmias and pulmonary hypertension.Accurate diagnosis and treatment of cardiac sarcoidosis often requires multimodality cardiovascular imaging. Check out these terrific videos from Cardiac Imaging Agora: 1) PET for inflammation/sarcoidosis and 2) Echo and CMR for sarcoidosis.While a pathological tissue diagnosis is the gold-standard, endomyocardial biopsy has a low sensitivity, weven when paired with image guidance. Remember to consider extra-cardiac sites for biopsy.Decisions regarding ablation of ventricular arrhythmia or ICD placement should be done individually with careful assessment of active inflammation secondary to cardiac sarcoidosis and possible response to immunosuppressive medications.Management of cardiac sarcoidosis has two basic principles: 1) Treat the underlying process with immunosuppression and 2) Treat the cardiac sequelae: heart failure, conduction abnormalities, ventricular arrhythmias, atrial arrhythmias, and pulmonary hypertension. Notes 1. The patient in this case was found to be in VT storm. Taking a step back, when we suspect a wide complex tachycardia (WCT) is VT, what are some etiologies we should keep in mind? Differentiating between a supraventricular vs. ventricular origin of a WCT will be a topic for a future episode! But after you have determined that the origin of WCT is ventricular, considerations for the underlying etiology should include ischemia-related, non-ischemic cardiomyopathy-associated, primary arrhythmia syndromes and idiopathic (in addition to common considerations such as medications and electrolyte abnormalities)Chronic ischemia-related WCT is typically scar-mediated, a result of re-entrant mechanism and more commonly presenting as monomorphic VT. WCT in the setting of acute ischemia is likely a result of combination increased automaticity and re-entry, typically manifesting as polymorphic VT. In fact, acute ischemia is the most common cause of polymorphic VT, not Torsades de Pointes, and should be our first consideration. Torsades de Pointes specifically occurs due to an early afterdepolarization in a patient with an acquired or congenital prolonged QT interval.Non-ischemic related WCT etiologies in structurally abnormal hearts include (but not limited to) cardiac sarcoidosis, myocarditis (specifically giant-cell myocarditis), hypertrophic cardiomyopathy, arrhythmogenic right ventricular cardiomyopathy, left dominant arrhythmogenic cardiomyopathy and Chagas disease. Especially in patients with dilated CM, if your initial evaluation does not reveal an etiology, then genetic testing should be considered to identify genetic sources of arrhythmogenic cardiomyopathies, such as laminin and desmoplakin mutations (See Episode 56: CNCR with Northwestern University!)Primary arrhythmia syndromes include, but are not limited to, Brugada, Long QT, Short QT, and catecholaminergic polymorphic VT (CPVT). Idiopathic WCT includes outflow tract, fascicular, or papillary muscle ventricular tachycardias (VT). 2. What is the underlying pathophysiology for the cardiac manifestations of sarcoidosis? Typically, the clinical manifestations of cardiac sarcoidosis depend on the extent and location of the inflammatory process and subsequent fibrosis. Granulomas can be found anywhere in the heart, though more commonly involve the interventricular septum and left ventricle.The most common presentations include conduction abnormalities (e.g., atrioventricular block, right bundle branch block), atrial and ventricular arrhythmias, and less commonly clinical heart failure. Of note, AV blocks and ventricular arrhythmia increase the risk of sudden cardiac death, which may be the first manifestation of cardiac sarcoid.Furthermore, RV involvement is common in cardiac sarcoid – whether it be from the hemodynamic consequences of extensive LV involvement, pulmonary hypertension (pre- and post-capillary mechanisms) or direct RV involvement. However, isolated RV involvement is rare.Sarcoidosis-associated pulmonary hypertension may be present in 5-20% of patients with sarcoidosis and is multifactorial with FIVE major etiologic categories:Cardiac: Group 2 (post-capillary) PH from elevated left-sided filling pressures related to heart failure.Parenchymal: Group 3 PH related to pulmonary parenchymal fibrosis.Vascular: vasculitis, arteritis, pulmonary embolism, pulmonary venoocclusive diseaseAnatomic: adenopathy compressing arteries, vascular distortion from pulmonary fibrosis, fibrosing mediastinitisComorbidities: portopulmonary hypertension (if there is hepatic involvement), anemia, OSA. 3. How do we utilize multi-modality imaging in the diagnosis of cardiac sarcoidosis? Multi-modality imaging aids in the diagnosis of cardiac sarcoidosis in two primary ways: (1) evaluating the extent and pattern of myocardial scar/fibrosis and (2) assessing for active inflammation.Cardiac magnetic resonance imaging (CMR) is utilized to delineate the pattern of scar if present. As discussed in EP #33, CMR is a powerful tool in the evaluation of cardiomyopathy, allowing quantification of RV/LV size, mass, global/regional function, and identification of myocardial scar by late gadolinium enhancement (LGE). Characteristic scar patterns of cardiac sarcoid include patchy, multifocal LGE typically in the mid-myocardium and sub-epicardium. While a positive CMR scan in the setting of biopsy-proven extracardiac sarcoid is indicative of probable cardiac sarcoid, a negative CMR scan does not exclude subclinical disease.PET/CT is also used for the evaluation of cardiac sarcoid, typically to identify the extent of active inflammation, guide immunosuppression therapy and/or if CMR is not available. 18-fluorodeoxyglucose (FDG)-PET/CT requires proper dietary preparation. Macrophages present in inflamed tissues will avidly take up 18F-FDG. But to avoid a false positive we need to suppress physiologic myocardial uptake of glucose to identify only pathologic WBC uptake. One way to suppress physiologic 18F-FDG is to give patients a high fat, ultra-low carb diet (instead of a prolonged fasting state alone), so myocytes preferentially rely on free fatty acids for fuel. PET imaging should be accompanied by an evaluation of myocardial perfusion, similar to the resting portion of a nuclear stress test, to evaluate for defects corresponding to areas of inflammation.Note, if 18F-FDG-PET scan reveals diffuse FDG uptake with no perfusion defect this can commonly indicate a false positive result from inadequate suppression of physiologic FDG uptake, as extensively inflamed myocardial should also lead to decreased perfusion in the involved region. See our upcoming Nuclear and Multi-Modality Imaging Series for more on imaging in Cardiac Sarcoid! 4. What is the role of endomyocardial biopsy in the diagnosis of cardiac sarcoidosis? Endomyocardial biopsy (EMB) historically has only a 25% success rate due to the patchiness of cardiac sarcoidosis. There are improved chances of success if EMB is done via an image-guided or electro-anatomical guided method, but sensitivity remains insufficient to rule out cardiac sarcoidosis even with guided biopsies.Importantly, to confirm the diagnosis of cardiac sarcoidosis, per the 2014 Heart Rhythm Society (HRS) Expert Consensus Recommendation, pathological tissue of non-caseating granulomas is needed. This can either be directly from the myocardium, via EMB, or from an extra-cardiac source when paired with at least one cardiac manifestation. Common places to biopsy include mediastinal lymph nodes via bronchoscopy or lymph nodes near the skin surface. Extra-cardiac sites can be identified on whole-body PET scans by FDG-uptake, as described above. 5. What is the role of VT ablation and ICD placement in cardiac sarcoid? Ventricular arrhythmia ablation is considered on an individual patient basis in cardiac sarcoidosis. Patients should be assessed for active inflammation, and if present, they should typically first be treated with immunosuppression as this may suppress the arrhythmias without ablation.

Jun 23, 2021

CardioNerds Academy Chief Fellows Dr. Rick Ferraro (FIT, Johns Hopkins) and Dr. Tommy Das (FIT, Cleveland Clinic) join Academy fellow Dr. Jessie Holtzman (soon, chief resident at UCSF internal medicine residency) to learn all about LDL physiology and function from Dr. Peter Toth! Low-density lipoprotein cholesterol (LDL-C) has been well established as a risk factor for atherosclerotic cardiovascular disease with an ever growing armamentarium of medications to lower LDL-C plasma levels. Yet, LDL-C also plays a number of key physiologic roles across mammalian species, such as cell membrane formation, bile acid synthesis, and steroid hormone production. In this episode, we discuss the definitions of high, normal, low, and ultra-low LDL-C, what functional assays are used to measure LDL-C, and what is considered the safe lower-limit of LDL-C, if there is one at all. Drawing upon experience from rare genetic conditions including abetalipoproteinemia and loss-of-function variants of the PCSK9 gene, we glean pearls that clarify the risks and benefits of low LDL-C. Relevant disclosure: Dr. Toth has served as a consultant to Amarin, Amgen, Kowa, Resverlogix, and Theravance; and has served on the Speakers Bureau for Amarin, Amgen, Esperion, and Novo Nordisk. Pearls • Quotables • Notes • References • Guest Profiles • Production Team CardioNerds Lipid Series PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls 1. Lipoproteins are processed via two major pathways in mammals: 1) exogenous fat metabolism that digests ingested lipids and 2) endogenous fat metabolism that synthesizes lipids in the liver and small intestine. High density lipoprotein (HDL)-mediated reverse transport also brings lipids from the periphery back to the liver. 2. LDL-C comprises ~70% of plasma cholesterol due to its long half-life of 2-3 days. It is one of 5 major lipid particles in plasma including chylomicrons, very low-density lipoproteins (VLDL), intermediate-density lipoproteins (IDL), LDL, and HDL. The liver degrades 40-60% of LDL, while no other tissues in the body make up more than 10% of LDL. LDL-C is energy-poor and cholesterol rich, such that peripheral tissues may not utilize these particles as a fuel source. 3. Preserved functions of LDL-C across mammalian species include cell membrane formation, bile acid synthesis, and steroid hormone production. In other mammalian species, LDL-C levels are found in the 35-50 mg/dL range (Way lower than found in the general human population, and likely more representative of baseline human physiology!). 4. Large, randomized control trials do not consistently demonstrate major adverse effects associated with lower serum LDL-C levels, including risks of cognitive decline, hemorrhagic stroke, reduced bone density, or impaired immune function. 5. Initiation of, and education on LDL-lowering therapy remains insufficient, both in terms of long-term adherence to therapy and achieving current guideline directed goals of LDL-C 150mg/dL).All measurement equations are measured against the gold standard of direct measurement via preparative ultracentrifugation, though this method is far more costly and time intensive. This method is preferred with triglycerides >400 mg/dL, where estimates become less accurate.Non-fasting cholesterol measurements may be more reflective of the “real-world” state as patients are most often post-prandial throughout the day, and are generally recommended as reliable lipoprotein measurement per recent guidelines (the two major exceptions being those undergoing evaluation with a family history of premature cardiovascular disease, and those having eaten a very high-fat meal in the previous 8 hours). 4. How low of an LDL-C is still considered safe? What adverse effects are associated with lower LDL-C levels? As above, recent evidence supports lowering LDL-C to <70 mg/dL in those at high cardiovascular risk, <55 mg/dL in those at very high cardiovascular risk, and even <40 mg/dL in those with a repeat cardiovascular event within two years based on recent U.S. and European Guidelines.The Fourier Trial compared LDL cholesterol reduction with a PCSK9 monoclonal antibody vs placebo and found a 59% reduction from baseline to a median of 30 mg/dL There was no statistically significant difference in adverse events (apart from injection site reactions) in individuals with ultra-low LDL.There is no lower limit of LDL cholesterol that is known to be unsafe. Meta-analyses of primary prevention data demonstrate a linear relationship between LDL-C and ischemic coronary event, so the prevailing philosophy currently remains – when it comes to LDL-C, lower is better.Modern studies have suggested that lower LDL-C is not associated with risk of increased cognitive impairment or hemorrhagic stroke. The ODYSSEY trial in 2019 demonstrated that for patients with recent ACS and dyslipidemia, PCSK-9 therapy decreased the risk of stroke, regardless of LDL-C levels achieved. The PROSPER trial additionally did not demonstrate any significant difference in cognitive function with statin therapy.There is currently no RCT data to suggest impaired immune function or bone density associated with lipid lower therapy. In fact,

Jun 13, 2021

CardioNerds (Amit Goyal and Daniel Ambinder) are joined by Dr. LaPrincess Brewer and Dr. Norrisa Haynes for a Narratives in Cardiology episode, with a special introduction by Dr. Sharonne Hayes. They discuss health inequities especially in communities of color, impact of projects utilizing community based participatory research (including FAITH! and SHARP founded by Dr. Brewer and Dr. Haynes respectively), and their experiences as underrepresented minority women physician-scientists. This special discussion is brought to you in collaboration with the Association of Black Cardiologists (ABC). The ABC’s mission is to “Promote the Prevention and Treatment of Cardiovascular Disease, including Stroke, in Blacks and other Diverse Populations and to Achieve Health Equity for all through the Elimination of Disparities.” You may join and support the ABC at abcardio.org. Claim free CME just for enjoying this episode! Cardionerds Narratives in Cardiology PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll Subscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Show notes for Health Equity, Community Based Participatory Research, & Underrepresented Minority Women Physician-Scientists 1. What healthcare disparities exist in communities of color? The life expectancy of black Americans on average is 3.4 years shorter than that of white Americans. CVD is estimated to explain over 32% of the mortality difference between AA and white men and 43% of the difference between AA and white women. Together these conditions contributed to > 2 million years of life lost in the AA population between 1999-2010. (1)The impact of COVID-19 on minority communities has caused disproportionate morbidity and mortality and devastating health and financial hardship. According to the CDC, black Americans are 1.9x as likely as whites to die from COVID-19. (2) Additionally, at the beginning of the pandemic, a staggering 41% of black owned businesses closed due to COVID-19 as compared to 17% of white owned businesses. (3) 2. Community engagement & Community based participatory research (CBPR) - what is it? CBPR often has a public health bend that focuses on and attempts to address social, structural and environmental inequities through active involvement of community members in all aspects of the research process (from conception to implementation). Community partners provide their unique expertise to enhance understanding of the community and facilitate implementation. (4) 3. What is FAITH!? The Fostering African American Improvement in Total Health (FAITH) program was started by the phenomenal Dr. LaPrincess Brewer. FAITH is a cardiovascular health and wellness program that uses a CBPR approach to promote heart health in the African American faith-based community.Participants in the FAITH program have shown significant improvement in heart health knowledge. Participants have also had improvement in key heart disease risk factors such as blood pressure. The FAITH app was created in collaboration with community members to achieve easy access and easy usability. It provides vital information and a community network that provides support and motivation for participants. 4. Specifics of SHARP? SHARP stands for Safe Haircuts as We Reopen Philadelphia. SHARP was started to assist local barbershops and salons implement proper COVID-19 safety practices to keep their businesses, clients, and staff safe. In partnership with community members, a safety blueprint was created to meet CDC and Philadelphia Health Department guidelines. Through donations from UPenn and Accenture, SHARP was able to distribute a significant number of PPE items to 30 businesses in West and Southwest Philadelphia. Additionally, due to the financial toll that the pandemic has had on small businesses, SHARP organized grant writing sessions through the Netter Center at Penn to help the coalition of businesses in West Philadelphia apply for governmental financial relief. Through collaboration with local mental health professionals, SHARP has also been able to offer free therapy to community members. SHARP is currently working with the coalition of businesses to assist them in becoming positive COVID-19 vaccine ambassadors. 5. What is the concept of #MeWho? #ME_WHO is a brilliant piece authored by Dr. Michelle Albert that was published in Circulation in 2018. In this piece, Dr. Albert eloquently describes how underrepresented minorities and specifically underrepresented minority women physician-scientists (URMWP) are tasked with maintaining an arduous balance.In her words “URMWP are faced with walking a tight rope in academic medicine that requires expertise and excellence in both clinical and scholarly domains, typically with insufficient academic support, social capital, and attainment of senior leadership roles that would turn their zeal and commitment into progress.”Dr. Albert then goes on to provide solutions which include: an inclusive ecosystem, academic institutions and professional organizations functioning as drivers of change through partnerships in their communities to elevate the professional and social climate, and federal entities and private funders committing to nurturing a diverse healthcare workforce committed to providing the best possible care to all communities. (5) CardioNerds Narratives in Cardiology The CardioNerds Narratives in Cardiology series features cardiovascular faculty representing diverse backgrounds, subspecialties, career stages, and career paths. Discussing why these faculty chose careers in cardiology and their passion for their work are essential components to inspiring interest in the field. Each talk will feature a cardiology faculty from an underrepresented group, within at least one of several domains: gender, race, ethnicity, religion, national origin, international graduate status, disadvantaged backgrounds, etc. Featured faculty will also represent a variety of practice settings, academic ranks, subspecialties (e.g. clinical cardiology, interventional cardiology, electrophysiology, etc), and career paths (e.g. division chief, journal editor, society leadership, industry consultant, etc). Faculty will be interviewed by fellows-in-training for a two-part discussion that will focus on: 1) Faculty's content area of expertise2) Faculty's personal and professional narrative As part of their narrative, faculty will discuss their unique path to cardiology and their current professional role with particular attention to challenges, successes, and advice for junior trainees. Specific topics will be guided by values relevant to trainees, including issues related to mentorship, work-life integration, and family planning. To help guide this important initiative, the CardioNerds Narratives Council was founded to provide mentorship and guidance in producing the Narratives series with regards to guests and content. The CardioNerds Narratives Council members include: Dr. Pamela Douglas, Dr. Nosheen Reza, Dr. Martha Gulati, Dr. Quinn Capers, IV, Dr. Ann Marie Navar, Dr. Ki Park, Dr. Bob Harrington, Dr. Sharonne Hayes, and Dr. Michelle Albert. The Narratives Council includes three FIT advisors who will lead the CardioNerds’ diversity and inclusion efforts, including the current project: Dr. Zarina Sharalaya, Dr. Norrisa Haynes, and Dr. Pablo Sanchez. Guest Profiles - Health Equity, Community Based Participatory Research, & Underrepresented Minority Women Physician-Scientists Dr. LaPrincess C. Brewer Dr. La Princess Brewer is an assistant professor and preventative cardiologist at the Mayo Clinic college of medicine. She is an innovative physician-scientist whose research focuses on creating visionary strategies to reduce heart disease and health disparities in minority populations and underserved communities. Dr. Laprincess Brewer also leads the Fostering African-American Improvement in Total Health (FAITH) program which she started as a cardiology fellow and has since brought to the Mayo clinic. The Faith program has since grown and evolved. It is now a mobile application which continues to improve cardiovascular health through the use of technology and digital health but now also focuses on COVID-19 education and COVID-19 mitigation in the African American Community. Dr. Brewer is also a member of the Association of Black Cardiologists (ABC). Dr. Norrisa Haynes Dr. Norrisa Haynes is a senior cardiology fellow at the University of Pennsylvania (UPenn). She attended Yale University for her undergraduate studies where she received a Bachelor of Science (BS) in Molecular and Cellular Biology. She went on to complete her medical school and internal medicine training at Columbia University College of Physicians and Surgeons. During medical school, she received a Master of Public Health (MPH) from Harvard University. After residency, she worked for Partners in Health (PIH) in Haiti for 2 years at Hôpital Universitaire de Mirebalais (HUM) as a junior attending. During those two years, she also worked as a Harvard Medical School instructor and Brigham hospitalist. After spending 2 years in Haiti, she started cardiology fellowship at UPenn. She is interested in imaging and is currently obtaining a Master of Science in Health Policy (MSHP). Dr. Haynes is a member of the ACC/AHA joint guidelines committee and is a member of UPenn’s Women in Cardiology group (WIC). Dr. Haynes also serves the fellow representative to the board of the Association of Black Cardiologists (ABC). References Carnethon MR, Pu J, Howard G, Albert MA, Anderson CAM, Bertoni AG, et al. Cardiovascular health in african americans: A scientific statement from the american heart association. Circulation. 2017 Nov 21;136(21):e393–423.

Jun 7, 2021

CardioNerds (Amit Goyal and Daniel Ambinder), join cardiology fellows from Indiana University cardiology fellows (Dr. Asad Torabi, Dr. Michelle Morris, and Dr. Sujoy Phookan) to discuss a case of a patient who developed a nagging cough post PCI and is ultimately diagnosed with Dressler Syndrome. This case describes the work up and management of post infarct pericarditis and briefly reviews the dilemma of utilizing triple anti-thrombotic therapy with high dose aspirin in the post myocardial infarction period. Indiana University faculty and expert, Dr. Julie Clary provides the E-CPR for this episode. Claim free CME just for enjoying this episode! Disclosures: None Jump to: Patient summary - Case media - Case teaching - References CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Patient Summary A 56-year-old man with recent anterior STEMI and new heart failure with reduced ejection fraction presented with fevers, persistent cough, and pleuritic chest pain following percutaneous coronary intervention for the past two weeks. He was ultimately found to have post cardiac injury syndrome - post infarct pericarditis (formerly known as Dressler syndrome) with elevated inflammatory markers, a small pericardial effusion, and incidentally noted to have an apical left ventricular thrombus. This case describes the work up and management of post infarct pericarditis and briefly reviews the dilemma of utilizing triple anti-thrombotic therapy with high dose aspirin in the post myocardial infarction period. Case Media CXREKGClick to Enlarge Episode Teaching Pearls 1. Post cardiac injury syndrome (PCIS) following myocardial infarction can be very debilitating and recurrence is the concern when treatment is not pursued. 2. Acute pericarditis is a clinical diagnosis which does not require imaging and can have a wide spectrum on presentation ranging from fever/cough to the classic positional chest pain. 3. PCIS following myocardial infarction is less common in the post PCI era but we are starting to see more cases in late presenters. 4. We have good level of evidence to suggest the use of colchicine to reduce the recurrence of PCIS. COPPS and COPPS-2, are two such randomized placebo control trials, which show benefit in the cardiac surgical patient. 5. While triple therapy on high dose aspirin is not discussed in the 2013 ACCF/AHA STEMI guidelines, carefully assess your patient’s bleeding risk and invoke patient shared decision making whenever possible. Notes 1. What is Post-Cardiac Injury Syndrome (PCIS) and what are the clinical manifestations? PCIS is an umbrella term for specific clinical scenarios which may result in symptomatic acute pericarditis.PCIS encompasses:Post-myocardial infarction pericarditis which may be early or late (Dressler syndrome – the focus of this case)Post-pericardiotomy syndrome (PPS)Post-traumatic pericarditis including traumatic and iatrogenic (following most percutaneous procedures such as ablations, PCI, lead placement, etc). 2. How is PCIS (or post infarct pericarditis) diagnosed? This is a clinical diagnosis, made when ≥ 2 of the following are present:Fever without alternative causePericarditic or pleuritic chest painFriction rubPericardial effusionPleural effusion with elevated CRPNote this is different from the diagnostic criteria for other causes of acute pericarditis which requires 2 of the 4 following features:Pericarditic chest painFriction rubNew widespread ST-elevations or PR depressions on ECGPericardial effusion (new or worsening)Supporting findings for pericarditis include:Elevation of inflammatory markers (CRP, ESR, WBC)Pericardial inflammation on cross sectional cardiac imaging (CT, CMR) 3. What are the complications of not treating Dressler syndrome? Imazio et al published an excellent case series in 2009 which answers this question. Overall the prevalence of complications for early and late post-infarct pericarditis was low. No cases of constrictive pericarditis were observed but the incidence of recurrent pericarditis was observed at 3.2%.The 2015 ESC pericardial guidelines recommend considering careful follow-up after PCIS to exclude possible evolution towards constrictive pericarditis with echocardiography every 6-12 months according to clinical features and symptoms (Class IIa). 4. What is the evidence for high dose Aspirin in Dressler syndrome? This is a class 1b evidence in the 2013 ACCF/AHA STEMI guidelines. This evidence comes from data from a small case series of 24 patients which compared aspirin to indomethacin head-to-head. Overall aspirin was non-inferior with similar bleeding risk. The guidelines recommend the use of high dose aspirin because of NSAIDS may interfere with DAPT and there is also concern regarding scar thinning and infarct expansion. The 2015 ESC pericardial guidelines recommend aspirin as a first choice for anti-inflammatory therapy of post-myocardial infarction pericarditis and those who are already on antiplatelet therapies (Class I). 5. What is the role of colchicine for MI, for chronic coronary disease, for pericarditis, and for PCIS? Following MI (without pericarditis): the COLCOT trial showed that colchicine is effective at preventing major adverse cardiac events after MI. In this randomized, double-blind, placebo-controlled trial, a total of 4,745 patients (within 30 days of MI and following intended coronary revascularization) were randomized to colchicine 0.5mg daily or to placebo. After a median follow-up of 22.6 months, there was a significant reduction in the primary efficacy outcome (cardiovascular death, MI, CVA, resuscitated cardiac arrest, or urgent hospitalization for UA leading to revascularization) (HR 0.77, 95% CI 0.61-0.96, p = 0.02).Chronic coronary disease (without pericarditis): the LoDoCo2 trial showed that colchicine is effective in reducing major adverse cardiac events in patients with chronic coronary disease. In this randomized, double-blind, placebo-controlled trial, a total of 5,522 patients were randomized to colchicine 0.5mg daily or to placebo. After a median follow-up of 28.6 months, there was a significant reduction in CV mortality, MI, ischemic stroke, or coronary revascularization driven by ischemia events in the treatment arm (HR 0.69, 95% CI 0.57-0.83, p < 0.001).Acute pericarditis: the unblinded COPE trial and blinded randomized placebo-controlled ICAP trial demonstrated benefit of colchicine in the first episode of pericarditis, added to NSAID therapy. The CORP trial (blinded RCT) demonstrated benefit of colchicine in recurrent pericarditis.Post-pericardiotomy syndrome: the COPPS and COPPS-2 trials showed efficacy of colchicine when initiated 3 days following or 2-3 days preceding surgery respectively, at the cost of increased gastrointestinal side effects. The 2015 ESC pericardial guidelines recommend:Class IIA: Colchicine added to aspirin or NSAIDs should be considered for the therapy of PCIS, as in acute pericarditis.Class IIA: Colchicine should be considered after cardiac surgery using weight-adjusted doses (i.e. 0.5 mg once for patients ≤70 kg and 0.5 mg twice daily for patients .70 kg) and without a loading dose for the prevention of PPS if there are no contraindications and it is tolerated. Preventive administration of colchicine is recommended for 1 month. 6. What is the recommended approach to triple anti-thrombotic therapy in patient with MI s/p PCI and an indication for anticoagulation? The duration for triple therapy should be limited to the shortest duration possible/needed (the duration of aspirin in this regimen remains controversial. In the 2020 ACC expert consensus pathway, a short duration of no more than 30 days is recommended. Clopidogrel is the P2Y12 inhibitor of choice in this regimen to minimize the risk of bleeding and aspirin should be limited to <100 mg.However, the guidelines do not specifically address approach to Dressler syndrome in a post-MI patient treated with PCI who has an indication for anticoagulation (as with apical thrombus in this case) where high dose aspirin would be recommended for pericarditis, DAPT for stent, and warfarin for the thrombus. As with all cases, shared decision making with careful weighing of risks and benefits is advised, in concert with an experienced heart team. References Berman J, Haffajee CI, Alpert JS. Therapy of symptomatic pericarditis after myocardial infarction: retrospective and prospective studies of aspirin, indomethacin, prednisone, and spontaneous resolution. Am Heart J. 1981 Jun;101(6):750-3. doi: 10.1016/0002-8703(81)90610-4. PMID: 7234652. https://pubmed.ncbi.nlm.nih.gov/7234652/ Imazio M, Negro A, Belli R, Beqaraj F, Forno D, Giammaria M, Trinchero R, Adler Y, Spodick D. Frequency and prognostic significance of pericarditis following acute myocardial infarction treated by primary percutaneous coronary intervention. Am J Cardiol. 2009 Jun 1;103(11):1525-9. doi: 10.1016/j.amjcard.2009.01.366. Epub 2009 Apr 8. PMID: 19463510. https://pubmed.ncbi.nlm.nih.gov/19463510/ Tardif JC, Kouz S, Waters DD, Bertrand OF, Diaz R, Maggioni AP, Pinto FJ, Ibrahim R, Gamra H, Kiwan GS, Berry C, López-Sendón J, Ostadal P, Koenig W, Angoulvant D, Grégoire JC, Lavoie MA, Dubé MP, Rhainds D, Provencher M, Blondeau L, Orfanos A, L'Allier PL, Guertin MC, Roubille F. Efficacy and Safety of Low-Dose Colchicine after Myocardial Infarction. N Engl J Med. 2019 Dec 26;381(26):2497-2505. doi: 10.1056/NEJMoa1912388. Epub 2019 Nov 16. PMID: 31733140. https://pubmed.ncbi.nlm.nih.gov/31733140/ Imazio M, Trinchero R, Brucato A, Rovere ME, Gandino A, Cemin R, Ferrua S, Maestroni S, Zingarelli E, Barosi A, Simon C, Sansone F, Patrini D, Vitali E, Ferrazzi P, Spodick DH,

Jun 1, 2021

CardioNerds (Amit Goyal and Daniel Ambinder), Dr. Pablo Sanchez (CardioNerds Ambassador, Stanford University Medical Center), Dr. Maria Pabon (CardioNerds Ambassador, Brigham and Women’s Hospital), and Karen Malacon (Student doctor and LMSA co-chair at Stanford University Medical Center) join Dean for Students at Harvard Medical School, Dr. Fidencio Saldana, for an important discussion about Latinx representation in cardiology. We established the multifaceted benefits of diversity in healthcare, including improving access, cultural competency, and quality of care delivered. We also talked about the need to increase the number of underrepresented minority students in medicine in addition to the importance of removing barriers to improve education. By providing appropriate resources as well as early mentorship and exposure to the medical field, we can address the "leaky pipeline," or as Dr. Saldana reframed it, "the clogged pipeline.” Then, we dove into Dr. Saldana’s experiences in medical school, the barriers he overcame, and how his parents’ hard work and generosity motivated him to become the cardiologist he is now. This event hosted the ACC Massachusetts Chapter. Stay tuned for a message by chapter Governor Dr. Malissa Wood. The PA-ACC & CardioNerds Narratives in Cardiology is a multimedia educational series jointly developed by the Pennsylvania Chapter ACC, the ACC Fellows in Training Section, and the CardioNerds Platform with the goal to promote diversity, equity, and inclusion in cardiology. In this series, we host inspiring faculty and fellows from various ACC chapters to discuss their areas of expertise and their individual narratives. Join us for these captivating conversations as we celebrate our differences and share our joy for practicing cardiovascular medicine. We thank our project mentors Dr. Katie Berlacher and Dr. Nosheen Reza. Audio editing by CardioNerds Academy Intern, Dr. Gurleen Kaur. Video Version • Quotables • Notes • References • Production Team The PA-ACC & CardioNerds Narratives in Cardiology PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Video version https://www.youtube.com/watch?v=cpq2wVgG8mA Quotable We strive to ensure that we have a diverse set of college students and a diverse set of medical students and residents and fellows. But I think it's also just as important to ensure that we have the resources to ensure that those individuals that we've recruited and have done so hard to recruit, continue to succeed. I've realized that you can teach mentoring, you can teach advising. And I think it's important to be able to create that culture and expectation. Some people may be a little bit better at it than others, but I think it's important to place an emphasis on that at each level of training, so that you can train to be a better mentor and a better advisor. Show Notes 1. How is the LatinX representation in medicine compared to in the general population? Based on the most recent data from the US census Bureau, as of 2019, the Hispanic proportion of the US population is about 18.5%.A recent report by the AAMC showed that for the academic year 2020-21, of around 22,000 medical school matriculants, only 11% were from LatinX background, although this number was higher compared to 2017 where only 9.8% of the matriculants were of LatinX origin. 2. How does increasing workforce diversity improve quality of care? Cultural competency forms an important cornerstone of high-quality and equitable care for a diverse population, and it is learned not by lecture but by exposure, experience, and atmosphere.Medicine involves not only knowledge but meaningful connection and having a physician with a common background enhances the patient-doctor interaction by a spectrum of constructive effects.Inasmuch as research questions are guided by interests of investigators, the inclusion of underrepresented minorities among the pool of investigators stands to better delineate problems and articulate solutions. Actuating the gears of change at state/local governments and health systems to solve issues of access and quality of care will be only benefited by inclusion of medical-trained underrepresented minorities at the table. 3. How do can we promote diversity in fellowship programs? Participate in and support efforts to promote recruitment of underrepresented minorities for residency and fellowship programs as well as retention at the faculty level.Participate in initiatives focused on mentoring underrepresented minorities early on (high school or college students).Educate ourselves and others about the barriers that underrepresented minorities must overcome such as inadequate housing, food insecurity, and/or financial support. 4. What is the role of mentorship in diversity and inclusion? Mentorship is one of the pillars to diversify our health care workforce. Mentoring one single medical student will translate into exponential beneficial effects for patients.Mentors can help to overcome internal and systemic barriers that students may encounter during their path as early as during high school and college education.Mentorship does not stop after training is complete and should continue at the faculty level.Mentorship and advising can be taught and should be an expectation during training. References Weinstein DF, Saldana F. DACA and the Dream of Becoming a Physician. N Engl J Med. 2017 Nov 16;377(20):1913-1915. doi: 10.1056/NEJMp1713102. Epub 2017 Oct 25. PMID: 29068757. Cohen JJ, Gabriel BA, Terrell C. The case for diversity in the health care workforce. Health Aff (Millwood). 2002 Sep-Oct;21(5):90-102. doi: 10.1377/hlthaff.21.5.90. PMID: 12224912. AAMC, Matriculants to US medical schools by race. 10/26/2020. https://www.aamc.org/media/6031/download Production Team Daniel Ambinder, MDAmit Goyal, MDGurleen Kaur, MD

May 28, 2021

CardioNerds (Amit Goyal and Daniel Ambinder), Cardio-OB series co-chair and University of Texas Southwestern Cardiology Fellow, Dr. Sonia Shah, and episode lead and Columbia University Cardiology Fellow Dr. Ersilia DeFilippis discuss hypertensive disorders of pregnancy (HDP) with Dr. Jennifer Lewey from the University of Pennsylvania. In this episode, we cover chronic hypertension, gestational hypertension, and pre-eclampsia—all of which encompass HDP and complicate approximately 5-10% of all pregnancies. We also review risk factors for HDP, diagnostic criteria, peripartum and postpartum management, and much more! Be sure to tune in to hear Dr. Lewey discuss the future impact of HDP on cardiovascular disease for women later in life and strategies that can help improve care. Finally Dr. DeFilippis shares her perspectives from her ACC.org FIT Section article titled “Shattering the Glass” including strategies to shattering the glass and tackling imposter syndrome in improving the representation of women in medicine. Audio editing by CardioNerds Academy Intern, Leticia Helms. Claim free CME for enjoying this episode! Pearls • Quotables • Notes • References • Guest Profiles • Production Team CardioNerds Cardio-Obstetrics Series PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls To make a diagnosis of HDP, blood pressure should be measured on at least 2 occasions at least 4 hours apart.Hypertension diagnosed before 20 weeks gestation is considered chronic hypertension whereas hypertension after 20 weeks is categorized as gestational hypertension.Always check for warning signs for pre-eclampsia!One of the key treatments for pre-eclampsia is delivery but pre-eclampsia can occur still in the postpartum period.Aspirin use in pregnancy during second and third trimesters can reduce the risk of pre-eclampsia among women at risk. Quotables “Ideally a lot of these conditions come down to prevention and addressing potential cardio-obstetrics issues before they reach the cardio-obstetrics specialist.” “Blood pressure can continue to be elevated even after delivery.” “Pregnancy complications not only increase cardiovascular risk in the middle age population but also in the postmenopausal population.” “Women feel so relieved when they know that their care team is dedicated to taking care of women with cardiovascular disease when they are pregnant.” Show notes Why should CardionNrds learn and know about hypertensive disorders of pregnancy? Hypertensive disorders of pregnancy (HDP) complicate about 5-10% of all pregnancies. HDP is a term that encompasses chronic hypertension, gestational hypertension, pre-eclampsia, and pre-eclampsia superimposed on chronic hypertension. Women with history of HDP are at increased risk for stroke, ischemic heart disease, and cardiovascular death later in life. It is important to include obstetric history as part of our assessment of cardiovascular risk. This obstetric history should include the number of pregnancies, history of gestational diabetes, gestational hypertension, history of pre-eclampsia as well as history of pre-term birth. Following delivery, these women need close monitoring for development of chronic hypertension as well as primary prevention of cardiovascular disease. 2. How is gestational hypertension distinguished from chronic hypertension? The key factor in distinguishing gestational hypertension from chronic hypertension is the timing of diagnosis. Before 20 weeks gestation, elevated blood pressure (defined as a reading > 140/90 on two occasions at least 4 hours apart) is considered chronic hypertension. After 20 weeks gestation, elevated blood pressures signify a pregnancy-induced process, namely gestational hypertension or pre-eclampsia if blood pressure elevation is severe enough or there is evidence of end-organ damage. Blood pressure is often lower in the 1st and 2nd trimesters due to lower systemic vascular resistance. We think the process of gestational hypertension and pre-eclampsia result from how spiral arteries implant in the uterus. There are a whole host of local factors that lead to an increase in blood pressure later on in pregnancy. 3. What are warning signs of pre-eclampsia? Pre-eclampsia is diagnosed in the setting of high blood pressure, usually after 20 weeks, in the setting of proteinuria or end-organ dysfunction. End-organ dysfunction most commonly includes thrombocytopenia, transaminitis, right upper quadrant pain, headaches, pulmonary edema, and symptoms and signs that are not explained by other causes. Notably, blood pressure readings greater than > 160/110 mm Hg are sufficient for the diagnosis in the absence of other findings. 4. What are risk factors for pre-eclampsia or pre-eclampsia superimposed on chronic hypertension? Risk factors for pre-eclampsia include a personal or family history of pre-eclampsia in prior pregnancies, chronic hypertension, older age, multiple gestation, obesity, and Black race. 5. When do we start treatment for hypertension during pregnancy? For women who are newly diagnosed with hypertension during pregnancy, the threshold to begin treatment is 160 mm systolic and 110 mm diastolic. The caveat to this is for women with known cardiovascular disease or other comorbidities, a lower blood pressure goal should be targeted closer to 120-130 mm Hg systolic over 80 mm diastolic. Typically, a higher blood pressure is tolerated in order to avoid uteroplacental hypoperfusion which can impact the growth of the baby. The CHIPS randomized trial was published in the NEJM in 2015 and compared less tight control (targeting diastolic blood pressure of 100 mm Hg) or tight control (targeting diastolic blood pressure of 85 mm Hg). Although tight control decreased the rate of severe maternal HTN, there was no significant difference in the risk of pregnancy loss or overall maternal complications. How can we modify risk in women with hypertension during pregnancy? Low dose aspirin use (81 mg daily) in pregnancy during second and third trimesters can reduce the risk of pre-eclampsia among women at risk. The USPTF recommends the use of aspirin as preventative medication after 12 weeks of gestation in women at high risk for pre-eclampsia (Grade B). Risk factors that qualify someone as high risk include history of pre-eclampsia, multifetal gestation, chronic hypertension, type 1 or 2 diabetes, renal disease, and/or autoimmune disease. ACOG also recommends aspirin prophylaxis initiated between 12 and 28 weeks of gestation, optimally before 16 weeks and continued daily until delivery. 7. What is the best approach to anti-hypertensive medication use in pregnancy? First line agents used during pregnancy for treatment of hypertension include labetalol and nifedipine. Hydralazine is a second-line agent that may be used. Although methyldopa classically appears on board exams, it is less effective and has side effects including depression and fatigue. For women with a history of hypertension prior to pregnancy that is well-controlled on agents such as amlodipine or hydrochlorothiazide, these can be continued since limited evidence suggests they are safe although there is just less available evidence. For women on angiotensin-converting enzyme inhibitors, angiotensin-receptor blockers, or mineralocorticoid antagonists, these must be stopped given their teratogenic effects. This table from a recent JACC review by Halpern et al summarizes nicely safety of antihypertensive medications in pregnancy and during breastfeeding. 8. How do we treat pre-eclampsia? Treatment of pre-eclampsia depends on severity and gestational age. Management is primarily two-fold: 1) using intravenous medications such as labetalol and hydralazine to lower the blood pressure; 2) magnesium sulfate for seizure prophlaxis. Delivery may help resolve the symptoms of pre-eclampsia and may be considered following 37 weeks gestational age. References Halpern et al. Use of Medication for Cardiovascular Disease During Pregnancy: JACC State-of-the-Art Review. JACC 2019;73(4):457-476. ACOG Committee Opinion. Low Dose Aspirin-Use During Pregnancy. July 2018. Magee et al. Less-Tight versus Tight Control of Hypertension in Pregnancy. NEJM 2015;372:407-417. Wang Y-X, Arvizu M, Rich-Edwards JW, et al. Hypertensive disorders of pregnancy and subsequent risk of premature mortality. J Am Coll Cardiol. 2021;77(10):1302-1312. doi.org/10.1016/j.jacc.2021.01.018. Guest Profiles Dr. Jennifer Lewey Dr. Jennifer Lewey is an Assistant Professor at the University of Pennsylvania, Director of Penn Women’s Cardiovascular Health Program, and Co-Director of the Pregnancy and Heart Disease Program. Dr. Silia DeFilippis Ersilia DeFilippis is a third-year general cardiology fellow at Columbia University Irving Medical Center in New York City. She will be beginning her fellowship in advanced heart failure and transplant cardiology next academic year at Columbia. Her research and clinical interest are in sex differences in advanced heart failure management and outcomes, racial disparities in heart failure outcomes, and cardio-obstetrics. CardioNerds Cardioobstetrics Production Team Natalie Stokes, MDSonia Shah, MDAmit Goyal, MDDaniel Ambinder, MD

May 24, 2021

In the last episode, episode 126, we discussed pregnancy and aortic disorders as part of The CardioNerds Cardio-obstetrics Series. This episode brought to mind episode 76, where our colleagues from the Cleveland Clinic taught us about a woman named Lizzie Gasser, who at the young age of 27 tragically presented with postpartum pulmonary edema, found to have papillary muscle rupture, and was ultimately diagnosed with Vascular Ehlers Danlos Syndrome (VEDS) at autopsy. This case has been published in JACC Case Reports: CardioNerds Corner. Now, in this very special episode, we meet Lizzie Gasser, beyond her heart disease through the eyes of her loving husband, Todd Gasser. Her legacy underscores the importance of seeing our patients as people beyond their illness, in the context of their lives, values, and loved ones. This powerful discussion is led by Dr. Erika Hutt (cardiology fellow at the Cleveland Clinic) and Dr. Eunice Dugan, (internal medicine resident at Johns Hopkins Hospital). Dr. Harry “Hal” Dietz (professor of pediatrics, an associate professor of medicine and an assistant professor of neurological surgery at the Johns Hopkins University School of Medicine and a leading authority on genetic aortopathies (including Loeys-Dietz Syndrome which carries his name). Audio editing by CardioNerds Academy Intern, Dr. Maryam Barkhordarian. This episode is brought to you in collaboration with the VEDS Movement. The VEDS Movement’s mission is to save lives and improve the quality of life of individuals with Vascular Ehlers-Danlos Syndrome (VEDS). By pursuing the most innovative research, educating the medical community, general public and affected individuals, and providing support to patients, families, and caregivers, The VEDS Movement, which is a division of The Marfan Foundation, charges forward and improves the outcomes for those living with VEDS. Individuals affected with VEDS can access medical webinars presented by the experts, join support groups, get involved in events and research, and donate by visiting TheVEDSMovement.org. Providers can also find resources, including CME opportunities, at TheVEDSMovement.org. CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Photos & Youtube videos featuring Lizzie Gasser and her family https://www.youtube.com/watch?v=W4sVuctrUZs&t=1s Video from the VEDS movement that Lizzie's family is interviewed in. Their interview is from 7m30s - 17m16s https://www.youtube.com/watch?v=6CeXYnZHhbg Video of Lizzy's life life that a friend put together. Episode Guests Dr. Erika HuttDr. Eunice DuganDr. Harry “Hal” Dietz CardioNerds Case Report Production Team Karan Desai, MDAmit Goyal, MDDaniel Ambinder, MD

May 19, 2021

CardioNerd Amit Goyal, Cardio-OB series co-chair and University of Texas Southwestern Cardiology Fellow, Dr. Sonia Shah, and episode lead and Johns Hopkins University Cardiology Fellow, Dr. Anum Minhas, discuss pregnancy and aortic disorders with Dr. Nupoor Narula of Weill Cornell Medical College. Special introduction by Sukrit Narula. In this episode we discuss the presentation and management of aortopathies during pregnancy. We begin by examining the pathophysiology of aortic disease during pregnancy, followed by a review of the heritable aortopathies and their risk of dissection. We then discuss preconception evaluation and antepartum care of women with aortopathies. We end with addressing management at the time of labor and delivery. Claim free CME for enjoying this episode! Abstract • Pearls • Quotables • Notes • References • Guest Profiles • Production Team CardioNerds Cardio-Obstetrics Series PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Episode Abstract - Pregnancy and Aortic Disorders In this episode we discuss the presentation and management of aortopathies during pregnancy. We begin by examining the pathophysiology of aortic disease during pregnancy, followed by a review of the heritable aortopathies and their risk of dissection. We then discuss preconception evaluation and antepartum care of women with aortopathies. We end with addressing management at the time of labor and delivery. Pearls - Pregnancy and Aortic Disorders 1. Assessment of aortic root and ascending aortic measurements should be performed prior to conception in women with known aortopathies, connective tissue diseases with high risk for aortopathies, bicuspid aortic valve or familial thoracic aortic syndromes. Dimensions should always be verified with multi-modality imaging prior to decision-making. 2. It is important to recognize that the immediate postpartum period is a high risk period for aortic dissection in women with aortopathies. 3. Goal systolic blood pressure is 4.0 cm.The 2018 ESC guidelines advise against pregnancy for aortic root diameter > 4.5 cm.The decision to intervene prophylactically during pregnancy is highly individualized and complex, and we must weight patient factors including gestational age and rapidity of growth while balancing risk/benefits to the fetus and mother. Ehlers-Danlos syndrome (EDS)Vascular EDS patients are at high risk of arterial and uterine rupture, and the 2018 ESC Guidelines recommend against pregnancy. If after shared-decision making a patient decides to proceed with pregnancy, the patient should be cared for in a specialized center with a multi-disciplinary Cardio-Ob team.Loeys-Dietz syndromeThere is limited data is available, and it is insufficient to make any clear recommendations regarding pregnancy. Most centers will generally approach prophylactic aortic root surgery in Loeys-Dietz syndrome similar to Marfan disease and consider elective repair at 4.0 to 4.5 cm.More frequent intrapartum echocardiograms may be considered given some suggestion of increased risk of dilatation during pregnancy.Turner SyndromeThere is a strong association with bicuspid aortic valve (present in 15-30% of patients). Generally, we consider elective surgery in patients with an aortic size index (ASI) (ascending aortic root size indexed to body surface area) of > 2.5 cm/m2 and that pregnancy should be avoided at this ASI cutoff. During pregnancy, prophylactic aortic surgery can be considered with a dilated aorta (> 2.5 cm/m2 or rapid enlargement > 3mm)Many women with Turner syndrome require assisted reproductive therapy (ART) and assisted reproductive therapy may increase the risk of cardiovascular complications.Imaging of the thoracic aorta and heart are recommended within two years prior to pregnancy or assisted reproductive therapy.Imaging should be performed at least once per 20 weeks if there is no increased ASI or other cardiovascular risk factors (e.g., family history of dissection or sudden death, bicuspid aortic valve, coarctation, elongation of the transverse arch).Imaging should be performed every 4-8 weeks for those with ASI > 2.0 cm/m2 or additional risk factors during pregnancy, and once during the first month after delivery. Subsequent imaging intervals depend on the severity of the aortic enlargement.Bicuspid aortic valve (BAV)Up to 50% of patients with BAV also have ascending aortic dilatationESC guidelines recommend elective aortic surgery if the ascending aorta is > 5.0 cm prior to pregnancy.Familial Thoracic aortic aneurysmsFamily history is present in 20% of patients.A series in 53 women with ACTA2 mutations and total of 137 pregnancies showed 8 pregnancy-associated dissections (6 were type A) .Evidence is limited, however, and no clear recommendations for pregnancy are available. What are some delivery considerations for women with aortopathies?The overall goal is to decrease the cardiovascular stress of the delivery process, and risk for both the mother and baby need to be considered jointly with the Maternal Fetal Medicine team.For Marfan Syndrome and aortic root between 4-4.5 cm,

May 13, 2021

CardioNerds (Amit Goyal & Karan Desai) join University of Minnesota fellows, Dr. Julie Power, Dr. Sasha Prisco, and Dr. Abdisamad Ibrahim for a riveting discussion in which they were pressured to diagnose a young woman with syncope. The fellows expertly take us through the next steps in the differential diagnosis, and management of pulmonary hypertension in this young patient! University of Minnesota faculty and expert in right ventricular (RV) failure in pulmonary arterial hypertension (PAH) Dr. Kurt Prins provides the E-CPR for this episode. With this episode, the CardioNerds family warmly welcomes The University of Minnesota to the CardioNerds Healy Honor Roll. The CardioNerds Healy Honor Roll programs support and foster the the CardioNerds spirit and mission of democratizing cardiovascular education. Healy Honor Roll programs nominate fellows from their program who are highly motivated and are passionate about medical education. The University of Minnesota fellowship program director, Dr. Jane Chen has nominated Dr. Julie Power for this position. In addition to being a CardioNerds Ambassador, Julie has already done amazing CardioNerds work as part of the CardioNerds Academy fellowship. Claim free CME just for enjoying this episode! Disclosures: None Jump to: Patient summary - Case media - Case teaching - References CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Patient Summary- Syncope and Pulmonary Hypertension A Somali woman in her mid-30s with no significant past medical history presented with shortness of breath and exertional syncope. EKG revealed evidence of RV strain. CTA-PE protocol did not show PE. However, there was RV dilation and subsequent echocardiogram demonstrated normal LV, but moderately reduced RV function with evidence of RV pressure and volume overload. RVSP was estimated to be 188 mmHg! Case Media ABCDEFGHClick to Enlarge A. CXR, B. ECG, C. PA measurements: Main PA measures 2.4 cm, right PA measures 2.3 cm, left PA measures 1.9 cm, D. Tricuspid valve Doppler, E. RA tracing, F. RV tracing, G. PA tracing, H. Wedge tracing CTA PE: No PE, markedly dilated pulmonary trunk at 4.7 cm. Right main pulmonary artery measures 3.1 cm. TTE: Parasternal long axis: Moderate right ventricular dilation compressing left ventricle. Global right ventricular function is moderately reduced. TTE: Parasternal long axis- RV view: Right ventricular dilation with mild pulmonary regurgitation TTE: Mild pulmonary regurgitation with dilation of main PA TTE: Paradoxical septal motion consistent with right ventricular pressure and volume overload. TTE: Apical 4 chamberParadoxical septal motion consistent with right ventricular pressure and volume overload. Moderate right ventricular dilation.Global right ventricular function is moderately reduced.Severe right atrial enlargement. Paradoxical septal motion consistent with right ventricular pressure and volume overload.Moderate right ventricular dilation.Global right ventricular function is moderately reduced.Severe right atrial enlargement.Moderate to severe tricuspid regurgitation. TTE: Positive bubble study Episode Teaching Pearls Pulmonary hypertension (PH) can generally be categorized as pre-, post-, or combined pre- and post-capillary PH. Isolated pre-capillary pulmonary hypertension is characterized by: mean pulmonary artery pressure (mPAP) ≥ 20 mmHg, a pulmonary capillary wedge pressure (PCWP) ≤ 15 mmHg, and a pulmonary vascular resistance (PVR) ≥ 3 Woods units (WU). Pulmonary arterial hypertension (PAH) (WHO Group 1) falls under pre-capillary pulmonary hypertension.Schistosomiasis is the most common cause of PAH (WHO Group I) worldwide. Approximately 7% of patient with hepatosplenic schistosomiasis have PAH. Some studies suggest that treatment of with praziquantel reverses vascular remodeling; however, there is point of no return, beyond which, anthelmintic therapies are ineffective to prevent progression.Exertional syncope and pericardial effusion are both risk factors for higher mortality in PAH.Women with severe PAH have extremely high risk of maternal morbidity and mortality. Endothelin receptor antagonists are contraindicated in pregnancy due to teratogenicity. Therefore, a pregnancy test must be obtained monthly while on this therapy.Patients with a lower socioeconomic status, based on median household income, have more advanced PAH at the time of diagnosis. Notes 1. How do you approach syncope? Syncope is a sudden transient loss of consciousness associated with absence of postural tone followed by complete and usually rapid recovery. There should be not be clinical evidence of “non-syncope” conditions including seizures, hypoglycemia, drug or alcohol intoxication, concussion due to head trauma and so forth. One approach to determining the etiology of the syncope is to consider 4 major categories: orthostatic, reflex-mediated, cardiac-obstructive, or cardiac-electrical.Reflex-mediated (neurocardiogenic) syncope typically has a prodrome and encompasses vasovagal syncope, situational syncope, and carotid hypersensitivity.Orthostatic syncope is syncope occurring when rising from recumbency. It is generally associated with an orthostatic SBP drop by more than 20 mmHg or DBP drop by more than 10 mmHg with a compensatory rise in heart rate. We most commonly think of dehydration or hypovolemia causing orthostasis. Being post prandial can cause orthostasis as well. Neurogenic orthostatic hypotension (OH) involves excessive pooling of blood volume in the splanchnic and/or leg circulation. Upon standing, there is decreased venous return to the heart with a subsequent decrease in cardiac output and cerebral perfusion. The autonomic nervous system can typically increase vascular tone, inotropy and chronotropy; however, in neurogenic OH these mechanisms are inadequate. Conditions where neurogenic OH is relatively common include multiple system atrophy, Parkinson’s disease, Huntington’s disease, peripheral neuropathies (e.g., diabetes, amyloidosis), and spinal cord injury, amongst other etiologies. Finally, common medications associated with orthostatic syncope include diuretics, alpha blockers, and tricyclic antidepressants.Cardiac-obstructive syncope may occur from structural obstruction (i.e., aortic stenosis, HCM, mitral stenosis, pulmonary embolism) or other lesions which limit the stroke volume (i.e., pericardial tamponade, pulmonary hypertension.Cardiac-electrical syncope include both tachyarrhythmias and bradyarrhythmias, often without a prodrome. 2. What are the different types of pulmonary hypertension (PH)? What are the hemodynamic definitions of pulmonary hypertension? The WHO separates PH into 5 groups:Group 1: Pulmonary arterial hypertension (e.g., idiopathic, heritable [BMPR2], anorexigen associated, drug or toxin-associated, HIV, connective tissue disease associated, schistosomiasis, portal hypertension, congenital heart disease, amongst other causes)Group 2: Pulmonary hypertension due to left sided heart disease (e.g., HFrEF, HFpEF, left-side valvular heart disease)Group 3: Pulmonary hypertension due to lung disease or hypoxia: (e.g.,COPD, ILD, OSA, hypoxia without lung disease such as high altitude, developmental lung disorders)Group 4: PH due to pulmonary artery obstructions most commonly Chronic Thromboembolic Pulmonary Hypertension (CTEPH)Group 5: Multifactorial causes such as hematologic disorders (chronic hemolytic anemia, as with myeloproliferative disorders), metabolic disorders (e.g., Gaucher disease, glycogen storage diseases, CKD), and systemic disorders (e.g., pulmonary Langerhans cell histiocytosis, neurofibromatosis, sarcoidosis) When we consider the hemodynamics of pulmonary hypertension, we break down PH into isolated pre-capillary, isolated post-capillary, or combined pre-and post-capillary pulmonary hypertension. Mean Pulmonary Artery Pressure (mmHg)Wedge Pressure (mmHg)Pulmonary Vascular Resistance (Woods Units)WHO GroupsPre-capillary> 20≤ 15≥ 31, 3, 4, 5Post-capillary> 20> 15 20> 15≥ 32, 5, multifactorial PAH falls under pre-capillary pulmonary hypertension, which is defined as mean pulmonary artery pressure (mPAP) ≥ 20 mmHg, a pulmonary capillary wedge pressure (PCWP) ≤ 15 mmHg, and a pulmonary vascular resistance (PVR) ≥ 3 Woods units (WU). 3. How do you work up suspected PAH? To start investigating for PAH, as always, we start with a thorough history and physical. The most common presenting symptom of pulmonary hypertension in general is exertional dyspnea/reduced exercise tolerance. Symptoms of PH can be nonspecific, especially early in its course, and thus there can be a delay in diagnosis. Remember, some patients have increased risk of developing PH and should be screened. These are patients with known risk factors for developing PAH, including relatives of patients with BMPR2 mutations, HIV, connective tissue disease (especially systemic sclerosis), portal hypertension, etc.Other accompanying symptoms may include chest pain, fatigue, and lightheadedness. Manifestations of more advanced disease include syncope, abdominal distension, and significant lower extremity edema attributable to right ventricular (RV) failure.Physical exam may reveal a loud P2, murmur of tricuspid regurgitation, an RV S3, jugular venous distension with or without Kussmaul’s sign, liver pulsatility, ascites, and/or peripheral edema.Review the CXR and EKG for findings consistent with pulmonary hypertension. Common EKG findings include right atrial enlargement, right axis deviation, RBBB, and an RV strain pattern in the right precordial leads.

May 9, 2021

CardioNerd (Amit Goyal), cardioobstetrics series co-chair Dr. Sonia Shah (FIT, UT Southwestern) and episode lead Dr. Kayle Shapero (FIT, UPMC) discuss pregnancy in patients with pulmonary hypertension with Dr. Candice Silversides, Associate Professor of Medicine and the Director of the Pregnancy and Heart Disease program and head of the Obstetric Medicine program at the University of Toronto. Disclosures: None Claim free CME for enjoying this episode! Abstract • Pearls • Quotables • Notes • References • Guest Profiles • Production Team CardioNerds Cardio-Obstetrics Series PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Episode Abstract In this episode we discuss the important and challenging topic of pulmonary hypertension in pregnancy. We’ll start by discussing the prevalence of pulmonary hypertension in pregnancy, as well as the associated maternal morbidity and mortality associated with each WHO class. We will use a case to help us illustrate the appropriate workup for pulmonary hypertension patients and to help us broach the challenging topic of pregnancy termination. In this case we will further explore advanced management options including pulmonary vasodilators, anti-coagulation, and the use of mechanical support. Don’t miss this opportunity to hear Dr. Silversides’ share her wisdom on the importance of a multidisciplinary care team to plan both the delivery as well as post-partum care to help prevent adverse outcomes for both the mother and baby. Pearls Pregnancy in pulmonary hypertension, regardless of the class, is considered high risk. Even women who appear hemodynamically stable at baseline can easily decompensate in pregnancy, and thus the overall mortality and morbidity are very high.Due to the high risk of maternal morbidity and mortality during pregnancy for women with pulmonary arterial hypertension, the option of termination of pregnancy should be discussed. Multidisciplinary care teams are the key to achieving optimal pregnancy outcomes in these patients. It is critical to create a team of experts with experience in pulmonary hypertension and plan for constant communication over the course of pregnancy.Pulmonary vasodilators including CCBs, phosphodiesterase inhibitors, and prostacyclin analogues should be initiated early to mitigate adverse outcomes.The majority of the complications in pulmonary hypertension patients occur after delivery, and so having a clear and safe postpartum plan is critical to a positive outcome. Quotables “We will someday identify the women who maternal morbidity and mortality is perhaps lower and we'll be able to give a better, risk assessment. But we're not quite there yet. And so currently, any woman who has pulmonary hypertension, true pulmonary hypertension in particular, pulmonary arterial hypertension, should be advised to avoid pregnancy.“ – Dr. Silversides“Women with PH can be falsely reassuring because they can walk in and look pretty good. And they're young, you know, they're not like the normal 70-year-old you might see on the ward. And so, you think they're going to be okay, but they can spiral downward very quickly. So I do think you also have to have a very high, um, uh, level of. Uh, caution in these patients.“- Dr. Silversides on assessing PH patients in pregnancy “I would tell you that I still think honesty is the best policy. I think you should offer women as much information as we currently know, so they can make informed decisions that are right for them. I think you also do have to really be sensitive to how you're delivering this information, because remember (for) some women it will have never occurred to them that they can't have a pregnancy. They may have been planning on having a kids and family and this information can really derail them. So you do have to use sensitivity, but I think you have to do it to accommodate to the patient that you're seeing. I don't think there can be a one size fits all approach.”- Dr. Silversides on the challenging topic of how to approach pregnancy termination conversations“… continue to optimize your care, the better shape the woman is going into delivery. The better outcomes you'll have at the time of labor and delivery.”- Dr. Silversides Show notes 1. How do we define pulmonary hypertension (PH) and why is it such a big deal in pregnancy? According to recent guidelines pulmonary hypertension is a mean pulmonary artery pressure ≥ 20 mmHg.The WHO separates PH into 5 groups:Group 1: Pulmonary arterial hypertension (e.g., idiopathic, heritable [BMPR2], anorexigen associated, drug or toxin-associated, HIV, connective tissue disease associated, schistosomiasis, portal hypertension, congenital heart disease, amongst other causes)Group 2: Pulmonary hypertension due to left sided heart disease (e.g., HFrEF, HFpEF, left-side valvular heart disease)Group 3: Pulmonary hypertension due to lung disease or hypoxia: (e.g.,COPD, ILD, OSA, hypoxia without lung disease such as high altitude, developmental lung disorders)Group 4: PH due to pulmonary artery obstructions most commonly Chronic Thromboembolic Pulmonary Hypertension (CTEPH)Group 5: Multifactorial causes such as hematologic disorders (chronic hemolytic anemia, as with myeloproliferative disorders), metabolic disorders (e.g., Gaucher disease, glycogen storage diseases, CKD), and systemic disorders (e.g., pulmonary Langerhans cell histiocytosis, neurofibromatosis, sarcoidosis) The prevalence of pulmonary hypertension and pregnancy is somewhere between 0.011 and 0.02%2. Although rare, this number has been rising due to the number of congenital patients living to childbearing age, as well as the emergence of effective pulmonary vascular therapy.Complications of PH during pregnancy include:The normal physiologic changes of pregnancy (increased plasma volume, increased stroke volume, increased cardiac output, decreased systemic vascular resistance), are poorly tolerated in PH due to an inability to decrease pulmonary vascular resistance and accommodate this increased plasma volume. This can lead to increased right ventricular overload.Decrease in systemic vascular resistance and associated drop in blood pressure can also lead to decreased RV perfusion, contributing to RV failure and making it increasingly difficult to accommodate the extra afterload demand.Pregnancy is both a prothrombotic and a pro-arrhythmic state, and maternal morbidity and mortality may also be related to complications from DVT/PE/arrhythmias, all of which are poorly tolerated by a failing RV with the increased afterload of PH and possible decreased perfusion from lower SVR.Abnormal maternal hemodynamics in PH also contribute to increased fetal and neonatal complications including preterm birth, fetal and neonatal death. 2. How does the severity of PH or the patient’s WHO group impact maternal outcomes? MortalityOverall mortality for PH patients during pregnancy is quite high: Two major systematic reviews covering a time span of 30 years in nearly 200 pregnancies cited total mortality to range between 25-38%. The majority of patients died within the first month after delivery and major causes of death were heart failure, sudden cardiac death and pulmonary embolism4,5 MorbidityA comprehensive study looking at approximately 1500 pregnant women with PH from the national inpatient sample (spanning from 2003-2012) found that the rate of major adverse cardiovascular events was around 24.8%.6Karen et al assessed outcomes in ~150 pregnancies from the ROPAK study according to PH etiology (idiopathic PAH, PH due to congenital heart disease, PH due to left sided disease). Morbidity and mortality were highest in women with idiopathic PAH, and lowest in women with PH due to left sided heart disease. Complications were also higher in patient with severe PH (RVSP >70mmHg).7Meng et al assessed 49 pregnancies from four large centers and found mortality to vary according to PH subgroup: 23% mortality in Group 1 patients, as compared to a 5% mortality in all other WHO groups. Similarly, patients with severe PH (RVSP >50mmHg) had a higher need for advanced therapies as compared to women with mild PH.1Several variables determine risk during pregnancy related to PH, including the WHO group, etiology of PH, functional class, need for PAH medications at baseline, as well as cardiac size and function. 3. What is the recommended initial workup to help identify and risk stratify patients with PH? Helpful baseline information includes BNP, prior echocardiograms, as well as hemodynamics from prior right heart catheterizations.For those patients previously treated for PH, it is important to identify which medications were used in the past or are currently being prescribed. This particularly important to identify teratogenic medications like endothelin antagonists.One of the most important factors is to identify the patient’s functional status including assessing six-minute walk tests, including O2 saturation, desaturation, and distance walked.Of note, while a RHC helps define the hemodynamic profile, the entire vascular bed is more fragile during pregnancy than in a non-pregnant state, and there have been reports of pulmonary artery rupture with interventions during pregnancy.8 This must be kept in mind when assessing the need for RHC. 4. How do you approach management of patients with PH during pregnancy? Frequent follow-ups and communication with the entire multidisciplinary team are vital. This team should include cardiology, a PH specialist and/or team, high risk obstetrics, and OB anesthesia.Patients should be monitored serially throughout pregnancy with the use of BNP, echocardiography, and assessment of functional status/symptoms.While every patient situation will be different,

May 4, 2021

CardioNerd (Amit Goyal), cardioobstetrics series co-chair Dr. Natalie Stokes, Cardionerds Duke University CardioNerds Ambassador and episode lead fellow, Dr. Kelly Arps, join Dr. Andrea Russo, Director of Electrophysiology and Arrhythmia Services at Cooper Medical School of Rowan University and immediate past president Heart Rhythm Society, for a discussion about pregnancy and arrhythmia. Stay tuned for a message from Dr. Sharonne Hayes about WomenHeart. Audio editing by Gurleen Kaur. Claim free CME for enjoying this episode! Dr. Russo's disclosures: Johnson and Johnson, Medtronic, Inc., Boston Scientific Corporation, Kestra, Medilynx, Up-to-Date, and ABIM. Abstract • Pearls Notes • References • Guest Profiles • Production Team CardioNerds Cardio-Obstetrics Series PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Episode Abstract Pregnant patients may have exacerbation of underlying arrhythmic syndromes or unmasking of previously undiagnosed arrhythmic syndromes. Management of atrial and ventricular tachyarrhythmias should proceed with increased urgency in pregnant patients due to risk of adverse hemodynamic events in the mother and fetus. Cardioversion of atrial and ventricular arrhythmias is safe in pregnancy. Preferred antiarrhythmic agents in pregnant patients include metoprolol, propranolol, verapamil, flecainide, propafenone, sotalol, procainamide, and lidocaine. Management of arrhythmias in pregnancy should include collaboration with obstetrics and maternal-fetal medicine teams. Pearls Pre-conception counseling is a shared decision making process; include obstetrics and maternal-fetal medicine colleagues in challenging cases. Have a high sense of urgency for acute arrhythmias in pregnancy due to risk of impaired fetal perfusion. Goals of acute arrhythmic management should include rapid treatment while avoiding hypotension. In scenarios when beta blockers are indicated, metoprolol and propranolol are first choice. Avoid atenolol as this drug has the highest risk of fetal bradycardia and intra-uterine growth retardation in the class. Lidocaine or procainamide should be first line for ventricular arrhythmias in pregnancy. Amiodarone is potentially teratogenic and should not be used in pregnant patients unless all other options have been exhausted. Show notes 1. What are the expected electrophysiologic changes associated with pregnancy? Increase in resting heart rate which peaks in third trimesterPR shorteningECG axis shift leftward and upwardNon-specific ST and T wave changes These changes, along with increased cardiac output and volume with increased stretch in all chambers, increase the risk of re-entrant arrhythmias in those who are predisposed. ↑ atrial volume -> ↑ stretch -> ↑ ectopy -> ↑ risk for re-entrant arrhythmias 2. What is the approach to pre-conception counseling for patients with known arrhythmias or arrhythmic syndromes? Anticipate frequency and potential severity of adverse arrhythmic outcomes during pregnancy and post-partum periodConsider available options for rhythm control and anticoagulation therapy, as appropriate, during the pre-conception, pregnancy, and post-partum periodsConsider catheter ablation prior to pregnancy, particularly for curable arrhythmias such as Wolff-Parkinson-White (WPW) and AVNRT Offer genetic counseling about hereditary risk to fetus for inherited arrhythmias such as Brugada syndrome and Long QT syndrome 3. What is the management of SVT in pregnancy? Consider the increased risk of tachyarrhythmias in pregnancy: Typically benign arrhythmias can lead to more rapid decompensation in mother due to increased baseline cardiac output. Typically benign arrhythmias can lead to rapid danger to the fetus due to maternal hypotension and shortened diastolic filling time, both of which contribute to impaired fetal perfusion. Treatment algorithm is identical to that of non-pregnant patients Attempt vagal maneuversAdenosine is safeCardioversion is safe: monitor the fetus during and after cardioversionIn stable arrhythmias, choose nodal blocking agents with the best safety profile: metoprolol, propranolol, and verapamil. Evaluation of the pregnant patient with new onset SVT Have a high index of suspicion for underlying structural heart disease such as peripartum cardiomyopathy in a pregnant women with new diagnosis of SVT – presence of structural heart disease significantly increases the risk of maternal morbidity and mortality. Pregnancy can be the first presentation of inherited arrhythmia syndromes that commonly present in young adults such as WPW, Brugada Syndrome, Catecholaminergic Polymorphic VT (CPVT), Long QT Syndrome (LQTS), Arrhythmogenic Right Ventricular Cardiomyopathy / Dysplasia (ARVC/D), and Hypertrophic Cardiomyopathy (HCM). 4. What are some special considerations for acute management of VT in pregnancy? Cardioversion is safe. First line pharmacologic therapy: lidocaine or procainamide Lidocaine has been associated fetal bradycardia but has been used safely without reported teratogenic effectBrugada syndrome: consider quinidine in Brugada syndromeFascicular VT: use verapamilOnly use amiodarone if absolutely necessary, and after the first trimester 5. What is the approach to chronic arrhythmia management in pregnancy? Preferred rate control agents: MetoprololPropranololDigoxinVerapamil AVOID: atenolol (increased risk of fetal bradycardia and intrauterine growth restriction; note that this risk is present with all beta blockers*) Preferred rhythm control agents: Flecainide (if no structural heart disease)Propafenone (if no structural heart disease)SotalolLidocaineProcainamideQuinidine AVOID: amiodarone; use only in a patient with refractory unstable arrhythmias after the first trimester (due to fetal thyroid and neurodevelopmental issues) AVOID: dronedarone; Category X in pregnancy Catheter ablation in the pregnant patient Best delayed until late in pregnancy or after deliveryMaternal-fetal medicine colleagues should be involved in procedural planningMinimize fluoroscopic timeShield the pelvis during fluoroscopy and use electroanatomic mapping *Surveillance for pregnant patients on beta blockers: Serial growth ultrasounds in the third trimesterAntenatal testing of for bradycardia and hypoglycemiaPostnatal monitoring for: BradycardiaApneaGrowth retardation 6. What is the approach to antiarrhythmic therapy in the breastfeeding patient? All antiarrhythmic drugs are passed into breast milk Preferred rate control agents: metoprolol, propranolol (watch for fetal bradycardia)Rhythm control agents: weigh risks and benefits; read dosing adjustments on prescribing instructions carefully AVOID: atenololAVOID amiodaroneAVOID: dronedarone 7. What is the approach to anticoagulation in pregnancy and breastfeeding? Use the CHAD2S2-VASc score to estimate stroke risk for pregnant patients with AF and AL Risk of stroke with AF and AFL in pregnancy are uncertain, as women of childbearing age were minimally represented in large studies evaluating prophylactic antithrombotic drug treatment. Pregnancy Low molecular weight heparin is preferred in the first trimester and around the time of delivery.Warfarin should be avoided during the first trimester (especially at doses >5 mg daily), but may be used in the second and beginning of the third trimester.Avoid DOACs Breastfeeding Use warfarin or LMWH AVOID: DOACs may be excreted in breast milk and should not be used during breast feeding. 8. What is the approach to specific arrhythmic syndromes? AVNRT: recommend catheter ablation prior to conception if prior diagnosis. Manage acute events if they occur during pregnancy. WPW: recommend catheter ablation prior to conception if prior diagnosis. Use procainamide for acute arrhythmic events and avoid nodal blocking agents. LQTS:recommend beta blockers (metoprolol or propranolol) through pregnancy and at least through the post -partum period CPVT: recommend beta blockers (metoprolol or propranolol) through pregnancy and at least through the post-partum period 9. What is the approach to management of cardiac arrest in the pregnant patient? ACLS should be performed per ACLS guidelines, including chest compressions and defibrillation. Positioning: aim to avoid IVC compression and impaired venous return to the heart in the supine pregnant patient. Patients with a pulse: left lateral decubitusNo pulse: Manually displace the uterus to the leftAll patients: place IVs above the diaphragm Be prepared for difficult airway in mother due to airway edema Call OB and neonatal teams immediately to determine need for emergency C-section if no ROSC within the first several minutes. References Lindley KJ, Judge N. Arrhythmias in Pregnancy. Clin Obstet Gynecol. 2020;63(4):878-892. doi:10.1097/GRF.0000000000000567 Vaidya VR, Arora S, Patel N, et al. Burden of Arrhythmia in Pregnancy. Circulation. 2017;135(6):619-621. doi:10.1161/CIRCULATIONAHA.116.026681 Seth R, Moss AJ, McNitt S, et al. Long QT syndrome and pregnancy. J Am Coll Cardiol. 2007;49(10):1092-1098. doi:10.1016/j.jacc.2006.09.054 Hodes AR, Tichnell C, Te Riele AS, et al. Pregnancy course and outcomes in women with arrhythmogenic right ventricular cardiomyopathy. Heart. 2016;102(4):303-312. doi:10.1136/heartjnl-2015-308624 European Society of Gynecology (ESG); Association for European Paediatric Cardiology (AEPC); German Society for Gender Medicine (DGesGM), et al. ESC Guidelines on the management of cardiovascular diseases during pregnancy: the Task Force on the Management of Cardiovascular Diseases during Pregnancy of the European Society of Cardiology (ESC).

Apr 26, 2021

CardioNerd (Amit Goyal), Narratives in Cardiology FIT representative Dr. Zarina Sharalaya and Cleveland Clinic fellow Dr. Gregory Ogunnowo join Dr. Quinn Capers IV, UTSW as Professor of Medicine, Associate Dean of Faculty Diversity, and the inaugural Vice Chair of Diversity, Equity, and Inclusion in the Department of Internal Medicine, for an important and moving discussion about diversity, implicit bias, and #BlackMenInMedicine. Special thanks to Dr. Kimberly Manning for her introductory remarks for Dr. Capers. Audio editing by CardioNerds Academy Intern, Dr. Maryam Barkhordarian. Claim free CME just for enjoying this episode! Click here to see Dr. Caper's tweet regarding his daughter's original peice Cardionerds Narratives in Cardiology PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll Subscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! https://twitter.com/DrQuinnCapers4/status/1277715623246733317?s=20 CardioNerds Narratives in Cardiology The CardioNerds Narratives in Cardiology series features cardiovascular faculty representing diverse backgrounds, subspecialties, career stages, and career paths. Discussing why these faculty chose careers in cardiology and their passion for their work are essential components to inspiring interest in the field. Each talk will feature a cardiology faculty from an underrepresented group, within at least one of several domains: gender, race, ethnicity, religion, national origin, international graduate status, disadvantaged backgrounds, etc. Featured faculty will also represent a variety of practice settings, academic ranks, subspecialties (e.g. clinical cardiology, interventional cardiology, electrophysiology, etc), and career paths (e.g. division chief, journal editor, society leadership, industry consultant, etc). Faculty will be interviewed by fellows-in-training for a two-part discussion that will focus on: 1) Faculty's content area of expertise2) Faculty's personal and professional narrative As part of their narrative, faculty will discuss their unique path to cardiology and their current professional role with particular attention to challenges, successes, and advice for junior trainees. Specific topics will be guided by values relevant to trainees, including issues related to mentorship, work-life integration, and family planning. To help guide this important initiative, the CardioNerds Narratives Council was founded to provide mentorship and guidance in producing the Narratives series with regards to guests and content. The CardioNerds Narratives Council members include: Dr. Pamela Douglas, Dr. Nosheen Reza, Dr. Martha Gulati, Dr. Quinn Capers, IV, Dr. Ann Marie Navar, Dr. Ki Park, Dr. Bob Harrington, Dr. Sharonne Hayes, and Dr. Michelle Albert. The Narratives Council includes three FIT advisors who will lead the CardioNerds’ diversity and inclusion efforts, including the current project: Dr. Zarina Sharalaya, Dr. Norrisa Haynes, and Dr. Pablo Sanchez. Guest Profiles - Physician Scientists Women Electrophysiology Dr. Quinn Capers, IV Dr. Quinn Capers, IV grew up in Dayton Ohio and left his hometown to do his undergraduate training at Howard University. He began his journey in medicine at The Ohio State University and went on to do residency, cardiology fellowship, and interventional cardiology training at Emory University. After graduation he worked for 8 years in private practice, and made the switch back to academics and came back to Ohio State to continue his career. In 2009, he was named associate dean of admissions and in 10 years, the College of Medicine went from 13% underrepresented minorities to 26% of the 2019 entering class, and in the last 6 years women have outnumbered men in the incoming classes. In 2019 he was promoted to Vice Dean for Faculty Affairs, received the award for professor of the year, and the Diversity Champion Award from the institution. Most recently, the state of Texas gained a gem as Dr. Capers has moved to join the UTSW as Professor of Medicine, Associate Dean of Faculty Diversity, and the inaugural Vice Chair of Diversity, Equity, and Inclusion in the Department of Internal Medicine. He has an expansive list of accolades and awards. Dr. Capers was awarded the AHA Laennec Clinician Educator Award in 2018. He was recognized as the 2020 recipient of the Exemplary Leadership Award of the Group on Diversity and Inclusion from the Association of American Medical Colleges (AAMC). He is an inaugural member of the American College of Cardiology’s Diversity and Inclusion Task Force. In 2021 he received the Pamela S. Douglas Distinguished Award for Leadership in Diversity and Inclusion. He has had an impactful presence on social media where he created the hashtags #BlackMenInMedicine and #TakeAWomanToTheCathLab. Dr. Capers is a passionate advocate for enhancing diversity and inclusion, a champion for improving health equity, and a devoted mentor to countless trainees. Dr. Zarina Sharalaya Dr. Zarina Sharalaya is an interventional cardiology fellow at the Cleveland Clinic. She completed medical school at The Ohio State University and then completed her residency at The University of North Carolina Chapel Hill. She moved back to her home state of Ohio to do general cardiology fellowship at The Cleveland Clinic. Zarina has been very involved with the Ohio ACC and this year has served as co-chair of the FIT Council. She is passionate about the Women in Cardiology initiative has been able to help formulate the first WIC chapter for Ohio ACC. She enjoys traveling, music, and spending time with her husband and new puppy Zuma. Dr. Greg Ogunnowo Dr. Gregory Ogunnowo (Dr_GregoryO) is a cardiology fellow at the Cleveland Clinic. He completed medical school at the University of South Carolina School of Medicine in Columbia, South Carolina. He went on to complete internal medicine residency at Washington University School of Medicine in St. Louis where he stayed on as faculty in the Department of Hospital Medicine for a year prior to pursing fellowship. His interests include outcomes research in interventional cardiology and medical education In his spare time, Greg enjoys traveling, exercising, and experiencing new cultures through their food. When he’s not in the hospital, you can find Greg planning a trip with close friends and family. References Ellis J, Otugo O, Landry A, Landry A. Interviewed while Black. N Engl J Med. 2020 Dec 17;383(25):2401-2404. doi: 10.1056/NEJMp2023999. Epub 2020 Nov 11. PMID: 33176078. Amit Goyal, MDDaniel Ambinder, MD

Apr 26, 2021

CardioNerds (Amit Goyal & Daniel Ambinder) join Dr. Rayan Jo Rachwan, Dr. Anupama Joseph, and Dr. Mohammed Merchant from the University of Wisconsin-Madison for a classic Madison dinner cruise! They discuss the following case: Mixed shock secondary to severe right ventricular outflow tract obstruction with Gemella Haemolysans prosthetic pulmonary valve endocarditis in a young patient with Shone Complex (syndrome). Dr. Ford Ballantyne III provides the E-CPR segment for this episode. Special introductory music composed by Dr. Rayan Jo Rachwan. We are excited to welcome University of Wisconsin- Madison to the CardioNerds Healy Honor Roll and Dr. Rayan Jo Rachwan as the CardioNerds Ambassador. Claim free CME just for enjoying this episode! Jump to: Patient summary - Case media - Case teaching - References CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Patient Summary A 26-year-old male with history of bicuspid aortic valve and Shone Complex (syndrome)—status post coarctation repair, subaortic resection and Ross-Konno operation—presenting with 3 months of constitutional and respiratory symptoms. Initial evaluation demonstrated that patient was in a state of mixed shock due to a large pulmonary Melody valve thrombus with superimposed Gemella Haemolysans prosthetic valve endocarditis. He required treatment with inotropes, pressors, followed by intubation and extracorporeal membrane oxygenation (ECMO). Patient was treated initially via right heart catheterization with balloon dilation and stent placement to his right ventricle-to-pulmonary artery conduit, which lead to significant improvement in his hemodynamics. Patient was then decannulated from ECMO, extubated, weaned off pressor support and later underwent a successful surgical resection of the infected pulmonary homograft and Melody valve/stents and replacement with pulmonary-valved conduit. He was also discharged on a prolonged course of antibiotics. Case Media - Shone Complex A B C D Click to Enlarge A. CXR, B. ECG, C. TV Doppler, D. PV Doppler CTA Chest •Melody pulmonic valve repair with large thrombus arising from the mid-distal valve extending into the main pulmonary artery and proximal left pulmonary artery. Evaluation for distal subsegmental pulmonary emboli is limited. •Tiny focus of air in the thrombus may be related to contrast injection. Infection is less likely. •Enlarged right heart chambers, may be in part chronic right heart enlargement and/or new right heart strain. No pulmonary infarct. CT chest abdomen and pelvis with contrast •Findings suggestive of acute hepatitis and acute pancreatitis. No pancreatic hypoenhancement or peripancreatic fluid collection. •No abscess within the abdomen or pelvis. •Small caliber of the infrarenal abdominal aorta and bilateral iliac arteries, probably congenital. TTE 1 TTE 2 TTE 3 TTE 4 TTE 5 TTE 6 RHC with balloon dilation of the RV-PA conduit and evidence of multiple levels of stent fracture. Pulmonary angiogram showing no evidence of distal embolization or significant pulmonary embolism and no evidence of perforation. There is evidence of moderate pulmonary insufficiency into a dilated right ventricle. Episode Teaching - Shone Complex Pearls 1. Patients with congenital heart disease are more predisposed to infective endocarditis (IE). Therefore, there should be a low-threshold for infectious workup in the case of unexplained fever or malaise without associated symptoms for >72 hours. Every routine visit should screen for symptoms and signs of IE. 2. Treatment of right ventricular (RV) outflow tract obstruction with balloon dilation +/- stenting can be considered as a bridge to valve replacement in the case of severe hemodynamic compromise; thus, restoring RV and pulmonary artery coupling. As with many complex decisions this should be made in consultation with an experience heart team and shared decision making with the patient or proxy. 3. Patients with RV volume and/or pressure overload from right-sided valve etiology should be assessed serially (i.e., yearly) with transthoracic echocardiography. 4. When precise quantitative data about the RV is required to make important clinical decisions (e.g., when to recommend pulmonary valve replacement), cardiac magnetic resonance imaging (CMR) remains the diagnostic modality of choice. 5. Repairing or replacing the pulmonary valve should be considered when RV end-diastolic volume >160 mL/m2 and/or RV end-systolic volume >80 mL/m2 on CMR. Notes What is Shone syndrome? Shone syndrome (a.k.a. Shone anomaly, Shone complex) is a rare congenital abnormality that accounts for 0.6% of all congenital abnormalities.It is characterized by a series of left-sided obstructive lesions. The diagnosis is made with the presence of at least 3 of 8 described lesions.The 8 described lesions are:Cor TriatriatumSupramitral ringParachute mitral valveSubaortic stenosisBicuspid aortic valve and small aortic valve annulusCoarctation of the aortaHypoplastic (stiff) left ventricle.Small aortic archSupravalvular mitral ring, parachute mitral valve, subaortic stenosis, and coarctation of the aorta were the first four described lesions and constitute the classic constellation of Shone complex.Incomplete forms involve an LV inflow lesion plus at least one LV outflow lesion.Frequently, coarctation of the aorta is recognized before the other defects are detected. The coarctation may mask the effects of the other lesions and some patients with Shone syndrome are only diagnosed when symptoms persist after coarctation repair. How does Shone syndrome manifest? The symptoms associated with Shone syndrome are mostly symptoms of congestive heart failure (which can occur in the first week of life), potentially presenting in early childhood as fatigue, rapid breathing and wheezing, faster than normal heart rate, poor oral intake, poor weight gain, fluid retention (edema) in the legs, pallor (anemia), and frequent pneumonias.In a series of 28 adult patients with Shone syndrome followed for a median of 8 years (Aslam et al., CJC 2016), nearly half had cardiovascular hospitalizations during adulthood, mostly for arrhythmias or heart failure.The severity and prognosis depend on the individual lesions involved and the degree of obstruction to flow they cause. How is Shone syndrome diagnosed? Diagnosis involved multimodality imaging predominantly with TTE, as well as TEE, CMR, and/or cardiac CTA as useful adjuncts depending on the lesions and patient age.Invasive hemodynamics and angiography are important adjuncts, particularly while planning repair. How is Shone syndrome treated? It is treated by addressing each of the constituent defects. For example:Coarctation of the aorta:Treated surgically with excision with end-to-end anastomosis or subclavian flap angioplasty. Alternatively, it can be treated with transcatheter balloon angioplasty, particularly in the case of re-coarctation after surgical repair.Subaortic stenosis:Treated surgically by excising the excess tissue below the aortic valve. If other forms of aortic stenosis are present, surgical repair may involve the replacement of the aortic valve.Mitral stenosis (caused by “parachute” mitral valve and by supravalvular mitral membrane):Treated by surgery (valve replacement vs. valve repair). What is the prognosis of patients with Shone syndrome? The long-term prognosis for patients with Shone syndrome is difficult to predict and is extremely variable depending on the lesions involved and degree of obstruction.It depends on the extent of mitral valve disease, the degree to which the left ventricle is hypoplastic, and the cumulative effects of surgical treatments.Moreover, patients who develop pulmonary arterial hypertension (PAH) have a poorer prognosis. Early surgical intervention is important to prevent the adverse consequences of long-standing obstruction and ensuing PAH. How are patients with Shone syndrome followed-up? With regard to right ventricular (RV) assessment, echocardiography (more widely available) provides useful diagnostic information in many clinical circumstances that affect the right heart.However, when precise quantitative data is required to make important clinical decisions (e.g., when to recommend pulmonary valve replacement), cardiac magnetic resonance imaging (CMR) remains the diagnostic modality of choice.Repairing or replacing a dysfunctional pulmonary valve should be considered when RV end-diastolic volume (RVEDV) >160 mL/m2 and/or RV end-systolic volume (RVESV) >80 mL/m2 on CMR.RV normalization could be achieved with pulmonary valve replacement when preoperative RVEDV is ≤160 mL/m2 or RVESV is ≤80 mL/m2 on CMR. What is the Melody valve and what is it used for? The Melody valve consists of bovine jugular vein sewn within a platinum-iridium stent.Transcatheter pulmonary valve placement with the Melody valve is effective in the short term for relief of right ventricular outflow tract (RVOT) obstruction and pulmonary regurgitation in patients with surgically implanted right ventricle–to–pulmonary artery conduits.Melody stent fracture (MSF) with valve dysfunction is the most common indication for reintervention after Melody valve placement.MSF is more likely in patients with severely obstructed RVOT conduits and when the Melody valve is directly behind the anterior chest wall and/or clearly compressed.Pre-stenting of the conduit before valve implantation improves the durability of the implanted valve. Congenital heart disease (CHD) and infective endocarditis (IE)?

Apr 25, 2021

CardioNerds (Amit Goyal, Daniel Ambinder, Carine Hamo, and Karan Desai) are honored to bring to you the Braunwald Chronicles. These are stories of discovery, innovation, accidents, perseverance, and more…truly these are the stories of cardiology, directly from a father of modern cardiology himself, Dr. Eugene Braunwald. Dr. Braunwald’s life and stories together are the saga which have brought us to this day in modern cardiology. So please join us for this wonderful series, as we journey through the history of cardiology, across 6 extraordinary chapters. We complete The CardioNerds Braunwald Chronicles with Chapter 6 where Dr. Braunwald discusses triple threats, randomized controlled trials, textbooks & digital education. He reflects on the impact he has had through education through text books and how being an educator has been just as gratifying to him as being a scientist. We thank Dr. Karan Desai, Editorial APD with the CardioNerds Academy, and fellow at University of Maryland, for all the work he put into designing the Braunwald Chronicles. Audio editing by Pace Wetstein. CardioNerds Braunwald Chronicles Series PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron!

Apr 23, 2021

CardioNerds (Amit Goyal, Daniel Ambinder, Carine Hamo, and Karan Desai) are honored to bring to you the Braunwald Chronicles. These are stories of discovery, innovation, accidents, perseverance, and more…truly these are the stories of cardiology, directly from a father of modern cardiology himself, Dr. Eugene Braunwald. Dr. Braunwald’s life and stories together are the saga which have brought us to this day in modern cardiology. So please join us for this wonderful series, as we journey through the history of cardiology, across 6 extraordinary chapters. We continue with Chapter 5 where Dr. Braunwald discusses his discoveries related to carotid sinus stimulation, limitation of infarct size & the open artery hypothesis. The open artery hypothesis has revolutionized the way we take care of patients with myocardial infarction. We thank Dr. Karan Desai, Editorial APD with the CardioNerds Academy, and fellow at University of Maryland, for all the work he put into designing the Braunwald Chronicles. Audio editing by Pace Wetstein. Dr. Braunwald's favorite paper: (Please note the very last paragraph)Kjekshus JK. Factors influencing infarct size following coronary artery occlusion. JOslo City Hosp. 1974;24(11-12):155-175. CardioNerds Braunwald Chronicles Series PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron!

Apr 23, 2021

CardioNerds (Amit Goyal, Daniel Ambinder, Carine Hamo, and Karan Desai) are honored to bring to you the Braunwald Chronicles. These are stories of discovery, innovation, accidents, perseverance, and more…truly these are the stories of cardiology, directly from a father of modern cardiology himself, Dr. Eugene Braunwald. Dr. Braunwald’s life and stories together are the saga which have brought us to this day in modern cardiology. So please join us for the Braunwald Chronicles, as we journey through the history of cardiology, across 6 extraordinary chapters. We continue with Chapter 4 where Dr. Braunwald discusses his discoveries related to the A "Royal Screw-up" & The Discovery of Hypertrophic Cardiomyopathy. There are hypertrophic cardiomyopathy centers of excellence sprinkled throughout the world. Comprehensive ACC/AHA guidelines for hypertrophic cardiomyopathy that came out in 2020, there's incredible drug discovery and randomized controlled trials looking at innovations in the management of HCM. We had a whole series on CardioNerds for hypertrophic cardiomyopathy where we taught about the four "Ps" or four preventions of hypertrophic cardiomyopathy management; prevent symptoms, prevent stroke in atrial fibrillation, prevent sudden cardiac death in the patient and prevent sudden cardiac death in the family. How fortunate are we to now hear all about how hypertrophic cardiomyopathy was discovered. We thank Dr. Karan Desai, Editorial APD with the CardioNerds Academy, and fellow at University of Maryland, for all the work he put into designing the Braunwald Chronicles.Audio editing by Pace Wetstein. CardioNerds Braunwald Chronicles Series PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron!

Apr 22, 2021

CardioNerds (Amit Goyal, Daniel Ambinder, Carine Hamo, and Karan Desai) are honored to bring to you the Braunwald Chronicles. These are stories of discovery, innovation, accidents, perseverance, and more…truly these are the stories of cardiology, directly from a father of modern cardiology himself, Dr. Eugene Braunwald. Dr. Braunwald’s life and stories together are the saga which have brought us to this day in modern cardiology. So please join us for the Braunwald Chronicles, as we journey through the history of cardiology, across 6 extraordinary chapters. We continue with Chapter 3 where Dr. Braunwald discusses his discoveries related to the natural history of aortic stenosis, beta-blockers in heart failure and times when seizing the moment led to important contributions to the world of cardiology. Dr. Braunwald also shares insights on mentorship as he speaks fondly of his relationship with the cardiac surgeon, Dr. Andrew "Glenn" Morrow. We thank Dr. Karan Desai, Editorial APD with the CardioNerds Academy, and fellow at University of Maryland, for all the work he put into designing the Braunwald Chronicles. Audio editing by Pace Wetstein. CardioNerds Braunwald Chronicles Series PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron!

Apr 20, 2021

CardioNerds (Amit Goyal, Daniel Ambinder, Carine Hamo, and Karan Desai) are honored to bring to you the Braunwald Chronicles. These are stories of discovery, innovation, accidents, perseverance, and more…truly these are the stories of cardiology, directly from a father of modern cardiology himself, Dr. Eugene Braunwald. Dr. Braunwald’s life and stories together are the saga which have brought us to this day in modern cardiology. So please join us for the Braunwald Chronicles, as we journey through the history of cardiology, across 6 extraordinary chapters. We continue with Chapter 2 where Dr. Braunwald discusses his Camelot years, discoveries with regards to myocardial oxygen consumption & how the transseptal approach was developed. We hear about the incredible environment at the NIH during his early days, his delineation of the variables that result in myocardial oxygen demand and the discovery of the transseptal approach, which is so key to so many of our percutaneous interventions today. We thank Dr. Karan Desai, Editorial APD with the CardioNerds Academy, and fellow at University of Maryland, for all the work he put into designing the Braunwald Chronicles. Audio editing by Pace Wetstein. CardioNerds Braunwald Chronicles Series PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron!

Apr 19, 2021

CardioNerds (Amit Goyal, Daniel Ambinder, Carine Hamo, and Karan Desai) are honored to bring to you the Braunwald Chronicles. These are stories of discovery, innovation, accidents, perseverance, and more…truly these are the stories of cardiology, directly from a father of modern cardiology himself, Dr. Eugene Braunwald. Dr. Braunwald’s life and stories together are the saga which have brought us to this day in modern cardiology. So please join us for the Braunwald Chronicles, as we journey through the history of cardiology, across 6 extraordinary chapters. We begin with Chapter 1: At The Right Place, At The Right Time & With The Right People. We learn about how serendipitous events in Dr. Braunwald’s early days, paired with his incredible grit & brilliance got him to the NIH where he quickly became the chief of cardiology at the of age 31, the precipice to an illustrious career ahead. We thank Dr. Karan Desai, Editorial APD with the CardioNerds Academy, and fellow at University of Maryland, for all the work he put into designing the Braunwald Chronicles. A very special thanks Dr. Randall Starling, advanced heart failure faculty at the Cleveland Clinic, former President of HFSA, and a dedicated mentor and support to CardioNerds for introducing us to Dr. Eugene Braunwald and for providing the following introduction. Audio editing by Pace Wetstein. CardioNerds Braunwald Chronicles Series PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron!

Apr 16, 2021

CardioNerds Amit Goya and Daniel Ambinder, cardioobstetrics series co-chair Dr. Natalie Stokes, and episode lead Dr. Priya Kothapalli (University of Texas at Austin, Dell Medical School) discuss pregnancy and coronary artery disease with Dr. Malissa Wood, co-founder and co-director of the Corrigan Woman’s Heart Health center at Massachusetts General Hospital. They discuss the differential diagnosis of chest pain in the pregnant patient, the diagnostic approach and management of acute coronary syndromes in the patient population, and manifestations and management of SCAD in pregnancy. Episode introduction by Dr. Julie Power. Claim free CME for enjoying this episode! Guest Profiles • Production Team CardioNerds Cardio-Obstetrics Series PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Guest Profiles - Episode 114. Pregnancy Coronary Disease Dr. Malissa Wood Dr. Malissa Wood is a cardiologist at MGH, where she is one of the founders and co-director of the Corrigan Woman’s Heart Health center at MGH. She has authored two books “Smart at Heart” and “Thinfluence” and she’s made substantial contributions globally in promoting awareness of gender disparities in cardiovascular disease. She is the incoming chair elect for the ACC board of governors and current Governor of the Massachusetts ACC chapter, and is one of the leading experts in the world of Spontaneous Coronary Artery Dissection, or SCAD. Dr. Priya Kothapalli Dr. Priya Kothapalli is a second-year cardiology fellow at The University of Texas at Austin, Dell Medical School. Her clinical interests include endothelial dysfunction and vulnerable plaque. She looks forward to advanced training in interventional cardiology. CardioNerds Cardioobstetrics Production Team Natalie Stokes, MDSonia Shah, MDAmit Goyal, MDDaniel Ambinder, MD

Apr 12, 2021

CardioNerds (Amit Goyal and Daniel Ambinder), cardioobstetrics series co-chair Dr. Natalie Stokes, Northwestern University CardioNerds Ambassador Dr. Loie Farina, and episode lead fellow, Dr. Agnes Koczo (University of Pittsburgh) join Dr. Julie Damp of Vanderbilt University Associate Director of the VUMC Cardiovascular Disease Fellowship for a discussion about pregnancy, heart failure, and peripartum cardiomyopathy. Episode introduction by Dr. Luis Calderon. Audio editing by Pace Wetstein. Claim free CME for enjoying this episode! Abstract • Pearls • Quotables • Notes • References • Guest Profiles • Production Team CardioNerds Cardio-Obstetrics Series PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Episode Abstract In this episode we discuss the presentation of peripartum cardiomyopathy (PPCM), tips for examining a late antepartum patient, and review management of pregnancy complicated by cardiogenic shock. Weaved throughout the case, we discuss important concepts including the role of prolactin in PPCM which factors into both treatment decisions like prescribing bromocriptine (what!) as well as counseling on breastfeeding. Be sure to tune in to hear Dr. Damp’s review of the latest evidence regarding the diagnosis and management of PPCM, as well as her personal experience counseling patients on heart failure therapies and ICD placement in the context of important factors like breastfeeding status, contraception and future pregnancies. Pearls 1) PPCM most typically presents in the early postpartum period and is defined as an LVEF 50%) by 1 year following diagnosis. However, none of the patients with both LVEF 6 cm at presentation recovered to normal LVEF. For those who do not recover normal cardiac function, studies show nearly 50% will go on to further deterioration with a subsequent pregnancy and are at the highest WHO classification risk for pregnancy.Progesterone-releasing subcutaneous implants are first line for contraception, but likely all contraceptive methods have a benefit which outweighs potential risks of a subsequent pregnancy with abnormal baseline cardiac function. References Davis, M et al. Peripartum Cardiomyopathy. J Am Coll Cardiol. 2020 Jan 21;75(2):207 221. Koczo A, Marino A, Jeyabalan A, Elkayam U, Cooper LT, Fett J, Briller J, Hsich E, Blauwet L, McTiernan C, Morel PA, Hanley-Yanez K, McNamara DM; IPAC Investigators. Breastfeeding, Cellular Immune Activation, and Myocardial Recovery in Peripartum Cardiomyopathy. JACC Basic Transl Sci. 2019 Jun 24;4(3):291-300. Elkayam U, Schäfer A, Chieffo A, Lansky A, Hall S, Arany Z, Grines C. Use of Impella heart pump for management of women with peripartum cardiogenic shock. Clin Cardiol. 2019 Oct;42(10):974-981. Olson TL, O'Neil ER, Ramanathan K, Lorusso R, MacLaren G, Anders MM.

Apr 5, 2021

CardioNerds (Amit Goyal and Daniel Ambinder) join Dr. Gina Lundberg (Associate Professor of Medicine at Emory University School of Medicine, Clinical Director of the Emory Women's Heart Center, and Chair Elect for the ACC WIC Section) and Dr. Zarina Sharalaya (interventional cardiology fellow at CCF, CardioNerds Narratives FIT Council Member) for a Narratives in Cardiology episode. Dr. Lundberg highlights the disparities that exists with representation of women in cardiology and cardiology subspecialties, and how to navigate the challenges that exist for women in cardiology. Dr. Lundberg takes us through her career journey and gives several pearls for fellows-in-training regarding achieving career goals, networking, mentorship, and the use of social media to further your career. Special message from Dr. Annabelle Volgman. Audio editing and episode introduction by Gurleen Kaur. Quotables • Show notes • Guest profiles • About Narratives in Cardiology • Production team Claim free CME just for enjoying this episode! Cardionerds Narratives in Cardiology PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll Subscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Quotables “Improving the work environment for women is going to be really important for job retention and for encouraging more women to go into EP, interventional cardiology, and heart failure...” “One of the words of wisdom I say to a lot of early career women is slow down. You don't have to drink the whole thing in your first 10 years. You can just slowly ease into it- there's a time and a place for everything, a season for everything.” “So start building your network. Build your ‘otter raft’ and by otter, I mean that group of people, men or women who really support you and lift you up, who might recommend you for a position or a lecture that might share opportunities with you” Show notes What are some strategies to improve female representation in cardiology? Practicing cardiologists, both men and women, need to mentor and sponsor trainees to attract more female into the field.Improving the work environment is key to retention of women in cardiology (allowing for more flexibility to meet needs such as child-care etc.).We need to build the pipleline to start recruiting females early on, even in high school. 2. What are some strategies to network as a fellow-in-training? Start building your network early - attend ACC and AHA meetings. The ACC Legislative Conference is great because it’s a bit smaller and allows for more opportunities to meet leaders in the ACC.Share your story with other people (example your old high school or sorority/fraternity) as an opportunity to mentor and inspire others.Build your “otter raft”… that group of people who really support you and lift you up, who might recommend you for a position or a lecture that might share opportunities with you. 3. What is the role or value of social media for professional development? Social medial democratizes the landscape, giving everyone a voice regardless of level of training, background, or beliefs.It is invaluable for connecting and networking, on a global scale.It empowers individuals to share – be it powerful stories, their thoughts, and of course education.We of course need to be responsible with protecting our patient’s privacy, be discerning consumers, and be professional in our interactions. CardioNerds Narratives in Cardiology The CardioNerds Narratives in Cardiology series features cardiovascular faculty representing diverse backgrounds, subspecialties, career stages, and career paths. Discussing why these faculty chose careers in cardiology and their passion for their work are essential components to inspiring interest in the field. Each talk will feature a cardiology faculty from an underrepresented group, within at least one of several domains: gender, race, ethnicity, religion, national origin, international graduate status, disadvantaged backgrounds, etc. Featured faculty will also represent a variety of practice settings, academic ranks, subspecialties (e.g. clinical cardiology, interventional cardiology, electrophysiology, etc), and career paths (e.g. division chief, journal editor, society leadership, industry consultant, etc). Faculty will be interviewed by fellows-in-training for a two-part discussion that will focus on: 1) Faculty's content area of expertise2) Faculty's personal and professional narrative As part of their narrative, faculty will discuss their unique path to cardiology and their current professional role with particular attention to challenges, successes, and advice for junior trainees. Specific topics will be guided by values relevant to trainees, including issues related to mentorship, work-life integration, and family planning. To help guide this important initiative, the CardioNerds Narratives Council was founded to provide mentorship and guidance in producing the Narratives series with regards to guests and content. The CardioNerds Narratives Council members include: Dr. Pamela Douglas, Dr. Nosheen Reza, Dr. Martha Gulati, Dr. Quinn Capers, IV, Dr. Ann Marie Navar, Dr. Ki Park, Dr. Bob Harrington, Dr. Sharonne Hayes, and Dr. Michelle Albert. The Narratives Council includes three FIT advisors who will lead the CardioNerds’ diversity and inclusion efforts, including the current project: Dr. Zarina Sharalaya, Dr. Norrisa Haynes, and Dr. Pablo Sanchez. Guest Profiles Dr. Gina Lundberg Gina Price Lundberg MD FACC FAHA is an Associate Professor of Medicine at Emory University School of Medicine and has served as the Clinical Director of the Emory Women’s Heart Center since it was founded in 2013. She is a Preventive Cardiologist and specializes in heart disease in women, lipid abnormalities and cardiovascular risk reduction. She founded the first women’s heart prevention program in the state of Georgia in 1998. Dr Lundberg’s service at Emory University includes improving outcomes for women with cardiovascular disease but also improving gender equity for women in cardiology and encouraging more women to choose cardiology for their careers. She attended the Medical College of Georgia at Augusta University and trained in Internal Medicine at Atlanta Medical Center. Her cardiology fellowship was at Rush University in Chicago. She is active with the ACC, AHA, and NLA. She is the Chair-elect for the ACC Women in Cardiology Leadership Council and is the co-chair for the WIC Communications and Social Media Committee. She is the Co-chair for the NLA Social Media and Communications committee and the co-Chair for NLA DE&I Committee. She serves on the AHA Clinical Cardiology Communications and Social Media committee and the AHA Familial Hypercholesterolemia and Hyperlipidemia working group. And she serves as the Social Media Supervisor for JACC Case Reports. Dr. Zarina Sharalaya Dr. Zarina Sharalaya is an interventional cardiology fellow at the Cleveland Clinic. She completed medical school at The Ohio State University and then completed her residency at The University of North Carolina Chapel Hill. She moved back to her home state of Ohio to do general cardiology fellowship at The Cleveland Clinic. Zarina has been very involved with the Ohio ACC and this year has served as co-chair of the FIT Council. She is passionate about the Women in Cardiology initiative has been able to help formulate the first WIC chapter for Ohio ACC. She enjoys traveling, music, and spending time with her husband and new puppy Zuma. Narratives in Cardiology Production Team Gurleen KaurAmit Goyal, MDDaniel Ambinder, MD

Mar 31, 2021

CardioNerd Amit Goyal, cardioobstetrics series co-chair Dr. Natalie Stokes, and episode lead Dr. Daniela Crousillat discuss normal cardiovascular physiology in pregnancy with Dr. Garima Sharma, Director of the Cardio-Obstetrics Program and the Ciccarone Center ‘s Associate Director of Preventive Cardiology Education in the Division of Cardiology. They discuss physiology from conception to post-partum, including the key hemodynamic, hormonal, and structural changes associated with normal pregnancy in the absence of pre-existing cardiovascular disease. Series introduction by Dr. Sharonne N. Hayes. Claim free CME for enjoying this episode! Abstract • Pearls • Quotables • Notes • References • Guest Profiles • Production Team CardioNerds Cardio-Obstetrics Series PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Episode Abstract Join us for a thrilling ride with our expert as we dive into the normal cardiovascular physiology of women through pregnancy. We discuss physiology from conception to post-partum, including the key hemodynamic, hormonal, and structural changes associated with normal pregnancy in the absence of pre-existing cardiovascular disease. We discuss how these physiologic changes manifest the history, physical exam, and key diagnostic testing (ECG, laboratory markers, and echocardiogram). Armed with these basic principles, we join Dr. Garima Sharma on patient consults to learn about potential signs and symptoms of cardiovascular disease in pregnancy and appropriate ways to risk stratify women with pre-existing or acquired cardiovascular disease in pregnancy. Importantly, we delve deeper into the importance of the growing field of cardio-obstetrics in the context of rising maternal mortality and staggering racial disparities in the care and outcomes of women in pregnancy. Pearls In normal pregnancy, plasma volume increases by up to 50% resulting in an adaptive decrease in systemic vascular resistance (SVR) by 25% and an increase in cardiac output (CO) by ~50% by the 2nd trimester.Brisk carotid upstrokes, an S3 gallop, soft systolic ejection murmurs, pedal edema, and a mildly elevated jugular venous pressure (JVP) can all be normal physiologic findings in pregnancy in the context of no other signs/symptoms to suggest heart failure.A normal NT-proBNP among pregnant patients with pre-existing cardiovascular disease has a high negative predictive value for predicting adverse maternal cardiac outcomes.Pregnancy risk predictor tools (mWHO, CARPREG II, ZAHARA) are a crucial component of pre-conception counseling to help predict which women with existing cardiovascular disease are at highest risk for adverse maternal outcomes.The U.S. ranks 1st in the world for maternal mortality among developed nations and cardiovascular disease is the leading cause of pregnancy-associated mortality in the U.S. Non-Hispanic Black are 3.5 times more likely to die from pregnancy as compared to White women. Quotables “You don’t know where you are going until you know where you have been” - Dr. Garima Sharma on the importance of holding on to hope when encountering difficult situations in our training and career pathways. “Do not fear the pregnant patient! The pregnant patient is going through a normal physiologic process in her life, and the more we are familiar with it, the less we fear it” - Dr. Garima Sharma on taking care of pregnant patients. “If you are going to move the needle on maternal mortality and in making a long-term sustainable change in the lives of these women, you have to focus on prevention” - Dr. Garima Sharma on the importance of prevention in reducing maternal mortality. “Be empathetic. For most women, pregnancy is a normal state. These women need your help!” - Dr. Garima Sharma on the importance of taking care of women in pregnancy. Show notes What are the normal hemodynamic changes that occur in pregnancy? Let’s talk physiology! Pregnancy, nature’s most grueling stress test, is a dynamic process associated with significant hemodynamic and physiological adaptations in the cardiovascular system which have evolved to support the needs of a developing fetus.Predictable and expected hemodynamic changes occur during pregnancy for all women. Healthy women can adapt without significant consequences, whereas in women with underlying cardiac conditions, these changes may unmask a previously unknown condition or exacerbate existing abnormal hemodynamics. Adaptive Physiologic Changes of the Cardiovascular System (1) Source: Me Mehta LS, Warnes CA, Bradley E et al. Cardiovascular Considerations in Caring for Pregnant Patients: A Scientific Statement From the American Heart Association. Circulation 2020;141:e884-e903. Supplemental Table 1: Physiologic Changes Throughout Normal Pregnancy Compared to Pre Pregnancy State (2) Plasma volumeIncreases by about 50-75% by the 2nd trimester of pregnancy to meet greater circulatory needs of placenta and maternal organsErythropoietin causes an increase in red cell mass by 20-30% leading to relative dilution and “physiologic” anemia of pregnancy Systemic vascular resistance (SVR)To accommodate the increase in plasma volume, vasodilatation and vascular remodeling occur with a reduction in SVRSVR decreases starting early in the 1st trimester and falls by 25-30% in the 2nd trimester potentiated by progesterone and estrogen-induced vasodilatationDecreased SVR results in activation of the renal angiotensin-aldosterone system (RAAS) to maintain blood pressure and salt/water balance Cardiac output (CO)Increases by ~ 50% during pregnancy (up to 75% for a twin gestation!), starting at 5 weeks of gestation, and peaks at about 18-24 weeks in the 2nd trimesterCO (stroke volume (SV) x heart rate (HR)) increases predominantly via an increase in SV, but also an increase in HR by about 10-15 bpm by the 3rd trimester due to activation of the sympathetic system There are a multitude of other physiological changes that allow our cardiovascular systems to adapt to the normal hemodynamics of pregnancy. Respiratory: Increase in metabolic rate & O2 consumption, minute ventilation and tidal volume resulting in a mild compensatory respiratory alkalosis.Renal: Systemic vasodilation results in 50% increase in renal plasma flow and glomerular filtration rate (GFR), activation of RAAS to maintain fluid and electrolyte balance.Hematologic: “Physiologic” anemia of pregnancy due to increase in plasma volume > red blood cell mass, increased production of coagulation factors with promotion of a pro-thrombotic state.Endocrine: Increase in total cholesterol, triglycerides, LDL (by 50%) and decrease in HDL; mild insulin resistance. Labor & Delivery and Post-Partum Period: Labor: The maximum CO associated with pregnancy occurs during labor and immediately post-partum.Repeated Valsalva maneuvers with a doubling of CO (up to 10L!) in active laborEach uterine contraction displaces about 300-500 mL of blood back into the maternal systemic circulation Post-partum: Immediate: Caval decompression from evacuation of gravid uterus leads to marked increase in venous return (“auto transfusion”) back into the maternal systemic circulationTwo weeks post-partum: Maternal hemodynamics largely return to the pre-pregnancy state! 2. How are the normal physiological changes of pregnancy reflected in the physical exam and diagnostic cardiac testing? When should we worry? Physical Exam (2)Heart rate: Increases by 10-15 bpm by 3rd trimester, mild sinus tachycardiaBlood pressure: Decrease of 10-15 mm Hg in both SBP and DBP, nadiring in 2nd trimester, improving to pre-pregnancy state in 3rd trimesterWeight: 25-35 lbs considered normal total gestational weight gain in patients who are normal weight pre-partumCardiac exam: Mildly elevated jugular venous pressure with more prominent x and y descents, brisk carotid upstrokes, soft, systolic ejection murmur (flow murmur), S3 gallop, mild pedal edema, varicose veins, mammary flow murmurECG:Mild sinus tachycardiaInfrequent premature atrial and ventricular atrial contractionsLeftward axis deviationQ waves in inferior (II, III, aVF) and/or lateral (V4-V6) leads due to heart’s spatial shift left, anterior, and in the transverse plane to accommodate the gravid uterusCardiac BiomarkersNT-proBNPIncrease up to two-fold in pregnancy but should remain within normal rangeImportant clinical utility in patients with pre-existing cardiac disease to serially assess changes throughout pregnancyBNP <100 pg/nL among women with cardiovascular disease has a 100% negative predictive value for identifying cardiac events during pregnancy (3)NT pro BNP <128 at 20 weeks has 97% NPV for maternal complications (4)Echocardiography: (5)Increase in LV volumes (but remaining within normal limits) and 50% increase in LV and RV mass as response to increased blood volume and CO“Physiologic” left ventricular hypertrophyLeft ventricular ejection fraction remains unchangedMild increase in aortic root diameterTrivial MR, TR, and PR (not typically AR!)Trace, physiologic pericardial effusion (can be normal in up to 40%) When should we worry? Diastolic murmursSigns of congestive heart failure (crackles, elevated JVP/Kussmaul’s sign, marked lower extremity edema or weight gain)Loud P2 or RV heave which could signal elevated pulmonary pressures/pulmonary HTNElevated NT-proBNPLarge pericardial effusion or symptoms of pericarditis 3. What are the available pregnancy risk predictor scores for the risk stratification of women with pre-existing cardiovascular disease who are interested in achieving pregnancy? Modified World Health Organization (mWHO) Classification (6)

Mar 25, 2021

CardioNerds (Amit Goyal and Karan Desai) enjoy a picnic at Charm City’s Inner Harbor with Dr. Manu Mysore, Dr. Shawn Samanta, and Dr. Rawan Amir from the University of Maryland division of Cardiology as they dive into important case discussion about a patient with of non-ischemic cardiomyopathy s/p orthotopic heart transplantation who presents with dyspnea due to cell mediated rejection. Dr. Gautam Ramani Medical Director of Clinical Advanced Heart Failure at the University of Maryland, provides the e-CPR segment. Claim free CME just for enjoying this episode! Jump to: Patient summary - Case media - Case teaching - References CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Patient Summary A 58 year old woman with a history of non-ischemic cardiomyopathy s/p orthotopic heart transplantation in 2015 presented with worsening dyspnea upon exertion. Dyspnea in a post cardiac transplant brings forth a wide differential diagnosis spanning all the typical causes of dyspnea as well as causes more specific or common to the patient with a heart transplant. In this particular case, TTE showed newly reduced ejection fraction and valvular disease. Cell mediated rejection was considered highest on the differential and confirmed on endomyocardial biopsy. Given hemodynamic compromise with multiple foci of myocyte damage on biopsy, she was started on high dose steroids and anti-thymocyte globulin for treatment of rejection. Early identification and management of cell mediated rejection is crucial to the survival of patients like ours. Final diagnosis: orthotopic heart transplantation rejection. Case Media - Orthotopic heart transplant rejection Chest x-ray: Status post sternotomy. Patchy peripheral opacities in the bilateral lower lobes. Blunting of the costophrenic angles consistent with pleural effusion. Sinus tachycardia, HR 111, RBBB, Sub millimeter STE in leads 1, aVL. STD in infero-posterior leads TTE: Short axis TTE: Long axis TTE: Apical 4 Chamber Coronary angiography: RCA Coronary angiography: LAD/LCx Episode Education Pearls New onset heart failure in a post cardiac transplant patient should raise concern for acute cardiac allograft rejection, as well as all the usual culprits in nontransplant patients.Younger African American women and those with elevated HLA mismatches are key risk factors for cell mediated rejection.Treatment for cell-mediated (i.e., T-Cell mediated) rejection includes steroids and antithymocyte immunoglobulin and regimens are based on the severity ofclinical and histologic features.Though infrequent as an initial presentation of acute cellular rejection, new onset arrhythmias in a post cardiac transplant patient should raise concern for rejection as a possible etiology. Reversal of rejection should be verified with endomyocardial biopsy following treatment for rejection. The timing and frequency of biopsy will likely depend upon whether corticosteroids and/or antithymocyte therapy was utilized. Notes - Cell mediated rejection and more! 1) What are some common complications of cardiac transplantation? Common complications following cardiac transplantation can be divided into two major categories: graft-related complications and non-graft-related complications. Graft-related complications include:Early graft dysfunction (EGD) – reversible and irreversible injury related to organ procurement and reperfusion. Remember it is common for transplant patients to require inotropic and vasopressor support coming off cardiopulmonary bypass. Furthermore, LV diastolic dysfunction is also common after transplantation usually reflecting reversible ischemia or reperfusion injury and normally resolves over days to weeks, depending on the severity of reperfusion.Primary graft dysfunction (PGD) is a severe form of EGD that presents as a left, right or biventricular dysfunction occurring within the first 24 hours of transplantation for which there is no identifiable secondary cause (e.g. hyperacute rejection, prolonged ischemic time from massive intra-operative bleeding. The etiology is likely multifactorial including but not limited to reperfusion injury, the effect of donor brain death, and pre-existing donor heart disease.Early RV dysfunction related to pulmonary vascular resistance and fluid shifts early post-transplant may be particularly challenging. The RV is exposed to similar reperfusion injury or ischemic insults as the LV and typically RV dysfunction post-transplant includes RV dilation, subsequent poor coaptation of the tricuspid valve and tricuspid regurgitation. The “untrained” donor RV has to overcome potentially increased afterload (due to increased pulmonary vascular resistance) in the recipient, and as has been covered in previous Cardionerds episodes, the RV systolic function is highly sensitive to changes in afterload.Acute allograft rejection – either cellular-mediated rejection or antibody-mediated rejection, occurring due to the recipient’s immune system reacting against graft antigens (e.g., mainly, but not only, the human leukocyte antigen (HLA) mismatches). Hyperacute rejection is rare and commonly fatal complication of cardiac transplantation. It is mediated by preformed anti-donor antibodies and can lead to diffuse hemorrhage and thrombosis in the allograft. In the current era of panel-reactive antibody screening (PRA) where we screen for preformed anti-HLA recipient antibodies to donor lymphocytes, hyperacute rejection is rare but remains a possibility (especially in highly sensitized patients and/or depending on the technique of obtaining PRAs). See more below on antibody- and cell-mediated rejection.Cardiac Allograft Vasculopathy – an important cause of morbidity and mortality late following heart transplant related to both immune- and nonimmune-mediated coronary injury causing accelerated atherosclerosis and fibroproliferation with diffuse intimal hyperplasia resulting in allograft ischemia. For a detailed discussion on CAV, enjoy Ep #69.Non-Graft-Related ComplicationsInfections – related both to nosocomial exposures and immunosuppression, the typical infectious agents and syndromes predictably vary according to time from transplant. Early following transplant, the recipient is particularly susceptible due to post-operative nosocomial exposures (e.g., surgical wound, vascular access, urinary catheter, etc) and high dose peri-transplant immunosuppression. As such, wound/line/urinary infections and infections involving fungal and multidrug resistant bacterial organisms are common in the early phase (<1 month). In the mid-term (1-6 months), pneumonia, UTIs, and viral infections (CMV, HSV, VZV) are common. In the late-term, after the first post-transplant year, opportunistic infections become less common, and the typical community-based pathogens predominate.Acute and chronic renal injury – renal dysfunction is a common and important complication post-cardiac transplantation. Etiologies are varied and interrelated and include pre-transplant renal dysfunction, acute injury pre-operatively, calcineurin inhibitor toxicity, cardiorenal syndromes related to graft dysfunction, and chronic injury due to long-term metabolic complications (diabetes, hypertension).Malignancies – major problem in transplant recipients with rising cumulative risk over time. Post-transplant cancer risk is related to both immunosuppression dulling the normal immune system’s cancer surveillance and viral triggers for carcinogenesis. Common malignancies include lung cancer (especially as a significant proportion of patients with ischemic cardiomyopathy have a history of tobacco use), skin cancer, lymphomas, and breast and colon cancer. Post-transplant lymphoproliferative disorder (PTLD) is an EBV-associated proliferation of B-lymphocytes that is typically related to the degree of immunosuppression. 2) What are acute cell mediated rejection and antibody mediated rejection? Acute cell mediated rejection (ACR) is a host T cell lymphocyte response directed towards allograft tissue, leading to T-cell mediated cytotoxicity of myocardial tissue. It can be seen anywhere from weeks to months after transplantation. Risk factors include younger donor and/or recipient age, African American ethnicity, and history of significant HLA mismatches. Acute antibody mediated rejection (AMR) constitutes graft injury by circulating antibodies (immunoglobulin M or G) targeting antigens expressed by graft endothelial cells. Injury may be complement mediated or complement independent (e.g., by other inflammatory pathways within endothelial cells and/or by natural killer cells). 3) What are clinical manifestations of acute cell mediated rejection? Ideally, ACR is diagnosed prior to overt clinical manifestations from surveillance endomyocardial biopsies or Allomap testing (a blood test of gene-expression profiling of peripheral blood mononuclear cells used in select patients).Clinical manifestations of acute cell mediated rejection typically include symptoms of LV dysfunction including dyspnea, PND, orthopnea, palpitations, syncope or near-syncope. Signs of RV dysfunction causing right-sided congestion may include gastrointestinal symptoms such as nausea which could be a marker of hepatic congestion! Occasionally, patients can present with new onset atrial arrhythmias including atrial fibrillation or atrial flutter.Ultimately, cardiac transplant rejection is a form of myocarditis and so progressively severe forms may result in any of the manifestations of fulminant myocarditis including cardiogenic shock, atrial and ventricular arrhythmias, and conduction abnormalities. Thankfully,

Mar 22, 2021

CardioNerd Amit Goyal is joined by Dr. Erika Hutt (Cleveland Clinic general cardiology fellow), Dr. Aldo Schenone (Brigham and Women’s advanced cardiovascular imaging fellow), and Dr. Wael Jaber (Cleveland Clinic cardiovascular imaging staff and co-founder of Cardiac Imaging Agora) to discuss nuclear and complimentary multimodality cardiovascular imaging for the evaluation of multimodality imaging evaluation for cardiac amyloidosis. Show notes were created by Dr. Hussain Khalid (University of Florida general cardiology fellow and CardioNerds Academy fellow in House Thomas). To learn more about multimodality cardiovascular imaging, check out Cardiac Imaging Agora! Collect free CME/MOC credit just for enjoying this episode! CardioNerds Multimodality Cardiovascular Imaging PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll Subscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Show Notes & Take Home Pearls - Nuclear and Multimodality Imaging: Cardiac Amyloidosis Episode Abstract: Previously thought to be a rare, terminal, and incurable condition in which only palliative therapies were available, multimodality imaging has improved our ability to diagnose cardiac amyloidosis earlier in its disease course. Coupled with advances in medical therapies this has greatly improved the prognosis and therapeutic options available to patients with cardiac amyloidosis. Multimodality imaging involving echocardiography with strain imaging, 99mTc-PYP Scan, and cardiac MRI can help diagnose cardiac amyloidosis earlier, monitor disease progression, and even potentially differentiate ATTR from AL cardiac amyloidosis. Five Take Home Pearls Cardiac amyloidosis results from the deposit of amyloid fibrils into the myocardial extracellular space. The precursor protein can either be from immunoglobulin light chain produced by clonal plasma cells (in the setting of plasma cell dyscrasias) or transthyretin (TTR) produced by the liver (which can be “wild type” ATTR caused by the deposition of normal TTR or a mutant ATTR which is hereditary). These represent AL Cardiac Amyloidosis and ATTR Cardiac Amyloidosis respectively.Remember that amyloidosis can affect all aspects of the heart:the coronaries, myocardium, valves, electrical system, and pericardium! Be suspicious in a patient with history of HTN who has unexpected decrease in the need for antihypertensive agents with age or presents with a lower-than-expected blood pressure.Multimodality imaging can assist with the diagnosis of cardiac amyloidosis in patients with a high clinical suspicion, monitor disease progression, and even potentially differentiate ATTR from AL cardiac amyloidosis.Strain imaging assessment of global longitudinal strain (GLS) in patients with amyloid may demonstrate relatively better longitudinal function in the apex compared to the base, termed “apical sparing” or “cherry on top” (though in advanced stages the base to apex strain difference tends to become smaller). This has a 93% sensitivity and 82% specificity in identifying patients with cardiac amyloidosis and is particularly helpful with differentiating true cardiac amyloidosis from “mimics” such as hypertrophic cardiomyopathy, aortic stenosis, or hypertensive heart disease.When the clinical suspicion for cardiac amyloidosis is high, a semiquantitative grade ≥ 2 (myocardial uptake ≥ bone) on 99mTc-PYP Scan combined with negative free light chain and immunofixation assays (to rule out AL cardiac amyloidosis) can diagnose ATTR cardiac amyloidosis and exclude AL cardiac amyloidosis w/ 100% PPV! Furthermore, this can circumvent the need for endomyocardial biopsy. Echocardiography and cardiac MRI (CMR) are helpful for building the clinical suspicion for cardiac amyloidosis.When there is suspicion for AL cardiac amyloidosis, tissue biopsy is mandatory. Quotable: - Nuclear and Multimodality Imaging: Cardiac Amyloidosis “Even if you’re starting fresh, you should not do this test (technetium pyrophosphate scan) without a SPECT CT; you could be sending patients to therapy that costs anywhere between $25,000 to $250,000 per year for a disease that they don’t have.” --13:22 Detailed Show Notes 1. What is amyloidosis? What are the main precursor proteins in cardiac amyloidosis? Amyloidoses are protein-folding disorders in which proteinaceous deposits known as amyloid can infiltrate multiple organs. Cardiac amyloidosis is typically secondary to two main subtypes: 1) immunoglobulin light chain produced by clonal plasma cells (AL cardiac amyloidosis), and 2) transthyretin produced by the liver (ATTR cardiac amyloidosis). AL and ATTR account for >95% of cardiac amyloidosis. Rare precursors include serum amyloid A (AA) and apolipoprotein A-1 (ApoA-1).AL cardiac amyloidosisOverall incidence of AL amyloidosis is estimated to be 8.0-14.4 million persons per year in the USA with cardiac involvement in ~50% of patients. Median survival of patients with cardiac AL amyloidosis is 6 months from the onset of heart failure. Survival has improved with earlier detection and advancements in oncologic treatments.AL may deposit in any tissue outside the CNS and so patients often have multiorgan involvement (kidneys, liver, etc).ATTR cardiac amyloidosisATTR typically results in cardiac amyloidosis, peripheral neuropathy, and MSK sequelae (i.e., bilateral carpal tunnel, lumbar spinal stenosis, biceps tendon rupture) with relative proportions dependent on the mutant variant.Transthyretin amyloidosis can occur secondary to the deposition ofnormal TTR (known as “ATTR wild type” or “ATTRwt”) or a mutant form (hereditary form known as “ATTR mutant” or “ATTRm”).ATTRwtHas a 15:1 male to female prevalence ratio and usually occurs in older patients (>65 y.o.)Almost always involves the heartMay be responsible for as many as 30% of heart failure with preserved ejection fraction (HFpEF) cases in patients >75 years old!ATTRmHas only a slight male predominance and occurs in younger patients (>40 y.o.)Inherited in an autosomal dominant fashion with multiple genotypes with variable degrees of penetrance and cardiac involvementThere are more than 100 genetic variants of ATTR that are associated with amyloidosis. However, only a few of these variants, including Val30Met, Thr60Ala, Ser77Tyr, and Val122Ile, are responsible for the majority of cases of hereditary ATTRAs stated in Podcast Episode #7, the specific mutation is closely linked with the age of onset, natural history, and phenotype of the affected individual!The Val122Ile mutation is the most common variant in the USA and a has prevalence of 3-4% in the US African American population. It is associated with cardiac amyloidosis with minimal neuropathy.Thr60Ala is the 2nd most common variant in the USA and is seen most commonly in those of Irish descent. It is associated with a mixed cardiomyopathy and neuropathy phenotype.Val30Met causes a prototypical hATTR polyneuropathy (heriditary ATTR with polyneuropathy also known as “Familial Amyloid Polyneuropathy”The specific genetic variant affects treatment decision and screening is indicated for individuals with known or suspected familial amyloidosis presenting w/ new symptomatic heart failure. 2. What are some classic cardiac and extracardiac manifestations of amyloidosis? For fantastic case presentations of cardiac amyloidosis including suggestive history and physical exam findings, diagnostic considerations, and recommended management, tune in to CardioNerds Podcast Episodes #7-10 and #54! As described in Podcast Episode #7, amyloidosis is associated with many classic extracardiac findings based on which organ it deposits in, and can also deposit in every layer of the heart—coronary, ventricular, valvular, electrical, and pericardial tissues! Below is a brief outline of some of the classic extracardiac and cardiac manifestations of amyloidosis.Extracardiac:ATTR: peripheral nerves (sensorimotor and autonomic defects) and musculoskeletal sequelae (bilateral carpal tunnel syndrome, lumbar spinal stenosis, biceps tendon rupture). Degree of cardiac vs nerve involvement differs by mutant variant as above. A prior Cleveland Clinic study showed Congo red staining of tenosynovial tissue detected amyloid deposits in 10.2% of patients undergoing carpal tunnel release surgeryAL: any tissue outside the CNS. For instance, typical organs involved include the kidneys (nephrotic syndrome), liver, intestines, and nervous system. On exam one may find macroglossia and periorbital bruising.Cardiovascular:Decreased antihypertensive medication requirements with increasing age or presenting with lower than expected blood pressurePostural hypotensionCoronary microvascular diseaseChronically elevated but flat troponin (infiltration into the coronary microvasculature)Almost all patients with cardiac amyloidosis have significantly reduced peak stress myocardial blood flow (<1.3 ml/g/min) which may explain symptoms of angina in these patients with absence of epicardial coronary artery diseaseMyocardialSigns and symptoms of both left and right heart failureRestrictive physiologyLVH tends to be greater in ATTR than in AL by time of symptom onset. This is because AL is also directly toxic, thereby causing a toxic-infiltrative cardiomyopathy. ATTR is more likely to deposit asymmetrically and thus may more closely mimic hypertrophic cardiomyopathyValvularThickened AV valves and interatrial septumParadoxical low-flow, low-gradient severe aortic stenosis (~15% of patients who undergo transcatheter aortic valve replacement have ATTRwt). The low flow and low gradient are because of restrictive filling and significant diastolic dysfunctionElectricalAV Block, Bundle Branch BlockAtrial fibrillation from infiltration of the atria (especially ATTR), chronically high left atrial pressure, and/or aging.Low voltage EKG[NJ1] [GU2] (in most cases,

Mar 16, 2021

CardioNerds (Amit Goyal and Daniel Ambinder) join Dr. Christine Albert (Professor of Medicine, Founding Chair of the Department of Cardiology at Cedars-Sinai, and President of Heart Rhythm Society) and Dr. Rachita Navara (FIT at Washington University, soon to be EP fellow at UCSF) for a Narratives in Cardiology episode. We learn from their experiences as physician scientists and women in cardiology, and specifically in electrophysiology. Claim free CME just for enjoying this episode! Cardionerds Narratives in Cardiology PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll Subscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Show notes 1. Over the last several decades, what have we learned about the contribution of lifestyle factors to atrial fibrillation? Particularly in women, the development of obesity (BMI > 30 kg/m2) is associated with a 41% increase in the risk of developing atrial fibrillation (AF). Even short-term weight gains are associated with a 18% increased risk of developing AF. Fortunately, losing weight could modify or even reverse this elevated risk [1]Exercise is beneficial for reducing the risk of AF, but higher frequency of vigorous exercise is actually associated with an increased risk of developing AF in young men and joggers. This risk decreases with age, and is offset by the other benefits of vigorous exercise on AF risk factors [2]The link between alcohol consumption and AF was first described in 2008: for healthy middle-aged women, consuming two or more alcoholic drinks is associated with a statistically increased risk of developing AF [3]The recent VITAL trial is the largest and longest randomized trial on primary prevention of AF, following over 25,000 men and women over five years. As recently presented at AHA 2020, Dr. Christine Albert and her study team found that neither vitamin D nor fish oil prevents the development of AF [4] 2. What is some practical advice on giving presentations and preparing research grants from Dr. Albert, renowned physician-scientist, and leader in electrophysiology? Whenever possible, Dr. Albert recommends memorizing your presentation to avoid referencing notes frequently, and to allow for continued eye contact with the audience. Practice delivering your presentation multiple times prior to the scheduled talk.When preparing a grant, start early and seek feedback and edits from those in and out of your field.In many cases, a grant review involves individuals who may not be in your exact scientific field, so the priority is to interest the grant readers regardless of their scientific background. 3. Whether in research or clinical care, what are the common features of a well-oiled clinical team? In an ideal team, every individual adds value and has a clear role. Team members show mutual respect and provide the autonomy for other team members to demonstrate their expertise.Don’t be intimidated by the individuals on your team who are extremely talented or experienced in a given domain – this in turn elevates you by being on the same team!Leaders are most successful when they enable others to succeed. The spirit of collaboration and respect comes from the top, so leaders need to demonstrate respect for every team member and give each person a role, eliminating the need for team members to compete with each other. 4. What is some advice for female trainees navigating a male-dominated field (e.g. electrophysiology)? What makes a good mentor and mentee? It is very important to seek female or otherwise relatable role models in your field. While representation increases, it can also be valuable to seek female mentors outside your specific field.It is just as important for male mentors to continue to support female trainees, especially in fields where females are underrepresented.Often, as a mentee you may change your area of interest or seek a new area of specialization that may no longer be fully aligned with your mentor’s expertise. A good mentor will continue to mentor you and connect you with those who can help you explore your new interests.A good mentee also recognizes that mentors often have very limited time, so it is best to package all of your questions together and prepare for each meeting so that shared time is most high yield. CardioNerds Narratives in Cardiology The CardioNerds Narratives in Cardiology series features cardiovascular faculty representing diverse backgrounds, subspecialties, career stages, and career paths. Discussing why these faculty chose careers in cardiology and their passion for their work are essential components to inspiring interest in the field. Each talk will feature a cardiology faculty from an underrepresented group, within at least one of several domains: gender, race, ethnicity, religion, national origin, international graduate status, disadvantaged backgrounds, etc. Featured faculty will also represent a variety of practice settings, academic ranks, subspecialties (e.g. clinical cardiology, interventional cardiology, electrophysiology, etc), and career paths (e.g. division chief, journal editor, society leadership, industry consultant, etc). Faculty will be interviewed by fellows-in-training for a two-part discussion that will focus on: 1) Faculty's content area of expertise2) Faculty's personal and professional narrative As part of their narrative, faculty will discuss their unique path to cardiology and their current professional role with particular attention to challenges, successes, and advice for junior trainees. Specific topics will be guided by values relevant to trainees, including issues related to mentorship, work-life integration, and family planning. To help guide this important initiative, the CardioNerds Narratives Council was founded to provide mentorship and guidance in producing the Narratives series with regards to guests and content. The CardioNerds Narratives Council members include: Dr. Pamela Douglas, Dr. Nosheen Reza, Dr. Martha Gulati, Dr. Quinn Capers, IV, Dr. Ann Marie Navar, Dr. Ki Park, Dr. Bob Harrington, Dr. Sharonne Hayes, and Dr. Michelle Albert. The Narratives Council includes three FIT advisors who will lead the CardioNerds’ diversity and inclusion efforts, including the current project: Dr. Zarina Sharalaya, Dr. Norrisa Haynes, and Dr. Pablo Sanchez. Guest Profiles - Physician Scientists Women Electrophysiology Dr. Christine M. Albert Dr. Christine Albert is currently President of Heart Rhythm Society. She recently transitioned from Professor of Medicine at Harvard and Director of the Center of Arrhythmia Prevention at the Brigham to now Founding Chair of the Department of Cardiology at Cedars-Sinai. She is an Epidemiologist and R01-grant funded physician scientist with over 200 peer-reviewed publications – with landmark contributions demonstrating the role of lifestyle and genetics on heart rhythm disorders. She has served as PI for numerous large-scale award-winning clinical trials, her latest studying primary prevention of cardiovascular disease and cancer in 25,000 patients across the country. She has served as the associate editor for Circulation, and continues to serve on the editorial board of numerous journals in not only cardiology but also epidemiology, clinical nutrition, and endocrinology and metabolism. Dr. Rachita Navara Dr. Rachita Navara is a bioengineer and senior cardiology fellow at Washington University in St. Louis. She is excited to enter her dream specialty of electrophysiology at UCSF, the birthplace of catheter ablation for arrhythmias. Her interest in EP emerged during bioengineering training at the innovative Olin College of Engineering. She went on to medical school at UT Southwestern, where she was the lead singer of her med school band “The Pacemakers.” Dr. Navara completed her internal medicine training at Stanford University, where she was accepted into the inaugural Biodesign Pathway of Distinction and researched complex atrial fibrillation mechanisms under the mentorship of Dr. Sanjiv Narayan. She joined cardiology fellowship at Wash U, where she researched novel noninvasive cardiac radioablation under the mentorship of Dr. Phillip Cuculich. Dr. Navara’s startup company “SafeBeat Rx LLC” was competitively selected into BioGenerator’s Grants-to-business program, and she recently submitted her first NIH STTR grant. She was appointed as the youngest member of the National ACC EP Leadership Council, and she is currently an HRS representative to the AMA. Dr. Navara aims to lead a research lab conducting trials on EP devices and mapping/ablating technologies she has designed herself. In her free time, she enjoys painting, singing and tandem biking with her husband, and competitive scrabble tournaments (nerd level: ultimate). References - Physician Scientists Women Electrophysiology Tedrow, Usha B., David Conen, Paul M. Ridker, Nancy R. Cook, Bruce A. Koplan, JoAnn E. Manson, Julie E. Buring, and Christine M. Albert. "The long-and short-term impact of elevated body mass index on the risk of new atrial fibrillation: the WHS (Women's Health Study)." Journal of the American College of Cardiology 55, no. 21 (2010): 2319-2327.Aizer, Anthony, J. Michael Gaziano, Nancy R. Cook, Joann E. Manson, Julie E. Buring, and Christine M. Albert. "Relation of vigorous exercise to risk of atrial fibrillation." The American journal of cardiology 103, no. 11 (2009): 1572-1577.Conen, David, Usha B. Tedrow, Nancy R. Cook, M. V. Moorthy, Julie E. Buring, and Christine M. Albert. "Alcohol consumption and risk of incident atrial fibrillation in women." Jama 300, no. 21 (2008): 2489-2496.VITamin D and OmegA-3 TriaL (VITAL) results presented at AHA 2020 ahead of publication: https://www.cedars-sinai.org/newsroom/study-vitamin-d-fish-oil-dont-lower-atrial-fibrillation-risk/ Amit Goyal,

Mar 15, 2021

Join Thomas Jefferson University FITs, Drs. Sean Dikdan, Rachel Debenham and Harsh Doshi, as well as Cardionerds, Dan Ambinder and Karan Desai, on this incredible story of a young man who presented with ventricular arrhythmias and cardiogenic shock. The TJU Cardionerds expertly walk us through a rare diagnosis, his course over several years and his ultimate treatment with heart transplantation. From the evaluation of cardiogenic shock to the role of endomyocardial biopsy to facing inequities in organ allocation, there are learning pearls for every listener! CME is unavailable for this episode. Jump to: Patient summary - Case media - Case teaching - References Episode Graphic by Dr. Carine Hamo CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Patient Summary A 35 year old healthy male presents with cardiogenic shock and new heart failure with reduced ejection fraction. He has ventricular instability and is diagnosed with giant cell myocarditis by endomyocardial biopsy. His course over several years includes LVAD bridge to heart transplantation. He then has a recurrence of giant cell myocarditis in the transplanted heart which is successfully treated with high dose immunosuppression. Case Media ABClick to Enlarge A. ECG, B. CXR Episode Schematics & Teaching CardioNerds Myocarditis, updated 1.20.21 Giant Cell Myocarditis Pearls Giant cell myocarditis (GCM is a rare – and often fatal - cause of acute myocarditis. A hallmark of GCM is the presence of multinucleated giant cells; however, these may take 1-2 weeks to appear and can also be seen in sarcoidosis.Most etiologies of fulminant myocarditis do not have bradyarrhythmias as a prominent feature, and their presence should increase the suspicion for sarcoidosis, Chagas disease, or GCM.While non-specific, a clue to the diagnosis of GCM amongst other causes of myocarditis could be rapid clinical deterioration with minimal response to guideline directed therapy, including a lack of spontaneous recovery on mechanical support which more commonly occurs in fulminant lymphocytic myocarditis.Mechanical support is typically needed in the management of GCM, either as a bridge to transplantation or recovery.GCM can recur in the transplanted heart. This happens in up to 25% of transplant patients and warrants aggressive immunosuppression which usually is sufficient to ensure disease remission. Notes - Giant Cell Myocarditis What is Giant Cell myocarditis (GCM)?Giant cell myocarditis (GCM) is an extremely rare – and often fatal – cause of acute non-infectious myocarditis. The pathophysiology of GCM is poorly understood, but thought to be a T-cell mediated autoimmune process leading to diffuse or multifocal inflammatory infiltrate, including lymphocytes with multinucleated giant cells (note multinucleated giant cells are not exclusive to GCM and can be seen in sarcoidosis as well). It has been estimated to occur at a rate of 0.13 cases per 100,000 people (one in a million).It typically affects the myocardium in isolation and may not have any extracardiac manifestations, presenting with rapid hemodynamic deterioration, ventricular arrhythmias, and at times bradyarrhythmias. The rate of death or cardiac transplantation has been estimated at 89%, with a median survival of 5.5 months from the onset of symptoms to the time of death or transplantation.When should you be suspicious of GCM?The classic presentation is in a middle-aged Caucasian male who develops acute or subacute nonischemic cardiomyopathy (NICM) with clinical heart failure that progressively worsens. These patients often develop cardiogenic shock or arrhythmic instability – including both ventricular arrhythmia and conduction delays/heart block. See our prior episodes on the basics of building a clinical suspicion for myocarditis and the differential diagnosis (Episodes 29-33).While non-specific, a clue to the diagnosis of GCM amongst other causes of myocarditis should be rapid clinical deterioration with minimal response to guideline directed therapy, including a lack of spontaneous recovery on mechanical support which more commonly occurs in fulminant lymphocytic myocarditis. Furthermore, bradyarrhythmias are less common in myocarditis and should raise the suspicion for GCM, sarcoidosis or Chagas disease.How is GCM diagnosed?Definitive diagnosis of GCM requires endomyocardial biopsy (EMB). Similar to other rare forms of myocarditis like sarcoidosis or eosinophilic myocarditis, GCM requires pathology for diagnosis. Typically, a Class I indication (based on a joint statement 2007 statement from the AHA/ACC/ESC) for performing an EMB are (1) unexplained acute cardiomyopathywith < 2 weeks duration that is associated with hemodynamic compromise or (2) unexplained cardiomyopathy between 2 weeks’ to 3 months’ duration associated with a dilated LV and new bradyarrhythmia, new ventricular arrhythmias or lack of response to GDMT within 1 to 2 weeks of initial diagnosis. The specific pathology will naturally include multinucleated Giant cells, but it will also include a high count of CD3 cells and usually a higher CD8 to CD4 ratio. The characteristic giant cells make typically take 1-2 weeks to appear and thus EMB in the first few days of the illness may render a false negative. Furthermore, because myocardial involvement in GCM can be patchy, repeat biopsy may be needed if the clinical suspicion remains high. Finally, multinucleated cells can also be seen in sarcoidosis; however, granulomas and fibrosis tend to be more striking features in cardiac sarcoid.MRI can aid the diagnosis of GCM, however, many of these patients are too unstable to undergo MRI. When an MRI is able to be obtained, it will generally show diffuse abnormalities in T1 and T2 imaging and mapping.How is GCM treated?In addition to GDMT as tolerated, treatment includes multi-drug immunosuppression that typically involve some combination of cyclosporine, azathioprine, and high dose steroids. Antithymocyte immunoglobulin and the T-cell specific monoclonal antibody, muromonab, have been used as well. Even after treating the underlying myocarditis with aggressive immunosuppression, ventricular arrhythmias may persist.Mechanical circulatory support (MCS) is often needed as a bridge to heart transplantation or recovery. Options typically include intra-aortic balloon pump (IABP), IMPELLA (both RV and/or LV support devices), LVAD, RVAD, and ECMO. In patients with fulminant myocarditis, our goal is to maintain tissue perfusion while ensuring that we reduce LV workload and LVEDP. For this reason, peripheral VA ECMO alone is generally not used as it can increase afterload.IABP is typically not useful in a patient with a rapid and severe decrease in cardiac output, as it offers an additional 0.5L to 1 L/min of support. In this patient, LVAD and RVAD support were pursued. Surgical RVAD implantation involves cannulation of the right atrium or RV as well as pulmonary artery and is connected to an extracorporeal centrifugal flow pump. Another option for percutaneous RV support is a novel axial-flow pump. This device utilizes a catheter-mounted microaxial flow pump with the inflow just below the right atrium-inferior vena cava junction and the outflow into the pulmonary artery after insertion via the femoral vein due to the design of the system, internal jugular placement and ambulation are not possible.What are the expected outcomes in patients with GCM?Outcomes are generally poor without a heart transplant. With transplantation, however, 5-year survival is estimated at around 71%, which is similar to transplant survival rates in patients of other disease. Of note, GCM can recur in the transplanted heart. This happens in up to 25% of transplant patients. Recurrence warrants aggressive immunosuppression which is typically sufficient for disease remission. References 1. Ammirati E, Cipriani M, Moro C, Raineri C, Pini D, Sormani P, Mantovani R, Varrenti M, Pedrotti P, Conca C, Mafrici A, Grosu A, Briguglia D, Guglielmetto S, Perego GB, Colombo S, Caico SI, Giannattasio C, Maestroni A, Carubelli V, Metra M, Lombardi C, Campodonico J, Agostoni P, Peretto G, Scelsi L, Turco A, Di Tano G, Campana C, Belloni A, Morandi F, Mortara A, Cirò A, Senni M, Gavazzi A, Frigerio M, Oliva F, Camici PG; Registro Lombardo delle Miocarditi. Clinical Presentation and Outcome in a Contemporary Cohort of Patients With Acute Myocarditis: Multicenter Lombardy Registry. Circulation. 2018 Sep 11;138(11):1088-1099. doi: 10.1161/CIRCULATIONAHA.118.035319. PMID: 29764898. 2. Heymans S, Eriksson U, Lehtonen J, Cooper LT Jr. The quest for new approaches in myocarditis and inflammatory cardiomyopathy. J Am Coll Cardiol. 2016;68:2348-2364. 3. Rosenstein ED, Zucker MJ, Kramer N. Giant cell myocarditis: most fatal of autoimmune diseases. Semin Arthritis Rheum. 2000 Aug;30(1):1-16. 4. Cooper LT Jr, Berry GJ, Shabetai R. Idiopathic giant-cell myocarditis--natural history and treatment. Multicenter Giant Cell Myocarditis Study Group Investigators. N Engl J Med. 1997 Jun 26;336(26):1860-6. 5. Cooper LT, Baughman KL, Feldman AM, Frustaci A, Jessup M, Kuhl U, Levine GN, Narula J, Starling RC, Towbin J, Virmani R; American Heart Association; American College of Cardiology; European Society of Cardiology. The role of endomyocardial biopsy in the management of cardiovascular disease: a scientific statement from the American Heart Association, the American College of Cardiology, and the European Society of Cardiology. Circulation. 2007 Nov 6;116(19):2216-33. 6. Kociol, R. D. et al. (2020). Recognition and Initial Management of Fulminant Myocarditis. Circulation, 141, E69-E92. 7. Kandolin R, Lehtonen J, Salmenkivi K, Räisänen-Sokolowski A,

Mar 8, 2021

CardioNerds (Amit Goyal & Karan Desai) join Dr. Alex Pipilas (FIT, Boston University) and Dr. Danny Pipilas (FIT, MGH) for in Boston, MA. Adult congenital heart disease expert Dr. Keri Shafer (Brigham and Women’s Hospital) provides the E-CPR expert segment. They discuss a case of heart failure secondary to sinus venosus defect with partial anomalous pulmonary venous return. Claim free CME just for enjoying this episode! Jump to: Patient summary - Case media - Case teaching - References CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Patient Summary A 78-year-old woman with atrial fibrillation and heart failure with preserved ejection fraction presented with recurrent dyspnea and volume overload. A transthoracic echocardiogram demonstrated severe right ventricular enlargement and dysfunction. A CT pulmonary angiogram demonstrated partial anomalous pulmonary venous return and a transesophageal echocardiogram revealed a sinus venosus defect with left to right shunting. A right heart catheterization with oximetry saturation (“shunt run”) demonstrated pulmonary hypertension and a large left to right shunt (Qp/Qs ~ 3). She was referred for cardiac surgery and underwent repair of the sinus venosus defect and baffling of the anomalous pulmonary venous flow to the left atrium. Case Media ABCClick to Enlarge A. CXR, B. ECG, C. TR Velocity TTE: PLAX TTE: RV Outflow TTE: AP4 TEE: Sinus Venosus ASD TEE: Sinus Venosus ASD 2 Episode Schematics & Teaching Figure 1Figure 2 Pearls It is critical to determine whether there is more to a diagnosis of heart failure with a preserved ejection fraction. Utilize all available clinical data and risk calculators to determine if there are more appropriate diagnoses causing the patients symptoms, especially when certain aspects of the presentation does not add up.Right ventricular failure may be related to pressure overload (i.e., pulmonary hypertension, PV stenosis), volume overload (i.e., tricuspid regurgitation, left to right shunt lesions), or primary myocardial process (i.e., ischemia, infiltration, ARVC). In cases of severe right ventricular enlargement and dysfunction without apparent cause, look for a left to right shunt lesion (i.e., VSD, ASD, PAPVR). Sometimes further imaging (TEE, cardiac CT, cardiac MRI) is necessary to detect these lesions if not visualized on TTE.Left to right shunts can be quantified in the cardiac catheterization laboratory by measuring oxygen saturation in each chamber and detecting an O2 “step up” (increase in oxygen saturation from one chamber to the next). Large left to right shunts are quantified using the Fick principle and comparing the ratio of pulmonary blood flow (Qp) to systemic blood flow (Qs).Large left-to-right shunts can cause right ventricular volume overload and pulmonary hypertension. Patients often present with signs and symptoms of right ventricular failure including shortness of breath, exercise intolerance, volume overload, atrial arrhythmias, and recurrent heart failure. Some may develop right-to-left shunting and possible paradoxical embolism.ACC/AHA guidelines recommend closure of a sinus venosus defect if the PA systolic pressure is 2/3 of systemic systolic pressure and/or PVR >2/3 SVR. Quotable: About ACHD - “As we go through this physiology, I just want to remind all of the listeners out there that you have the opportunity to apply the knowledge you have from medical school about physiology to the adult human heart. You can’t make assumptions as we sometimes do in the setting of normal cardiac anatomy. We really need to think about the compliances of the downstream structures and where is the blood flow.” – Keri Shafer, MD Notes What are features and causes of RV failure? The clinical symptoms of right ventricular failure include fatigue, dyspnea, lower extremity edema, elevated JVP, early satiety, and abdominal swelling. Although there is overlap between the symptoms of right ventricular failure and left ventricular failure, in isolated right ventricular failure orthopnea, paroxysmal nocturnal dyspnea, and pulmonary edema are typically absent.It is convenient to break down the etiologies of right heart failure into “buckets”. Specifically, volume overload, pressure overload, and primary cardiomyopathic processes. Causes of right ventricular volume overload include valvular disease (tricuspid regurgitation, pulmonic insufficiency) and left-to-right shunts (ASD, VSD, sinus venosus defect, coronary sinus defect, PAPVR). Causes of right ventricular pressure overload, or excessive afterload, include pulmonary arterial hypertension, pulmonary embolism and chronic thromboembolic pulmonary hypertension, pulmonic stenosis, chronic hypoxemia, and longstanding elevated left atrial pressure causing group 2 PH (mitral regurgitation/stenosis, HFrEF, HFpEF). Cardiomyopathic processes include cardiac amyloidosis, right ventricular myocardial infarction, post-transplant right ventricular dysfunction, and arrhythmogenic right ventricular cardiomyopathy. Also, keep in mind that these disease processes often overlap. 2. What is partial anomalous pulmonary venous return (PAPVR)? Normally, the four pulmonary veins return oxygenated blood to the left atrium.Partial anomalous pulmonary venous return is a spectrum of congenital heart defects when one or more (but not all) of the pulmonary veins return oxygenated blood from the lungs to the systemic venous system (typically the SVC, IVC, or RA).The most common PAPVRs are LUPV (left upper pulmonary vein) à ascending vertical vein à innominate vein or RUPV à SVC. The latter is often associated with a concurrent sinus venosus defect connecting the RA and LA.Scimitar syndrome is a subtype of PAPVR in which part or all of the blood from the right lung is returned into the IVC. On chest X-ray, the outline of the anomalous drainage and associated congestion gives the appearance of a scimitar. 3. What is a sinus venosus defect? What is the sinus venosus? Early in development, the atria are one single chamber. The sinus venosus is the posterior entryway for blood returning to this primitive atrium.Eventually, the sinus venosus closes and moves rightward due to hemodynamic shifts during development.In adults, the sinus venous becomes the smooth posterior wall of the adult right atrium called the sinus venarum and is separated from the anterior wall of the RA by the cristae terminalis.If a persistent channel through the sinus venosus remains into adulthood, it can result in an intra-cardiac shunt. This is termed a sinus venosus defect and accounts for 10-15% of all inter-atrial shunts.Typically, this shunt is left-to-right and may lead to right ventricular volume overload, dysfunction and pulmonary hypertension. Some patients may develop right-to-left shunting or paradoxical embolism. Arrhythmias are an important complication.As above, sinus venosus defects are associated with PAPVR with RUPV à SVC.NOTE: a sinus venosus defect is NOT a defect in the atrial septum and so is not an “ASD”. Rather it is a defect connecting either the SVC-RA junction (more common) or the IVC-RA junction to the LA. The former is associated with a RUPV PAPVR and the latter is associated with a RLPV PAPVR. 4. What are the imaging modalities that are used to identify sinus venosus defects? Sinus venosus defects are poorly visualized on transthoracic echocardiography (TTE).If there is clinical suspicion for an inter-atrial shunt not visualized on TTE, then a transesophageal echocardiogram (TTE) should be performed. Additional imaging modalities include cross-sectional imaging with cardiac CT or cardiac MRI, which may also identify the presence of concomitant PAPVR.In cases of RV dilation and dysfunction without know etiology, evaluation for sinus venosus defect +/- PAPVR should be pursued. 5. What is the role for right heart catheterization in characterizing shunt defects? A right heart catheterization is useful for multiple reasons.Intracardiac pressure measurements serve as a surrogate for volume status.One can also obtain oxygen saturation in each cardiac chamber to identify the presence of a “step up”, or unexpected increase in oxygen saturation, which signifies a left-to-right shunt. To simplify, a left-to-right shunt is when oxygenated blood from the systemic circulation (left) inappropriately mixes with the pulmonary circulation (right), increasing the oxygen concentration. This can occur via anomalous pulmonary veins, defects at the atrial or ventricular level, or sometimes systemic arterio-venous fistulas.To obtain pressure measurements, a balloon-tipped catheter (Swann-Ganz catheter, PA catheter) is inserted through a vein and advanced through the heart and “wedged” in the pulmonary artery to estimate left atrial pressure. Normal pressure measurements are as follows (in mmHg): Right atrium < 8, right ventricle 25/5 (systolic/end diastolic pressure), pulmonary artery 25/15 (systolic/diastolic), and pulmonary capillary wedge pressure 8-12. Cardiac output can also be measured by thermodilution and via the Fick principle.In our case, the patient’s pressure measurements were: RA 20, RV 72/24, PA 68/36 (47), PCWP 26.As the catheter is passed through the great vessels and cardiac chambers and into the pulmonary artery, small amounts of blood can be sent for oximetry. Blood can be taken from the proximal and distal SVC, proximal and distal IVC, right atrium (low, mid, high), RV, PA and aorta.

Mar 3, 2021

CardioNerds (Amit Goyal and Daniel Ambinder) join Dr. Bryan Smith (Advanced Heart Failure and Transplant Cardiologist at the University of Chicago) and Dr. Shirlene Obuobi (rising cardiology fellow, CardioNerds ambassador for the University of Chicago, and creator of ShirlyWhirl, M.D.) They discuss the story of a patient with end stage heart failure due to peripartum cardiomyopathy that highlights racial disparities in healthcare and advanced heart failure. They emphasize the importance of providing mentorship for Black and Indigenous People of Color (BIPOC) and share personal stories of their journey to Cardiology. Dr. Andi Shahu joins us to read his AHA blog titled "Let’s Ban the Phrase “Social Issues”: Social Justice and Advanced Heart Failure Therapies". Audio editing by CardioNerds Academy intern, Pace Wetstein. Collect free CME/MOC credit just for enjoying this episode! Cardionerds Narratives in Cardiology PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll Subscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Quotables: “One of the reasons why I went into Heart Failure is because I connected a lot with these young patients, a lot of these young black men and black women who were terrified of the hospital. As a resident and a fellow I would go talk to them and really understand their fears and where they are coming from. I think a lot of times these patients can be labeled as ‘noncompliant,’ or ‘withdrawn,’ or ‘aggressive,’ but a lot of times you just have to understand where they’re coming from. And I really found that just sitting down to talk to them, and to get to know them, I was able to help get them better, or a lot of them went on to get VADs or transplant. And, to be perfectly honest, I’m in touch with a lot of these patients who I met as a fellow who...I feel are part of my life....You have to meet patients where they are. Meaning you need to text them, interact with them on social media, and really connect with them in a way they understand.” Dr. Bryan Smith (12:10) “Being black in America means not getting the benefit of doubt. ...I can’t help but wonder if unconscious bias among providers is imposing...unreasonable scrutiny on patients of color.” Shirlene (21:15) “There are many different ways to combat [racial] disparities. As a Heart Failure physician we have these multidisciplinary meetings where we discuss patients for transplant. And I think it’s...important to highlight to our providers that how we discuss patients really matters. Language definitely matters. Heart failure is art in addition to science. ...Sometimes when discussing these patients...charged words are used, like ‘withdrawn,’ or ‘aggressive,’ or ‘ghetto’ even. And it’s all coded, racist language. ...Part of our responsibility is to educate everyone with implicit bias training....and to make sure we’re able to advocate for patients in the right way.” Dr. Bryan Smith (22:30) “I’ve felt like I’ve been paying the minority tax...which is doing the necessary but unpaid and frequently seldom recognized labor of mentorship, community engagement, etc, and also of being hyper visible and acting as a symbol...” - Shirlene (24:52) “It’s really easy when patients are in the hospital to think of them only as patients and forget that they’re people too, and that people are complex, they have complex emotions, they have reactions to things, sometimes those reactions aren’t necessarily what we would think are appropriate for their medical situation, but they’re what make us human.” - Shirlene (9:50) Notes: 1. What are some of the racial disparities in diagnosis and outcomes of peri-partum cardiomyopathy, and what are some factors that might be contributing to those disparities? CVD disease is the leading cause of pregnancy-associated mortality in the US. Black and American Indian/ Alaskan Native women are 3-4x more likely to die from a pregnancy-related cause than white women. (1,2)The incidence of peripartum cardiomyopathy (PPCM) is 4x higher in black women than in white women. Black women may make up to 40% of the cases. (3,4)Black women with PPCM have lower LVEF at the time of diagnosis, lower rates of recovery of LVEF, higher incidence of mortality and need for LVAD/ transplant. (1,2)Studies looking for genetic reasons for this disparity have come up short.Black women are more likely to have comorbid conditions (i.e., gestational HTN, preeclampsia). 2. What is it like taking care of younger patients with LVEF, especially young black patients? Working in Advanced Heart Failure gives cardiologists the opportunity to work with younger patients due to the prevalence of CMs that present at younger ages.Younger patients tend to feel more invincible, and to have more distrust of the medical system.It is important to get to know these patients, meet them where they are, and communicate with them in ways they understand (text, social media). 3. How can we help to break the black patients’ distrust in the medical system? Understand the history: medicine has historically excluded and abused black patients. (ie. the Tuskegee study withheld treatment from black sharecroppers, gynecological surgery experimentations on black slave women, a legacy of segregation, etc.)Listen to our patients and try to meet them where they are.Understand the social determinants of health (SDOH) that may influence their ability to “adhere” to therapy/ appointments (i.e., difficulty finding childcare, employment restrictions)Partner with community initiatives (i.e., Urban Health Initiative at University of Chicago)Hire and train members of the community to work in the hospital!Invest in Pipeline programs and mentorship. 4. Why is diversity in the medicine important? Concordance of race between providers and patients improves trust, quality of care, and improves patient outcomes! (5)Black patients are less likely to be referred for catheterization, AICDs, etc., despite our best efforts to provide equitable care.Language is important! Consider the use of coded language and racially disparate expectations for patients when discussing issues such as transplant candidacy.Recruit physicians who are interested in disparities research, and make research into disparities a basis for promotion. 5. How do we engage the rest of the cardiology community to be invested in the recruitment and mentorship of underrepresented minorities in medicine (URiMs)? URiMs frequently pay the “minority tax,” or the necessary but unpaid and seldom recognized labor of mentorship, community engagement, etc. That can be a heavy load to carry, especially considering only 5% of cardiology fellows identify as being Black.“You can’t really be what you can’t see” - there’s a responsibility that URMs have in cardiology to be visible to inspire future generations.However, mentorship of URiMs should not be limited to only URiM faculty. Centers should try to recruit and establish a culture that values diversity.Diversity shouldn’t be limited to just attributes like race/ gender, but also in interest. Without diversity of thought, you may not have adequate mentorship and community engagement. Show notes updated as of 3.2.2021 CardioNerds Narratives in Cardiology The CardioNerds Narratives in Cardiology series features cardiovascular faculty representing diverse backgrounds, subspecialties, career stages, and career paths. Discussing why these faculty chose careers in cardiology and their passion for their work are essential components to inspiring interest in the field. Each talk will feature a cardiology faculty from an underrepresented group, within at least one of several domains: gender, race, ethnicity, religion, national origin, international graduate status, disadvantaged backgrounds, etc. Featured faculty will also represent a variety of practice settings, academic ranks, subspecialties (e.g. clinical cardiology, interventional cardiology, electrophysiology, etc), and career paths (e.g. division chief, journal editor, society leadership, industry consultant, etc). Faculty will be interviewed by fellows-in-training for a two-part discussion that will focus on: 1) Faculty's content area of expertise2) Faculty's personal and professional narrative As part of their narrative, faculty will discuss their unique path to cardiology and their current professional role with particular attention to challenges, successes, and advice for junior trainees. Specific topics will be guided by values relevant to trainees, including issues related to mentorship, work-life integration, and family planning. To help guide this important initiative, the CardioNerds Narratives Council was founded to provide mentorship and guidance in producing the Narratives series with regards to guests and content. The CardioNerds Narratives Council members include: Dr. Pamela Douglas, Dr. Nosheen Reza, Dr. Martha Gulati, Dr. Quinn Capers, IV, Dr. Ann Marie Navar, Dr. Ki Park, Dr. Bob Harrington, Dr. Sharonne Hayes, and Dr. Michelle Albert. The Narratives Council includes three FIT advisors who will lead the CardioNerds’ diversity and inclusion efforts, including the current project: Dr. Zarina Sharalaya, Dr. Norrisa Haynes, and Dr. Pablo Sanchez. Guest Profiles Dr. Bryan Smith Dr. Bryan Smith is an Advanced Heart Failure and Transplant Cardiologist at University of Chicago. Dr. Smith completed his medical school training, residency and Cardiology fellowship at University of Chicago, then traversed Lake Shore Drive to complete his advanced HF fellowship at Northwestern. At University of Chicago, he serves as the director of the hemodynamic Cath lab, on the Chicago board for AHA, and as a faculty mentor for SNMA (Student National Medical Association.) Dr.

Mar 1, 2021

CardioNerd Amit Goyal is joined by Dr. Erika Hutt (Cleveland Clinic general cardiology fellow), Dr. Aldo Schenone (Brigham and Women’s advanced cardiovascular imaging fellow), and Dr. Wael Jaber (Cleveland Clinic cardiovascular imaging staff and co-founder of Cardiac Imaging Agora) to discuss nuclear and complimentary multimodality cardiovascular imaging for the evaluation of abnormal coronary anatomy including anomalous coronary arteries and myocardial bridges. Show notes were created by Dr. Hussain Khalid (University of Florida general cardiology fellow and CardioNerds Academy fellow in House Thomas). To learn more about multimodality cardiovascular imaging, check out Cardiac Imaging Agora! Collect free CME/MOC credit just for enjoying this episode! CardioNerds Multimodality Cardiovascular Imaging PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll Subscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Show Notes & Take Home Pearls Five Take Home Pearls Anomalous coronaries are present in 1-6% of the general population and predominantly involve origins of the right coronary artery (RCA). Anomalous origination of the left coronary artery from the right sinus, although less common, is consistently associated with sudden cardiac death, especially if there is an intramural course. Sudden cardiac death can occur due to several proposed mechanisms: (1) intramural segments pass between the aorta and pulmonary artery making them susceptible to compression as the great vessels dilate during strenuous exercise; (2) an acute angle takeoff of the anomalous coronary can create a “slit-like” ostium making it vulnerable to closure. Anomalous left circumflex arteries are virtually always benign because the path taken behind the great vessels to reach the lateral wall prevents vessel compression.Myocardial bridging (MB) is a congenital anomaly in which a segment of the coronary artery (most commonly, the mid-left anterior descending artery [LAD]) takes an intramuscular course and is “tunneled” under a “bridge” of overlying myocardium. In the vast majority of cases, these are benign. However, a MB >2 mm in depth, >20 mm in length, and a vessel that is totally encased under the myocardium are more likely to be of clinical significance, especially if there is myocardial oxygen supply-demand mismatch such as with tachycardia (reduced diastolic filling time), decreased transmural perfusion gradient (e.g. in myocardial hypertrophy and/or diastolic dysfunction), and endothelial dysfunction resulting in vasospasm.PET offers many benefits over SPECT in functional assessment of MB including the ability to acquire images at peak stress when using dobutamine stress-PET, enhanced spatial resolution, and quantification of absolute myocardial blood flow. For pharmacologic stress in evaluation of MB, we should preferentially use dobutamine over vasodilator stress. Its inotropic and chronotropic effects enhance systolic compression of the vessel, better targeting the pathological mechanisms in pearl 2 above that predispose a MB to being clinically significant.CCTA can help better define the anatomy of MB as well as anomalous origination of the coronary artery from the opposite sinus (ACAOS), help with risk stratification, and assist with surgical planning.Instantaneous wave-free ratio (iFR) measures intracoronary pressure of MB during the diastolic “wave-free” period – the period in the cardiac cycle when microvascular resistance is stable and minimized allowing the highest blood flow. This allows a more accurate assessment of a functionally significant dynamic stenosis than fractional flow reserve (FFR) – which can be falsely normal due to systolic overshooting. Detailed Show Notes What are some examples of abnormal coronary anatomies and how often do they lead to clinical events?Abnormal coronary anatomy can relate to the origin (e.g. anomalous origination of coronary artery from the opposite sinus [ACAOS]), course (e.g. myocardial bridging [MB]), intrinsic properties (e.g. aneurysm or hypoplasia), or termination (e.g. fistula) of the coronary artery. In this episode and in these notes, we examine MB and ACAOS in more detail. For an excellent case discussion of anomalous left coronary artery from the pulmonary artery (ALCAPA) by the team from Massachusetts General Hospital, listen to CardioNerds Podcast Episode 81!MB –Myocardial BridgingMB is a congenital anomaly in which a segment of the coronary artery (most commonly, the mid-left anterior descending artery [LAD]) takes an intramuscular course and is “tunneled” under a “bridge” of overlying myocardium.MB was originally identified at autopsy by Reyman in his dissertation, “Disertatio de vasis cordis propriis “ in 1737. In the largest subsequent autopsy study by Risse et al. involving 1056 patients, MB was demonstrated in 26% of patients.Because it is so prevalent, it is difficult to determine its clinical significance. In most patients, MB is an incidental finding with an excellent survival rate (97% at 5 years); however, there are associations with myocardial ischemia, infarction, stress cardiomyopathy, arrhythmia, and sudden cardiac death (SCD).MB can generally be classified into two subtypes: a “superficial” variant which represents 75% of cases and a “deep” variant in which the LAD deviates towards the right ventricle (RV) and dives into the intraventricular septum. The overlying muscle bundle in the deep variant is typically at an oblique or transverse angle resulting in twisting of the tunneled segment and more commonly compromised coronary flow.One of the longest MB usually occurs in association with ACAOS! In this case, the left coronary artery comes off the right coronary cusp. The Left Main (LM) is around 3-4x longer in this instance and dives into the interventricular septum and takes a trans-septal course behind the pulmonary artery before emerging on the other side.There is increased prevalence in certain patient populations: hypertrophic cardiomyopathy (HCM), patients with spontaneous coronary artery dissection (SCAD) +/- fibromuscular dysplasia (FMD), and heart transplant recipientsACAOS - anomalous origination of coronary artery from the opposite sinusAnomalous coronaries are present in 1-6% of the general population and predominantly involve the origin of the right coronary artery (RCA)Anomalous origination of the left coronary artery from the right sinus, although less common, is consistently related to SCD. Separate studies have shown the incidence of SCD may be as high as 23% or 59% of cases in athletes under the age of 20 years.In a large Armed Forces Institute of Pathology (AFIP) study of 6.3 million military recruits, the autopsies of recruits who suffered nontraumatic deaths over a 25-year period were reviewed and ACAOS was found to be the most common cause. It accounted for 33% (64 of 126) of nontraumatic deaths and all cases involved a left coronary artery with an interarterial course. What features predispose MB or ACAOS to become clinically significant? What is the pathophysiology behind development of ischemia in those with clinically significant MB or ACAOS?MB – myocardial bridgingGiven the majority of MB is benign, correlating MB as causative in myocardial ischemia and its consequences has been a diagnostic challenge.In systole, the portion of the artery that is tunneled under the MB (bridge segment) is compressed. This can manifest clinically as angina, acute coronary syndrome, left ventricular (LV) dysfunction, arrhythmias, and SCD. However, the majority of myocardial perfusion occurs in diastole which is why MB is usually benign. Nonetheless, certain conditions in patients with MB can set up an oxygen supply-demand mismatch severe enough to lead to myocardial ischemia:Exercise-related stress leads to tachycardia which can decrease diastolic filling time for the coronary arteries and lead to more of the cardiac cycle to be spent in systoleMyocardial hypertrophy and diastolic dysfunction can affect the transmural perfusion gradient increasing supply-demand mismatch. Furthermore, LV hypertrophy can compress the microvasculature and reduce the microvascular reserve.Endothelial dysfunction (driven by metabolic changes secondary to hypoxia) can contribute to coronary compression and lead to the development of accelerated atherosclerosis and/or coronary vasospasm (leading to compression of the epicardial coronary artery throughout the cardiac cycle, not just during systole)There has been a recognized multiplier-effect described by Klues et al. in which the greater the degree of systolic narrowing of the MB, the greater the reduction in diastolic vessel diameter. This is also associated with increased retrograde flow in the coronary artery (which not only reduces perfusion but can introduce shear wall stress and predispose to plaque formation) and reduced flow reserve.Myocardial ischemia can also occur due to “branch steal.” The LAD may have septal perforators that arise from the tunneled segment. When there is compression of the vessel under the MB, there can be “steal” from these septal branches due to the Venturi effect. The septal branches are essentially depressurized because as the vessel narrows, velocity increases but the fluid (coronary blood flow) exerts less pressure. Thus, mild to moderate MB severity typically demonstrates septal ischemia (due to branch steal) rather than distal ischemia downstream from the compression.The vessel segment proximal to the bridge appears to develop atherosclerosis at increased rates approaching 90% -- likely as the sequela of shear stress. In contrast,

Feb 22, 2021

CardioNerds (Amit Goyal & Daniel Ambinder) join University of Maryland cardiology fellows (Manu Mysore, Adam Zviman, and Scott Butler) for some cardiology and an Orioles game in Baltimore! They discuss a rare cause of postpartum angina and cardiac arrest due to coronary vasculitis. Program director Dr. Mukta Srivastava provides the E-CPR expert segment and a message for applicants. Episode notes were developed by Johns Hopkins internal medicine resident Rick Ferraro with mentorship from University of Maryland cardiology fellow Karan Desai. This case has been published in JACC Case Reports! Collect free CME/MOC credit just for enjoying this episode! Jump to: Patient summary - Case media - Case teaching - References Episode graphic by Dr. Carine Hamo CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Patient Summary A woman in her early 30s with a past medical history of Hashimoto's thyroiditis and one prior miscarriage at <8 weeks presented with chest pain about 6 weeks postpartum from the birth of her third child. In the ED, she continued to report intermittent sharp chest discomfort and found to have a diastolic decrescendo murmur at the left upper sternal border and labs demonstrating a troponin-I of 0.07 ng/dL. Join the UMD Cardionerds for the incredible course and story of this young patient as we go through the differentia and approach to postpartum chest pain and ultimately arrive in a very rare diagnosis! For a detailed course, enjoy the JACC case report. Case Media Visit the JACC Case Reports to review the case media! Episode Schematics & Teaching The CardioNerds 5! – 5 major takeaways from the #CNCR case 1. How Do We Evaluate Chest Pain in Younger Patients Start with the same things as everyone else! Think broadly about the big three concerning etiologies of chest pain: Cardiac, Gastric, and Pulmonary (The excellent Clinical Problems Solvers 4+2+2 construct here is always a great resource. Find them at: https://clinicalproblemsolving.com/dx-schema-chest-pain/). Of course it is important to think about non-life threatening etiologies as well – esophageal spasm, gastric ulcer, rib fracture, skin lesion, among many others - given that high-risk chest pain is less likely in younger adults. While less common, acute coronary syndrome is not uncommon in young patients, as 23% of patients with MI present at age <55 years. 2. What About Chest Pain in Women? As has been discussed on the Cardionerds podcast (Listen to episodes with Dr. Nanette Wenger, Dr Martha Gulati, and Dr. Leslie Cho), women generally present with acute coronary syndrome at a later age, with a higher burden of risk factors than men, and with greater symptom burden but are less likely to be treated with guideline-directed medical therapies, undergo cardiac catheterization and receive timely reperfusion. In one study of young patients with acute MI, women – 19% of cases overall – were less likely to undergo revascularization or receive guideline-directed therapy The construct of classifying chest pain as "typical" and "atypical" likely leads to misdiagnosis or delayed diagnosis of acute myocardial infarction in women. Rather, it is important to recognize that while symptoms may not be "typical" for angina, coronary disease can manifest in many different ways. While many women will presents with chest pain suggestive of angina, women are more likely than men to present with dyspnea, indigestion, weakness, nausea/vomiting and/or fatigue. Note, shoulder pain and arm pain are twice as predictive of an acute myocardial infarction diagnosis in women compared with men. Furthermore, while obstructive epicardial disease remains the primary cause of acute MI in young women, it is also important to keep other causes of chest pain such as MINOCA, SCAD (see the UCLA episode), peripartum cardiomyopathy (see the Penn and MCW episodes), or coronary vasculitis on the differential. While these etiologies are rare, they are disproportionately represented in young women. 3. How do we think about categorizing vasculitis? Vasculitis is a broad term encompassing many forms of vessel wall (including arteries, veins or capillaries) inflammation. This can be secondary to autoimmunity, infection, drug reaction, and malignancy to name a few underlying causes. Generally vasculitis is divided by large vessel (e.g., Takayasu, Giant Cell), medium vessel (e.g., Polyarteritis Nodosa), and small vessel etiologies (e.g., Granulomatosis with Polyangitis, Eosinophilic Granulomatosis with Polyangiitis, Microscopic Polyangitis, Immune-mediated Vasculitis, amongst others). This characterization follows the 2012 Revised International Chapel Hill Consensus Conference Nomenclature of Vasculitis. Other important categories includes variable vessel vasculitis (e.g., Behcet's Disease, Cogan's Syndrome) and vasculitis associated with systemic disease (e.g., Lupus vasculitis, Rheumatoid vasculitis, Sarcoid vasculitis). 4. What Does Vasculitis Look Like in the Heart? While inflammation can occur throughout the heart – e.g., pericarditis or myocarditis – vasculitis in the heart refers specifically to inflammation of the coronary arteries. This is a relatively rare process, with <10% of vasculitis patients exhibiting cardiac involvement. Patients with coronary vasculitis rarely present with isolated coronary involvement and typically have systemic manifestations, such as constitutional symptoms in addition to cardiac symptoms (e.g., angina, heart failure, arrhythmia). Examination may reveal asymmetric pulses or BP readings between limbs and arterial bruits, with imaging revealing multi-organ infarcts without a clear embolic origin. Amongst the vasculitides, Takayasu Arteritis (TA) is one of the more frequent etiologies of coronary arteritis. In Takayasu Arteritis (TA), the affected arteries are typically the aorta and its major branches. In contrast to giant cell arteritis (GCA), TA is quite rare and tends to have onset <40 years age; however, for both diagnoses coronary involvement is rare. TA patients will typically have constitutional symptoms and may have diminished/absent arterial pulses often accompanied by bruits. Weakness of the arterial walls may lead to aneurysms and specifically aortic root aneurysm may result in aortic valve insufficiency. When involving the coronaries, there are three main type of TA lesions: stenosis or occlusion of the ostia/proximal segments (Type 1); diffuse or focal coronary vasculitis involving all the epicardial branches or focal areas (Type 2); coronary aneurysms (Type 3). 5. What Are the Complications of Coronary Vasculitis? The consequences of coronary vasculitis are variable and much of the data we have comes from case reports. As in the case presented, severe coronary ischemia and its complications, including arrhythmia and cardiac arrest, are a major concern. However, cardiac arrest is rarely the first presentation of coronary vasculitis, especially if it is detected early. The manifestations of coronary vasculitis are also going to be dependent on the specific etiology of the arteritis. Amongst the medium vessel vasculitis and specifically polyarteritis nodosa, 15-20% of patients will have cardiac involvement, with major complications including heart failure, myocardial infarction, or arrhythmia. Amongst the small vessel vasculitis, eosinophilic granulomatosis with polyangiitis is the most common culprit for cardiac involvement, primarily secondary to eosinophilic toxicity. Cardiac involvement is a major cause of mortality and poor prognostic sign in EGPA. The CardioNerds Cardiology Case Reports series shines light on the hidden curriculum of medical storytelling. We learn together while discussing fascinating cases in this fun, engaging, and educational format. Each episode ends with an “Expert CardioNerd Perspectives & Review” (E-CPR) for a nuanced teaching from a content expert. We truly believe that hearing about a patient is the singular theme that unifies everyone at every level, from the student to the professor emeritus. We are teaming up with the ACC FIT Section to use the #CNCR episodes to showcase CV education across the country in the era of virtual recruitment. As part of the recruitment series, each episode features fellows from a given program discussing and teaching about an interesting case as well as sharing what makes their hearts flutter about their fellowship training. The case discussion is followed by both an E-CPR segment and a message from the program director. References Kostner, M. J., & Warrington, K. J. (2019, March 13). Vasculitis of the Coronary Arteries. ACC.org. Ward, E. V., Nazari, J., & Edelman, R. R. (2012). Coronary artery vasculitis as a presentation of cardiac sarcoidosis. Circulation, 125(6), e344-e346. Awad, H. H., McManus, D. D., Anderson Jr, F. A., Gore, J. M., & Goldberg, R. J. (2013). Young patients hospitalized with an acute coronary syndrome. Coronary Artery Disease, 24(1), 54-60. Bugiardini, R., Cenko, E. (2020). Sex differences in myocardial infarction deaths. Lancet, 396:72–73 DeFilippis, E.M., Collins, B.L., Singh A., et. al Women who experience a myocardial infarction at a young age have worse outcomes compared with men: the Mass General Brigham YOUNG-MI registry, European Heart Journal, ehaa662 Miloslavsky, E., & Unizony, S. (2014). The heart in vasculitis. Rheumatic Disease Clinics, 40(1), 11-26. Mehta LS, Beckie TM, DeVon HA et al; American Heart Association Cardiovascular Disease in Women and Special Populations Committee of the Council on Clinical Cardiology, Council on Epidemiology and Prevention, Council on Cardiovascular and Stroke Nursing,

Feb 14, 2021

CardioNerd Amit Goyal is joined by Dr. Erika Hutt (Cleveland Clinic general cardiology fellow), Dr. Aldo Schenone (Brigham and Women’s advanced cardiovascular imaging fellow), and Dr. Wael Jaber (Cleveland Clinic cardiovascular imaging staff and co-founder of Cardiac Imaging Agora) to discuss nuclear and complimentary multimodality cardiovascular imaging for the evaluation of myocardial viability. Show notes & #Tweetorial were created by Dr. Hussain Khalid (University of Florida general cardiology fellow and CardioNerds Academy fellow in House Thomas). To learn more about multimodality cardiovascular imaging, check out Cardiac Imaging Agora! Collect free CME/MOC credit just for enjoying this episode! CardioNerds Multimodality Cardiovascular Imaging PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Show Notes & Take Home Pearls In response to ischemia the myocardium can dynamically change along a spectrum from myocardial stunning to myocardial hibernation to myocardial necrosis. The goals of viability testing are to identify patients who may benefit from revascularization as hibernating or stunned myocardium are potentially reversible causes of LV dysfunction. There are numerous imaging modalities available for the evaluation of myocardial viability. The broad range of ways in which myocardial viability is assessed speaks to the complexity of the disease spectrum and the difficulty in creating a unifying definition of viability to assess in clinical trials. Five Take Home Pearls 1. In response to an acute episode of ischemia with subsequent reperfusion, the myocardium can be exposed to a large flux of oxygen free radicals or calcium overload that affects the cellular membrane and contractile apparatus. This phenotypically results in decreased contractility of the affected region of myocardium that can persist for weeks, labeled myocardial stunning 2. Repeated episodes of myocardial stunning or chronic low myocardial blood flow can lead to cellular changes such as resorption of the contractile apparatus in order to decrease oxygen demand and allow the myocardial cells to survive. Phenotypically, this might appear as regions of hypokinesis or akinesis at rest with a fixed perfusion defect on myocardial perfusion imaging. This is typically considered hibernating myocardium. 3. The goal of myocardial viability testing is to be able to differentiate between stunned, hibernating and necrosed myocardium. In patients with known epicardial coronary disease, this differentiation allows us to identify who may benefit from revascularization with improved LV systolic function and overall survival. 4. There are several imaging modalities that can be used in the assessment of myocardial viability. The most sensitive modalities are FDG-PET and CMR. The addition of Dobutamine or first pass perfusion with Gadolinium additionally increases the specificity of CMR. These modalities are more expensive and not as widely available. 5. The dynamic nature of the myocardial hibernation and the lack of a unifying definition/phenotypic expression of myocardial hibernation and viability have made it difficult for clinical trials to show that re-establishing myocardial blood flow to hibernating myocardium is beneficial. As Dr. Jaber stated in the episode in his spin on the classic opening phrase from Leo Tolstoy’s masterpiece, Anna Karenina, “All normal hearts are normal in the same way, and all abnormal hearts are abnormal in different ways.” 6. The PARR-2 trial was one of the few randomized, controlled trials of patients with LV systolic dysfunction and coronary artery disease who were randomized to either FDG-PET guided management or standard care with respect to whether to pursue revascularization. Overall, there was not a significant reduction in the primary composite endpoint between the FDG-PET arm and the standard care arm. However, not all patients received the revascularization strategy recommended by imaging. In patients whom the PDG-PET recommendation for revascularization was followed, there was a significant benefit compared to the standard care group. Quotable: “All normal hearts are normal in the same way, All abnormal hearts are abnormal in different ways”—0:54 Detailed Show Notes What is myocardial hibernation and myocardial stunning? How do these concepts fit into the discussion of myocardial viability? A common scenario encountered in clinical practice is the patient who has depressed LV systolic function and known obstructive epicardial coronary disease. For these patients, we may wonder if the myocardium supplied by the epicardial coronary arteries with obstructive lesions is living (viable) or dead(scarred), and whether there would be a benefit to revascularization. If the LV systolic function is decreased with hypokinesis or akinesis and perfusion deficits, then the myocardium is either dead (scarred), stunned, or hibernating! This is a spectrum. Stunned myocardium and hibernating myocardium were originally described in the late 1970s and popularized in the 1980s — stunned myocardium by Dr. Braunwald and Dr. Kloner and hibernating myocardium by Dr. Diamond and Dr. Rahimtoola. When first described, myocardial stunning was thought of as a “hit” (episode of severe ischemia), “run” (relief of ischemia before irreversible injury) and “stun” (a relatively long period of post-ischemia LV dysfunction). What are stunned myocardium and hibernating myocardium? When a region of myocardium becomes ischemic and that ischemia is severe and prolonged, myocardial necrosis occurs, there is no return of contractile function, and the myocardium is replaced by scar tissue. If, however, there is reperfusion and relief of the ischemia before necrosis occurs, the myocardium can become “stunned”. Myocardial stunning is a transient period of post-ischemic dysfunction that can persist for days to weeks prior to recovery of myocardial function. There are a variety of hypotheses as to why this occurs. Some of the leading hypotheses are: In response to ischemia, there can be a flux of oxygen free radicals that disrupt cellular membranes and the contractile apparatus of the cell. Calcium overload that affects myofilament responsiveness to calcium or leads to sarcoplasmic reticulum dysfunction. Phenotypically, this may manifest as hypokinesis or akinesis of the corresponding area of myocardium. If there are repetitive episodes of myocardial stunning or if there is chronic low myocardial blood flow to a region of the myocardium, this can lead to myocardial hibernation. Essentially, the myocardium undergoes metabolic adaptations and downregulation of function (e.g. resorption of the intracellular contractile apparatus) that allows the myocardium to survive by reducing myocardial oxygen demand. Phenotypically, this results in contractile abnormalities at rest that may manifest as hypokinesis or akinesis of the corresponding area of myocardium. This dysfunction may persist weeks to months even after revascularization as the contractile apparatus replenishes. As referenced in the episode, Dr. Rahimtoola popularized the concept of hibernating myocardium in a published report in the 1980s of a patient who had chronic angina, single vessel obstructive epicardial coronary disease in the LAD, depressed LV systolic function, and an anteroapical myocardial wall motion abnormality (WMA). After administration of nitroglycerin, the patients LV systolic function and WMA improved suggesting that this area of the myocardium was viable. The patient underwent coronary bypass surgery and their LV systolic function and wall motion eventually normalized—confirming that this area of myocardium was viable all along. As described by Dr. Kloner in a recent review, an analogy to hibernating myocardium is a broken arm that is casted. As the muscles are not being used, we can expect some atrophy and similarly with hibernating myocardium, the cardiac muscle is not contracting and some level of atrophy is not unexpected. As with a broken arm that is casted will need some time to recover near full function, revascularization will not lead to immediate normalization of cardiac function. What are our goals when it comes to viability testing? In which patients should we pursue viability testing (evaluation for myocardial stunning or myocardial hibernation)? The primary goals of viability testing are: To avoid attempting to revascularize dead myocardium as this would unnecessarily expose them to the risks of an invasive procedure. To identify patients who may have an improvement in LV systolic function with revascularization. To potentially improve survival. There are certain patient populations in whom we should not pursue viability testing as the information provided by testing would not change our management: Patients who have normal coronary arteries or nonobstructive disease. Patients with obstructive epicardial coronary disease that is not amenable to revascularization. Patients with normal LV systolic function. There are different modalities we can use to assess for myocardial viability. How can we conceptualize the different modalities and what are the advantages/disadvantages of each one? We can broadly differentiate the modalities used to assess for myocardial viability into those that are looking for “signs of life” (e.g., evidence of inducible contractility, cell membrane integrity, metabolic activity) and those that are looking for “signs of death” (e.g., myocardial wall thinning, presence of scar). How to look for signs of life: Dobutamine Stress Echocardiography With DSE, we are trying to prove that areas of the myocardium that are hypokinetic or akinetic have some reserve and contractile function.

Feb 7, 2021

CardioNerd Amit Goyal is joined by Dr. Erika Hutt (Cleveland Clinic general cardiology fellow), Dr. Aldo Schenone (Brigham and Women’s advanced cardiovascular imaging fellow), and Dr. Wael Jaber (Cleveland Clinic cardiovascular imaging staff and co-founder of Cardiac Imaging Agora) to discuss nuclear and complimentary multimodality cardiovascular imaging for the evaluation of coronary microvascular disease. To learn more about multimodality cardiovascular imaging, check out Cardiac Imaging Agora! Collect free CME/MOC credit just for enjoying to the episode! CardioNerds Multimodality Cardiovascular Imaging PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll Subscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Guest Profiles Wael Jaber, MD Wael Jaber, MD, is a staff cardiologist in the Section of Cardiovascular Imaging, Robert and Suzanne Tomsich Department of Cardiovascular Medicine, at the Sydell and Arnold Miller Family Heart, Vascular & Thoracic Institute at Cleveland Clinic. Dr. Jaber specializes in cardiac imaging (both nuclear cardiology and echocardiography) and valvular heart disease. Dr. Jaber attended college at the American University in Beirut, graduating with a Bachelor of Science in biology. He then went on at the American University to receive his medical degree while making the Dean's honor list. He completed his residency in internal medicine at the St. Luke's-Roosevelt Hospital Center at Columbia University College of Physicians and Surgeons, where he also completed fellowships in cardiovascular medicine and nuclear cardiology. Dr. Jaber is currently is the Medical Director of the Nuclear Lab and of the Cardiovascular Imaging Core Laboratory in C5Research. He is fluent in English, French and Arabic. He is the author of Nuclear Cardiology review: A Self-Assessment Tool and cofounder of Cardiac Imaging Agora. Dr. Aldo L Schenone Dr. Aldo L Schenone is one of the current Chief Non-Invasive Cardiovascular Imaging Fellows at the Brigham and Women's Hospital. He completed medical school at the University of Carabobo in Valencia, Venezuela, and then completed both his Internal Medicine residency and Cardiology fellowship at the Cleveland Clinic where he also served as a Chief Internal Medicine Resident. Dr. Erica Hutt Dr. Erika Hutt @erikahuttce is a cardiology fellow at the Cleveland Clinic. Erika was born and raised in Costa Rica, where she received her MD degree at Universidad de Costa Rica. She then decided to pursue further medical training in the United States, with the goal of becoming a cardiologist. She completed her residency training at Cleveland Clinic and went on to fellowship at the same institution. Her passions include infiltrative heart disease, atrial fibrillation, valvular heart disease and echocardiography among many. She is looking forward to a career in advanced cardiovascular imaging. References and Links Kaski, J.-C., Crea, F., Gersh, B. J., & Camici, P. G. (2018). Reappraisal of Ischemic Heart Disease. Circulation. https://doi.org/10.1161/circulationaha.118.031373Jaber, W., & Gimelli, A. (n.d.). Cardiac Imaging Agora. https://www.cardiacimagingagora.com/list/Taqueti, V. R., & Di Carli, M. F. (2018). Coronary Microvascular Disease Pathogenic Mechanisms and Therapeutic Options: JACC State-of-the-Art Review. In Journal of the American College of Cardiology. https://doi.org/10.1016/j.jacc.2018.09.042 Wael Jaber, MD Dr. Aldo L SchenoneDr. Erika Hutt Dr. Madiha KhanAmit Goyal, MD

Feb 4, 2021

CardioNerds (Amit Goyal & Carine Hamo) discuss the past, present, and future of Women's Heart Health & Women in Cardiology with Dr. Nanette Wenger, Professor of Medicine in the Division of Cardiology at the Emory University School of Medicine. Dr. Wenger is a true leader in the field of women’s heart health and a strong proponent for women in cardiology and medicine. Her passion, dedication, and advocacy have inspired countless trainees to carry this torch and continue to build on her truly impactful work. Special introduction by Dr. Martha Gulati. This is a special encore in recognition of the Go Red campaign and celebration of women's health. Collect free CME/MOC credit for enjoying this episode! Episode graphic by Dr. Carine Hamo The Cardionerds CV prevention series includes in-depth deep dives on so many prevention topics including the ABCs of prevention, approach to obesity, hypertension, diabetes mellitus and anti-diabetes agents, personalized risk and genetic risk assessments, hyperlipidemia, women’s cardiovascular prevention, coronary calcium scoring and so much more! CardioNerds Prevention PageCardioNerds Women's Cardiovascular Health PageCardioNerds Episode PageSubscribe to our newsletter- The Heartbeat CardioNerds AcademyCardionerds Healy Honor RollCheck out CardioNerds SWAG!Become a CardioNerds Patron! This episode initially ran as part of the CardioNerds Prevention Series which we produced in collaboration with the American Society for Preventive Cardiology! The ASPC is an incredible resource for learning, networking, and promoting the ideals of cardiovascular prevention! Cardionerds Cardiovascular Prevention Series References and Links 1. Wenger NK (2005) Women in cardiology: The US experience. Heart. 2. Douglas PS, Rzeszut AK, Noel Bairey Merz C, Duvernoy CS, Lewis SJ, Walsh MN, Gillam L (2018) Career preferences and perceptions of cardiology among us internal medicine trainees factors influencing cardiology career choice. JAMA Cardiol. 3. Wenger NK, Speroff L, Packard B (1993) Cardiovascular Health and Disease in Women. N Engl J Med. 4. Burgess S, Shaw E, Zaman S (2019) Women in Cardiology. Circulation. Meet Dr. Wenger! Dr. Nanette Wenger is Professor of Medicine in the Division of Cardiology at the Emory University School of Medicine. Dr. Wenger received her medical degree from Harvard Medical School in 1954 as one of their first female graduates followed by training at Mount Sinai Hospital where she was the first female to be chief resident in the cardiology department. She is among the first physicians to focus on heart disease in women with an expertise in cardiac rehabilitation and geriatric medicine. Dr. Wenger has received numerous awards including the Distinguished Achievement Award from the Scientific Councils of the American Heart Association and its Women in Cardiology Mentoring Award, the James D. Bruce Memorial Award of the American College of Physicians for distinguished contributions in preventive medicine, the Gold Heart Award, the highest award of the American Heart Association, a Lifetime Achievement Award in 2009 and the Inaugural Bernadine Healy Leadership in Women’s CV Disease Distinguished Award, American College of Cardiology. She chaired the U.S. National Heart, Lung, and Blood Institute Conference on Cardiovascular Health and Disease in Women, is a Past President of the Society of Geriatric Cardiology and is past Chair, Board of Directors of the Society for Women’s Health Research. Dr. Wenger serves on the editorial boards of numerous professional journals and is a sought-after lecturer for issues related to heart disease in women, heart disease in the elderly, cardiac rehabilitation, coronary prevention, and contemporary cardiac care. She is listed in Best Doctors in America. Carine Hamo, MDAmit Goyal, MD

Jan 31, 2021

CardioNerd Amit Goyal is joined by Dr. Erika Hutt (Cleveland Clinic general cardiology fellow), Dr. Aldo Schenone (Brigham and Women’s advanced cardiovascular imaging fellow), and Dr. Wael Jaber (Cleveland Clinic cardiovascular imaging staff and co-founder of Cardiac Imaging Agora) to discuss nuclear and complimentary multimodality cardiovascular imaging for the evaluation of coronary ischemia. Show notes were created by Dr. Hussain Khalid (University of Florida general cardiology fellow and CardioNerds Academy fellow in House Thomas). To learn more about multimodality cardiovascular imaging, check out Cardiac Imaging Agora! Collect free CME/MOC credit for enjoying this episode! CardioNerds Multimodality Cardiovascular Imaging PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll Subscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Show Notes & Take Home Pearls Five Take Home Pearls 1. We can broadly differentiate non-invasive testing into two different categories—functional and anatomical. Functional tests allow us to delineate the functional consequence of coronary disease rather than directly characterizing the burden of disease. Anatomical tests such as coronary CTA, on the other hand, allow us to directly visualize obstructive epicardial disease. 2. In general PET imaging provides higher quality images than SPECT imaging for a variety of reasons, including a higher “keV” of energy in PET radiotracers 3. If using a SPECT camera, we should use cameras that have attenuation correction. Without attenuation correction, the specificity of a SPECT camera drops to 50-60%. 4. In evaluating ischemic heart disease, cardiac nuclear imaging can provide a wide range of information including myocardial perfusion (rest and stress), ejection fraction assessment (rest and stress), absolute myocardial blood flow with quantitative flow reserve in all coronary territories (PET), assessment of myocardial viability (PET), and calcium score with CT attenuation correction. 5. To select the best non-invasive test, we should consider a variety of factors such as pretest probability of obstructive epicardial disease, patient-specific factors (e.g., ability to exercise) and whether a functional or an anatomical test will provide the best answer for our clinical question. Detailed Show Notes What are the basic non-invasive testing categories for evaluation of coronary artery disease? We have a variety of different non-invasive testing modalities that can be broadly separated into functional tests and anatomical tests. The basic principle underlying functional stress testing is to induce ischemia or coronary vasodilation (discussed below), followed by a functional assessment by different techniques (e.g., EKG, echocardiography, radionuclide imaging) to detect flow-limiting obstructive coronary artery disease. These tests delineate the functional consequence of the coronary disease, rather than directly characterizing the burden of disease itself. Functional tests can also allow us to assess the nature of a patient’s symptoms. For example, by having a patient exercise on a treadmill we can evaluate whether we can reproduce a patient’s chest pain syndrome. Anatomical tests allow us to visualize the presence of obstructive epicardial disease. For example, obtaining a Coronary Computed Tomography Angiography (CCTA) for a patient with chest pain would allow you to directly visualize possible obstructive epicardial disease. How do we induce ischemia for functional stress testing? To induce ischemia (and/or coronary vasodilation), we have many different stressors that can be broadly separated into exercise stressors and pharmacologic stressors. Treadmill exercise via standardized protocols is the most common method for inducing ischemia and has the advantage of assessing functional capacity, which has prognostic information. Supine bicycle is another common exercise modality that is utilized. There are also several pharmacologic stressors that vary in their mechanisms of action. Dobutamine is a synthetic catecholamine that stimulates myocardial beta-1 and beta-2 receptors to increase heart rate, contractility, and consequently myocardial oxygen demand with a small decrease in systemic vascular resistance. Adenosine and adenosine derivatives (e.g. regadenoson) induce coronary vasodilation and take advantage of differences in coronary flow reserve. With obstructive coronary lesions, the vessels distal to the obstruction are already dilated at baseline and have little flow reserve. Adenosine (and its derivatives) induce vasodilation and increase flow in normal coronary beds, but much less so in areas supplied by an obstructive lesion. Consequently, we can see disparate radiotracer uptake that correlates with different coronary territories. Once we’ve induced ischemia, we can assess it via electrocardiogram (EKG) alone or in conjunction with an imaging modality such as echocardiography, MRI, or nuclear imaging -- such as Single Photon Emission Computed Tomography (SPECT) or Positron Emission Tomography (PET). What is the difference between SPECT and PET imaging quality? What are the advantages of using PET imaging? SPECT and PET imaging both use gamma cameras that detect gamma rays produced by the injected radionuclide tracer. SPECT utilizes a single-crystal camera to acquire multiple 2D images to be reconstructed into a 3D image, while PET imaging utilizes a multi-crystal camera which can detect more counts (e.g., quantification of radioactivity). SPECT studies usually use Technetium-based tracers which have nuclei that emit 140 keV of energy. PET studies usually use Rubidium or Ammonia which have nuclei that emit around 510 keV of energy. Either of these studies can also use Thallium which have nuclei that emit 68 keV of energy. In general, the higher the “keV”, the better the image quality. So, using thallium may result in poorer quality images and is not recommended as a first-line agent. Rubidium has a half-life of 76 seconds and Ammonia has a half-life of 10 minutes—so it is possible to do an exercise stress test if using Ammonia but not with using Rubidium! Because the radiotracers used for PET imaging have higher “keV” than those used in SPECT imaging, PET image quality is generally better with a higher resolution. If using a SPECT camera, you should use a camera that has attenuation correction. Attenuation artifact can occur when you have tissue such as breast or diaphragm that overlies the myocardium and decreases the intensity/strength of signal prior to reaching the myocardium. This can result in the false appearance of a myocardial perfusion defect in that region. Without attenuation correction, the specificity of a SPECT camera drops to 50-60%. In addition to improved spatial resolution and higher quality images resulting from using radiotracers with higher “keV”, PET cameras also do not require physical collimation. This allows for even further increase in spatial resolution and image quality. A collimator is a piece of lead with holes that absorb and stop most photons except for those that arrive almost perpendicular to the detector face. This allows the camera to accurately localize the radiotracer in the patient’s body over the organ of interest. Overall, PET has better sensitivity, specificity, and better accuracy to diagnose 50% and 70% lesions than SPECT! However, maintaining PET scanners comes at increased cost compared to SPECT. What diagnostic information can cardiac nuclear imaging provide us? What are some unique uses of nuclear imaging? In the evaluation of coronary disease, some diagnostic information provided by SPECT and PET imaging include: Assessment of myocardial perfusion and blood flow at both rest and stress Ejection fraction assessment at both rest and stress Quantitative flow reserve in all coronary territories (PET) Assessment of myocardial viability (PET) Prognostication Calcium Score with CT Attenuation Correction If using CT for attenuation correction, you should also use it for calcium score. A high coronary calcium score can change management—there is also data that shows that just showing patients the plaque on CT imaging can improve outcomes! There are many uses of nuclear imaging, and novel uses are continuously being described. In addition to its use in noninvasive stress testing and ischemic heart disease, we can also use it to assess etiology of cardiomyopathies: In patients with suspected cardiac sarcoidosis, fluorodeoxgylocse(FDG)-PET imaging with Rubidium can be utilized to detect sarcoid and prognosticate. Enjoy the upcoming discussion about sarcoidosis imaging as well as the CNCR from the University of Chicago! Nuclear scintigraphy with 99m-Technetium pyrophosphate can be used to assess for cardiac amyloidosis. Stay tuned for more on this as part of the amyloidosis imaging discussion. FDG PET and whole-body-white blood cell scan can be used to help evaluate for prosthetic valve endocarditis or LVAD-associated infections, which we will also discuss later in this imaging series! FDG-PET can help evaluate and differentiate aortopathies in patients presenting with chest pain Many novel uses of nuclear stress testing are being described for patients admitted to the cardiac intensive care unit (CICU). CT imaging and MRI require significant patient cooperation. MRI additionally is sometimes limited by patient compatibility issues. A full PET study can be done in 20-25 minutes, however, independent of renal and hepatic function. In patients admitted to the CICU with an intra-aortic balloon pump (IABP), exercise can be simulated by reducing the IABP support ratio from 1:1 to 1:3. A PET stress test can then be conducted using this “exercise” to evaluate for myocardial ischemia. How do you select the best non-invasive test?

Jan 25, 2021

CardioNerds (Carine Hamo, Amit Goyal and Daniel Ambinder) discuss personalized risk assessment for cardiovascular prevention with Dr. Amit Khera, the immediate past president for the American Society for Preventive Cardiology and Director of the Preventive Cardiology and Professor of Medicine at the University of Texas, Southwestern Medical School in Dallas, Texas. They dive into an illuminating discussion about traditional and next generation personalization of risk assessment which covers the need for personalization, traditional risk stratification, applying risk enhancing factors for decision making, biomarkers, familial hypercholesterolemia, and the use of -Omics. This episode is the 13th and final part of our in-depth prevention series produced in collaboration with the American Society for Preventive Cardiology! Stay tuned for a bonus segment at the end of the episodeas we talk to Dr. Ankur Kalra, interventionist at the Cleveland Clinic, Podcast host of Parallax by Ankur Kalra, and founder of the non-profit startup, makeadent.org for a discussion about the CHAI (Cardiovascular Health in Asian Indians) Collaborative, an initiative that aims to identify genetic markers of heightened atherosclerosis in South Asians. Episode graphic by Dr. Carine Hamo CardioNerds Cardiovascular Prevention PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll Subscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Show notes Coming soon! Cardionerds Cardiovascular Prevention Series The Cardionerds CV prevention series includes in-depth deep dives on so many prevention topics including the ABCs of prevention, approach to obesity, hypertension, diabetes mellitus and anti-diabetes agents, personalized risk and genetic risk assessments, hyperlipidemia, women’s cardiovascular prevention, coronary calcium scoring and so much more! We are truly honored to be producing the Cardionerds CVD Prevention Series in collaboration with the American Society for Preventive Cardiology! The ASPC is an incredible resource for learning, networking, and promoting the ideals of cardiovascular prevention! This series is kicked off by a message from Dr. Amit Khera, President of the American Society for Preventive Cardiology and President of the SouthWest Affiliate of the American Heart Association. Guest Profiles Amit Khera, MD, MSc, FACC, FAHA, FASPC Dr. Amit Khera is Professor of Medicine at the University of Texas, Southwestern Medical School in Dallas, Texas where he serves as Director of the Preventive Cardiology, and holder of the Dallas Heart Ball Chair in Hypertension and Heart Disease. He is also currently President of the American Society for Preventive Cardiology and President of the SouthWest Affiliate of the American Heart Association. His clinical and research interests include the primary and secondary prevention of coronary artery disease, focusing on risk assessment and risk factor modification in those with premature and familial disease. Dr. Khera received his undergraduate degree in American History from the University of Pennsylvania, with magna cum laude honors. He obtained his medical degree from Baylor College of Medicine where he served as class president and was inducted into the Alpha Omega Alpha honor medical society. He completed an Internal Medicine Residency at Brigham and Women’s Hospital, Harvard Medical School, followed by a Cardiology Fellowship at the University of Texas, Southwestern Medical Center. He also completed his Masters degree in Epidemiology at the Harvard School of Public Health. He has published over 150 publications in the field of preventive cardiology and has served on numerous local and national committee and leadership roles for the American Heart Association, American College of Cardiology, and American Society for Preventive Cardiology. He is currently Digital Strategies Editor and an Associate Editor for the journal Circulation. Dr. Khera has been named Best Doctor in Dallas and Texas SuperDoctor every year since 2014 and was previously the Program Director for the Cardiology Fellowship at UT Southwestern from 2011-2019. References and Links Coming soon! Amit Khera, M.D.Carine Hamo, MDAmit Goyal, MDDaniel Ambinder, MD

Jan 18, 2021

CardioNerds (Amit Goyal and Daniel Ambinder) are joined by Cleveland Clinic cardiology fellow Dr. Gregory Ogunnowo to discuss hypertension with Dr. Luke Laffin, cardiology faculty in the division of Preventive Cardiology and Rehabilitation and Medical Director of Cardiac Rehabilitation at the Cleveland Clinic. Part 2 of this discussion covers the evaluation for secondary causes of HTN, approach to resistant HTN, interventional anti-hypertensive procedures, and a note on cardiac rehabilitation. Part 1 covered the definition of hypertension, correct measurement of blood pressure, nonpharmacologic HTN management, initial choice of BP agents, and hypertensive disorders of pregnancy. Episode graphic by Dr. Carine Hamo CardioNerds Cardiovascular Prevention PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll Subscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Show notes Coming soon! Cardionerds Cardiovascular Prevention Series The Cardionerds CV prevention series includes in-depth deep dives on so many prevention topics including the ABCs of prevention, approach to obesity, hypertension, diabetes mellitus and anti-diabetes agents, personalized risk and genetic risk assessments, hyperlipidemia, women’s cardiovascular prevention, coronary calcium scoring and so much more! We are truly honored to be producing the Cardionerds CVD Prevention Series in collaboration with the American Society for Preventive Cardiology! The ASPC is an incredible resource for learning, networking, and promoting the ideals of cardiovascular prevention! This series is kicked off by a message from Dr. Amit Khera, President of the American Society for Preventive Cardiology and President of the SouthWest Affiliate of the American Heart Association. Guest Profiles Dr. Luke Laffin, serves as cardiology faculty in the division of Preventive Cardiology and Medical Director of Cardiac Rehabilitation at the Cleveland Clinic. Dr. Laffin attended medical school at Vanderbilt University School of Medicine. He trained in internal medicine and cardiology at the University of Chicago where he completed a dedicated fellowship in hypertensive diseases. He is a clinical specialist in hypertension designated by the American Society of Hypertension – which has now merged with the AHA. Dr. Gregory Ogunnowo is a cardiology fellow at the Cleveland Clinic. He completed medical school at the University of South Carolina School of Medicine in Columbia, South Carolina. He went on to complete internal medicine residency at Washington University School of Medicine in St. Louis where he stayed on as faculty in the Department of Hospital Medicine for a year prior to pursing fellowship. His interests include outcomes research in interventional cardiology and medical education In his spare time, Greg enjoys traveling, exercising, and experiencing new cultures through their food. When he’s not in the hospital, you can find Greg planning a trip with close friends and family. References and Links Coming soon! Luke Laffin MDGreg Ogunnowo, MDAmit Goyal, MDDaniel Ambinder, MD

Jan 11, 2021

CardioNerds (Amit Goyal and Daniel Ambinder) are joined by Cleveland Clinic cardiology fellow Dr. Gregory Ogunnowo to discuss hypertension with Dr. Luke Laffin, cardiology faculty in the division of Preventive Cardiology and Rehabilitation and Medical Director of Cardiac Rehabilitation at the Cleveland Clinic. Part 1 of this discussion covers the definition of hypertension, correct measurement of blood pressure, nonpharmacologic HTN management, initial choice of BP agents, and hypertensive disorders of pregnancy. Be sure to follow-up with Part 2 to learn about evaluation for secondary causes of HTN, approach to resistant HTN, interventional anti-hypertensive procedures, and a note on cardiac rehabilitation. Episode Graphic by Dr. Carine Hamo CardioNerds Cardiovascular Prevention PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll Subscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Show notes Coming soon! Cardionerds Cardiovascular Prevention Series The Cardionerds CV prevention series includes in-depth deep dives on so many prevention topics including the ABCs of prevention, approach to obesity, hypertension, diabetes mellitus and anti-diabetes agents, personalized risk and genetic risk assessments, hyperlipidemia, women’s cardiovascular prevention, coronary calcium scoring and so much more! We are truly honored to be producing the Cardionerds CVD Prevention Series in collaboration with the American Society for Preventive Cardiology! The ASPC is an incredible resource for learning, networking, and promoting the ideals of cardiovascular prevention! This series is kicked off by a message from Dr. Amit Khera, President of the American Society for Preventive Cardiology and President of the SouthWest Affiliate of the American Heart Association. Guest Profiles Dr. Luke Laffin, serves as cardiology faculty in the division of Preventive Cardiology and Medical Director of Cardiac Rehabilitation at the Cleveland Clinic. Dr. Laffin attended medical school at Vanderbilt University School of Medicine. He trained in internal medicine and cardiology at the University of Chicago where he completed a dedicated fellowship in hypertensive diseases. He is a clinical specialist in hypertension designated by the American Society of Hypertension – which has now merged with the AHA. Dr. Gregory Ogunnowo is a cardiology fellow at the Cleveland Clinic. He completed medical school at the University of South Carolina School of Medicine in Columbia, South Carolina. He went on to complete internal medicine residency at Washington University School of Medicine in St. Louis where he stayed on as faculty in the Department of Hospital Medicine for a year prior to pursing fellowship. His interests include outcomes research in interventional cardiology and medical education In his spare time, Greg enjoys traveling, exercising, and experiencing new cultures through their food. When he’s not in the hospital, you can find Greg planning a trip with close friends and family. References and Links Coming soon! Luke Laffin MDGreg Ogunnowo, MDAmit Goyal, MDDaniel Ambinder, MD

Jan 1, 2021

CardioNerds (Amit Goyal and Daniel Ambinder) introduce the CardioNerds Narratives in Cardiology Series which will feature the stories of amazing cardiovascular faculty and trainees representing diverse backgrounds, subspecialties, career stages, and career paths. To kick this series off, Dr. Pamela Douglas, who heads the Diversity and Inclusion task force for the American College of Cardiology, provides valuable insights in the field and shares her personal story. We are joined by the CardioNerds Narratives #FIT Advisors, Dr. Zarina Sharalaya, Dr. Norrisa Haynes and Dr. Pablo Sanchez for this very important discussion. Special messages by: Dr. Vanessa Blumer, Dr. Robert Harrington, Dr. Richard Chazal, Dr. Nosheen Reza, Dr. Neha Pagidipati, Dr. Mary Norine (Minnow) Walsh, Dr. Melissa Daubert, Dr. Gerald Bloomfield, Dr. Angela Lowenstern, Dr. Ralph Brindis, Dr. Michael Valentine, Dr. Anna Lisa Crowley, Dr. Malissa Wood and Dr. Geoffrey Ginsberg. Cardionerds Narratives in Cardiology PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll Subscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Show notes What is "Diversity" & "Inclusion"?Facets of diversity are all aspects of human differences. These include gender, race, ethnicity, age, physical ability, gender identity, national origin, language, religion, sexual orientation, socioeconomic status, and more.Inclusion is making everyone feel welcomed and included.Inclusion requires having a culture & environment where everyone can thrive regardless of background differences. This inclusive culture fosters respect & belonging in which we hear, appreciate, & value everyone and their perspectives.Inclusive organizations work with individuals to recognize and eliminate both explicit and implicit biases. They may do this with intentional efforts like professional & skills development as well as addressing awareness, education, and policy. Diversity measures representation by counting the presence of varying identities and characteristics. But Diversity itself is not the final goal.Diversity is the metric while Inclusion is the goal. For now, while representation is so disparate among certain groups, diversity is an important metric. It’s hard to be truly inclusive with such professional inequities. “Ultimately what we want is for people to belong. So not just be asked to the dance and sitting around and staring at everybody else but really feeling like you can go out on that dance floor and dance, like nobody's watching and it's fine because this is your community.” - Pamela Douglas Why is achieving diversity important?Diversity is a virtue in and of itself. But more than that, diverse groups make better decisions, are more innovative, are better at problem solving, and have an expanded talent pool.Cardiovascular medicine benefits from having a diverse workforce. Science performed by diverse groups has greater scientific novelty and produces higher impact papers in higher impact journals. Is there a link between professional diversity and healthcare inequities?YES!Physician diversity reduces healthcare disparities and improves healthcare quality.Physicians who train in diverse environments are more culturally competent when treating underrepresented groups.Underrepresented physicians are more likely to serve underrepresented populations.Underrepresented patients are more likely to follow the recommendations of physicians who look like them. This enhanced trust is critical to an effective patient-physician relationship. In the context of clinical trials and guidelines, underrepresented physician scientists help diversify our clinical trial participants, resulting in a more robust and representative evidence base. How are we doing in cardiology with respect to diversity?There have been improvements but we have a long way to go.Women comprise 43% of internal medicine resident physicians by only 22% of general cardiology fellows and even lower proportions within procedural fields.Underrepresented minorities--specifically Blacks, Hispanics, and Native Americans--make up about 32% of the US population but only 13% of general cardiology fellows.Benchmarks for other racial and ethnic groups and for other facets of diversity like socioeconomic status, sexual orientation, gender identity, IMG status, and others are even less clear.Inequities amplify in advanced career and leadership positions. Only 11%, 9%, 11%, and 24% of Asian, black, Hispanic, and white women, respectively, are full professors compared with 21%, 18%, 19%, and 36% of Asian, black, Hispanic, and white men, respectively (Albert 2018).In the top 40 ranked cardiology programs, there are no female cardiology chiefs (Albert 2018).There were no women editors-in-chief for US general cardiology journals between 1998 and 2018 and only 1 woman editor-in-chief for a general European cardiology journal (Balasubramanian et al., 2020).Such benchmarks are helpful for measuring representation, but remember the ultimate goal is Inclusion. We want to be more holistic in our approach to Inclusion.Let’s focus on competency and quality. Given the benefits of a diverse workforce discussed above, Diversity itself is a competency. If someone brings a different background & perspective, they are valuable to the group, just as someone else with specific leadership and interpersonal skills. How do we create a more diverse Cardiology?This requires a multi-pronged approach that spans deep pipeline projects through to career ascension.We must deliberately address implicit bias and both systemic racism & sexism.Among other efforts (detailed below), we have to create a welcoming environment, showcase a culture conducive to work-life integration, and ensure equity in compensation, opportunities, and promotion. According to a survey of internal medicine trainees, the top perceptions of cardiology careers were adverse job conditions, interference with family life, and lack of diversity. Women and those residents who had already chosen noncardiology careers more strongly valued work-life balance and had more negative perceptions of cardiology than men or future cardiologists. Compared with men, women trainees placed greater value on stable hours, family friendliness, female friendliness, and positive role models (Douglas et al., 2018).Understanding these perceptions was a key motivator for the CardioNerds Narratives in Cardiology series! The CardioNerds “Narratives in Cardiology” series will feature cardiovascular faculty representing diverse backgrounds, subspecialties, career stages, and career paths. The faculty will be interviewed by fellows-in-training (FITs) to discuss both their clinical expertise and their individual career narratives with the goals of showcasing diversity within the profession, inspiring interest in the field, and demonstrating the more positive culture of modern cardiology.See the ACC’s approach below (Figure 1 - Poppas et al., 2020) and the approach by Albert 2018 (Figure 2). Show notes updated as of 12.30.2020 Figure 1 Figure 2 Click to enlarge. (Figure 1 - Poppas et al., 2020, Figure 2 - Albert 2018. CardioNerds Narratives in Cardiology The CardioNerds Narratives in Cardiology series features cardiovascular faculty representing diverse backgrounds, subspecialties, career stages, and career paths. Discussing why these faculty chose careers in cardiology and their passion for their work are essential components to inspiring interest in the field. Each talk will feature a cardiology faculty from an underrepresented group, within at least one of several domains: gender, race, ethnicity, religion, national origin, international graduate status, disadvantaged backgrounds, etc. Featured faculty will also represent a variety of practice settings, academic ranks, subspecialties (e.g. clinical cardiology, interventional cardiology, electrophysiology, etc), and career paths (e.g. division chief, journal editor, society leadership, industry consultant, etc). Faculty will be interviewed by fellows-in-training for a two-part discussion that will focus on: 1) Faculty's content area of expertise2) Faculty's personal and professional narrative As part of their narrative, faculty will discuss their unique path to cardiology and their current professional role with particular attention to challenges, successes, and advice for junior trainees. Specific topics will be guided by values relevant to trainees, including issues related to mentorship, work-life integration, and family planning. To help guide this important initiative, the CardioNerds Narratives Council was founded to provide mentorship and guidance in producing the Narratives series with regards to guests and content. The CardioNerds Narratives Council members include: Dr. Pamela Douglas, Dr. Nosheen Reza, Dr. Martha Gulati, Dr. Quinn Capers, IV, Dr. Ann Marie Navar, Dr. Ki Park, Dr. Bob Harrington, Dr. Sharonne Hayes, and Dr. Michelle Albert. The Narratives Council includes three FIT advisors who will lead the CardioNerds’ diversity and inclusion efforts, including the current project: Dr. Zarina Sharalaya, Dr. Norrisa Haynes, and Dr. Pablo Sanchez. Guest Profiles Dr. Pamela Douglas Pamela S Douglas MD is the Ursula Geller Professor of Research in Cardiovascular Diseases in the Department of Medicine at Duke University. She has led several landmark and pivotal multicenter randomized clinical trials and outcomes research studies funded by government, professional societies, and industry. She is renowned for her scientific and policy work in improving the quality and appropriateness of imaging in clinical care, clinical trials, and registries and through development and dissemination of national standards for imaging quality, utilization, informatics, and analysis.

Dec 28, 2020

CardioNerds (Amit Goyal & Karan Desai) join University of Illinois at Chicago cardiology fellows (Brody Slostad, Kavin Arasar, and Mary Rodriguez-Ziccardi) for a cup of tea from atop Hancock Tower! They discuss an illuminating case of altered mental status & electrical instability due to digitalis poisoning. Program director Dr. Alex Auseon and APD Dr. Mayank Kansal provide the E-CPR and a message for applicants. Episode notes were developed by Johns Hopkins internal medicine resident Tommy Das with mentorship from University of Maryland cardiology fellow Karan Desai. Jump to: Patient summary - Case media - Case teaching - References Episode graphic by Dr. Carine Hamo CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor RollSubscribe to our newsletter- The HeartbeatSupport our educational mission by becoming a Patron!Check out CardioNerds SWAG! Cardiology Programs Twitter Group created by Dr. Nosheen Reza Patient Summary A woman in her late 80s with history of systemic arterial hypertension and dementia presented with 2 weeks of nausea, vomiting, confusion, and yellow-tinted vision. When she presented to the hospital, initial history was limited as her caregiver was unaware of her medications and medical history. An initial ECG showed isorhythmic A-V dissociation and scooping ST segments laterally. Given her clinical history, this raised the suspicion for Digoxin toxicity, and a serum digoxin level was significantly elevated. However, this was not a home medication for the patient, nor did she have access to it! Listen to the episode now as the UIC Cardionerds masterfully take us through this case that would surely stump Dr. House! Case Media through the Differential ABCDEFClick to Enlarge A. Initial ECGB. CXR- Patchy opacities of the left lower lobe consistent with pulmonary edema and/or aspiration​ pneumonia.C. Repeat ECG: AF with AV block, persistent scooped T waves​D. Post arrest ECG: Flutter/fib with AV block, VERY LONG PAUSES up to 6 secondsE. ECG post TVP: A flutter, slow V response (pacing picking up), intrinsic ventricular rate 20-40, PM set to 50 bpmF. Most recent ECG: Normal sinus rhythm TTE Episode Schematics & Teaching The CardioNerds 5! – 5 major takeaways from the #CNCR case 1) This episode featured a challenging case of digitalis toxicity. Cardionerds, what is the mechanism of action of cardiac glycosides? Cardiac Glycosides (such as digoxin, digitalis, and oubain), inhibit the myocardial Na/K ATPase pump. This leads to an increased concentration of intracellular sodium, which then drives the influx of calcium into cardiac myocytes via the Na/Ca exchanger. This increase in intracellular calcium leads to further calcium release from the sarcoplasmic reticulum making even more calcium available to bind to troponin, increasing contractility. In addition to their effect on inotropy, cardiac glycosides increase vagal tone, reducing SA node activity and slowing conduction through the AV node by increasing the refractory period 2) The first published account of digitalis to treat heart failure dates back to the 18th century, when botanist and physician William Withering published "An account of the Foxglove and some of its medical uses with practical remarks on dropsy, and other diseases". A lot has changed over the years; what are some of the uses of digoxin in the modern day? The DIG trial (1997) demonstrated a reduction in hospitalizations in patients with HFrEF treated with digoxin. However, no impact on mortality was shown. A major limitation from randomized trials of digoxin is the lack of contemporary background HF treatment (e.g., ARNI, SGLT2i, MRA, Device Therapy). Thus, its role in modern HFrEF management is typically limited to reducing hospitalizations in patients with persistent NYHA Class III or IV symptoms despite maximally tolerated guideline-directed medical therapy Digoxin can also be used for acute or chronic rate control in atrial fibrillation, and may be particularly useful in patients with RVR refractory to beta blockers/calcium channel blockers or in those patients who cannot tolerate these agents due to hypotension. Notably, data from the ARISTOTLE trial (2018) showed a significant mortality increase was seen in patients with a digoxin level ≥1.2 ng/ml, while no increase in mortality was seen with levels <0.9 ng/ml. Recent data from the small, randomized RATE-AF trial showed no difference in quality of life and similar heart rate control in older patients with permanent atrial fibrillation and heart failure symptoms. Thus, while the therapeutic window may be limited, there remains a role for digoxin in the treatment of HFrEF, Afib, or both. 3) While digoxin can be given in HFrEF and/or AF, its use is limited by its side-effects and potential toxicity. What are the clinical manifestations of digitalis toxicity? Arrhythmia: Digitalis toxicity can cause virtually any atrial or ventricular arrhythmia. More to come in take-away #4! GI: Acute toxicity is associated with nausea, vomiting, abdominal pain. Meanwhile, chronic toxicity can be more subtle with less pronounced nausea, anorexia and weight loss developing over weeks to months. Neuro: Alterations in color vision (chromatopsia), particularly seeing a yellow hue, can be specific for digitalis poisoning. Headache, fatigue, lethargy and altered mental status can also occur. 4) Lets dig a little deeper into digoxin induced arrhythmias; why is digoxin so arrhythmogenic, and what are the most common electrical manifestations? By inhibiting the Na/K ATPase pump, digoxin increases intracellular sodium and calcium levels, as well as extracellular potassium. These electrolytes shifts, in addition to the increased parasympathetic activity, lead to Digoxin's arrhythmogenicity. Generally, younger patients develop bradyarrythmias due to increased vagal tone, while older patients who may have pre-existing cardiac disease are more likely to develop tachyarrythmias. Influx of calcium into the cardiac myocyte leads to delayed afterdepolarizations in phase 4 of the ventricular action potential, which can trigger ventricular tachycardia. Digoxin also increases atrial pacemaker cell automaticity, leading to an increase in atrial arrythmias. This occurs via an increase in the slope of phase 4 of the pacemaker action potential (decreasing the time to depolarization), lowering the depolarization threshold, and increasing the resting potential. While ectopic atrial tachycardia with AV block and bidirectional VT are associated with digoxin toxicity, virtually any arrhythmia can be seen in digitalis toxicity. However, atrial fibrillation and flutter are less likely to be induced by digoxin toxicity. 5) Now that we've established all the effects and side-effects of digoxin, lets wrap up with some points on treating cardiac glycoside toxicity! The mainstay of therapy for acute and/or severe digoxin toxicity is digoxin-specific antibody (Fab) fragments. Empiric treatment for adults with imminent cardiac arrest or ingestion of an unknown amount of digoxin consists of 10 vials, with each vial binding approximately 0.5mg of digoxin. Indications for Fab fragments aside from acute overdose include: Hemodynamically unstable arrythmias Hyperkalemia Evidence of end-organ damage from hypoperfusion Notably, the serum digoxin concentration alone does not dictate Fab fragment treatment. Additionally, in patients with severe renal impairment, Fab fragments may be ineffective and may provide a false sense of benefit. The manifestations of digoxin toxicity may improve initially in these patients given Fab; however, recurrent toxicity can occur weeks later as digoxin moves from peripheral tissues. While other cardiac glycosides have cross-reactivity with digoxin and can be treated with Fab fragments, dosing can be challenging due to lack of correlation between serum digoxin level and cardiac glycoside activity. Potassium homeostasis in digoxin toxicity is nuanced. Hyperkalemia, as a result of Na-K ATPase inhibition, is a predictor of mortality in acute toxicity. After Fab fragments are given, hyperkalemia is often rapidly corrected, and over-aggressive treatment of hyperkalemia in the setting of acute toxicity may ultimately lead to hypokalemia once Fab fragments are given. References Digitalis Investigation Group (1997). The effect of digoxin on mortality and morbidity in patients with heart failure. The New England journal of medicine, 336(8), 525–533. Lopes, R. D., Rordorf, R., De Ferrari, G. M., et al. (2018). Digoxin and Mortality in Patients With Atrial Fibrillation. Journal of the American College of Cardiology, 71(10), 1063–1074. Chen, J. Y., Liu, P. Y., Chen, J. H., & Lin, L. J. (2004). Safety of transvenous temporary cardiac pacing in patients with accidental digoxin overdose and symptomatic bradycardia. Cardiology, 102(3), 152–155. Taboulet, P., Baud, F. J., Bismuth, C., & Vicaut, E. (1993). Acute digitalis intoxication--is pacing still appropriate?. Journal of toxicology. Clinical toxicology, 31(2), 261–273. The CardioNerds Cardiology Case Reports series shines light on the hidden curriculum of medical storytelling. We learn together while discussing fascinating cases in this fun, engaging, and educational format. Each episode ends with an “Expert CardioNerd Perspectives & Review” (E-CPR) for a nuanced teaching from a content expert. We truly believe that hearing about a patient is the singular theme that unifies everyone at every level, from the student to the professor emeritus. We are teaming up with the ACC FIT Section to use the #CNCR episodes to showcase CV education across the country in the era of virtual recruitment. As part of the recruitment series,

Dec 21, 2020

CardioNerds (Carine Hamo, Amit Goyal, and Daniel Ambinder) discuss the obesity epidemic and how it relates to the cardiovascular system with Dr. Chiadi Ndumele, cardiologist and epidemiologist at The Johns Hopkins Hospital and chairs the obesity subcommittee of the American Heart Association (AHA). They cover obesity definitions, epidemiology, strengths and limitations of different biometrics, including BMI, impact on myocardial structure and function, and current pharmacologic & surgical options for weight loss. They also discuss the practical approach to addressing obesity with patients. This episode was produced by Dr. Carine Hamo. Show notes & references by Dr. Daniel Ambinder. Episode graphic by Dr. Carine Hamo Cardionerds Cardiovascular Prevention PageCardioNerds Episode PageSubscribe to our newsletter- The HeartbeatSupport our educational mission by becoming a Patron! Show notes 1. What is obesity and how do we define it at the personal and population level? Obesity is when there is an excess and often dysfunctional adipose tissue that contributes to morbidity and to premature mortality The metric used to define obesity is Body Mass Index (BMI), defined as a person's weight in kilograms divided by the square of the person's height in meters (kg/m2) See WHO BMI classification below 2. What is the current epidemiology of obesity and are there certain populations that are affected more than others? Rates of obesity are climbing. Currently, around 70% of the population meets criteria for being either overweight or obese and ~40% are at the level of obesity. Minorities such as African Americans, Native Americans, and Latinos have higher rates of obesity. Higher rates of obesity are also seen in groups with lower socioeconomic status. Certain populations, such as Southeast Asians, tend to develop severe metabolic consequences of obesity such as insulin resistance and cardiovascular consequences with less excess weight than other populations. Adult weight is very important but weight history (long standing obesity) plays a role as well when it comes to cardiovascular risk associated with obesity. 3. Currently the WHO classifies obesity based on BMI. What are the limitations to using BMI as a measure of obesity? Are their benefits to measuring waist circumference instead? BMI is a far from a perfect measure but it correlates nicely at the population level with cardiovascular events and premature mortality BMI is more accessible than a direct quantitative or functional measure of adipose tissue A major limitation of BMI is that it does not reflect body composition. Body composition is very important in understanding risk associated with obesity. For example, football players may fall into the category of grade 1 obesity if just using BMI to classify their weight status. Waist circumference (WC) is a good way of getting a sense of body composition. Abdominal obesity is most closely linked to insulin resistance and various metabolic consequences such as diabetes, hypertension, and inflammation. This is why WC is incorporated into the metabolic syndrome construct. Adding WC measurements to the BMI measurements, particularly for individuals in the overweight and grade 1 obesity group (BMI 25-29.9, and 30-34.9) provides significant prognostic information about the development of cardiovascular disease. 4. How do obesity and metabolic syndrome impact myocardial structure and function? How does obesity and increased adiposity fit into the larger scheme of metabolic risk and metabolic syndrome? Obesity is independently associated with myocardial remodeling and with increased heart failure risk. This contrasts with coronary heart disease (CAD) and stroke. For CAD and stroke, most associations with obesity are largely mediated by diabetes, hypertension and dyslipidemia. However, in heart failure, there is a strong unexplained association that remains after you consider those associated conditions. The independent association of obesity with heart failure pertains almost exclusively to heart failure with preserved ejection fraction (HFpEF) and not heart failure with reduced ejection fraction (HFrEF). The mechanism for this independent association is not well understood and is an area of active research. In mice that are predisposed to obesity have several inflammatory processes that occur locally in the myocardium and systemically that likely contribute to cardiac risk. At the local level, lipotoxicity occurs within the myocardium as it does in nonalcoholic fatty liver disease. At the systemic level, adipose tissue releases adipokines and cytokines that are linked to myocardial damage, injury, and fibrosis. There is a spectrum of metabolic risk among individuals with excess weight. And when obesity is associated with metabolic syndrome in individuals, the risk for cardiovascular disease markedly rises. 4. What are some core tenants of addressing obesity when working with patients when it comes to exercise and diet? A core tenant of discussing obesity with patients is to discuss it! Obesity is generally under-addressed and under-discussed. Motivation by being positive about risk reduction with a healthier lifestyle can be very effective. Help patients “take time to invest in themselves”. Having them put items on the calendar that include exercise activities, such as taking a walk or going to the gym, can be a useful strategy for patients who are particularly busy with work or school. Stress reduction is an important component to diet and exercise. Smaller activities, a brisk walk or taking the stairs at work can help reduce the activation energy required for exercise and can make exercise feel more attainable to patients. Meal planning and meal timing are both very important aspects to counseling for patients when it comes to healthy eating. 5. What are some tips and tricks on broaching the subject of obesity with patients given the sensitivity of the subject. It is important to check biases in this space. Obesity should not be considered an individual failing when there is a systemic and societal based issue. We need to think of obesity as a multi-factorial disease that has a behavioral component but also has a more complex societal and biological contribution as well. Approaching the patient with a plan for partnership of management of obesity as a disease, like other diseases such as hypertension and diabetes can be very helpful. Patients want to lose weight, it just becomes very challenging for a variety matters. The weight of the clinician can have an impact as to the discussion of weight in the clinic. For example, clinicians with a higher weight than the patient tend to avoid discussing obesity during clinic visits. Clinicians who have healthy weight statuses can used stigmatizing language when counseling patients. Appreciate that weight management can be challenging and there'll be stops and starts but there can be great outcomes with long-term partnerships with patients. 6. What are the current pharmacologic options for weight loss and when should these agents be considered? Pharmacological agents should be considered once physical activity and social stressors are addressed. Pharmacological therapy can be a nice adjunct to lifestyle modification, particularly when BMI remains above 30 or when BMI remains >27 with comorbidities. There are a variety of agents such as Orlistat, Liraglutide, Phentermine, Topiramate, and Bupropion. These medications are generally underutilized due to cost and side effects. Some agents have cannot be used long term which may limit their use. The only agent that has been related to cardiovascular risk reduction is Liraglutide. 7. What do we know about the role of bariatric surgery in cardiovascular disease prevention and does weight loss through bariatric surgery provide differential benefit over other forms of weight loss? Bariatric surgery is probably the most powerful weapon in our obesity arsenal. There are two major subtypes of bariatric surgery. There is a restrictive subtype, such as a sleeve gastrectomy, and a malabsoptive subtype, such as a gastric bypass surgery. The Roux-en-Y gastric bypass has both the malabsorptive and restrictive components. There is prospective data that shows that bariatric surgery is associated with more weight loss than lifestyle modifications. Bariatric surgery is also shown to be associated with a reduction in comorbidities like hypertension, diabetes and dyslipidemia. Bariatric surgery is also associated with a reduction in pathophysiological processes like inflammation and endothelial dysfunction. Prospective studies with matched data, such as the Swedish Obesity study cohort, bariatric surgery has been associated with a reduced risk in cardiovascular disease events and a markedly improved survival. There have been significant risk reductions in heart failure as well. Most cardiovascular disease reductions seen with bariatric surgery occur through the profound weight loss that occurs after surgery. Risk calculators such as https://riskcalc.org/BariatricSurgeryComplications/ can help guide clinicians and patients when considering bariatric surgery. BMIWHO ClassificationBelow 18.5Underweight18.5-24.9 Normal weight25.0-29.9Pre-obesity 30.0-34.9Obesity class I35.0-39.9Obesity class 2> 40.0Obesity class 3 Cardionerds Cardiovascular Prevention Series The Cardionerds CV prevention series includes in-depth deep dives on so many prevention topics including the ABCs of prevention, approach to obesity, hypertension, diabetes mellitus and anti-diabetes agents, personalized risk and genetic risk assessments, hyperlipidemia, women’s cardiovascular prevention, coronary calcium scoring and so much more! We are truly honored to be producing the Cardionerds CVD Prevention Series in collaboration with the American Society for Preventive Cardiology!

Dec 15, 2020

CardioNerds (Amit Goyal and Daniel Ambinder) discuss diabetes mellitus with Dr. Dennis Bruemmer. This is a must-listen for anyone engaged in the case of the cardiovascular patient. Given the alarming obesity epidemic, we anticipate a rising worldwide tide of diabetes mellitus and ensuing cardiovascular disease. Here we discuss the epidemiology and approach to diabetes management, with emphasis on what CardioNerds need to know. Dr. Bruemmer is board-certified in both cardiology and endocrinology, and is the director of the Center for Cardiometabolic Health in the section of Preventive Cardiology and Rehabilitation at the Cleveland Clinic. Episode graphic by Dr. Carine Hamo Cardionerds Cardiovascular Prevention PageCardioNerds Episode PageSubscribe to our newsletter- The HeartbeatSupport our educational mission by becoming a Patron! Show notes Why should CardioNerds pay attention to diabetes mellitus (DM)? As a cardiovascular risk equivalent, DM is a key CVD risk factor, associated with a 2-4 fold increased risk. 70% of ACS patients have DM. Cardiologists will see more patient with DM given the rising prevalence of obesity, subsequent diabetes and ensuing CVD. Only 6% of patients with DM and cardiovascular disease (CVD) get appropriate care for DM and CVD. Historically, hypoglycemic agents improved microvascular outcomes (retinopathy, nephropathy, neuropathy), but not macrovascular outcomes (MI, CVA, PAD). However, this has changed with the advent of mandatory cardiovascular safety trials with positive data for GLP1 agonists and SGLT2 inhibitors! There aren't enough endocrinologists! They only see ~5% of DM patients. In 2012 the US generated 280 endocrinologists versus 100 million patient with DM or pre-DM. Primary care physicians are key allies in the care of these patients. So as CardioNerds, let's get over this therapeutic inertia and take ownership of our patients' DM as we already do for their HTN and HLD; in collaboration with a multidisciplinary team including the PCP, dietician, pharmacist, DM educators, +/- behavioral therapist, +/- endocrinologist, +/- metabolic surgeon. What is your global approach to the patient with DM? Optimize the non-DM CVD risk factors with lifestyle intervention and medical management: CVD risk factors are very common in patients with DM (sedentary lifestyle, unhealthy weight, HTN, HLD). The Steno-2 Study (Gaede et al., NEJM 2008) showed that in patients with T2DM & microalbuminuria, intensive intervention with multiple drug combinations and behavioral modification was better with regards to: vascular complications, death from any cause, and death from CV causes. Emphasize a healthy lifestyle - use a patient-centered approach with motivational interviewing and shared decision making, provide education, set realistic goals, identify barriers (socioeconomic, etc), engage family and a multidisciplinary team (nutritionist, exercise physiologist), utilize behavioral interventions. Pharmacologic intervention - medical weight loss for BMI > 27 and DM (enjoy upcoming Ndumele episode), anti-HTN (enjoy upcoming Laffin episode), and anti-HLD (enjoy the Navar-Shah episode). NOTE that statins have been shown to have a small effect on increasing incident or worsening DM, but the effect size is small and overcome by the benefit in whom statins are indicated. Treat the Hyperglycemia itself! Let's discuss this deeper… What is your approach to non-insulin DM management? First-line agents: US guidelines: in addition to lifestyle intervention, start with metformin as the first line agent. European guidelines: now give preference to GLP1 agonists and SGLT2 inhibitors in patients with or at risk for cardiovascular disease. Sulfonylureas: increase pancreatic insulin secretion. Dr. Bruemmer feels they obsolete for the preventive cardiologist from the standpoints of safety, efficacy, and cardiovascular disease. There is no efficacy data past 4 years and no cardiovascular benefit. In contrast data suggests increase all-cause mortality and possibly MACE events. Low cost may make these more affordable for some patients. Thiazolidinediones (aka: "glitazones"): increase insulin sensitivity, the primary defect in T2DM. Rosiglitazone is discouraged due to adverse cardiovascular outcomes. Pioglitazone has better data, especially in those who've had a stroke or TIA (IRIS Trial, NEJM 2016). They may have a role in those for whom other classes are contraindicated or cost-prohibitive. DPP4 Inhibitors: increase incretin levels (GLP-1 and GIP) which inhibit glucagon release, increase insulin secretion, and delay gastric emptying. They do not cause hypoglycemia or weight gain. These have a very modest glycemic effect and have no CV benefit. There was a signal for increased heart failure hospitalizations with saxagliptin and alogliptin, but not with sitagliptin. These should have very little, if any, role in your management. See Figures for the "Overall Approach" from the 2019 EASD-ADA update. Which anti-glycemic drugs have a proven cardiovascular outcomes benefit? GLP1 Agonists: bind to GLP1 receptor and promote glucose dependent insulin release, inhibit glucagon secretion, and delay gastric emptying. Note that patients should be counseled that these are injectables (oral semaglutide has not yet proven CV benefit). Liraglutide (LEADER trial) and injectable semaglutide (SUSTAIN-6) showed significant MACE reduction, but CV benefit does not appear to be a class effect. They likely have an anti-atherothrombotic effect as well as benefits on blood pressure, weight, and glycemic control without hypoglycemia. There is no apparent impact on heart failure hospitalizations. Warn of primarily GI side effects and infrequent risk of acute pancreatitis. Start low and slowly up-titrate as tolerated as GI symptoms typically abate with time. There is a black box warning for medullary thyroid cancer so AVOID if there is a family or personal history of this. SGLT2 Inhibitors: bind to and block the SGLT2 co-transporter in the renal proximal renal tubules, thereby inhibiting glucose reabsorption and increasing glucose loss via urine (glycosuria) along with osmotic diuresis as well as weight and blood pressure reduction. They have both cardiovascular and renal outcomes benefits. Importantly they reduce HF and cardiovascular death in those with HFrEF independent of hypoglycemic action and are now a key component for HFrEF optimal medical therapy (enjoy Ep #36 with Dr. Robert Mentz). Risks include: dehydration due to osmotic diuresis (consider reducing concurrent diuretic doses), genitourinary fungal infections (not UTIs including pyelonephritis; caution in those with urinary incontinence and poor perineal hygiene), euglycemic DKA (caution in T1DM and those with ketosis-prone T2DM), and a questionable risk of amputations and fractures associated with canagliflozin but not others in the class. NOTE: many patients with CVD remain on outdated hypoglycemic agents rather than on these newer agents with proven CV benefit. Much of this is related to cost and access. Whenever you see a patient with DM, review their med list and help them bring it up to speed with the latest data! What is the role of metabolic surgery in patients with DM?The prevalence of obesity is rising at an alarming rate and portrays an equally grim epidemiology for rising rates of diabetes and cardiovascular disease. By 2025, 1/5 of the world may be obese. Already, >1/3 of US adults are obese with stark differences based on race and socioeconomic status. The worldwide prevalence of diabetes is similarly expected to rise: >50% in the next decade! Rates of CV disease and mortality will follow suit. Preventing obesity via education, lifestyle, and policy is of the utmost importance. Managing obesity requires a multipronged approach with shared decision making including: promoting a healthy lifestyle with diet and exercise, +/- pharmacologic weight loss, +/- metabolic (bariatric) surgery. Behavioral intervention promoting a healthy lifestyle is the cornerstone for all overweight and obese patients as part of primary, secondary, and tertiary prevention. However the results are typically modest and inconsistently sustained over longer periods. Pharmacologic intervention for weight loss may provide added benefit over lifestyle alone and is indicated for individuals with BMI ≥30 kg/m2 or BMI ≥27 kg/m2 with at least 1 obesity-associated comorbidity who are motivated, but have failed to lose weight or maintain weight loss by using high-intensity lifestyle intervention alone. Obesity-associated comorbidities include: T2DM, HTN, HLD, ASCVD (CAD, CVA, PAD), CHF, Afib, VTE, OSA, and CKD. There are 5 antiobesity drugs approved by the US FDA: orlistat, lorcaserin, naltrexone-bupropion, phentermine-topiramate, and liraglutide. Of these, only liraglutide has proven CV benefit. Metabolic (bariatric) surgery is most effective for clinically significant and sustained weight loss and for diabetes remission in obese individuals. Surgical options include: Roux-en-Y gastric bypass (RYGB), sleeve gastrectomy (SG), adjustable gastric banding (AGB), and biliopancreatic diversion with duodenal switch (BPDDS). Metabolic surgery is recommended for patients with a BMI ≥40 kg/m2 without concomitant medical problems and in patients with a BMI ≥35 kg/m2 who have at least 1 severe obesity-associated comorbidity (e.g. T2DM). Interestingly, some of the cardiometabolic benefits of metabolic surgery are independent of weight loss and include mechanisms related to incretin levels, insulin secretion/sensitivity, inflammatory mediator profile, bile acid circulation, and gut microbiota. The peri-operative risk is low and has declined with improved technique. Nutritional deficiencies are the most common long-term complications and can be prevented with follow-up and supplementation. Show notes updated as of 12.13.2020

Dec 7, 2020

The CardioNerds (Carine Hamo and Daniel Ambinder) discuss aspirin as primary prevention, Vitamin D, Calcium, and omega 3 fatty acids supplementation with Dr. Erin Michos, director of women's cardiovascular health and the associate director of preventive cardiology with Johns Hopkins Ciccarone Center for the Prevention of Cardiovascular Disease. We are also joined by Dr. Michos' mentees, Dr. Rick Ferraro, Dr. Andi Shahu, and student doctor Sunyoung (Sarah) Jang for a discussion about mentorship and career development. This episode was produced by Dr. Rick Ferraro and Dr. Carine Hamo. Show notes & references by Dr. Amit Goyal. Episode graphic by Dr. Carine Hamo Cardionerds Cardiovascular Prevention PageCardioNerds Episode PageSubscribe to our newsletter- The HeartbeatSupport our educational mission by becoming a Patron! Show notes - Aspirin, Vitamin D, Calcium & Omega 3 Fatty Acids Supplementation What is the role of aspirin for primary ASCVD prevention? The Conundrum: ASCVD event rates are much lower in the primary prevention than in the secondary prevention population, BUT the bleeding rates are comparable. So in the primary prevention patients, the bleeding risk is just as high, but the propensity for benefit is lower. The Question: Does low dose aspirin have a place in the primary prevention of ASCVD events. The Data: ARRIVE Trial: in moderate risk nondiabetic patients without prior ASCVD events, there was no different in the composite ASCVD end point, but there was an increased risk of bleeding (mostly mild GI bleeding). Thus, in the moderate risk patients --> primary prevention aspirin has an unfavorable risk-benefit profile. The benefit in a higher risk (>10-20% estimated 10-yr risk) remains unclear. ASCEND Trial: In men and women age ≥ 40yrs with diabetes without prior ASCVD events, there was a modest benefit (NNT = 59 patients for 10 years to prevent 1 major ASCVD event) counterbalanced by a similar magnitude of harm (NNH = 77 patients for 10 years to cause 1 major bleeding event). Thus, in adults with diabetes --> primary prevention aspirin had a neutral risk-benefit profile. ASPREE Trial: in elderly patients (≥ 70 years; ≥ 65 years for Hispanic or Black patients) without prior ASCVD events, there was no difference in ASCVD events but there was a significant increase in bleeding events (NNH = 42 patients for 10 years to cause 1 major bleeding event). The trial was stopped early due to futility. Interestingly, there was higher all-cause mortality driven primarily by cancer. Importantly, patients had to have a life expectancy longer than 5 years and those with dementia, substantial physical disability, or high estimated bleeding risk were excluded. Thus, in elderly patients --> primary prevention aspirin led to overall harm. The Recommendations: There was insufficient evidence to recommend a specific risk threshold for starting primary prevention aspirin. This may be due to more widespread contemporary prevention strategies like lifestyle management, tobacco cessation, statin use, better blood pressure control, etc. Individualize the decision based on the totality of evidence for an individual's risk of ASCVD events versus bleeding events. Notably, those with higher ASCVD risk generally also have a higher bleeding risk. Class IIB: Low-dose aspirin (75-100 mg orally daily) might be considered for the primary prevention of ASCVD among select adults 40 to 70 years of age who are at higher ASCVD risk but not at increased bleeding risk. There may be a role for primary prevention aspirin in select adults with a high estimated ASCVD risk and low bleeding risk. CAC score ≥ 100 may help identify those might benefit from primary prevention aspirin. As always, shared decision making remains crucial. Class III: Low-dose aspirin (75-100 mg orally daily) should not be administered on a routine basis for the primary prevention of ASCVD among adults >70 years of age. Class III: Low-dose aspirin (75-100 mg orally daily) should not be administered for the primary prevention of ASCVD among adults of any age who are at increased risk of bleeding. What is the role of Vitamin D supplementation in preventing cardiovascular disease? The Conundrum: Low levels of Vit D is associated with increased risk of CV outcomes including myocardial infarction, stroke, heart failure, atrial fibrillation, and more. But while low Vit D seems to be a marker for bad outcomes, correlation ≠ causation. Notably, this correlation was not confirmed by Mendelian randomization studies, further refuting possible causation. Confounding factors include links between low Vit D levels and obesity and sedentary lifestyle, themselves risk factors for adverse CV outcomes. The Question: Given the association between low Vit D levels & CV disease --> can you prevent CV disease by identifying and treating low Vit D with supplementation. The Data: Randomized Clinical Trials --> treatment with vitamin D does not prevent CV disease. Women's Health Initiative: Calcium & Vit D supplementation had no effect on incident coronary or cerebrovascular events. But perhaps this was due to a low Vit D dose of only 400 IU daily. Would a higher dose have benefit? ViDA Study: monthly high-dose Vit D supplementation (100,000 IU of D3) did not prevent CV disease, including within the 25% of patients who had level 70: 800 IU daily Level 20 ng/mL is adequate for bone and overall health. But the optimal level remains contested. The Endocrine Society recommends aiming for level ≥ 30 ng/mL. What is the role of Calcium supplementation in preventing cardiovascular disease? The Conundrum: Calcium supplementation is common and important for bone health. However there is some concern that excess calcium may worsen adverse CV outcomes. The Question: Does calcium intake cause CV harm? The Data: The Auckland Calcium Study: raised concern that calcium supplementation may increase cardiovascular risk (secondary analysis of a study designed to assess impact on bone health). EPIC-Heidelberg, MESA, & other observational studies: calcium supplementation is associated with adverse cardiovascular events. In contrast, calcium intake from food sources does not seem to be associated with adverse CV events. Meta-analysis by Khan et al. 2019: calcium + Vit D was associated with an increased risk for stroke. These findings may be from the bolus effect of calcium supplementation whereby a sudden rise in serum calcium levels may result in vascular calcium deposition and interact with the coagulation cascade. The Recommendations: Use calcium supplementation cautiously, according to the recommended daily intake, and using food sources. Personalized approach using shared decision making considering CV risk and bone health. Avoid excess calcium supplementation. Recommended daily intake: Adults aged 19-50 years old & Men aged 51-70 years: 1000 mg/day Adults aged >70 years and Women aged 51-70: 1200 mg/day What is the role of Omega-3 Polyunsaturated Fatty Acids in preventing cardiovascular disease? The Conundrum: High triglyceride levels are associated with adverse CV events, but triglyceride-reducing agents like niacin and fibrates, have not been effective in reducing the risk of these events. The Question: Does intake of Omega-3 Fatty Acids improve CV health and if so, what is the appropriate formulation? The Data: ASCEND Omega-3 Trial & VITAL Trial: lower doses of EPA/DHA combination omega-3 fatty acids ~840mg daily are not beneficial in reducing CV events. REDUCE-IT Trial: 4g of icosapent ethyl (IPE - a pure EPA formulation) daily reduced MACE events in those with elevated triglyceride levels despite statin use. The Japanese JELIS trial also showed a CV benefit using a lower dose of pure EPA (1.8mg daily) among statin-treated adults with hyperlipidemia. STRENGTH Trial: 4g EPA/DHA Omega 3-fatty acid formulation failed to show CV benefit among statin-treated patients with dysplipidemia. The difference from REDUCE-IT trial may be due to the drug formulations (pure EPA vs EPA/DHA combination). Notably, in REDUCE-IT, the benefit had a dose-response relationship with blood levels of EPA; the higher the EPA, the greater the benefit. Dietary fish oil supplements may include a substantial portion of harmful saturated fats vs the beneficial polyunsaturated fats. Dietary supplements have been shows to contain far less Omega-3 fatty acids than indicated on the label! Furthermore, dietary supplements may get oxidized and contain harmful contaminants. The Recommendations: Use IPE 4g daily for patients ≥ 45 years old with established ASCVD or ≥ 50 years old with diabetes & other risk factor(s) who are on maximally tolerated statin and continue to have elevated Triglyceride level 135-499 mg/dL. The marked CV benefit from icosapent ethyl seen in the REDUCE-IT trial should not be extrapolated to other fish oil preparations! The Cardionerds CV prevention series includes in-depth deep dives on so many prevention topics including the ABCs of prevention, approach to obesity, hypertension, diabetes mellitus and anti-diabetes agents, personalized risk and genetic risk assessments, hyperlipidemia, women’s cardiovascular prevention,

Nov 18, 2020

CardioNerds (Amit Goyal) joins Thomas Jefferson cardiology fellows (Jay Kloo, Preya Simlote and Sean Dikdan - host of the Med Lit Review podcast) for some amazing craft beer from Independence Beer Garden in Philadelphia! They discuss a fascinating case of atrioesophageal fistula (AEF) formation after pulmonary vein isolation (PVI). Dr. Daniel Frisch provides the E-CPR and program director Dr. Gregary Marhefka provides a message for applicants. Johns Hopkins internal medicine resident Colin Blumenthal with mentorship from University of Maryland cardiology fellow Karan Desai. Jump to: Patient summary - Case media - Case teaching - References Episode graphic by Dr. Carine Hamo The CardioNerds Cardiology Case Reports series shines light on the hidden curriculum of medical storytelling. We learn together while discussing fascinating cases in this fun, engaging, and educational format. Each episode ends with an “Expert CardioNerd Perspectives & Review” (E-CPR) for a nuanced teaching from a content expert. We truly believe that hearing about a patient is the singular theme that unifies everyone at every level, from the student to the professor emeritus. We are teaming up with the ACC FIT Section to use the #CNCR episodes to showcase CV education across the country in the era of virtual recruitment. As part of the recruitment series, each episode features fellows from a given program discussing and teaching about an interesting case as well as sharing what makes their hearts flutter about their fellowship training. The case discussion is followed by both an E-CPR segment and a message from the program director. CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademySubscribe to our newsletter- The HeartbeatSupport our educational mission by becoming a Patron!Cardiology Programs Twitter Group created by Dr. Nosheen Reza Patient Summary A man in his mid-60s with a history of paroxysmal Afib presented to the ED after one week of chest pain and altered mental status. His afib had been difficult to rate and rhythm control, and thus he had undergone catheter ablation with pulmonary vein isolation 3 weeks prior to presentation. In the ED he was found to be febrile and had a witnessed seizure. Blood cultures returned positive for Strep agalactiae and his CT head showed multiple areas of intravascular air. Join the Thomas Jefferson University Cardionerds as they take us through an expert discussion on the differential of post-catheter complications, the diagnosis of atrial-esophageal fistula and ultimately management of this potentially fatal complication! Case Media ABCDEFClick to Enlarge A. ECG: Normal sinus rhythm HR 105 bpmB. CXRC. CT head: Multiple tiny foci of air throughout bilateral cerebral hemispheres. Appearance is most suggestive of intravascular air, although it is unclear if it is venous, arterial or both.D. MRI: 1. Restricted diffusion in bilateral cortical watershed zones, as well as in the posterior medial left cerebellar hemisphere, most consistent with recent infarctions.E. CT Chest: A small focus of air tracking along the left mainstem bronchus anterior to the esophagus, may represent a small amount of pneumomediastinum versus air in an outpouching of the esophagus. No air tracking more cranially along the mediastinal soft tissues. No definite soft tissue defect in the esophagus.F. Surgical repair of LA & Esophagus Episode Teaching The CardioNerds 5! – 5 major takeaways from the #CNCR case What is a pulmonary vein isolation? What are the most common complications? When is catheter ablation indicated?The majority of Afib triggers come from areas where the pulmonary veins attach to the left atrium. Approximately 15-20% of patients undergoing ablation will have non-pulmonary vein triggers. Guided by this anatomic and pathophysiologic underpinning, electrical isolation and ablation of these areas helps prevent propagation of the Afib impulses. The most effective method for pulmonary vein isolation (PVI) is ablation of the PV antrum, areas located near the PV ostia, using an oval mapping catheter to confirm ablation of electrical activity from the PV ostia.Vascular access complications (e.g. hematoma, pseudoaneurysm) are the most common complications following PVI and occur in approximately 1-4% (KD: I think complication rate is lower in studies I've reviewed) cases. Most other complications occur in less than 1% of cases and include cardiac tamponade/perforation, TIA/stroke, PV stenosis, pneumonia, phrenic nerve palsy, gastric motility disorders, atrial-esophageal fistula, and death.There is some growing evidence that catheter ablation may be superior to medical management alone in certain symptomatic populations (e.g., HFrEF). However, in the recent CABANA trial, catheter ablation did not significantly reduce death, disabling stroke, or serious bleeding compared to medical management in all comers with new-onset or untreated symptomatic Afib.The 2020 ESC guidelines on AFib give a Class I recommendation to Afib ablation for (1) symptom control in patients with paroxysmal or persistent AFib who have failed or are intolerant of at least one Class I or III antiarrhythmic drug (AAD); or (2) to reverse LV dysfunction in AFib patients when tachycardia-induced cardiomyopathy is highly probable regardless of their symptom status.What is an atrial esophageal fistula (AEF) and how does it form after a PVI?Esophageal perforation is a rare complication of PVI and occurs in 0.1-0.25% of procedures. If it goes undetected, an AEF can form, which is an abnormal connection between the esophagus and the left atrium. Overall it is the 2nd most common cause of death after PVI, with acute cardiac tamponade being the most common.In normal human anatomy, the esophagus runs just posterior to the LA, often coming within a few millimeters at its closest point. Regardless of modality (e.g. cryoablation, radiofrequency ablation), this close proximity can lead to damage of the esophagus via multiple mechanisms. First, all current ablation techniques use thermal injury, which can lead to direct mucosal damage the esophagus. Additionally, damage to the anterior esophageal plexus can impact gastric motility and emptying, which can increase reflux and lead to esophageal ulceration. Finally, thermal damage to the end arterioles can cause ischemic injury to the esophagus, which weakens the esophagus and predisposes it to ulcer and fistula formation.Though data is limited, ulceration of the esophagus appears to be the primary defect in AEF with the ulcer slowly propagating from the esophagus through the pericardium to the LA, forming a one way connection from the esophagus to the LA.What can be done to help avoid AEF formation during a PVI? What risk factors put patients at high risk for AEF formation?Esophageal temperature monitoring is frequently implemented to help reduce the risk of esophageal damage. In the 2017 HRS-led expert consensus statement on ablation of AFib, three-quarters of the writing group members terminate ablation if they observe a 1 C or 2 C rise in temperature from baseline, or a recorded temperature of 39C-40C in their practice. Temperatures above 41C increase the risk of AEF formation. Many providers also prescribe a PPI to reduce gastric acid secretion, a possible contributor to esophageal damage, but this data is not based clinical trial data.Multiple systems including esophageal cooling devices and methods to move the esophagus away from the LA are under development, but none have substantial clinical data to warrant widespread use.Risk factors for AEF formation include RF ablation (though can be seen with all ablation energy sources), higher esophageal temperature, and higher energy delivery (longer contact time, higher power, increased contact force, larger catheter tip, and higher irrigation flow).What are the most common signs and symptoms of an AEF and how is it diagnosed?Since AEFs start as an esophageal ulcer that progresses to a fistula, AEF formation typically takes 1-6 weeks (mean 20 days) from the time of ablation. Many of the common signs and symptoms are nonspecific and include fever, fatigue, AMS, chest pain, nausea, vomiting, dysphagia, hematemesis, melena, and dyspnea. Common complications include sepsis from bacteria (generally gram-positive organisms) entering the blood stream from the esophagus and stroke from air emboli.CT with oral and IV contrast or MRI imaging of the esophagus are the most useful diagnostic modalities. Occasionally this can show contrast extravasation from the LA to the esophagus, but more commonly it will show air from the esophagus into the pericardial space. Barium swallow can also be helpful as it has a very high specificity, but unfortunately a low sensitivity. Blood cultures and head CT are often obtained given the symptoms that patients present with and increase clinical suspicion if they demonstrate bacteremia or air emboli. Importantly, once AEF is suspected, EGD is contraindicated as insufflation of the esophagus can lead to a large air embolus and stroke.How are AEFs treated? What is the prognosis?Early diagnosis and treatment of AEFs is crucial as mortality is 100% without treatment. Esophageal ulceration or even pericardial esophageal fistulas have significantly better prognosis, highlighting the necessity for early identification. Esophageal stenting has not shown to be effective, and surgical repair with primary repair of the esophagus is the gold standard. Broad spectrum antibiotics should be utilized to treat or prevent the development of bacteremia and sepsis.Even with early identification and proper treatment, mortality is still very high with up to ~40% of patients dying after surgery. References Arruda, M. S., Armaganijan, L., Biase, L. D., Rashidi, R., & Natale, A. (2009).

Nov 17, 2020

CardioNerds (Amit Goyal & Daniel Ambinder) join Oregon Health & Science University cardiology fellows (Miranda Merrill, Timothy Simpson, Kris Kumar, and Stacey Howell) for a riverside chat at the Portland waterfront! They discuss a case of cardiac arrest associated with mitral valve prolapse (MVP) with mitral annular disjunction (MAD). Dr. Punag Divanji provides the E-CPR and program director Dr. Hind Rahmouni provides a message for applicants. Episode notes were developed by Johns Hopkins internal medicine resident, Eunice Dugan, with mentorship from University of Maryland cardiology fellow Karan Desai. Jump to: Patient summary - Case media - Case teaching - References Episode graphic by Dr. Carine Hamo The CardioNerds Cardiology Case Reports series shines light on the hidden curriculum of medical storytelling. We learn together while discussing fascinating cases in this fun, engaging, and educational format. Each episode ends with an “Expert CardioNerd Perspectives & Review” (E-CPR) for a nuanced teaching from a content expert. We truly believe that hearing about a patient is the singular theme that unifies everyone at every level, from the student to the professor emeritus. We are teaming up with the ACC FIT Section to use the #CNCR episodes to showcase CV education across the country in the era of virtual recruitment. As part of the recruitment series, each episode features fellows from a given program discussing and teaching about an interesting case as well as sharing what makes their hearts flutter about their fellowship training. The case discussion is followed by both an E-CPR segment and a message from the program director. CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademySubscribe to our newsletter- The HeartbeatSupport our educational mission by becoming a Patron!Cardiology Programs Twitter Group created by Dr. Nosheen Reza Patient Summary Coming soon! Case Media ABCDEFGClick to Enlarge A. CXRB. Rhythm Strips - ventricular fibrillationC. ECG: 1st degree AVB (PR ~ 215), borderline RAD, Qtc ~460 msec, slight ant. convexity with inferior terminal T waveD: TTE E: TTE with Pickelhaube Spike seen in mitral valve prolapse F-G: Cardiac MRI TTE 1 TTE 2 TTE 3 Cardiac MRI Episode Schematics & Teaching Coming soon! The CardioNerds 5! – 5 major takeaways from the #CNCR case Coming soon! References Coming soon! CardioNerds Case Reports: Recruitment Edition Series Production Team Bibin Varghese, MDRick Ferraro, MDTommy Das, MDEunice Dugan, MDEvelyn Song, MDColin Blumenthal, MDKaran Desai, MDAmit Goyal, MDDaniel Ambinder, MD

Nov 15, 2020

CardioNerd (Amit Goyal) join Emory University School of Medicine cardiology fellows (Sonali Kumar, John Lisko, and John Ricketts) for a lovely stroll on the BeltLine in Atalanta, GA. They discuss an interesting case of severe mitral stenosis treated with Valve-in-MAC transcatheter mitral valve replacement (TMVR) with LAMPOON. Drs. Vasilis Babaliaros and Adam Greenbaum provide the E-CPR and program director Dr. B. Robinson Williams III provides a message for applicants. Episode notes were developed by Johns Hopkins internal medicine resident Bibin Varghese with mentorship from University of Maryland cardiology fellow Karan Desai. Jump to: Patient summary - Case media - Case teaching - References Episode graphic by Dr. Carine Hamo The CardioNerds Cardiology Case Reports series shines light on the hidden curriculum of medical storytelling. We learn together while discussing fascinating cases in this fun, engaging, and educational format. Each episode ends with an “Expert CardioNerd Perspectives & Review” (E-CPR) for a nuanced teaching from a content expert. We truly believe that hearing about a patient is the singular theme that unifies everyone at every level, from the student to the professor emeritus. We are teaming up with the ACC FIT Section to use the #CNCR episodes to showcase CV education across the country in the era of virtual recruitment. As part of the recruitment series, each episode features fellows from a given program discussing and teaching about an interesting case as well as sharing what makes their hearts flutter about their fellowship training. The case discussion is followed by both an E-CPR segment and a message from the program director. CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademySubscribe to our newsletter- The HeartbeatSupport our educational mission by becoming a Patron!Cardiology Programs Twitter Group created by Dr. Nosheen Reza Patient Summary Coming soon! Case Media ABCDEFGHI JKClick to Enlarge A. CXRB. ECGC. TTE: Trasns-mitral PW Doppler D. Laceration in swineE-F: CT planningG. Transeptal catheters H. Trans-mitral PW Doppler (post procedure) I. LVOT gradients J-K. Post procedure CT TTE 1 TTE 2 TTE 3 TEE 1 TEE 2 Fluoroscopy 1 Fluoroscopy 2 Fluoroscopy 3 TEE 3 Fluoroscopy 4 TEE 4 TEE 5 Fluoroscopy 5 Fluoroscopy 6 Fluoroscopy 7 TEE 6 TEE 7 https://youtu.be/1gUyat6pg30 LAMPOON Procedure Episode Schematics & Teaching Coming soon! Click to enlarge! The CardioNerds 5! – 5 major takeaways from the #CNCR case Coming soon! References Coming soon! CardioNerds Case Reports: Recruitment Edition Series Production Team Bibin Varghese, MDRick Ferraro, MDTommy Das, MDEunice Dugan, MDEvelyn Song, MDColin Blumenthal, MDKaran Desai, MDAmit Goyal, MDDaniel Ambinder, MD

Nov 13, 2020

Aloha! CardioNerds (Amit Goyal & Karan Desai) join University of Hawaii cardiology fellows (Isaac Mizrahi, Nath Limpruttidham, Nishant Trivedi, and Shana Greif) for some shaved iced on the Big Island's north shore! They discuss a fascinating case of a patient presenting with decompensated heart failure found to have a giant coronary aneurysm. Program director Dr. Dipanjan Banerjee provides the E-CPR as well as a message for applicants. Episode notes were developed by Johns Hopkins internal medicine resident Tommy Das with mentorship from University of Maryland cardiology fellow Karan Desai. Jump to: Patient summary - Case media - Case teaching - References Episode graphic by Dr. Carine Hamo CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademySubscribe to our newsletter- The HeartbeatSupport our educational mission by becoming a Patron!Cardiology Programs Twitter Group created by Dr. Nosheen Reza Patient Summary A man in his early 60s with history of hypertension, peripheral arterial disease, atrial fibrillation, and AAA s/p repair presented with subacute fatigue, palpitations, shortness of breath, and lower extremity edema. On exam he was warm and well perfused, though hypotensive, tachycardic with an irregular rhythm, and had an elevated JVP. ECG showed AF with RVR without evidence of acute MI, and troponin was negative. TTE revealed a reduced LVEF and WMA in the inferolateral walls with akinesis of the basal mid septum; additionally, two large extracardiac structures were noted, one with heterogenous echotexture in the AV groove, and a second with an echolucent interior adjacent to the RA. The patient underwent coronary angiography, showing a dilated and calcified proximal LAD with high grade stenosis adjacent to the first septal perforator, a ectatic LCX that supplied left to right collaterals, and a giant RCA aneurysm with TIMI 0 flow distally. CCTA confirmed these findings, showing thrombosed aneurysms of the LAD, LCX, and RCA. Interventional cardiology and cardiac surgery both evaluated the patient's case, and determined that he was not a candidate for intervention. He was ultimately diuresed to euvolemia with significant improvement in symptoms, and plans to follow-up as an outpatient for heart transplant evaluation. Case Media ABCDClick to Enlarge A. CXRB. ECG: atrial fibrillation with RVR, left axis deviation, poor r wave progressionC. Wide complex tachycardia D. CT chest demonstrating giant aneurysm TTE Coronary Angiography Episode Schematics & Teaching The CardioNerds 5! – 5 major takeaways from the #CNCR case 1) This case featured a patient with a giant coronary aneurysm – how are coronary artery aneurysms defined and classified? Coronary artery aneurysms (CAA) are defined as a focal dilation of a coronary segment at least 1.5x the adjacent normal segment. Contrast this with coronary artery ectasia, which refers to a diffuse, as opposed to focal, coronary dilation. CAA morphology can be classified as either saccular (transverse > longitudinal diameter) or fusiform (transverse 20mm in diameter. Aortocoronary saphenous vein graft aneurysms have distinct characteristics and natural history compared to native coronary aneurysms. These aneurysms tend to present late (e.g., > 10 years following CABG) and tend to be larger than native CAA. IVUS can help differentiate between a true aneurysm with preserved integrity of all 3 vessel layers (intima, media, and adventitia) and a pseudoaneurysm with loss of wall integrity and damage to the adventitia. 2) Now that we have the language to define and classify coronary artery aneurysms, what are some causes these lesions? Atherosclerosis: lipid deposition, focal calcification, and fibrosis can weaken the vessel wall and predispose to subsequent coronary artery dilation. Up to 50% of CAAs are linked to arteriosclerosis. Autoimmune/inflammatory processes: Lupus and systemic vasculitis, such as Kawasaki's disease and Takayasu arteritis, can all lead to CAAs. Vasculitic CAAs usually affect more than one artery. Connective Tissue Disease: Marfan's syndrome and Ehlers-Danlos disease, for instance, are characterized by deficiencies in vessel wall integrity, leading to CAAs. Dynamic Wall Stress: Episodic hypertension and vasoconstriction, such as that seen in frequent cocaine use, can lead to wall stress, endothelial damage, and coronary artery aneurysms. Direct Vessel Wall Injury: Intracoronary interventions, such as angioplasty, stent delivery, and brachytherapy, can cause shear wall stress that leads to CAAs. Infectious Causes: Direct vessel wall invasion or immune complex deposition can be seen in bacterial, mycobacterial, fungal, and syphilitic infections. Septic emboli from infectious endocarditis can also lead to mycotic coronary aneurysms. Genetic susceptibility: Certain HLA class II genotypes are susceptible to CAAs. This may be the underlying pathology in certain idiopathic and congenital CAAs. 3) How do coronary artery aneurysms clinically present? Most CAAs are asymptomatic, and are found incidentally on coronary angiography or CCTA. Concomitant obstructive arteriosclerosis can cause angina or plaque rupture, and thrombosis in the aneurysm lumen can lead to distal embolization and myocardial infarction. Massive enlargement of CAAs and saphenous vein graft aneurysms can compress adjacent structures. CAA rupture is rare, though can cause cardiac tamponade. Stress-induced myocardial ischemia can also occur due to microvascular dysfunction 4) How do we diagnosis and assess CAAs? Most CAAs are evaluated via coronary angiography, though a complete angiographic evaluation can be complicated by delayed antegrade contrast filling, segmental back flow, and contrast stasis. In giant aneurysms, a forceful and prolonged contrast injection is needed to avoid misinterpreting slow aneurysmal filling as thrombosis. IVUS can help differentiate between true aneurysms, pseudoaneurysms, and coronary segments with aneurysmal appearance due to plaque rupture or stenosis. Furthermore, IVUS can assist in sizing aneurysm and planning for potential PCI. Coronary CTA noninvasively allows for a more accurate assessment of aneurysm size and degree of thrombus than angiography. CCTA is particularly useful in patients with giant CAA as it can provide an understanding of mechanical complications of these aneurysms. 5) How are coronary artery aneurysms managed? Notably, there is a lack of randomized and large-scale trial data to guide the treatment of CAAs; most recommendations are made on the basis of small case series and expert opinion. Medical Management: Given the association between CAA and arteriosclerosis, risk factor modification should be emphasized. The role of antiplatelet and anticoagulant agents is an area of ongoing debate, though there may be benefit in patients with multivessel ectasia. Furthermore, the context in which the patient presents (e.g., incidental finding vs. acute coronary syndrome) will guide the antiplatelet and/or anticoagulant strategy. Invasive (Percutaneous) Management: PCI of an aneurysmal vessel in the setting of acute MI is associated with lower rates of procedural success, and higher rates of distal embolization and no-reflow phenomenon. Additionally, these patients have higher rates of stent thrombosis and mortality. Given the higher thrombus burden in aneurysmal arteries, thrombectomy may be helpful in aiding PCI. Some case studies have additionally utilized intracoronary thrombolytics. Another strategy is a stent-assisted coil embolization technique in cases where covered stent placement is not possible due to tortuosity, calcification, or risk of side branch compromise. To date, there haven't been covered stents specifically designed for CAAs, but stents have been used off-label. Surgical Management: The most common operative strategy is to open the aneurysm, suture the afferent and efferent vessels, and finish with bypass grafting if possible. Other operative strategies include aneurysm ligation, resection, or marsupialization with interposition graft. References Thibodeau, J. T., & Drazner, M. H. (2018). The Role of the Clinical Examination in Patients With Heart Failure. JACC. Heart failure, 6(7), 543–551. Abou Sherif, S., Ozden Tok, O., Taşköylü, Ö., et al. (2017). Coronary Artery Aneurysms: A Review of the Epidemiology, Pathophysiology, Diagnosis, and Treatment. Frontiers in cardiovascular medicine, 4, 24. Kawsara, A., Núñez Gil, I. J., Alqahtani, F., et al. (2018). Management of Coronary Artery Aneurysms. JACC. Cardiovascular interventions, 11(13), 1211–1223. Newburger, J. W., Takahashi, M., & Burns, J. C. (2016). Kawasaki Disease. Journal of the American College of Cardiology, 67(14), 1738–1749. McCrindle, B. W., Rowley, A. H., Newburger, J. W., et al. (2017). Diagnosis, Treatment, and Long-Term Management of Kawasaki Disease: A Scientific Statement for Health Professionals From the American Heart Association. Circulation, 135(17), e927–e999. The CardioNerds Cardiology Case Reports series shines light on the hidden curriculum of medical storytelling. We learn together while discussing fascinating cases in this fun, engaging, and educational format. Each episode ends with an “Expert CardioNerd Perspectives & Review” (E-CPR) for a nuanced teaching from a content expert. We truly believe that hearing about a patient is the singular theme that unifies everyone at every level, from the student to the professor emeritus. We are teaming up with the ACC FIT Section to use the #CNCR episodes to showcase CV education across the country in the era of virtual recruitment. As part of the recruitment series,

Nov 12, 2020

CardioNerds (Amit Goyal & Daniel Ambinder) join Georgetown University/Washington Hospital Center cardiology fellows (Nitin Malik, AJ Grant, and Tsion Aberra) for some fresh Maryland blue crab cakes at the Georgetown waterfront in Washington, DC. They discuss a rare case of histoplasmosis pericarditis complicated by cardiac tamponade. Dr. Patrick Bering provides the E-CPR and program director Dr. Gaby Weissman provides a message for applicants. Johns Hopkins internal medicine resident Colin Blumenthal with mentorship from University of Maryland cardiology fellow Karan Desai. Jump to: Patient summary - Case media - Case teaching - References Episode graphic by Dr. Carine Hamo The CardioNerds Cardiology Case Reports series shines light on the hidden curriculum of medical storytelling. We learn together while discussing fascinating cases in this fun, engaging, and educational format. Each episode ends with an “Expert CardioNerd Perspectives & Review” (E-CPR) for a nuanced teaching from a content expert. We truly believe that hearing about a patient is the singular theme that unifies everyone at every level, from the student to the professor emeritus. We are teaming up with the ACC FIT Section to use the #CNCR episodes to showcase CV education across the country in the era of virtual recruitment. As part of the recruitment series, each episode features fellows from a given program discussing and teaching about an interesting case as well as sharing what makes their hearts flutter about their fellowship training. The case discussion is followed by both an E-CPR segment and a message from the program director. CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademySubscribe to our newsletter- The HeartbeatSupport our educational mission by becoming a Patron!Cardiology Programs Twitter Group created by Dr. Nosheen Reza Patient Summary A woman in her early 30s with a history of Crohn's disease on TNF-inhibitor therapy and chronic prednisone presented to the ED after two months of abdominal pain and fevers. She was found to have a perforated bowel and taken to emergent surgery and eventually found to have disseminated histoplasmosis. Post-surgery, her hypotension worsened. At this point, the Georgetown University Cardionerds were involved. Listen to the podcast now to learn about histoplasmosis, it's cardiac involvement, and management of acute effusive pericarditis! Case Media ABCDEClick to Enlarge A. Left: Admission chest x-ray (PA film), which was overall unremarkable. Right: Chest x-ray from hospital day 12 - which revealed pulmonary edema with bilateral perihilar haziness, increased prominence of pulmonary vascularity, and small-moderate bilateral pleural effusions. Note increased size of cardiac silhouette. At the corresponding time, pericardial effusion (without tamponade) had been diagnosed.B. EKG: Sinus tachycardia and low-voltage QRS complexes.C. CT abdomen/pelvis on hospital day 14. Free air noted within the abdomen (left). Moderate pericardial effusion also incidentally appreciated (right).D. Pulse-Wave Doppler of mitral inflow. Flow variation is present, but variation is less than 65, history of PUD) a PPI should be added for gastrointestinal protection. In patients with concomitant CAD, aspirin is often preferred. NSAIDs are often used for 1-2 weeks until symptoms resolve and/or CRP normalizes, after which they should be tapered off. Multiple RCTs, including the COPE and ICAP trials, support the addition of colchicine to NSAIDs to reduce symptoms and recurrence. Colchicine is typically given for 3 months after an acute episode.Corticosteroids can also be used as 2nd or 3rd line treatment for acute pericarditis, but they have been associated with longer course of disease and higher recurrence rates in meta-analyses. To reduce this risk, low dose steroids are preferred (i.e. prednisone 0.2-0.5 mg/kg/day) and they should be slowly tapered after symptoms resolve and CRP normalizes with close CRP monitoring to detect recurrence. Steroids can be beneficial as first line therapy in cases of autoimmune or immune checkpoint inhibitor-associated pericarditis.In patients with a lack of response to initial therapy with NSAIDs + colchicine, further workup might be required as these treatments are most effective in viral or idiopathic pericarditis. Treatment failure could indicate the presence of bacterial or malignant pericarditis, which often do not respond to the typical anti-inflammatories.In patients with recurrence of symptoms after resolution, multiple clinical trials, including the CORE and CORP trials, support the use of colchicine for recurrent pericarditis. Low dose steroids as described above are also often used in patients who had recurrence with first line therapy.Immunologic therapies like anakinra, an IL-1 antagonist, have shown benefit in RCTs even in patients who are resistant to colchicine and steroid dependent. In the recently published phase III RHAPSODY trial, rilonacept (an IL-1alpha and IL-1beta cytokine trap) led to resolution of recurrent pericarditis compared to placebo.How should pericardial effusions be managed in the setting of acute pericarditis? When should you consider draining a pericardial effusion?When a pericardial effusion is detected, the first step should be determining the size and hemodynamic significance with physical exam and echocardiography. For more on the relevant physical exam and echo findings, please see the show notes for Episode 72 on effusive-constrictive pericarditis! Hemodynamically significant effusions require urgent consultation for drainage. In this situation, pericardial drainage catheters should be left in place until drainage ceases, which improves apposition of the pericardial layers and reduces recurrence.Pericardiocentesis for diagnostic purposes is not routinely recommended. Patients who are resistant to initial treatment, or in whom a bacterial or neoplastic cause is suspected, should undergo pericardiocentesis with diagnostic studies to identify the underlying etiology.What is histoplasmosis? How does it usually present? What is the difference between histoplasmosis and disseminated histoplasmosis? How common in pericardial involvement?Histoplasma capsulatum is a dimorphic fungus and the most prevalent endemic mycosis in the US. Endemic to the Ohio and Mississippi River valleys, it is inhaled into the lungs as a mold where it will become a yeast in tissues at 37 degrees C. Once it the lungs it is consumed by macrophages leading to lymphatic and eventually hematogenous spread. Even with systemic spread, most cases are asymptomatic, but approximately 1 in 2000 cases can result in a severe infection. Most cases of severe infection occur in those with high-inoculum exposure, the elderly, or severely immunocompromised as T-cells and TNF play a vital role in host immune response.When symptoms do arise, they are usually mild, self limited, and resolve without treatment. The most common symptoms are fever, chills, myalgias, cough, pleuritic chest pain, and headache.Even among severe infections, isolated pulmonary manifestations are most common. When infection spreads to other organ systems outside of the lungs it is labeled disseminated histoplasmosis.Pericarditis associated with histoplasmosis is uncommon and occurs in around 5-10% of cases. It is most common in pulmonary histoplasmosis and is thought to be primarily an inflammatory response to the pulmonary disease rather than an invasion of the infection in to the pericardium.How is disseminated histoplasmosis treated? How does this differ from pulmonary histoplasmosis?Histoplasmosis can affect a wide range of organ systems including skin, GI tract, brain, bone marrow, and lungs.

Nov 11, 2020

CardioNerds (Amit Goyal & Karan Desai) join Medical University of South Carolina cardiology (MUSC) fellows (Carson Keck, Samuel Powell, and Ishan Shah) at MUSC Children's Hospital cafeteria overlooking the gorgeous Charleston Harbor. They reflect on an informative case of exertional intolerance due to tricuspid regurgitation. Dr. Ryan Tedford provides the E-CPR and program director Dr. Daniel Judge provides a message for applicants. Episode notes were developed by Johns Hopkins internal medicine resident, Eunice Dugan, with mentorship from University of Maryland cardiology fellow Karan Desai. Jump to: Patient summary - Case media - Case teaching - References Episode graphic by Dr. Carine Hamo The CardioNerds Cardiology Case Reports series shines light on the hidden curriculum of medical storytelling. We learn together while discussing fascinating cases in this fun, engaging, and educational format. Each episode ends with an “Expert CardioNerd Perspectives & Review” (E-CPR) for a nuanced teaching from a content expert. We truly believe that hearing about a patient is the singular theme that unifies everyone at every level, from the student to the professor emeritus. We are teaming up with the ACC FIT Section to use the #CNCR episodes to showcase CV education across the country in the era of virtual recruitment. As part of the recruitment series, each episode features fellows from a given program discussing and teaching about an interesting case as well as sharing what makes their hearts flutter about their fellowship training. The case discussion is followed by both an E-CPR segment and a message from the program director. CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademySubscribe to our newsletter- The HeartbeatSupport our educational mission by becoming a Patron!Cardiology Programs Twitter Group created by Dr. Nosheen Reza Patient Summary Coming soon! Case Media ABClick to Enlarge A. Tricuspid valve CW DopplerB. Hepatic vein flow TTE: TV inflow TTE: TV inflow with color Doppler TTE: Apical 4 chamber TTE: RV focused color Cardiac MRI - 4 chamber CINE Cardiac MRI - Short-axis stack CINE Episode Teaching The CardioNerds 5! – 5 major takeaways from the #CNCR case Coming soon! References Coming soon! CardioNerds Case Reports: Recruitment Edition Series Production Team Bibin Varghese, MDRick Ferraro, MDTommy Das, MDEunice Dugan, MDEvelyn Song, MDColin Blumenthal, MDKaran Desai, MDAmit Goyal, MDDaniel Ambinder, MD

Nov 11, 2020

CardioNerds (Amit Goyal & Daniel Ambinder) join Brown University cardiology fellows (Greg Salber, Vrinda Trivedi, and Esseim Sharma) for a gorgeous coastal boat ride in Providence, RI. They discuss an educational case of hypertrophic cardiomyopathy with superimposed stress cardiomyopathy. Dr. Katharine French provides the E-CPR and program director Dr. Raymond Russell provides a message for applicants. Episode notes were developed by Johns Hopkins internal medicine resident Evelyn Song with mentorship from University of Maryland cardiology fellow Karan Desai. Jump to: Patient summary - Case media - Case teaching - References Episode graphic by Dr. Carine Hamo The CardioNerds Cardiology Case Reports series shines light on the hidden curriculum of medical storytelling. We learn together while discussing fascinating cases in this fun, engaging, and educational format. Each episode ends with an “Expert CardioNerd Perspectives & Review” (E-CPR) for a nuanced teaching from a content expert. We truly believe that hearing about a patient is the singular theme that unifies everyone at every level, from the student to the professor emeritus. We are teaming up with the ACC FIT Section to use the #CNCR episodes to showcase CV education across the country in the era of virtual recruitment. As part of the recruitment series, each episode features fellows from a given program discussing and teaching about an interesting case as well as sharing what makes their hearts flutter about their fellowship training. The case discussion is followed by both an E-CPR segment and a message from the program director. CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademySubscribe to our newsletter- The HeartbeatSupport our educational mission by becoming a Patron!Cardiology Programs Twitter Group created by Dr. Nosheen Reza Patient Summary A man in his mid-70s with history of hypertension and diabetes presented with chest pain and ST elevation in V1-V3. Two weeks prior to his presentation he was diagnosed with HoCM after several months of progressive dyspnea. TTE at that time showed HCM with resting left ventricular outflow gradient of 35 mmHg and 83 mmHg with valsava and systolic anterior motion (SAM) of the mitral valve. Join the Brown University Cardionerds as they take us through the differential of chest pain in HCM, approach to wall motion abnormalities, and the fascinating management questions that arise. Case Media ABCDEClick to Enlarge A. ECG 2 weeks prior to current presentation B. Current ECG C. CXRD. M mode though the mitral valve demonstrating systolic anterior motion of the mitral valveE. LVOT CW Doppler tracings with a peak velocity ~ 5 m/s Coronary angiography - 1 Coronary angiography - 2 TTE - 1 TTE - 2 TTE - 3 TTE - 4 Cardiac MRI Episode Schematics & Teaching Hypertrophic Cardiomyopathy InfographicClick to enlarge! The CardioNerds 5! – 5 major takeaways from the #CNCR case What's the differential for LVH and what findings are more suggestive of HCM? Causes for LVH can be either pathological or physiological. Pathological causes include infiltrative diseases like hypertrophic cardiomyopathy (HCM), Amyloidosis, or Fabry disease and inflammatory diseases like myocarditis.Physiological causes are due to remodeling from increased cardiac output or workload like in athletic heart or from a high afterload state such as in aortic stenosis and hypertension.In hypertension, AS, and athletic heart, LV hypertrophy is more commonly concentric and rarely exceeds 15mm. In HCM, LV hypertrophy is more commonly asymmetric (basal anteroseptum > posterior wall), often >15mm, and typically involves the basal ventricular septum.Differentiating pathologic versus physiologic causes of LVH can typically be done from a detailed history and exam (e.g., evidence of hypertrophy out of proportion to pressure overload, multisystem involvement). Cardiac MRI can be used to differentiate between HCM and other phenocopies. In HCM, LGE is usually seen at the insertion point of the LV and RV or the most hypertrophied myocardial regions whereas in amyloidosis, endomyocardial LGE is more characteristic. What are some characteristic exam findings seen in HoCM? Systolic murmur at the left sternal border can be heard in patients with obstructive HCM (HoCM). The murmur is a result of LVOT obstruction due to systolic anterior motion (SAM) of the mitral valve and LV basal septal hypertrophy.Maneuvers that decrease preload, such as Valsalva or going from a sitting to upright position, will enhance the obstruction and increase the intensity of murmur.Maneuvers that increase the preload or afterload, such as squatting or handgrip, will decrease the intensity of murmur.Additionally, mitral valve pathology – whether a primary valve process or secondary to SAM/ abnormalities in the chordae – can lead to murmurs of mitral insufficiency. These murmurs will typically be best heard at the apex. The murmur associated with SAM will be mid to late peaking as the anterior leaflet is pulled away from the posterior leaflet, unlike the holosystolic murmur associated with intrinsic MV pathology.Pulsus bisferiens describes an aortic waveform with two peaks per cardiac cycle that's characteristic of dynamic LVOT. The onset of systole leads to the initial peak in aortic waveform. Then the narrowing of LVOT leads to a transient occlusion, causing a midsystolic dip in the aortic waveform. Lastly, towards the end of systolic, the ventricle overcomes the obstruction, leading to the second peak in the aortic waveform. What are the 4 Ps in management of HCM? Prevent symptoms: medical therapies with negative inotropy and chronotropy such as BB and CCB should be used. In the recent phase III EXPLORER-HCM, a cardiac myosin inhibitor, mavacamten, was shown to impressively reduce HF symptoms and LVOT gradient in patients with HoCM. In patients refractory to medical treatment, surgeries like myectomy or alcohol septal ablation are also options.Prevent stroke: HCM patients are at higher risk for atrial tachyarrhythmias and thus embolic stroke. All patients with atrial tachyarrhythmias should be anticoagulated regardless of their CHADSVASc score.Prevent sudden cardiac death (SCD) in family: HCM is an autosomal dominant genetic cardiomyopathy so all first relatives should undergo genetic testing and serial TTEs.Prevent SCD: HCM patients should undergo risk stratification for implantable cardiac defibrillators as VT/VF and SCD are major causes of morbidity and mortality in these patients. Some risk factors for primary prevention ICD include syncope without a clear cause, LV wall thickness > 30 mm, family history of SCD in a 1st-degree relative, repetitive episodes of NSVT on Holter, and failure to increase SBP > 20 mmHg with exercise. What's the Brockenbrough-Braunwald-Morrow sign? The Brockenbrough-Braunwald-Morrow sign is a useful catheterization laboratory maneuver that describes the characteristic LV pressure tracing pattern that's seen in dynamic LV outflow tract obstructive and can be used to differentiate obstructive HCM from other fixed valvular or subvalvular obstruction.Normally in patients without dynamic outflow obstruction, a compensatory pause after a PVC increases the filling time during diastole, leading to a higher stroke volume and arterial pulse pressure. Per the Frank-Starling mechanism, the expanded EDV also increases cardiac muscle stretch resulting in an increase in myocardial contractility, systolic aortic pressure, and thus an increase in pulse pressure.In patients with obstructive HCM, the augmented inotropic response after a PVC actually aggravates the obstruction. Thus, there is a rise in LV systolic pressure but also a rise in the LVOT gradient, resulting in a paradoxical decrease in systolic aortic pressure and pulse pressure. This is called the Brockenbrough-Braunwald-Morrow sign. How do we diagnose and treat Takotsubo cardiomyopathy? Takotsubo cardiomyopathy leads to transient heart failure caused by severe physical or emotional stress. Most patients will recover their EF but mortality is similar to that of anterior MI. 90% of cases occur in post-menopausal women. The Revised Mayo Clinic criteria, widely used to diagnose Takotsubo CM, include:Transient dyskinesis of LV midsegments, with or without apical involvementRegional wall motion abnormalities (WMA) extending beyond a single epicardial vascular distributionAbsence of obstructive coronary disease in the territory of WMA or angiographic evidence of acute plaque rupture.New EKG abnormalities or modest elevation in the cardiac troponin levelAbsence of pheochromocytoma and myocarditisTreatment is largely supportive and continues until the LV function recovers, usually within 21 days of onset. Anticoagulation should be started in patients with large areas of cardiac hypokinesis because major cerebral or vascular events are major complications. References Geske, J. B., Ommen, S. R., & Gersh, B. J. (2018). Hypertrophic Cardiomyopathy: Clinical Update. JACC. Heart failure, 6(5), 364–375.Boyd, B., & Solh, T. (2020). Takotsubo cardiomyopathy: Review of broken heart syndrome. JAAPA : official journal of the American Academy of Physician Assistants, 33(3), 24–29.Méndez, C., Soler, R., Rodríguez, E., Barriales, R., Ochoa, J. P., & Monserrat, L. (2018). Differential diagnosis of thickened myocardium: an illustrative MRI review. Insights into imaging, 9(5), 695–707.Lasam G. (2018). Brockenbrough-Braunwald-Morrow Sign: An Evaluative Hemodynamic Maneuver for Left Ventricular Outflow Tract Obstruction. Cardiology research, 9(3), 180–182.Cui, H., Nguyen, A., & Schaff, H. V. (2018). The Brockenbrough-Braunwald-Morrow sign. The Journal of thoracic and cardiovascular surgery, 156(4), 1614–1615.

Nov 10, 2020

In Episode #82, we met Jeremy Keck as a patient born with L-TGA and DILV treated with Fontan procedure. Now, in this very special episode, we meet Jeremy Keck beyond his heart disease through the eyes of his loving wife Ana Keck. His legacy underscores the importance of seeing our patients as people beyond their illness, in the context of their lives, values, and loved ones. We learn to appreciate the full life one can live with complex adult congenital heart disease but also of the work that remains to be done. This powerful discussion is led by Dr. Evelyn Song (internal medicine resident at Johns Hopkins Hospital), Dr. Pablo Sanchez (cardiology fellow at Stanford University), and Dr. Michael Landzberg (cardiovascular and palliative care faculty and former director of ACHD at Brigham and Women’s Hospital). ​ Jeremy's gofundme pageJeremy's case discussion - episode 82Jeremy's obituary page CardioNerds Case Reports PageCardioNerds Episode PageSubscribe to our newsletter- The HeartbeatSupport our educational mission by becoming a Patron! In Loving Memory of Jeremy Keck Jeremy Keck was a giant within the construction industry and accomplished so much in his 37 years of life. However, his greatest point of pride was his family. He is survived by his wife Ana, two young daughters, Emilee and Kaylee, his parents, Jeff and Terri Keck, brother Kevinn (Deana) Keck, nephews Jeremy and Payne, and nieces Taylore and Payge. Jeremy also had a heart for philanthropy. He was an active supporter of the Heart Center at Phoenix Children's Hospital. In an interview with The Arizona Republic in 2015, Jeremy said he wouldn’t change his experience even if he had the chance. “I have a perspective on life that you can't teach anybody," he said. “You can't even explain it to people. The small things that happen that might not go your way seem pretty minor.” Jeremy had such a positive impact on those around him, inspiring everyone to live life to the fullest. He will be deeply missed. Visit Jeremy's gofundme page for more information. Music AcknowledgementsEternal Hope by Kevin MacLeod is licensed under a Creative Commons Attribution 4.0 license. https://creativecommons.org/licenses/by/4.0/ Source: http://incompetech.com/music/royalty-free/index.html?isrc=USUAN1100238. Artist: http://incompetech.com/

Nov 6, 2020

CardioNerds (Amit Goyal & Daniel Ambinder) join Stanford cardiology fellows (Pablo Sanchez, Natalie Tapaskar, Jimmy Tooley) for tacos while enjoying the sunshine on the Stanford Oval! They recount the story of a man with adult congenital heart disease (ACHD): L-TGA (levo-transposed great arteries) with double inlet LV post-Fontan complicated by VF arrest. Dr. Christiane Haeffele provides the E-CPR and program director Dr. Joshua Knowles provides a message for applicants. Episode notes were developed by Johns Hopkins internal medicine resident Evelyn Song with mentorship from University of Maryland cardiology fellow Karan Desai and Cleveland clinic cardiology fellow Josh Saef. Jump to: Patient summary - Case media - Case teaching - References The CardioNerds Cardiology Case Reports series shines light on the hidden curriculum of medical storytelling. We learn together while discussing fascinating cases in this fun, engaging, and educational format. Each episode ends with an “Expert CardioNerd Perspectives & Review” (E-CPR) for a nuanced teaching from a content expert. We truly believe that hearing about a patient is the singular theme that unifies everyone at every level, from the student to the professor emeritus. We are teaming up with the ACC FIT Section to use the #CNCR episodes to showcase CV education across the country in the era of virtual recruitment. As part of the recruitment series, each episode features fellows from a given program discussing and teaching about an interesting case as well as sharing what makes their hearts flutter about their fellowship training. The case discussion is followed by both an E-CPR segment and a message from the program director. CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademySubscribe to our newsletter- The HeartbeatSupport our educational mission by becoming a Patron!Cardiology Programs Twitter Group created by Dr. Nosheen Reza Patient Summary A man in his mid-30s with past medical history notable for L-TGA (levo-transposed great arteries) with double inlet LV s/p Fontan palliation was playing golf when he suddenly collapsed. EMS arrived after three minutes of bystander CPR. An AED indicated the patient had suffered a VF arrest. ROSC was achieved after 1 round of Epi and 1 shock delivered. He was intubated and started on targeted temperature management protocol. Home medications were notable for digoxin 0.25mg daily, sotalol 120mg BID, and warfarin 5mg daily. Initial labs were notable for Na 127, K 5.4, Cr 1.0 (unknown baseline), INR 4.5, Lactate 4.6, Troponin-I 0.532, VBG 7.06/61, and random Digoxin level 2.7. EKG showed AV sequential pacing at a rate of 70 bpm. QTc prolonged at 571ms. No ischemic ST changes. Device interrogation showed sustained VT for 5 minutes prior to external shock. No internal shock was delivered. He was initially stabilized and his acidosis and hyperkalemia were corrected. Course was complicated by hemoptysis due to alveolar hemorrhagic and he was given concentrated prothrombin complex to reverse his coagulopathy. He eventually stabilized, and a formal TTE was obtained which showed a hypoplastic RV, single dilated LV with an akinetic posterior wall and hypokinetic lateral wall, all similar to his prior TTE in 2019. No obstruction noted at the IVC/Fontan anastomotic site. Coronary angiogram performed after his kidney function improved also did not show any significant obstructions or coronary anomalies. After multidisciplinary discussion, his VF arrest was attributed to a combination of prior ventricular fibrosis/scar, suspected digoxin toxicity, sotalol, dehydration, and renal failure. He had a subcutaneous ICD lead placed and was ultimately discharged home. Case Media ABClick to Enlarge A. CXRB. ECG Episode Schematics & Teaching The CardioNerds 5! – 5 major takeaways from the #CNCR case What's Transposition of the Great Arteries (TGA)? TGA is defined by a nontraditional ventricle-arterial relationship so that the aorta arises from the morphological RV and the pulmonary artery (PA) arises from the morphological LV There are two types of TGA, L or levo and D or dextro. D (rightward)-TGA: Systemic venous return flows into RA -> RV -> delivered to systemic circulation via Aorta, bypassing the lungs. The pulmonary veins flow into the LA -> LV-> delivered to the pulmonary circulation via the PA. The result is two parallel systems that fail to deliver oxygenated blood to the systemic circulation. This is not compatible with life unless another defect such as ASD, VSD, or PDA is present (or created) to allow mixing of deoxygenated and oxygenated blood. Patients with D-TGA usually require arterial switch procedures within 1 month of life. A simplified way to understand this is to say that the great vessels are malpositioned, leaving patients with two parallel circulation. L (leftward)-TGA: Deoxygenated blood flows into RA -> morphologic LV in the traditional RV position -> PA -> Lungs-> LA -> morphologic RV in the traditional LV position -> aorta to deliver oxygenated blood to the body. A simplified way to understand this is to say that the ventricles are malpositioned, leaving patients with two circulations in series (normal) with the pumps in the wrong places. There's no cyanosis at birth and patients may be completely asymptomatic for years. This is more rare than D-TGA and only occurs in ~7 per 100,000 births. The problem in L-TGA is that the morphologic RV, being the systemic ventricle, is not meant to withstand systemic afterload and can result in significant TR and ventricular dysfunction. Additionally, the majority of the cases (80%) are associated with an additional heart defect, such as VSD, pulmonary stenosis, RV hypoplasia, or DILV as in our case. What's Double Inlet Left Ventricle (DILV)? In DILV, both atrio-ventricular valves (mitral and tricuspid) lead into the LV and a large VSD is present to connect the LV and RV. DILV is very rare (~5 in 100,000 births). It coexists with L-TGA in about 65% of the cases. DILV leads to mixing of oxygenated and deoxygenated blood in the LV, resulting in inadequately oxygenated blood entering the systemic circulation and also over-circulation to the pulmonary system (increased Qp:Qs), resulting in LV congestion and heart failure over time. What's the Fontan procedure? The Fontan procedure is typically performed as a palliation procedure to direct flow of systemic venous return to the lungs without passing through a subpulmonic ventricle. It's typically performed in patients with complex congenital heart disease with a single functioning ventricle such as tricuspid atresia, pulmonary atresia, hypoplastic left heart syndrome, and DILV. In these conditions, intracardiac mixing of oxygenated and deoxygenated blood leads to cyanosis and ventricular volume overload without surgical intervention. The early variation of the Fontan procedure connected the pulmonary arteries to the RA. However, this led to RA dilation and loss of contractility, resulting in decreased pulmonary blood flow and increased risk for thrombus formation and arrhythmias. More modern Fontan palliation procedures connect both vena cavae directly to pulmonary arteries (via an intra- or extra-cardiac conduit), bypassing the RA and RV completely. Elevated pulmonary pressure is an absolute contraindication for the Fontan procedure since there's no ventricular contraction to pump blood through the lungs (it relies on passive flow). Therefore, the cavopulmonary Fontan circulation can't be created at birth given the normal high pulmonary vascular resistance in newborns. The modern Fontan palliation sequence is performed in a staged fashion to allow the patient's body to adapt to the different hemodynamic states and reduce overall surgical morbidity and mortality. Stage 1: systemic-pulmonary shunt; performed during neonatal period An artificial shunt is placed between a major systemic central vessel, usually subclavian artery, and proximal pulmonary artery. The goal of this step is to provide dedicated pulmonary blood flow to allow adequate oxygen delivery to tissues and pulmonary arterial growth. Stage 2: superior cavopulmonary connection (Glenn procedure); performed between 4-12 months Anastomosis is made between the SVC and proximal right PA. The previous systemic-pulmonary shunt is usually ligated. This allows priming of the pulmonary vasculature over time before completion of the Fontan circulation. Stage 3: completion of the Fontan circulation; performed between ages 1-5. Different surgical techniques are used, but the common endpoint is IVC anastomosis to the right PA. After the Fontan procedure, cardiac output is completely dependent on passive flow into the lungs. LV preload is central to Fontan physiology. Dehydration, an increase in pulmonary vascular resistance and/or worsening LV stiffness (and hence LV filling) can lead to decreased cardiac output. What are some complications associated with the Fontan procedure? RA dilatation was very common with the classic Fontan where atriopulmonary instead of cavopulmonary Fontan circulation was created, the RA is exposed to elevated pressure, leading to RA dilatation, thrombus formation, and arrhythmias. Ventricular failure usually develops after the first decade following completetion of the Fontan palliation. Patients will typically develop the classic symptoms of heart failure due to either HFrEF or HFpEF. Potential contributors to CHF include atrial tachycardia, valvular regurgitation, and volume-loading shunts. Atrioventricular valve (AVV) regurgitation can develop insidiously after the Fontan procedure and is a significant risk factor for long-term mortality post Fontan. AVV regurgitation can lead to volume overload, ventricular dilation, reduced ventricular contractility, and increased postcapillary and central venous pressures, compromising the Fontan circulation.

Nov 5, 2020

CardioNerds (Amit Goyal & Karan Desai) join Massachusetts General Hospital cardiology fellows (Daniel Pipilas, Rachel Frank and Kemar Brown) on a luxurious sailboat for iced coffees and Modern Pastry delicacies! They discuss a rare case of Anomalous Left Coronary Artery from the Pulmonary Artery (ALCAPA). Program director, Dr. Doreen DeFaria Yeh provides the E-CPR and a message for applicants. Episode notes were developed by Johns Hopkins internal medicine resident Evelyn Song with mentorship from University of Maryland cardiology fellow Karan Desai. Jump to: Patient summary - Case media - Case teaching - References Episode graphic by Dr. Carine Hamo CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademySubscribe to our newsletter- The HeartbeatSupport our educational mission by becoming a Patron!Cardiology Programs Twitter Group created by Dr. Nosheen Reza Patient Summary A women in her early 30s who's a Jehovah's witness presented with three days of intermittent chest pain. Past medical history included anxiety. Initial vitals and physical exam were unremarkable. Labs were notable for an elevated troponin T of 360 ng/L and a low TSH of 0.02 mIU/L with an elevated free T4 of 5.1 ng/dL. EKG demonstrated lateral and inferior ST depressions. TTE demonstrated a normal LVEF of 58% with a subtle anterolateral wall motion abnormality. Given her lack of conventional risk factors for CAD, resolution of her chest pain, and downtrending troponin, coronary CTA was obtained next which did not show any CAD but demonstrated an anomalous left main coronary artery (LMCA) arising from the main pulmonary artery with evidence of left to right shunting from the left main into the PA and extensive coronary and bronchial collateralization. The anterior wall hypokinesis was also seen on CT, consistent with ischemia due to myocardial steal phenomenon. Given the abnormal thyroid function tests, thyroid US was also obtained which showed patchy heterogeneity consistent with thyroiditis. Ultimately, the patient was diagnosed with ALCAPA and her chest pain was attributed to steal phenomenon due to hyperthyroidism and increased cardiac demand. She was treated with long-acting nitrates and beta-blocker with resolution of symptoms and was referred to cardiac surgery on discharge. After a multidisciplinary discussion involving the cardiac surgery team, patient underwent ligation of LMCA with SVG bypass to LAD. One month after operation, she developed palpitations and chest pain during exertion and was taken to the hospital. Labs showed an elevated hs-troponin T of 711 ng/L and she was treated for type 1 NSTEMI with aspirin, heparin drip, and statin. Repeat TTE demonstrated normal LVEF and lack of WMA. LHC showed occlusion of SVG graft and possible thrombus in LAD near the site of graft anastomosis. RCA was large and patent, providing adequate collaterals to the left coronary system. Ultimately, PCI was deferred and medical management was pursued because she had adequate collaterals from right coronary system. She was treated with DAPT, beta-blocker, and atorvastatin and has been doing well since. Case Media ABCDEFClick to Enlarge A. CXRB. ECG C. Follow up ECGD-F. Cardiac CT TTE 1 TTE 2 Angiography 1 Angiography 2 Angiography 3 Angiography 4 Angiography 5 Episode Schematics & Teaching The CardioNerds 5! – 5 major takeaways from the #CNCR case How are the coronary arteries formed during embryology and how are anomalous coronary arteries formed? During embryology, according to one theory, the coronary ostia and artery formation begins with ingrowth of a capillary plexus into the aortic sinuses. This complex process heavily depends on the proliferation and migration of cells that originate outside the heart at the sinus venosus and then differentiate into endothelial cells, vascular smooth muscle cells, and fibroblasts. Proper migration of these cells to aorta, creating the coronary ostia, depend heavily on expression of growth factors like FGF-2, PDGF, and VEGF. Anomalous origin of a coronary artery from the aorta or from the pulmonary artery have a common defect: the cells of the capillary plexus surrounding the aorta and pulmonary artery fail to reach and/or penetrate the normal sites of developing aorta. This can be caused by different mutations affecting the growth factor signaling pathways. What is ALCAPA? ALCAPA stands for anomalous left coronary artery (LCA) origin from the pulmonary artery. There's also ARCAPA which is anomalous RCA origin from the pulmonary artery. It occurs at an incidence of 1 in 300,000 live births or 0.25 to 0.5% of all congenital heart disease. It is difficulty to diagnose during infancy as it presents similarly to other more common pediatric conditions such as infantile colic, food intolerance, GERD, and bronchiolitis. The usual symptoms include inconsolable crying, poor feeding, rapid breathing, or symptoms of significant distress. Infants may develop myocardial infarction and CHF and a majority of them will die within the first year of life without surgical repair. Infants with ALCAPA rarely manifests in teenagers and adults, unlike the patient in our case. What are the hemodynamic consequences seen in ALCAPA? In fetal life, pulmonary artery pressure is the same as systemic pressure which allows adequate myocardial perfusion from the pulmonary artery to LCA. After birth, pulmonary vascular resistance falls precipitously and subsequently pulmonary artery pressure drops lower than systemic pressure. Furthermore, the pulmonary artery carries oxygen-poor blood; therefore, LCA is now perfused with desaturated blood at low pressure, resulting in inadequate perfusion to the myocardium, especially during exertion such as feeding or crying. Collateral vessels from a normally arising coronary artery can provide perfusion to the anomalous coronary; however, this can lead to "coronary steal" phenomenon and L-to-R shunt. The steal phenomenon and shunt occur because as the pulmonary resistance decreases further, the LCA and the collateral flow tends to pass into the low-pressure pulmonary artery rather than into the high-resistance myocardial blood vessels, resulting in coronary steal phenomenon and myocardial ischemia. When there are adequate collaterals, symptoms can be absent or very minor, allowing patients with ALCAPA to grow into adulthood. Adults with ALCAPA can either be asymptomatic or have exertional chest pain or even sudden cardiac death. What are some factors that will enable patients with ALCAPA to survive to adulthood? Factors that ultimately result in adequate perfusion of myocardium by the LCA will all enable patients survive to adulthood. These factors include: Abundant collateral vessels between the RCA and LCA allowing retrograde LV perfusion from the RCA system. Right dominant system which allows a smaller myocardial area to be supplied by the LCA, leading to less extensive myocardial ischemia. Ostial stenosis of the LCA or a restrictive opening into the pulmonary artery limits the left-to-right shunt and minimizes coronary steal from the pulmonary artery. Development of systemic blood supply to the LCA can occur when collaterals develop from the bronchial artery, providing adequate oxygenated blood flow and perfusion to the myocardium. What are some treatment options for ALCAPA? If an adult patient presents with CHF, medical management consists of the standard GDMT of afterload reduction, diuretics, and inotropic agents if needed. Once the patient is stabilized, surgical correction should be pursued. Previously, a simple ligation of the LCA at its origin was performed to prevent the steal phenomenon and myocardial ischemia. Essentially, the heart is converted to a one-vessel coronary system, entirely dependent on collaterals from the RCA. However, the one-vessel coronary system approach is no longer favored due to its high rate of complications such as recanalization of the ALCAPA, a greater risk of atherosclerosis, severe MR, and a persistent risk of SCD due to silent ischemia. Current surgical procedures are directed toward establishing a two-coronary vessel system through 3 main methods: Coronary button transfer which is direct reimplantation of the anomalous LCA into the aorta or left subclavian artery, after the pulmonary artery is transected. This is the most commonly used method in newborns. If done in adults, coronary friability increases the risk of tearing, bleeding, and kinking of the LCA. Takeuchi procedure which is creation of an aortopulmonary window - the pulmonary artery is opened and a baffle is created between the aorta and LCA. This method is commonly used in infants when coronary button transfer is not feasible but is rarely needed. Complications include supravalvular pulmonary stenosis, aortic insufficiency, and baffle obstruction or leaks. Placement of a coronary artery bypass graft (CABG) combined with ligation of the origin of LCA can be done to restore adequate perfusion. This is the preferred method in adults and what was done in this case. Complications include graft stenosis and occlusion which is what happened in this case. The CardioNerds Cardiology Case Reports series shines light on the hidden curriculum of medical storytelling. We learn together while discussing fascinating cases in this fun, engaging, and educational format. Each episode ends with an “Expert CardioNerd Perspectives & Review” (E-CPR) for a nuanced teaching from a content expert. We truly believe that hearing about a patient is the singular theme that unifies everyone at every level, from the student to the professor emeritus. We are teaming up with the ACC FIT Section to use the #CNCR episodes to showcase CV education across the country in the era of virtual recruitment. As part of the recruitment series,

Nov 4, 2020

CardioNerds (Amit Goyal & Daniel Ambinder) join Brigham and Women’s Hospital cardiology fellows (Mounica Yanamandala, Simin Lee and Maria Pabon Porras) for some fun times at the Charles River Esplanade! They discuss a complicated case of prosthetic valve endocarditis with aortic regurgitation. Dr. Dale Adler provides the E-CPR and program director Dr. Donna Polk provides a message for applicants. Episode notes were developed by Johns Hopkins internal medicine resident Bibin Varghese with mentorship from University of Maryland cardiology fellow Karan Desai. Jump to: Patient summary - Case media - Case teaching - References Episode graphic by Dr. Carine Hamo The CardioNerds Cardiology Case Reports series shines light on the hidden curriculum of medical storytelling. We learn together while discussing fascinating cases in this fun, engaging, and educational format. Each episode ends with an “Expert CardioNerd Perspectives & Review” (E-CPR) for a nuanced teaching from a content expert. We truly believe that hearing about a patient is the singular theme that unifies everyone at every level, from the student to the professor emeritus. We are teaming up with the ACC FIT Section to use the #CNCR episodes to showcase CV education across the country in the era of virtual recruitment. As part of the recruitment series, each episode features fellows from a given program discussing and teaching about an interesting case as well as sharing what makes their hearts flutter about their fellowship training. The case discussion is followed by both an E-CPR segment and a message from the program director. CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademySubscribe to our newsletter- The HeartbeatSupport our educational mission by becoming a Patron!Cardiology Programs Twitter Group created by Dr. Nosheen Reza Patient Summary A male in his mid-40s with history of HIV on ART (undetectable VL, CD4 320) and idiopathic thoracic ascending aortic aneurysm (TAAA) with AR s/p bioprosthetic valve replacement 10 years prior presented with acute onset lightheadedness and pre-syncope. He was diagnosed with an idiopathic TAAA at age 30 after he was noted to have an incidental murmur. Over the next few years, his aortic root increased to over 7 cm with severe AR, LV dilation, and reduced LVEF of 45%. He underwent bioprosthetic aortic valve replacement and root repair with a Medtronic freestyle porcine aortic root with subsequent recovery of his LVEF to 50% and improved LV dilation. Thereafter, he was doing well until he reported a flu like illness 3 weeks prior to presentation with reported fever up to 101.3 F and associated myalgias. He denied any sick contacts or recent travel and was adherent to his HIV regiment. On the day of presentation, he was walking his dogs when he developed acute onset lightheadedness with presyncope. On presentation, he had a low grade fever, tachycardia, tachypnea, and hypoxia. On exam, cardiac exam was notable for loud blowing diastolic murmur, non-distended JVP, decreased breath sounds, warm extremities with bounding pulses and without edema. There were no stigmata of endocarditis. Labs revealed elevated cardiac and inflammatory biomarkers. Blood cultures were initially NGTD. CXR corroborated the exam with bilateral interstitial and airspace opacification with effusions. TTE showed LVEF 35% with global hypokinesis, dilated LV with LVEDD 7.5 cm, mild RV systolic dysfunction, severe AR with holo-diastolic flow reversal in the abdominal aorta, no prosthetic stenosis, and aortic root 31 mm. TEE showed a well-seated AVR with leaflet thickening and several echodensities. CT surgery deemed patient to be high risk for the OR. After a few days, patient required intubation for increased work of breathing and acute decompensation requiring vasoactive infusions. After multidisciplinary discussions, the patient ultimately underwent ViV TAVR with successful placement of a 29 mm Edwards Sapien 3 valve. That day, he was weaned off pressors, and subsequently extubated. Infectious workup remained negative thereby resulting in a final diagnosis of prosthetic aortic valve culture-negative endocarditis vs sterile prosthetic valve deterioration. He was discharged on intravenous empiric antibiotics and was doing well in clinic 2 months later. Case Media ABCDEFClick to Enlarge A. CXR: Bilateral airspace and interstitial opacification. Small bilateral effusions. No pneumothorax.B. ECG C. CW Doppler across the aortic valve D. PW Doppler showing holodiastolic flow reversal in the descending thoracic aorta E. Pre-TAVR LV and aortic pressure tracings F. Post-TAVR LV and aortic pressure tracings TTE 1 TEE 1 TEE 2 TEE 3 TEE 4 TAVR implantation TEE - Post TAVR TEE - Post TAVR TEE - Post TAVR Episode Schematics & Teaching Coming soon! Pathophysiology of Aortic RegurgitationSevere Aortic RegurgitationClick to enlarge! The CardioNerds 5! – 5 major takeaways from the #CNCR case 1. The patient had an idiopathic ascending aortic aneurysm. How do you typically approach the etiology for a thoracic aortic aneurysm? Let us first differentiate the terminology for the aorta. The ascending aorta includes the aortic root (which contains the sinuses of Valsalva), the aortic arch which includes the great vessels. The descending aorta begins beyond the left subclavian artery. The isthmus is the point where the aortic arch and the descending aorta join (also the site of the ductus arteriosus which turns into the ligamentum arteriosum). The abdominal aorta begins distal to the diaphragm. Thoracic Aortic Aneurysms (TAA) include aneurysms that occur from the aortic root to the crus of the diaphragm. There are various etiologies for TAAs, but the most common cause is medial necrosis. This is a non-specific pathologic finding that may be found in a number of conditions. The underlying histologic findings include loss of elastic fibers and vascular smooth muscle in the media, with accumulation of a basophilic ground substance leading to a cystic appearance. There are several ways to approach the etiology of TAAs. The causes may be classified into degenerative, genetic, infectious, inflammatory, and other causes. Genetic causes include but are not limited to Marfan's Syndrome, Loeys-Dietz Syndrome, Ehlers-Danlos Type IV, Familial TAA, and Turner syndrome. Inflammatory conditions include giant cell arteritis, Takayasu arteritis, and HLA-B27 associated spondyloarthropathies. An important infectious cause includes syphilis as we have previously discussed on our CNCR Series: Ep #47 - Syphilitic Aortitis! Generally, aortopathies occurring proximal to the ligamentum arteriosum are more likely to be genetic while those occurring distally are more likely to be degenerative (related to atherosclerotic risk factors). Remember, in terms of management, TAAs tend to grow more rapidly as they become larger and depending on the etiology, there may be a lower cut-off for elective procedures as the guidelines suggest earlier intervention for specific conditions. For instance, patients with Loeys-Dietz (amongst other genetic syndromes), can be considered for elective TAA at aneurysms less than 50 mm given the high occurrence of dissection after 50 mm. The approach should be individualized to the patient's underlying condition, body size and sex (as there may be smaller absolute aortic root size and diameter in women). 2. The patient had well controlled HIV and developed a TAA. What are the known cardiovascular risks associated with HIV? Cardiovascular disease, including myocardial, pericardial, and vascular (including coronary) disease, has become a major cause of morbidity and mortality in patients with HIV Vascular disease likely has several causes including traditional risk factors (e.g., diabetes, hypertension) and chronic inflammation which leads to accelerated atherosclerosis. Recall from the CardioNerds Prevention Series that HIV is a key "risk-enhancing factor"! HIV is an important cause of heart failure, including HIV-associated dilated cardiomyopathy. Some data has suggested that the HIV-1 virus may infect myocardial cells directly in a patchy distribution leading to progressive damage and fibrosis. Furthermore , underlying ischemia, co-infection with other pathogens (e.g., EBV, CMV, coxsackievirus B), cardiac autoimmunity, and drug toxicities can contribute to the development of HF. Patients with HIV are additionally at higher risk of developing HFpEF. The mechanism remains to be elucidated, though the extent of chronic inflammation, T-cell activation, and loss of adaptive immunity likely all play a role. Pericardial disease and specifically pericarditis was the most common manifestation of HIV-associated cardiac disease prior to the advent of potent ART. Other manifestations include pulmonary arterial hypertension (WHO Group 1), increased risk of venous thromboembolism, and possibly sudden cardiac death. Infective endocarditis rates are similar to patients without HIV, once corrected for other exposures (e.g., IV drug use). 3. The patient developed a new loud decrescendo blowing diastolic murmur which was concerning for aortic regurgitation. What are the other physical exam findings associated with aortic regurgitation? As we reviewed in previous episodes (Ep #47 - Syphilitic Aortitis), the physical exam of patients with chronic AR is full of classic findings and eponyms! The classic murmur of AR is a diastolic, blowing, decrescendo murmur heard in the LUSB. The severity of AR correlates with the duration of the murmur more than the intensity. The increased blood flow across the AV can lead to a systolic flow murmur in the RUSB, and the regurgitant blood flow can limit opening of the MV causing a diastolic murmur best heard at the apex called the Austin-Flint murmur. Note,

Nov 3, 2020

CardioNerds (Amit Goyal & Daniel Ambinder) join University of Washington cardiology fellows (Shannon McConnaughey, Betty Ashinne and Andrew Perry - host of the AP Cardiology podcast) for some tacos and beer at the water and discuss a puzzling case of recurrent troponin elevation. Dr. Kelly Branch provides the E-CPR and program director, Dr. Rosario Freeman, provides a message for applicants. Episode notes were developed by Johns Hopkins internal medicine resident Eunice Dugan with mentorship from University of Maryland cardiology fellow Karan Desai. Jump to: Patient summary - Case media - Case teaching - References Episode graphic by Dr. Carine Hamo CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademySubscribe to our newsletter- The HeartbeatSupport our educational mission by becoming a Patron!Cardiology Programs Twitter Group created by Dr. Nosheen Reza Patient Summary A female is her late 50s with past medical history of alcohol use disorder and intravenous drug use complicated by hepatitis C presented with generalized weakness and was found to have lower extremity fractures. Cardiology was consulted for pre-operative management. When obtaining a cardiac history, she reported rare, intermittent, and non-anginal chest pain. She had no current chest pain or dyspnea. On chart review, she had multiple presentations over the past 3 years for various complaints - some were chest pain - during which she was found to have elevated troponin I values. Most of the elevations were in the 0.5 to 1 ng/mL range, but one time, her peak troponin was 32 ng/mL. At one of those presentations, she had a TTE that showed septal wall motion abnormalities. She underwent coronary angiography on two occasions, which both showed proximal and mid-LAD calcifications, but no significant stenosis and she was managed medically. At the current presentation, her vitals were within normal limits and her exam did not show any cardiopulmonary abnormalities. Labs were notable for troponin I of 10 ng/mL but CK-MB was normal. Interestingly, alkaline phosphatase was 3 times the upper limit of normal, and rheumatoid factor was 1156 IU/mL compared to 70 previously (normal range 0-20 IU/mL). EKG was without ischemic changes. TTE showed no wall motion abnormalities, normal LVEF, and no significant valvular disease. Cardiac catherization was deferred, and the patient was not interested in cardiac MRI. Due to an incongruent troponin elevation with the clinical presentation, there was concern for interference with the troponin assay due to the elevated rheumatoid factor and alkaline phosphatase levels. Upon further investigation, dilution of the troponin yielded results lower than factor of dilution or undetectable results. Mayo testing of the sample showed troponin-T of 0.024 ng/mL (normal 20%, there is likely myocardial necrosis and the test should be followed with imaging and possible intervention. If the elevation persists but is less than a 20% increase, then it is reasonable to see if your laboratory offers other assays for testing. If there is a mismatch in the second assay, then testing for interference in the first assay must be pursued. If there is no alternative assay, then investigation for chronic myocardial injury is warranted by ruling out structural heart disease or coronary heart disease. If there is no pathology, then it is reasonable to pursue analytical interferences. The most common reason for false positive results is cross-reacting antibodies (most commonly heterophile antibodies) that interact with the assay. A common way to remove the interferent is to perform dilution studies. The concentration of the mixed sample will not decrease with serial dilutions until the interferent is gone at which point the concentration will decrease steeply. References Fourth Universal Definition of Myocardial Infarction (2018).

Nov 1, 2020

CardioNerds (Amit Goyal) join University of Mississippi Medical Center cardiology fellows (Catherine Lowe, Chris Latour and Adi Sabharwal) as they sit at the reservoir enjoying a great view of the water at the Pelican Cove Grill in Jackson, MS. They discuss and educational case of decompensated heart failure and shock in the setting of severe functional mitral regurgitation treated with MitraClip. Dr. Kellan Ashley provides the E-CPR and program director Dr. Trey Clark provides a message for applicants. Episode notes were developed by Johns Hopkins internal medicine resident Richard Ferraro with mentorship from University of Maryland cardiology fellow Karan Desai. Jump to: Patient summary - Case media - Case teaching - References Episode graphic by Dr. Carine Hamo The CardioNerds Cardiology Case Reports series shines light on the hidden curriculum of medical storytelling. We learn together while discussing fascinating cases in this fun, engaging, and educational format. Each episode ends with an “Expert CardioNerd Perspectives & Review” (E-CPR) for a nuanced teaching from a content expert. We truly believe that hearing about a patient is the singular theme that unifies everyone at every level, from the student to the professor emeritus. We are teaming up with the ACC FIT Section to use the #CNCR episodes to showcase CV education across the country in the era of virtual recruitment. As part of the recruitment series, each episode features fellows from a given program discussing and teaching about an interesting case as well as sharing what makes their hearts flutter about their fellowship training. The case discussion is followed by both an E-CPR segment and a message from the program director. CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademySubscribe to our newsletter- The HeartbeatSupport our educational mission by becoming a Patron!Cardiology Programs Twitter Group created by Dr. Nosheen Reza Patient Summary A man his mid 70s with a history of non-ischemic heart failure status post CRT-D placement, A-Fib, and chronic kidney disease presented with progressive shortness of breath with limited exertion. The patient was found to have severe secondary mitral regurgitation. Listen to the episode now to learn about treatment options for severe mitral regurgitation in heart failure and specifically the evaluation for MitraClip! Case Media ABCDEClick to Enlarge A. Right atrial pressure B. Right ventricular pressureC. Pulmonary artery pressureD. Wedge pressureC. Pre and post MitraClip left atrial pressure Episode Teaching The CardioNerds 5! – 5 major takeaways from the #CNCR case 1. What is Comprehensive Disease Modifying Therapy in HFrEF? Comprehensive disease modifying therapy for heart failure with reduced ejection fraction (HFrEF) has become both more robust and better understood by practitioners inside and outside the cardiology community. Comprehensive therapy is generally considered to consist of beta-blockade, mineralocorticoid receptor antagonist (MRA), sodium-glucose cotransporter-2 inhibitors (SGLT2i) and angiotensin receptor neprilysin inhibitor (ARNI), with ARNI being the preferred agent over angiotensin converting enzyme inhibitor (ACEi) or angiotensin II receptor blocker (ARB). Despite a greater understanding of HFrEF therapy by the medical community, significant gaps remain with recent data showing few patients on concomitant beta blockade, MRA, SGLT2i and ACE/ARB/ARNI, and even fewer at target doses. Compared to ACE, BB, and MRA alone, comprehensive therapy with MRA, BB, SGLT2i and ARNI could add an additional 6 years for middle-aged patients. 2. What role does Mitral Valve Disease have in Heart Failure Exacerbations? For patients that remain symptomatic or with repeated hospitalizations for decompensated heart failure despite comprehensive therapy, it is important to look for additional pathology contributing to heart failure exacerbations. Mitral valve disease is one such etiology, particular secondary mitral valve regurgitation (MR) which can be seen in heart failure due to changes in left ventricular anatomy. Severe MR is associated with worsening left ventricular function and heart failure. For some time, however, it was an open question if functional MR was secondary to heart failure or an independent cause of heart failure exacerbations. Recent major trials suggest severe MR may act independently to worsen or lead to more frequent heart failure exacerbations. 3. How Do we Assess Mitral Valve Function in Heart Failure? MR is primarily quantified by echocardiography, which allows for close observation of regurgitant flow. Once a diagnosis of secondary MR has been established by evaluating mitral valve morphology and leaflet motion (e.g., Carpentier Classification), there are several parameters including objective quantification of MR hemodynamics that are utilized to assess MR severity. However, the AHA/ACC guidelines and the ESC guidelines have different thresholds for severe secondary MR. In the ACC/AHA guidelines, important quantitative measures include calculation of the effective regurgitant orifice area (EROA), regurgitant volume (RVol) and regurgitant fraction (RF). When the MR is holosystolic and accounting for several limitations of these measures, EROA ≥0.4cm2, regurgitant volume ≥60mL, regurgitant fraction ≥ 50% are highly specific for severe MR. Vena contracta, the narrowest diameter of the regurgitant jet, is a semi-quantitative measure of MR severity and ≥0.7 cm (with a single jet) is consistent with severe MR. Remember, MR is dynamic and is dependent on the loading conditions. Thus, it is critical to record the patient's blood pressure, estimated LV systolic pressure in the setting of aortic stenosis, rhythm and heart rate when reporting echocardiographic measures. 4. What are the Therapeutic Options for Mitral Valve Disease? Repair options generally include chordal-sparing mitral valve replacement (generally preferred in secondary MR rather than surgical mitral valve repair) and MitraClip. Mitral valve replacement is generally performed by surgeons, and with some exceptions is performed via open heart surgery. MitraClip placement consists of a small device that enters the left atrium via a trans-septal approach, and attaches to and approximates the mitral valve leaflets to reduce the burden of MR. 5. How Does the Data Substantiate these Options? The EVEREST II trial was the first major trial to show similar clinical improvement and improved safety of MitraClip placement as compared to conventional mitral valve replacement surgery. The MITRA-FR and COAPT trials subsequently looked specifically at GDMT versus GDMT with percutaneous mitral valve repair in the treatment of heart failure. While MITRA-FR did not exhibit improvement in hospitalization for heart failure or mortality, the COAPT trial did show exhibit improvement in these markers. While the topic is of much discussion, differences in heart failure severity and achievement of GDMT was suspected to drive in part the different findings in these two trials. Furthermore, the concept of proportionate and disproportionate MR is thought to also lead to differences in the two trials. Patients with "disproportionate" MR – the severity of the MR is unexpected to the degree of LV dilation – were more well-represented in the COAPT trial. These patients seemingly are more likely to respond to interventions on the valve in addition to GDMT. COAPT was therefore the first trial to show improvement in mortality and outcomes in patients with moderate-to-severe MR secondary to LV dysfunction. References Greene, S. J., Butler, J., Albert, N. M., et. al (2018). Medical therapy for heart failure with reduced ejection fraction: the CHAMP-HF registry. Journal of the American College of Cardiology, 72(4), 351-366.Feldman, T., Foster, E., Glower, D. D. et. al. (2011). Percutaneous repair or surgery for mitral regurgitation. New England Journal of Medicine, 364(15), 1395-1406.Obadia, J. F., Messika-Zeitoun, D., Leurent, G. et. al (2018). Percutaneous repair or medical treatment for secondary mitral regurgitation. New England Journal of Medicine, 379(24), 2297-2306.Stone, G. W., Lindenfeld, J., Abraham, W. T., et. Al (2018). Transcatheter mitral-valve repair in patients with heart failure. New England Journal of Medicine, 379(24), 2307-2318. CardioNerds Case Reports: Recruitment Edition Series Production Team Bibin Varghese, MDRick Ferraro, MDTommy Das, MDEunice Dugan, MDEvelyn Song, MDColin Blumenthal, MDKaran Desai, MDAmit Goyal, MDDaniel Ambinder, MD

Oct 28, 2020

CardioNerds (Amit Goyal & Daniel Ambinder) join Boston University cardiology fellows (Yuliya Mints, Anshul Srivastava, and Michel Ibrahim) for some hotdogs at Fenway Park in Boston, MA. They discuss an educational case of carcinoid heart disease with severe tricuspid regurgitation. Program director, Dr. Omar Siddiqi provides the E-CPR and APD Dr. Katy Bockstall provides a message for applicants. Episode notes were developed by Johns Hopkins internal medicine resident Bibin Varghese with mentorship from University of Maryland cardiology fellow Karan Desai. Jump to: Patient summary - Case media - Case teaching - References Episode graphic by Dr. Carine Hamo The CardioNerds Cardiology Case Reports series shines light on the hidden curriculum of medical storytelling. We learn together while discussing fascinating cases in this fun, engaging, and educational format. Each episode ends with an “Expert CardioNerd Perspectives & Review” (E-CPR) for a nuanced teaching from a content expert. We truly believe that hearing about a patient is the singular theme that unifies everyone at every level, from the student to the professor emeritus. We are teaming up with the ACC FIT Section to use the #CNCR episodes to showcase CV education across the country in the era of virtual recruitment. As part of the recruitment series, each episode features fellows from a given program discussing and teaching about an interesting case as well as sharing what makes their hearts flutter about their fellowship training. The case discussion is followed by both an E-CPR segment and a message from the program director. CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademySubscribe to our newsletter- The HeartbeatSupport our educational mission by becoming a Patron!Cardiology Programs Twitter Group created by Dr. Nosheen Reza Patient Summary A woman in her mid 60s with history of neuroendocrine tumor (NET) presented to the cardio-oncology clinic with chronic progressive SOB and fatigue. She was diagnosed with NET after presenting with a small bowel obstruction (SBO) several years prior. At the time, she was found to have liver and pulmonary metastasis with MR enterography showing thickening of the terminal ileum. Ileocecetomy and biopsy of the liver lesions confirmed metastatic NET. Despite treatment with octreotide and everolimus, follow up CT showed progression of liver lesions and she was eventually started on telotristat and enrolled in a clinical trial. On presentation, she was not tachycardiac, hypotensive or requiring oxygen supplementation (KD: Correct?). On exam, she demonstrated elevated JVP with a positive hepato-jugular reflex and a 3/6 holosytolic murmur loudest at the LLSB that increased with inspiration. Lab work revealed urinary 5-HIAA was 212 (nl 300 mmol/24 h conferred a 2- to 3-fold increased risk for developing or progression of carcinoid heart disease TTE is the imaging modality of choice for patients with signs and/or symptoms of carcinoid heart disease, in patients with elevated NT-proBNP , and any patient undergoing surgical liver or abdominal intervention. The findings of carcinoid heart disease are on a spectrum, but there are some characteristic findings as outlined above. TEE can be an additional test to fully characterize valvular involvement and/or for surgical planning. Furthermore, cardiac CT and CMR may be valuable as adjuncts 4. How do you manage carcinoid heart disease? The only definitive and effective therapy for carcinoid heart disease is valve intervention. Diuretics and aldosterone antagonists can be helpful to relieve symptoms, but typically only have temporary effectiveness. Telotristat ethyl, an oral tryptophan hydroxylase inhibitor used in combination with a somatostatin analog for management of diarrhea associated with carcinoid syndrome, has been used to try to prevent the development and progression of carcinoid heart disease. Surgical valve intervention should be considered in patients with severe valvular disease and/or signs of right heart failure, with at least 12 months of anticipated post-operative survival fromt heir NET disease. Symptomatic management primarily involves loops diuretics and aldosterone antagonists for relieving symptoms associated with RHF. Digoxin, vasodilators, and ACEi have no proven efficacy in this population. Bioprosthetic valves may be preferred over mechanical valves due to the inherent increased risk of bleeding in patients with advanced liver disease and hepatic dysfunction from carcinoid disease. However, bioprosthetic valves may be more prone to premature dysfunction and degeneration due to the underlying carcinoid process and thrombosis formation. A careful multi-disciplinary team and approach is needed to individualize valve choice for each patient. Transcatheter valve replacement has been undertaken for pulmonic valve involvement, but transcatheter tricuspid valve replacement is not common. 5. What is the overall prognosis of patients with carcinoid heart disease with and without surgical management? Carcinoid heart disease with NYHA III or IV symptoms have a poor prognosis and median survival is only 11 months. In carcinoid patients with cardiac symptoms and controlled systemic disease,

Oct 27, 2020

Oct 23, 2020

CardioNerds (Amit Goyal & Daniel Ambinder) join UCSF cardiology fellows (Emily Cedarbaum, Matt Durstenfeld, and Ben Kelemen) for some fun in San Francisco! They discuss a informative case of ST-segment elevation (STEMI) due to coronary vasospasm. Dr. Binh An Phan provides the E-CPR and program director Dr. Atif Qasim provides a message for applicants. Episode notes were developed by Johns Hopkins internal medicine resident Evelyn Song with mentorship from University of Maryland cardiology fellow Karan Desai. Jump to: Patient summary - Case media - Case teaching - References Episode graphic by Dr. Carine Hamo The CardioNerds Cardiology Case Reports series shines light on the hidden curriculum of medical storytelling. We learn together while discussing fascinating cases in this fun, engaging, and educational format. Each episode ends with an “Expert CardioNerd Perspectives & Review” (E-CPR) for a nuanced teaching from a content expert. We truly believe that hearing about a patient is the singular theme that unifies everyone at every level, from the student to the professor emeritus. We are teaming up with the ACC FIT Section to use the #CNCR episodes to showcase CV education across the country in the era of virtual recruitment. As part of the recruitment series, each episode features fellows from a given program discussing and teaching about an interesting case as well as sharing what makes their hearts flutter about their fellowship training. The case discussion is followed by both an E-CPR segment and a message from the program director. CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademySubscribe to our newsletter- The HeartbeatSupport our educational mission by becoming a Patron!Cardiology Programs Twitter Group created by Dr. Nosheen Reza Patient Summary A man in his mid-50s with alcohol use disorder, cirrhosis, atrial fibrillation, and alpha thalassemia complicated by iron overload presented with hematemesis. He was tachycardic and hypotensive. Labs were notable for Hgb 8.1 (baseline of 10.2), INR 1.3, lactate 4.2, and ferritin 4660. He was started on IV PPI and octreotide. Course was complicated initially by Afib with RVR with hypotension. Subsequently, the patient developed unstable VT requiring CPR. Post-code EKG showed inferolateral ST elevations. Troponin-I rose from 19 to 225 and his pressor requirement continued to increase despite resolution of his GIB. TTE showed LVEF 42% with new inferolateral wall motion abnormalities, normal RV systolic function, severe mitral regurgitation, and small pericardial effusion. After treatment of his GIB by IR and GI, he underwent an urgent LHC which showed 30% stenosis in proximal LAD, 70% in LADD2, and 95% in distal RCA. Coronary spasm was noted in all vessels. Intracoronary nitroglycerin and nicardipine were administered with significant improvement in spasm and resolution of STE on EKG. Vasopressors were quickly weaned off after. He was eventually stabilized, extubated, and started on an oral nitrate and calcium channel blocker. Repeat TTE showed normalized systolic function without any wall motion abnormalities. Case Media ABClick to Enlarge A. Baseline ECG - atrial fibrillationB. ECG with inferior STEMI CORS - left system CORS- RCA pre-vasodilator CORS- RCA post-vasodilator Episode Schematics & Teaching The CardioNerds 5! – 5 major takeaways from the #CNCR case What are the cardiac manifestations of hemochromatosis? Cardiac hemochromatosis encompasses cardiac dysfunction from either primary or secondary hemochromatosis. Initially, hemochromatosis leads to diastolic dysfunction and arrhythmias. In later stages, it can lead to dilated cardiomyopathy. Diagnosis of iron overload is established by elevated transferrin saturation (>55%) and elevated serum ferritin (>300 ng/mL). Genetic testing for mutations in the HFE gene should be pursued. Cardiac MRI with measurement of T2* relaxation times is the diagnostic test of choice as it can both detect and quantify myocardial iron overload. The iron content in the myocardial tissue is inversely proportional to the time constant of decay for relaxation time. Thus the higher the iron content, the shorter T2* relaxation time. What are the causes of ST-segment elevation on EKG besides acute plaque rupture or vasospasm? Pericarditis: in acute pericarditis, ST elevation can be seen diffusely in all leads, with PR segment depression (except lead aVR +/- V1). The diffuse ST elevations are due to involvement of subepicardial layer of the ventricular wall. The PR depressions are due to involvement of the subepicardial layer of the atrial wall. Stress CM: The ECG findings of stress cardiomyopathy may be indistinguishable from STEMI secondary to acute plaque rupture. Brugada syndrome: >2 mm ST-segment elevation in the right precordial leads followed be a negative T wave can be seen in patients with Type 1 Brugada. Type 2 and Type 3 Brugada will have STE as well but with different morphologic criteria. Electrolyte abnormalities: hyperkalemia can sometimes cause ST elevation. Other EKG findings of hyperkalemia include widened QRS, tall and peaked T waves, low-amplitude or lack of P waves, high grade AV Block, sine wave, and/or ventricular fibrillation or PEA. Pulmonary embolism: the classic EKG features of PE are S1Q3T3 with signs of RV strain (RBBB, RAD) though these are neither sensitive or specific. Sometimes, ST elevation in aVR and right-sided precordial are seen in massive PE due to RV overload, dilation, and/or ischemia (see the Cedars-Sinai episode for more details!). Cardioversion: striking ST-segment elevation, often >10mm, can be seen after cardioversion but only lasts 1-2 minutes. Raised ICP: can mimic acute myocardial infarction with widespread T-wave inversions +/- STE (or depression). Other non-cardiac causes, albeit rare causes, include significant gastrointestinal visceral distension, pneumonia, and pancreatitis. What are the two types of ischemic mitral regurgitation (IMR)? IMR is often a complication of ischemic heart disease and is associated with a worse prognosis across a variety of settings. Ischemic MR can occur due to a primary cause (e.g., abnormality of the valve apparatus and specifically papillary muscle rupture) or secondary cause (e.g., acutely from ischemia and chronically from a complex pathophysiologic changes). In chronic IMR, regional and/or global LV systolic dysfunction and ventricular remodeling can cause restricted leaflet motion. There can be outward papillary muscle displacement and when this happens, mitral leaflet coaptation moves apically away from the mitral annulus. Further, scarring of the papillary muscles may produce further mitral leaflet tethering and LV dilation can lead to mitral annular dilation. The posterior mitral annulus may contract less as well (which contributes to as much as 25% of the closure of the mitral orifice during systole). The ultimate results is poor leaflet coaptation and mitral regurgitation. MR secondary to papillary muscle rupture after an acute MI will almost certainly require surgery; while secondary MR from acute ischemia will often respond to revascularization. The treatment of chronic ischemic MR is a topic for another Cardionerds Episode so stay tuned! What's the pathogenesis of coronary vasospasm? In coronary vasospasm, the coronary arteries – and specifically the vascular smooth muscle layer – constricts due to various causes including emotional distress, changes in sympathetic tone, cocaine, or cigarette smoking, leading to myocardial ischemia. The causes and mechanisms of coronary vasospasms are still poorly understood but there are a few potential mechanisms proposed. Autonomic nervous system: increase in sympathetic tone can induce coronary vasospasms. Vasospasms more commonly occur at night during rapid eye movement sleep, when a reduction in vagal activity is associated with an increase in adrenergic activity. Inflammation: chronic inflammation and cigarette smoking are shown to be associated with vasospasm. Patients with vasospasm are found to have elevated hs-CRP, IL-6, and peripheral WBC. Other mechanisms have also been proposed including smooth muscle cell hypercontractility, oxidative stress, and genetics What's the treatment for coronary vasospasm? Any factor that may precipitate coronary vasospasm, especially smoking, should be avoided. There are additionally certain medications that should be avoided including non-selective beta blockers like propranolol and triptans. For medical treatment, long-acting calcium channel blockers can be used, especially taken at nighttime when attacks of coronary vasospasm are frequent Long-acting nitrates can also be added to prevent recurrent attacks if calcium channel blockers alone are inadequate References Gulati, V., Harikrishnan, P., Palaniswamy, C., Aronow, W. S., Jain, D., & Frishman, W. H. (2014). Cardiac involvement in hemochromatosis. Cardiology in review, 22(2), 56–68. Wang, K., Asinger, R. W., & Marriott, H. J. (2003). ST-segment elevation in conditions other than acute myocardial infarction. The New England journal of medicine, 349(22), 2128–2135. Báez-Ferrer, N., Izquierdo-Gómez, M. M., Marí-López, B., Montoto-López, J., Duque-Gómez, A., García-Niebla, J., Miranda-Bacallado, J., de la Rosa Hernández, A., Laynez-Cerdeña, I., & Lacalzada-Almeida, J. (2018). Clinical manifestations, diagnosis, and treatment of ischemic mitral regurgitation: a review. Journal of thoracic disease, 10(12), 6969–6986. Hung, M. J., Hu, P., & Hung, M. Y. (2014). Coronary artery spasm: review and update. International journal of medical sciences, 11(11), 1161–1171. Slavich, M., & Patel, R. S. (2016). Coronary artery spasm: Current knowledge and residual uncertainties. International journal of cardiology. Heart & vasculature, 10, 47–53.

Oct 22, 2020

CardioNerds (Amit Goyal & Daniel Ambinder) join Summa Health cardiology fellows (Jack Hornick, Phoo Pwint Nandar, and Sideris Facaros) for a hike on the Towpath Trail at Cuyahoga Valley National Park in Akron, Ohio! They discuss an informative case of Arrhythmogenic Right Ventricular Cardiomyopathy (ARVC) complicated by ventricular tachycardia & cardiogenic shock. Dr. Kenneth Varian provides the E-CPR and program director, Dr. Marc Penn provides a message for applicants. Episode notes were developed by Johns Hopkins internal medicine resident, Eunice Dugan, with mentorship from University of Maryland cardiology fellow Karan Desai. Jump to: Patient summary - Case media - Case teaching - References Episode graphic by Dr. Carine Hamo CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademySubscribe to our newsletter- The HeartbeatSupport our educational mission by becoming a Patron!Cardiology Programs Twitter Group created by Dr. Nosheen Reza Patient Summary A female in her 40s with no past medical history presented 6 years prior with acute onset dizziness, palpitations and fatigue without chest pain. She had no family history of arrythmias, SCD, or prior syncope. Her heart rate was 170 bpm and EKG showed wide complex, regular tachycardia felt to be VT. She underwent synchronized cardioversion to sinus rhythm. Her baseline EKG showed sinus bradycardia with low voltage, incomplete RBBB, and ventricular ectopy. Labs were unrevealing, and social history was negative for toxic insults or illicit substance abuse. TTE showed preserved LVEF and normal valves, but RV was dilated with decreased systolic function. LHC was without obstructive coronary disease. She was diagnosed with ARVC and received an ICD for secondary prevention. She was discharged on sotalol for arrythmia management. Her genetic testing later returned positive for uncertain significance in the DSP gene and JUP gene, both commonly implicated in ARVC. She was followed in the outpatient setting for 5 years with no apparent shocks. Six years later, she presented with acute onset dizziness and palpitations similar to her initial presentation. EKG showed a wide complex tachycardia at 170 bpm treated with amiodarone and cardioversion. On ICD interrogation, she was found to have had several episodes of VT, but at a rates below the VT detection zone programmed in the ICD. Subsequent RHC showed significantly depressed cardiac index and RV dysfunction. She underwent successful inpatient VT ablation. She was then discharged home with plans for close follow up; however, 2 days later, she started feeling nauseous with fatigue and abdominal pain. She was sent straight to the nearest transplant-capable hospital where she was found to be in cardiogenic shock. She was admitted to ICU and started on inotropes. Due to refractory shock, she was cannulated for VA ECMO and successfully underwent cardiac transplantation two days later. Case Media 123Click to Enlarge A. Post cardioversion ECG: NSR, low voltage, incomplete RBBB, PVCB. TTE: RV enlargement C. TTE: Tissue Doppler velocity (S') low TEE Episode Schematics & Teaching The CardioNerds 5! – 5 major takeaways from the #CNCR case What is ARVC? Arrhythmogenic Right Ventricular Cardiomyopathy/Dysplasia (ARVC/D) is a heritable cardiac muscle disorder that classically involves the RV (though LV involvement is increasingly being recognized) marked by loss of healthy myocardium and replacement with fibrofatty tissue predominantly due to genetic defects in both desmosomal and non-desmosomal proteins. Clinical manifestations include RV dysfunction, ventricular arrhythmias, and sudden cardiac death (SCD). This is a progressive disease that can affect the epicardium and/or mid-myocardium first and then move towards the sub-endocardium. It affects approximately 1 in 5000 individuals and is an important cause of (SCD) in young patients. 50% of patients have a positive family history and it is thought to be inherit in an autosomal dominant fashion, however prevalence is underestimated due to incomplete penetrance. Interestingly, males are more affected than females possibly due to interaction of sex hormones with pathophysiology or historically different levels of participation in competitive sports among men and women. The differential for ARVC should include Uhl's anomaly, myocarditis, sarcoidosis, and Brugada syndrome among other considerations. What genes are implicated and what is the pathophysiology? While 20-30% of ARVC is due to non-desmosomal gene variants (e.g., desmin, Titin) and non-genetic causes, 40-50% is due to autosomal dominant gene mutations that encode desmosomal proteins. These include plakophilin 2 PKP2 (in 10 to 45% of patients), followed by desmoplakin DSP (10 to 15%), desmoglein 2 DSG2 (7 to 10%), and desmocollin 2 DSC2 (2%). Rarely, there can be an autosomal recessive inheritance pattern, including Naxos disease (first recognized in the Cycladian Islands in the Aegean Sea) characterized by ARVC along with "wooly hair" and palmoplantar hyperkeratosis. Our understanding of the genetic underpinnings of ARVC continues to evolve. Desmosomes play a major role in intercellular adhesion and synchronized activation and signaling between myocytes. Defective desmosomes disrupt intercellular junctions which lead to myocyte detachment and myocyte death, and this process is especially exaggerated by mechanical stress like exercise. Athletes often have severe disease, possibly a result of high-intensity mechanical stress during exercise. Other resultant features of defective cardiac myocyte signaling is increased expression of adipogenic and fibrogeneic genes, resulting in the hallmark pathologic correlate of fibrofatty replacement of muscle tissue. The fibrofatty scar tissue that replaces the myocardium slows conduction and allows for formation of macro-entry circuits that lead to the propagation of arrythmias. Furthermore, dysregulation of otherwise synchronized excitability due to abnormal cellular connections increase propensity for fatal arrhythmias. What EKG findings may be seen in ARVC? EKG is an important tool in screening since 85-90% of patients will have at least one of the findings of ARVC. However, it is important to remember that the findings may evolve over time, including a normal ECG at presentation and thus serial re-assessment is crucial. ECG changes include inverted T-waves in the right precordial leads, which have been correlated with RV enlargement and risk for ventricular arrhythmias. T wave inversions (TWI) are present in up to 87% of adult patients with ARVC, but can be especially challenging to interpret in athletes who may have TWIs as normal variants in 5% of white athletes and 25% of black athletes. The preceding ST-segment may provide a clue as to whether the TWI is abnormal, as ARVC patients with precordial TWI often have an isoelectric ST-segment while athletes have preceding convex ST-segment elevation. Other findings include: (1) prolonged S-wave upstroke (≥55 milliseconds) in the absence of a RBBB (~90% of patients w/o a RBBB) (2) Epsilon wave (~ 5 to 30% of patients) which is a distinct positive deflection at the end of the QRS complex best seen in V1 and/or V2 reflecting delayed activation of some parts to of the RV. Fontaine bipolar precordial leads (repositioning of the limb leads) may help increase the sensitivity for detecting epsilon waves. Isoproterenol infusion can be used to induce ventricular arrhythmias in suspected patients How can we diagnose ARVC? In the "concealed phase," patients are often asymptomatic but are still at risk of sudden cardiac death, especially during exertion. Furthermore, in the early stages of disease, structural changes may be subtle (or even absent) and confined to a focal area of the RV. In the "electrical phase," patients can present with symptomatic ventricular arrhythmias and RV structural abnormalities that are detected by cardiac imaging. Sports and rigorous exercise increase risk of SCD and contribute to disease progression. Common first symptoms are palpitations and effort-induced syncope, though SCD can also be the first presentation. In the later stages, diffuse disease is possible with biventricular heart failure. In patients in whom there is a clinical suspicion for ARVC (e.g., positive family history, exercise-induced palpitations, unexplained right precordial TWI, patients who present with unexplained ventricular arrhythmias, and/or SCD), the diagnosis frequently requires multiple diagnostic tests. The 2010 revised Task Force Criteria is used to confirm the diagnosis of ARVC, though proposed changes continue to arise as our understanding of ARVC evolves. The criteria require a demonstration of structural, functional, and electrophysiological abnormalities that reflect underlying histological changes. Thus, the criteria include parameters defining (1) global and/or regional dysfunction and structural changes; (2) tissue characterization of the walls; (3) repolarization abnormalities on ECG; (4) depolarization/conduction abnormalities on ECG; (5) arrhythmias; and (6) family history. Criteria for diagnosis is based on meeting two major, one major and two minor, or four minor criteria. Cardiac MRI is the preferred imaging tool because it can quantitatively assess phenotypic structural and functional abnormalities such as global dilatation and/or systolic akinesia/dyskinesia. In suspected ARVC, late gadolinium enhancement can represent fibrofatty infiltration. It is important to note that endomyocardial biopsy is not indicated as routine testing, but may be considered to aid in securing a diagnosis amongst competing diagnoses. How is ARVC managed? In patients with suspected and/or confirmed ARVC, there are 5 pillars of management: Prevent sudden cardiac death.

Oct 20, 2020

CardioNerds (Amit Goyal & Daniel Ambinder) join Scripps cardiology fellows (Christine Shen and Andrew Cheng) for some Cardiology and California Burritos in San Diego! They discuss an informative case of Wet Beriberi and Stiff Left Atrial Syndrome. Dr. Thomas Heywood provides the E-CPR and program director Dr. Malhar Patel provides a message for applicants. Episode notes were developed by Johns Hopkins internal medicine resident Tommy Das with mentorship from University of Maryland cardiology fellow Karan Desai. Jump to: Patient summary - Case media - Case teaching - References Episode graphic by Dr. Carine Hamo The CardioNerds Cardiology Case Reports series shines light on the hidden curriculum of medical storytelling. We learn together while discussing fascinating cases in this fun, engaging, and educational format. Each episode ends with an “Expert CardioNerd Perspectives & Review” (E-CPR) for a nuanced teaching from a content expert. We truly believe that hearing about a patient is the singular theme that unifies everyone at every level, from the student to the professor emeritus. We are teaming up with the ACC FIT Section to use the #CNCR episodes to showcase CV education across the country in the era of virtual recruitment. As part of the recruitment series, each episode features fellows from a given program discussing and teaching about an interesting case as well as sharing what makes their hearts flutter about their fellowship training. The case discussion is followed by both an E-CPR segment and a message from the program director. CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademySubscribe to our newsletter- The HeartbeatSupport our educational mission by becoming a Patron!Cardiology Programs Twitter Group created by Dr. Nosheen Reza Patient Summary A woman in her mid-60s with history of rheumatic mitral stenosis s/p mechanical mitral valve replacement, HFpEF, and paroxysmal atrial fibrillation s/p ablation presents with subacute worsening dyspnea despite escalating diuretic doses. TTE shows an EF of 62%, normal gradients across the mitral valve without mitral regurgitation, and a dilated IVC. She is admitted with a presumed diagnosis of decompensated heart failure, and started given IV furosemide. Her symptoms slightly improve though do not resolve, and her creatinine increases from 1.4 to 2.1. In light of the unclear hemodynamic picture, a RHC is done, showing a RA pressure 9, RV pressure of 80/10, PAP 70/25 with mPAP 40, PCWP 30, SVR 872, CO 11 (by thermodilution), and CI 5.2. Notably, large V waves are noted on the RHC. Given concern for mitral regurgitation in the setting of large V waves, a TEE was pursued, which confirmed the lack of MR seen on TTE. Thus, her large V waves were felt to be due to stiff left atrial syndrome, and a cardiac CT showed a severely calcified "coconut left atrium". Labwork revealed a profoundly low thiamine level (21, with LLN of 70), raising concern for wet beri beri syndrome. The patient's unifying diagnosis was indolent left atrial syndrome that was exacerbated by high outout heart failure due to Wet Beri Beri syndrome. The patient received thiamine supplementation, and was diuresed to euvolemia with dramatic improvement in symptoms. A repeat RHC after thiamine replacement showed a CO of 5.7 and CI of 2.74 by thermodilution, demonstrating resolution of her high output heart failure. Case Media ABCDEFClick to Enlarge A. CXRB. ECGC. RHC: large V waves are noted on the RHCD. CO 11 and CI 5.2 by thermodilution pre-treatment E. Cardiac CT showed a severely calcified "coconut left atrium"F. Repeat CO of 5.7 and CI of 2.74 by thermodilution after thiamine replacement TTE 1 TTE 2 TEE 1 - Mitral Valve TEE 2 - Mitral Valve Cardiac CT Episode Schematics & Teaching Click to enlarge! The CardioNerds 5! – 5 major takeaways from the #CNCR case 1) This case featured a patient with Stiff Left Atrial Syndrome! Cardionerds, what the heck is that? Stiff Left Atrial Syndrome (SLAS) is fundamentally a disorder of atrial compliance, wherein a non-compliant left atrium (LA) leads to abnormal atrial diastole. During LV systole (atrial diastole), the LA receives blood from the low-resistance pulmonary veins. Under normal conditions, the LA pressures initially fall (x-descent). Then, as the atrium fills from both RV contraction and passive filling from the pulmonary veins, there is a steady and modest rise in LA pressure (v-wave). In patients with decreased LA compliance, the V-wave may be accentuated. In SLAS, left atrial compliance is significantly decreased, leading to very large v-waves that reflect the inability to accommodate LA filling and the steepened slope of the pressure-volume curve (see the below diagram from Urey et al). This leads to dramatically increased LA pressures during LV systole (especially in late LV systole), contributing to post-capillary pulmonary hypertension over time and symptoms of dyspnea on exertion. 2) Which patients are at risk of developing SLAS, how is it diagnosed, and how is it managed? Stiff Left Atrial Syndrome was first described in the late 1980s as a complication of mitral valve surgery, and has been increasingly recognized as a complication of left atrial ablation procedures leading to atrial fibrosis. While the condition is relatively rare (occurring in ~1.4% of patients following ablation), significant heart failure symptoms and pulmonary hypertension can develop. While no diagnostic criteria exist, SLAS should be considered in patients with HFpEF, a small or calcified LA on imaging, and risk factors including mitral valve surgery and/or prior left atrial ablations. Invasive hemodynamics will show large v-waves in the absence of mitral regurgitation (or disproportionate to the degree of MR) and an elevated PCWP out of proportion to the LVEDP. It is important to exclude pulmonary vein stenosis, another potential complication of ablation. Management consists primarily of diuretics and reducing ventricular afterload as tolerated, though an intra-atrial septostomy could be considered in refractory cases. Notably, SLAS may be asymptomatic in many patients due to the compliance of the pulmonary venous vascular system, which can store blood volume without significant increases in pressure. However, this compliance could become overwhelmed in certain stressed states or exercise. 3) Our patient experienced a stressor in the form of high output heart failure; what is the pathophysiology of high output heart failure, and what is your differential for high output heart failure? While a number of causes for high output heart failure exist, they share an underlying pathophysiology of excessively decreased systemic vascular resistance and increased metabolic demand. The persistently low SVR leads to decreased ventricular afterload, increased LV emptying and thus increased stroke volume and cardiac output. This subsequently leads to increased preload and symptoms of congestive heart failure. Furthermore, increased oxygen demands requires increased cardiac output. Additionally, the persistently low SVR causes low renal perfusion pressure (renal hypoperfusion) which leads to RAAS activation and volume expansion Diagnosis is based on echocardiographic evaluation, RHC hemodynamics, and an identified cause of a high output state. TTE may show normal or reduced ejection fraction; additional findings may include a dilated IVC, RV enlargement or dysfunction, elevated estimated pulmonary artery pressures, and/or LV enlargement. RHC typically shows a CO > 8 L/min or a CI > 4 L/min/m2, though these cutoffs are not absolute. The differential for high output heart failure includes etiologies secondary to predominantly low SVR (e.g., obesity, cirrhosis, AV fistula) versus those secondary to increased metabolic drive (e.g., hyperthyroidism, myeloproliferative disorders). See the CNCR episode from the Johns Hopkins Hospital for more details! 4) How does thiamine deficiency lead to high output heart failure? Thiamine is vital to aerobic metabolism in the Krebs cycle and the Pentose Phosphate Pathway. In states of thiamine deficiency, anaerobic metabolism is favored over aerobic metabolism, leading to increased levels of lactate and pyruvate. This leads to a decrease in adenosine triphosphate (ATP) and increase in adenosine monophosphate (AMP), which is released into skeletal muscle as adenosine. This release of adenosine leads to vasodilation and decreased systemic vascular resistance through shunt physiology. Arterial hypoperfusion of the kidneys leads to activation of the RAAS and expansion of plasma volume. Increased oxygen demand lead to an increased cardiac output. Importantly, CO by thermodilution and Fick may be discrepant in Beriberi! This is because mitochondria are unable to utilize O2 by performing aerobic metabolism. Thus, less oxygen is extracted from the blood, and venous oxygen saturations will be relatively elevated. This may leads to an erroneously elevated CO by Fick's method as compared to thermodilution! 5) Lets bring it all together! Cardionerds, what is your illness script for Beriberi? Pathophysiology: As detailed above, thiamine deficiency causes an increase in anaerobic metabolism, increased oxygen demand and systemic vasodilation through increased adenosine levels. Epidemiology: Patient populations at risk for severe thiamine deficiency include patients with severe malnutrition, chronic alcohol use, incarceration, social isolation, refugee populations, history of bariatric surgery, or chronic loop diuretic use. Notably, 90% of patients on diuretics can develop some level of thiamine deficiency. Signs/Symptoms: "Dry" beriberi involves symmetrical peripheral neuropathy, primarily in the distal extremities.

Oct 19, 2020

CardioNerds (Amit Goyal & Karan Desai) join University Hospitals Cleveland Medical Center cardiology fellows (Tarek Chami, Jamal Hajjari, and Haytham Mously) for some amazing pizza and coffee in Cleveland, Ohio! They discuss an important case of effusive constrictive pericarditis. Dr. Brian Hoit provides the E-CPR and assistant program director Dr. Claire Sullivan provides a message for applicants. We are grateful to chief fellow Scott Janus for his leadership in planning this episode! Episode notes were developed by Johns Hopkins internal medicine resident Colin Blumenthal with mentorship from University of Maryland cardiology fellow Karan Desai. Jump to: Patient summary - Case media - Case teaching - References Episode graphic by Dr. Carine Hamo The CardioNerds Cardiology Case Reports series shines light on the hidden curriculum of medical storytelling. We learn together while discussing fascinating cases in this fun, engaging, and educational format. Each episode ends with an “Expert CardioNerd Perspectives & Review” (E-CPR) for a nuanced teaching from a content expert. We truly believe that hearing about a patient is the singular theme that unifies everyone at every level, from the student to the professor emeritus. We are teaming up with the ACC FIT Section to use the #CNCR episodes to showcase CV education across the country in the era of virtual recruitment. As part of the recruitment series, each episode features fellows from a given program discussing and teaching about an interesting case as well as sharing what makes their hearts flutter about their fellowship training. The case discussion is followed by both an E-CPR segment and a message from the program director. CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademySubscribe to our newsletter- The HeartbeatSupport our educational mission by becoming a Patron!Cardiology Programs Twitter Group created by Dr. Nosheen Reza Patient Summary A woman in her mid-70s presented to clinic with subacute onset shortness of breath. Her past medical history includes metastatic breast cancer s/p mastectomy, chemo/radiation, and hormonal therapy. Exam notable for tachycardia without hypoxia, muffled heart sounds, JVD with Kussmaul's sign, and 1+ LE edema. The patient was sent to the ED for evaluation of possible pericardial effusion. CTA chest in ED did not demonstrate a PE, but did show bilateral pleural effusions, and a moderate pericardial effusion with evidence of metastatic disease extending into the mediastinum. TTE obtained showing normal LVEF, moderate pericardial effusion with thickened pericardium, and significant respirophasic tricuspid and mitral inflow variations. Pulsus paradoxus was manually checked and found to be 16 mmHg. Due to concern for cardiac tamponade, she was taken to the cath lab for a RHC and pericardiocentesis. RHC prior to pericardiocentesis showed elevated left and ride sided filling pressures, blunted y decent in the RA, and equalization of diastolic pressures. Pericardiocentesis yielded 200 cc of bloody fluid with improvement, but continued elevation, in her L and R sided pressures. Blunted y decent did give way to a now rapid y descent concerning for constrictive pericarditis. She then underwent a cardiac MRI showing respirophasic septal motion suggestive of interventricular dependence and >1 cm thick pericardium with LGE c/w inflammation. Unfortunately, cytology of pericardial fluid was c/w a malignant effusion and despite treatment with a few months of anti-inflammatory therapy her symptoms did not improve. She then underwent a pericardial stripping with subsequent resolution of her symptoms. As her symptoms and hemodynamics were related to both the effusion and constriction, she was ultimately diagnosed with effusive constrictive pericarditis. Case Media ABCDEFGHIJKLMNOClick to Enlarge A. ECGB. CXRC-F. TTE (inflow velocities (mitral and tricuspid), IVC sniff test G-L: Right heart catheterization tracings M-N: Post pericardiocentesis TTE: Tissue Doppler O: Cardiac MRI CT Scan TEE - 1 TTE - 2 TTE - 3 TTE -4 CMR -1 CMR - 2 Episode Schematics & Teaching Click to enlarge! The CardioNerds 5! – 5 major takeaways from the #CNCR case What is cardiac tamponade, what causes it, and how does it lead to hypotension? The pericardial cavity typically holds 50 cc of fluid, which acts as a lubricant for the beating heart. Accumulation of additional fluid in this space can increase intrapericardial pressure and cause compression of the cardiac chambers. Rapid accumulation of small amounts of fluid can lead to tamponade as the pericardium will not have time to expand. In instances of a slow accumulation, large volumes might accumulate before tamponade occurs as the pericardium will expand to accommodate the fluid. Many conditions can cause tamponade. The most common are malignancy (>50% of all cases), infection (viral most common, though TB is common in developing countries), trauma/post procedural (e.g. cardiac surgery, pacemaker placement), uremia, rheumatologic (e.g. SLE, RA), drug induced (e.g. hydralazine, procainamide), and radiation-induced. Note the epidemiology is different from causes of pericarditis without tamponade. Increasing pericardial pressure leads to a compensatory increase in diastolic pressure in all chambers until they become similar to the pericardial pressure. This happens more rapidly in the right side of the heart due to lower diastolic pressures in these chambers. The elevated intracardiac diastolic pressures reduces the driving pressure for filling (Flow = pressure gradient / resistance and so ↓∆P = ↓Flow ); this reduces diastolic filling (preload) and a causes a compensatory increase in contractility and heart rate to maintain stroke volume and cardiac output (CO = HR x SV so as SV decreases, the HR increases). As diastolic filling continues to decrease the transmural distending pressure of the RA and RV will also decrease and eventually lead to diastolic collapse. As reviewed in previous posts (Mayo and Tennessee), as ventricular interdependence worsens, left ventricular cardiac output can be further compromised and contribute to hypotension. Enjoy Episodes #58 and #59 discussing constrictive pericarditis. Tamponade can be a difficult clinical diagnosis. How is it diagnosed, what are some of the basic clinical markers of cardiac tamponade, and which are most useful in diagnosis? Though definitive diagnosis requires pericardiocentesis with hemodynamic and clinical improvement, there are many features that are useful for identifying tamponade. Unfortunately, no one clinical or echocardiographic feature is diagnostic of tamponade and a clinical diagnosis relies on the assimilation of multiple abnormalities. Beck's triad of hypotension, jugular venous distension, and muffled heart sounds Originally described in 1935 by Dr. Claude Beck, it focuses on these signs of tamponade, which were derived from surgical patients and are more characteristic of acute tamponade from trauma or cardiac/aortic rupture. Though ~90% of patients in trauma series have at least one of these findings, only about ~30% have all three. Muffled heart sounds and hypotension are both poorly sensitive findings, making the sensitivity of the overall triad poor. Tachycardia Though not specific, tachycardia is a very sensitive marker of cardiac tamponade as in some series it is present in 81-100% of patients with a pooled sensitivity of around 80%. Elevated JVP Elevated JVP is one of the key findings in tamponade and is present in almost all cases. Increased early diastolic pressure limits filling during this period, blunting the y descent. Studies show sensitivity ranges from 53-88% with a pooled average of 75%. Kussmaul's sign Kussmaul's sign is the failure of the JVP to fall during inspiration. This is rarely seen in cardiac tamponade; it is much more common in constrictive pericarditis, where it can be seen in up to 50% of cases. EKG findings of low voltage or electrical alternans As fluid builds around the heart it can insulate the heart's electrical activity from the EKG leads leading to low voltage on the EKG. Additionally, as the heart oscillates within the distended pericardial sack, the QRS amplitude can oscillate, which is called electrical alternans. As low voltage can be seen in a variety of conditions it is poorly specific, but sensitivity is around 70%. Electrical alternans on the other hand is rarely seen in tamponade, but if present it has a PPV > 95%. Enlarged cardiac silhouette on CXR The cardiac silhouette on a CXR does not appear enlarged until a pericardial effusion is around 200 mL. Given that many conditions also cause an enlarged silhouette it has both poor sensitivity and specificity. What is a pulsus paradoxus and what is the pathophysiology? How do you measure it and how clinically useful is it in the diagnosis of tamponade? What conditions might cause it to be absent in tamponade? In a normal heart, inspiration decreases intrathoracic pressure, thus increasing right-sided filling. As the RV stretches to accommodate the volume, the interventricular septum bulges towards the left causing reduced left-sided filling and therefore a drop in blood pressure (this is ventricular interdependence). During expiration the opposite happens and the blood pressure increases. This process is exaggerated in cardiac tamponade as both ventricles are completing for a limited amount of space, which leads to a larger than normal drop in blood pressure during inspiration. This exaggerated drop is called pulsus paradoxus (though pulsus exaggeratus may be a better name!). Pulsus paradoxus can be measured with a blood pressure cuff while a patient is breathing normally.

Oct 14, 2020

CardioNerds (Amit Goyal & Daniel Ambinder) join University of Michigan cardiology fellows (Apu Chakrabarti, Jessica Guidi, and Amrish Deshmukh) for some craft brews in Ann Arbor! They discuss a challenging case of Ventricular Septal Rupture after acute MI. Dr. Kim Eagle, editor of ACC.org & host of Eagle's Eye View Podcast, and Dr. Devraj Sukul provide the E-CPR and message for applicants. Episode notes were developed by Johns Hopkins internal medicine resident, Eunice Dugan, with mentorship from University of Maryland cardiology fellow Karan Desai. Jump to: Patient summary - Case media - Case teaching - References Episode graphic by Dr. Carine Hamo The CardioNerds Cardiology Case Reports series shines light on the hidden curriculum of medical storytelling. We learn together while discussing fascinating cases in this fun, engaging, and educational format. Each episode ends with an “Expert CardioNerd Perspectives & Review” (E-CPR) for a nuanced teaching from a content expert. We truly believe that hearing about a patient is the singular theme that unifies everyone at every level, from the student to the professor emeritus. We are teaming up with the ACC FIT Section to use the #CNCR episodes to showcase CV education across the country in the era of virtual recruitment. As part of the recruitment series, each episode features fellows from a given program discussing and teaching about an interesting case as well as sharing what makes their hearts flutter about their fellowship training. The case discussion is followed by both an E-CPR segment and a message from the program director. CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademySubscribe to our newsletter- The HeartbeatSupport our educational mission by becoming a Patron!Cardiology Programs Twitter Group created by Dr. Nosheen Reza Patient Summary A male in his 60s with medical history of obesity and GERD presents with five days of progressive chest pressure radiating to bilateral arms and associated with dyspnea on exertion. Due to worsening chest pain with new lightheadedness, he decided to come to the ED. His presentation to the hospital was delayed due to fear of contracting COVID-19. In the ED, patient was afebrile, blood pressure 96/56, HR 137, RR 22, and oxygen saturation 94% on room air. On exam, he was ill appearing, acutely distressed, and altered. He had a 3/6 mid systolic murmur loudest at L sternal border, JVP to 10 cm H2O and had crackles up to mid-lung fields. His extremities were cool to touch. Labs notable for Cr 1.5, High-Sensitivity Troponin-T up to 5756, and lactate 3.9. EKG showed incomplete RBBB, PVCs, and ST elevations in the inferior leads with depressions in lateral and precordial leads. Coronary Angiography showed mid-RCA occlusion with faint L to right collaterals. He underwent PCI with restoration of TIMI 3 flow. After PCI, he continued to be hypotensive requiring IABP and norepinephrine. PA catheter demonstrated (in mmHg): RA 26, RV 63/29 (31), 55/36 (44), PCWP 29, and CO 5 L/min, CI 2.2, and SVR 467. Shunt run of mixed venous O2 saturation showed: SVC 71%, RA 72%, RV 62%, PA 85% with oxygen step up in the R-sided circuit. Left ventriculogram then confirmed septal rupture with contrast extravasation from LV into RV. Due to worsening shock, he was stabilized on VA ECMO which was complicated by hemolysis and acute renal failure requiring CVVHD. On day 7 after presentation, he underwent surgery which revealed a large 6x6 cm ventricular septal defect on the posterior aspect of the septum and repaired with a large bovine pericardial path. He was eventually discharged after a prolonged stay and repeat TTE on follow up showed biventricular dysfunction and residual 1cm VSD. Case Media ABCDClick to Enlarge A. ECG: Incomplete RBBB, PVCs, and ST elevations in the inferior leads with depressions in lateral and precordial leads. B. Coronary angiography: mid-RCA occlusion with faint L to right collaterals.C-D. A large (6x6cm) VSD was found at the posterobasal aspect of the septum. Infarcted tissues were removed and a large bovine pericardial patch was used to repair the defect (due to the size of the defect, there was very little viable septum remaining and the patch had to be sewn directly into the LV and RV walls). LV gram performed showing a left to right shunt. TEE -1 TEE - 2 Episode Schematics & Teaching Click to enlarge! The CardioNerds 5! – 5 major takeaways from the #CNCR case Classification and Management of Post-AMI VSR Why and in whom should we worry about VSR? Ventricular Septal Rupture or VSR is rare in the era of early reperfusion strategies. Historical incidence of VSR after AMI was thought to be 1-2% and has decreased to between 0.17% and 0.3%. It can be attributed to early identification and restoration of flow in the infarct related artery (IRA). Although the incidence has decreased, the mortality remains high (41-80%). Risk factors include older age, female sex, history of heart failure, and chronic kidney disease. If VSR does occur it tends to be in a patients presenting with their first MI with delayed, failed or no reperfusion therapy. The presence of collaterals is likely protective against developing VSR and reducing size of infarct. How do we recognize and diagnose VSR after AMI? Abrupt hemodynamic compromise after revascularization or refractory shock with AMI should prompt suspicion for mechanical complications, including VSR. Note: some patients may be stable early in their course. The classic presentation would be recurrent chest pain and hypotension several days after an MI, along with a new harsh holosystolic murmur usually best heard at the left lower sternal border sometimes accompanied by a thrill. Identifying this murmur requires a thorough baseline examination and frequent re-evaluation. Note, the absence of this murmur does not rule out VSR as the murmur may not be audible in a large VSR. In terms of making the diagnosis of VSR, TTE is the starting point. The location of the VSR will likely depend on the infarct related artery (see below), but the two most common locations are basal inferoseptal and anteroapical septal walls. To identify the VSR it is critical to use color doppler in the area of interest and to lower the Nyquist limit to readily identify lower velocity flow with better definition. TTE is also critical to define worsening pulmonary hypertension and/or left and right ventricular dysfunction as these are prognostic factors. When there are poor image quality and the defect cannot be readily identified, TEE may be necessary. If a RHC is available, we can identify a left to right shunt via an oxygen step-up. Normal oxygen saturation in the RV is typically 64 to 68%. When there is an increase in oxygen saturation from RA to RV (or PA) of greater than 5% that can be suggestive of a VSR. Further, we can calculate the shunt fraction to quantify the extent of the shunt. During a left heart catheterization, LV ventriculography can identify the VSR When does VSR occur post AMI and how does IRA relate to VSR location? It is historically thought to occur between 3-6 days after AMI, however newer studies show earlier development with one study showing median time of 16 hours after AMI. This may be related to more awareness, increased access to echo, or a change in the presentation of VSR due to earlier reperfusion strategies. The LAD and the RCA are the arteries most commonly implicated in the development of a VSD. Remember, anatomically, the LAD supplies the apical portion of the ventricular septum and the RCA gives posterior septal perforators that supply the basal inferoseptal wall. These areas are the most common locations for VSR after a transmural infarct as they are located at the border zone of a myocardial infarct. Remember the defect can be simple or complex. A complex VSR is associated with multiple areas and various dissection planes that track along the myocardium. What is the pathophysiology and classification for VSR We can classify VSR in 2 ways: the Becker and Mantgem system and simple vs. complex. The Becker and Mantgem system was originally made for cardiac free wall rupture, but is also used for pathological classification of VSR. There are 3 mechanisms and pathophysiologic findings that correlate with temporal presentation. Type 1 : Occurs acutely ( 24 hours) typically shows slow erosion of infarcted myocardium due to neutrophilic infiltration of ischemic/necrotic tissue Type 3: Occurs late following an MI and after aneurysm formation and then subsequent rupture In the simple vs. complex VSR classification, we classify VSR as simple if there is a direct connection between the LV and RV. Meanwhile, a complex VSR is a serpiginous connection (multiple planes) and more likely caused by hemorrhage. What are the goals of management and definitive therapy? Surgical repair is the ideal definitive treatment, though mortality is very high. Patients with worse outcomes after surgery are female, older, RV dysfunction and have higher level of cardiac circulatory compromise. Newly infarcted tissue is weak and friable, may not hold sutures well, and is prone to repeat defects. Successful repair requires complete debridement of necrotic tissue and sparing of healthy tissue which may be difficult to differentiate in the early stages after infarction. Surgical mortality appear to be higher with basal inferoseptal rupture associated with inferior MI, as these patients may need concomitant mitral valve repair as they often have ischemic MR as well Timing of surgery is a complex issue and there are no clear guidelines for timing of surgery and therefore it is an individualized decision.

Oct 13, 2020

CardioNerds (Amit Goyal & Daniel Ambinder) join University of Connecticut (UCONN) cardiology fellows (Mansour Almnajam, Justice Oranefo, Yasir Adeel, and Srinivas Nadadur) as they enjoy the amazing view from the Heublein tower! They discuss a challenging case of left ventricular free wall rupture & pseudoaneurysm as a complication of a STEMI. Dr. Peter Robinson provides the E-CPR and program director Dr. Joyce Meng provides a message for applicants. Episode notes were developed by Johns Hopkins internal medicine resident Bibin Varghese with mentorship from University of Maryland cardiology fellow Karan Desai. Jump to: Patient summary - Case media - Case teaching - References Episode graphic by Dr. Carine Hamo The CardioNerds Cardiology Case Reports series shines light on the hidden curriculum of medical storytelling. We learn together while discussing fascinating cases in this fun, engaging, and educational format. Each episode ends with an “Expert CardioNerd Perspectives & Review” (E-CPR) for a nuanced teaching from a content expert. We truly believe that hearing about a patient is the singular theme that unifies everyone at every level, from the student to the professor emeritus. We are teaming up with the ACC FIT Section to use the #CNCR episodes to showcase CV education across the country in the era of virtual recruitment. As part of the recruitment series, each episode features fellows from a given program discussing and teaching about an interesting case as well as sharing what makes their hearts flutter about their fellowship training. The case discussion is followed by both an E-CPR segment and a message from the program director. CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademySubscribe to our newsletter- The HeartbeatSupport our educational mission by becoming a Patron!Cardiology Programs Twitter Group created by Dr. Nosheen Reza Patient Summary A man in his mid 50s with no significant PMH presented with a 10-day history of chest pain that progressed to acute pleuritic pain and shortness of breath in the past 24 hours. On arrival, he was hypothermic, in rapid atrial fibrillation with HR in the 130-150s, and an initial BP was not able to be obtained. He was tachypneic with labored breathing, lethargic, and cyanotic. Exam revealed markedly elevated JVP, cool extremities, and diminished breath sounds with bibasilar rales. Labs demonstrated leukocytosis, significantly elevated liver enzymes, troponin-I at 10.91, elevated NT-proBNP, and lactate at 6. ECG demonstrated tall, broad R-waves in V1-V4 with downsloping STD and upright T-waves concerning for a posterior infarct. He was immediately intubated, cardioverted into NSR, and started on vasopressors. Bedside echocardiogram demonstrated diffuse LV hypokinesis with akinesis of the inferolateral wall, LVEF 25-30%, and pericardial fluid with hyperechoic material adherent to the inferior wall as well as tamponade physiology. Chest CTA was negative for aortic dissection and confirmed hemopericardium. He was taken to the OR where he underwent a subxiphoid pericardial window. They found significant clot burden (both old and new), but no frank rupture. Adherent clot was not removed to prevent further hemodynamic compromise. Intraoperative TEE additionally demonstrated severe eccentric MR with partial posteromedial papillary muscle rupture. An IABP was placed and inotropic and vasoactive support was continued to temporize pending definitive therapy and the patient improved hemodynamically. Repeat TTE prior to surgery demonstrated a large apical and inferolateral pseudoaneurysm. Coronary angiogram revealed proximal occlusion of the LCx and diffuse three vessel coronary disease otherwise. He ultimately underwent CABG, mechanical mitral valve replacement, and pericardial patch repair of the ventricular pseudoaneurysm. Final diagnosis: Free Wall Rupture & Pseudoaneurysm. Thankfully, the patient ultimately made a complete recovery! Case Media ABCDEFClick to Enlarge A. ECG: tall, broad R-waves in V1-V4 with downsloping STD and upright T-wavesB. CXRC. CT angiogram thoracic aorta: Moderate sized hemopericardium with tamponade physiology. Transmural infarction of LV base to mid inferior wall. Circumflex occlusion just beyond the first obtuse marginal. Normal aorta without dissection or aneurysm.D-F. Coronary angiogram: LCx is occluded proximally, distal vessel fills via faint collaterals from the right, OM1: Fills via right to left collaterals. LAD: 70%, mid; 90%, apical, 1st diagonal: 50%, ostial; 60-70%, proximal; 90% of inferior subdivision, bifurcating vessel. RCA: (Dominant); 50%, mid: 40%, distal. PDA: 60%, proximal, small-caliber vessel. PLV: 60-70%, proximal TEE: Trans-gastric views TEE TEE: MV with color CORS: Occluded Lcx CORS: Obstructive CAD in LAD CORS: RCA TTE: PLA TTE: A4C TTE: A4C with contrast demonstrating an LV pseudoaneurysm Episode Schematics & Teaching Click to enlarge! The CardioNerds 5! – 5 major takeaways from the #CNCR case This patient presented with EKG showing a posterior myocardial infarction. Why was he not taken to the cath lab immediately for revascularization? Duration of ischemia, its relationship to infarct size, and the mortality benefit from reperfusion therapies are crucially related to time in the very early course of STEMI. However, this relationship breaks down in patients presenting late after a STEMI. In OAT (Occluded Artery Trial), hemodynamically stable patients who presented late (3-28 days) after a myocardial infarction with high risk features (e.g., proximal LAD occlusion with TIMI 0 to 1 flow) were randomized to PCI + optimal medical therapy (OMT) within 24 hours or OMT alone. There was no difference in the primary endpoint of all-cause mortality, nonfatal MI, or NYHA class III to IV heart failure. These findings are reflected in the ACC/AHA guidelines, where delayed PCI of a totally occluded infract artery >24 hours after STEMI in hemodynamically and electrically stable patients is given a Class III recommendation (no benefit). Although the patient presented with EKG findings concerning for a posterior STEMI, this was likely 10 days after his acute insult. In addition, his hemodynamic instability and bedside POCUS raised the concern for a mechanical complication of a STEMI. In a patient with suspected mechanical complication of acute MI, such as free wall rupture and acute MR, the priority of therapy is to rapidly identify the mechanical problem and perform emergency surgical therapy. Furthermore, the need for antiplatelet therapy following any PCI would complicate surgical planning. PCI may be helpful in patients with ischemia induced papillary muscle dysfunction ("ischemic MR"). However there is no role for immediate PCI when the mechanical integrity of the mitral valve has been compromised. This patient presented with hemodynamic instability and bedside POCUS revealed pericardial fluid with tamponade physiology. What are some causes of acute hemorrhagic pericardial effusion? When thinking about hemorrhagic pericardial effusions, expedited evaluation is critical. While there is overlap with traditional causes of pericardial effusion, some causes may need immediate intervention. Amongst these considerations are iatrogenic complication of cardiac surgery, cardiac catheterization, or electrophysiologic procedures. Other etiologies include complications of myocardial infarction including free wall rupture/pseudoaneurysm, complication of aortic dissection, and trauma. As with serous pericardial effusions, malignancy should remain on the differential, as well as tuberculosis in endemic areas. A CTA of the aorta ruled out dissection but showed a moderate sized hemopericardium raising concern for a mechanical complication of posterior MI, specifically a free wall rupture (FWR). What are the risk factors for a FWR after an MI? Ventricular free wall rupture is quite uncommon in the reperfusion era; however, if it does occur, mortality rates are high. FWR typically occurs acutely or sub-acutely, occurring within 2 weeks for 90% of patients. Risk factors include first myocardial infarction, poor collateralization of the infarcted territory, older age, female sex, persistent ST elevation and delayed presentation/unsuccessful revascularization. When patients present acutely, patients will typically develop tamponade, rapidly progress to pulseless electrical activity, and/or sudden cardiac death. When patients develop subacute FWR or contained rupture (i.e., pseudoaneurysm), they may present with signs and symptoms of pericarditis and subacute hypotension. When FWR occurs, it typically involves the anterior, posterior, or lateral left ventricular wall. The pathophysiology of ventricular free wall rupture is related to the timing of the rupture. Rupture will typically occur at the border of the necrotic and healthy (and often hyperkinetic) myocardium and in areas of the greatest shear stress. In the left ventricle, this tends to be near the anterior and posterior papillary muscles, regardless if they are compromised in the infarct. Note, pericardial effusions can be a common finding in the setting of an acute MI (~15-25% of patients in the acute setting); however, a rapidly expanding pericardial effusion associated with significant wall thinning along the infarcted region should raise the suspicion for LV free wall rupture. The patient was stabilized after surgical evacuation of pericardial fluid in the OR. When should you consider pericardiocentesis vs surgical management? In cases of cardiac tamponade with concern for circulatory collapse there are no absolute contraindications to pericardiocentesis. The goal is urgent drainage of pericardial fluid and how we drain the fluid will depend on the etiology, acuity, and available providers.

Oct 13, 2020

CardioNerds (Amit Goyal & Daniel Ambinder) join University of California San Diego (UCSD) cardiology fellows (Harpreet Bhatia, Dan Mangels, and Quan Bui) for a relaxing beach bonfire in the beautiful city of San Diego! They discuss a challenging case of post-transplant cardiac allograft vasculopathy. Dr. Hao (Howie) Tran provides the E-CPR and program director Dr. Daniel Blanchard provides a message for applicants. Episode notes were developed by Johns Hopkins internal medicine resident Richard Ferraro with mentorship from University of Maryland cardiology fellow Karan Desai. Jump to: Patient summary - Case media - Case teaching - References The CardioNerds Cardiology Case Reports series shines light on the hidden curriculum of medical storytelling. We learn together while discussing fascinating cases in this fun, engaging, and educational format. Each episode ends with an “Expert CardioNerd Perspectives & Review” (E-CPR) for a nuanced teaching from a content expert. We truly believe that hearing about a patient is the singular theme that unifies everyone at every level, from the student to the professor emeritus. We are teaming up with the ACC FIT Section to use the #CNCR episodes to showcase CV education across the country in the era of virtual recruitment. As part of the recruitment series, each episode features fellows from a given program discussing and teaching about an interesting case as well as sharing what makes their hearts flutter about their fellowship training. The case discussion is followed by both an E-CPR segment and a message from the program director. CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademySubscribe to our newsletter- The HeartbeatSupport our educational mission by becoming a Patron!Cardiology Programs Twitter Group created by Dr. Nosheen Reza Patient Summary A man in his late 20s with a past medical history of orthotopic heart transplant, presents with one-week of progressive lower extremity edema and dyspnea with NYHA class IV symptoms. 5 years prior, he underwent orthotopic heart transplant for arrhythmogenic right ventricular cardiomyopathy. Subsequently, he has had multiple episodes of rejection or recurrent graft dysfunction. On presentation, he was normotensive and borderline tachycardic. Exam revealed elevated JVP, decreased breath sounds, and pitting edema. Labs demonstrated leukocytosis, acute kidney injury, and elevated pro-BNP. TTE demonstrated LVEF 35%, apical akinesis, and grade III diastolic dysfunction (all similar to prior). He was initially diuresed and RHC/EMB was performed to evaluate for rejection. Early in his course, the patient unfortunately suffered a PEA arrest with ROSC was quickly achieved after 1 minute of CPR. He was intubated and cannulated for VA ECMO. EMB demonstrated ISHLT Grade 1R cellular rejection and he was ultimately listed for re-transplant. Shortly thereafter, the patient received an OHT. His pathology demonstrated intimal thickening of all his coronaries, consistent with coronary artery vasculopathy, felt to be the major contributor to his presentation. Case Media ECG Episode Schematics & Teaching Click to enlarge! The CardioNerds 5! – 5 major takeaways from the #CNCR case 1. What is CAV? CAV stands for cardiac allograft vasculopathy. Within the transplanted heart, CAV is the proliferation of vascular smooth muscle and intimal thickening in the epicardial coronary arteries and microvasculature leading to diffuse narrowing. CAV is common, present in greater than 30% of patients at 5 years post-transplant. It is a significant contributor to post-transplant mortality after the first year. CAV, in contrast to typical atherosclerotic lesions, is diffuse and concentric while atherosclerosis tends to be focal with eccentric luminal narrowing and heterogenous plaque composition. Patients s/p OHT can still develop typical coronary artery disease, likely developed from pre-existing disease in the donor heart. CAV should be high on the differential for the cause of graft dysfunction, especially after the first year post-transplant. 2. How and Why Does CAV Occur? CAV has multiple contributing factors. There are immunologic and non-immunologic factors, but it appears the immunologic components play the larger role given that the pan-vasculopathy develops in the donor heart and not in the recipient's vasculature. In CAV, there is chronic immune-mediated injury creating a persistent inflammatory state in the donor coronary endothelium leading to a neointimal proliferative process in the coronaries. Amongst immunologic factors, it appears the number of episodes of cellular rejection correlates with the development of CAV. CAV occurs when foreign antigens are recognized by the host immune system as "non-self," a process termed allorecognition. T-cells are subsequently activated, and release a number of inflammatory cytokines that leads to additional T-cell stimulation, inflammatory cell proliferation, and endothelial cell propagation. Ultimately this inflammatory cascade leads to smooth muscle cell advancement and intimal growth into the arterial lumen. Other immunologic factors include HLA mismatch and antibody-mediated rejection. There are numerous non-immunologic factors, including older donor age, CMV infection, hyperlipidemia, insulin resistance, donor brain death secondary to intracranial hemorrhage, and prolonged ischemic time. 3. How Do Patients with CAV Present? Donor hearts are denervated at explantation, and so post-transplant patients typically will not develop classic anginal symptoms as seen with typical atherosclerotic coronary disease. Thus, routine surveillance is necessary (see below). If not diagnosed early, the clinical presentation may include LV dysfunction (with or without symptoms), acute myocardial infarction, heart block, arrhythmias, syncope, or sudden cardiac death. 4. How Do We Diagnose CAV? Routine surveillance is necessary because patients are generally asymptomatic and there is a high incidence of CAV posttransplant. The most common method for screening includes coronary angiography, but its sensitivity is reduced compared to traditional atherosclerotic disease as CAV is diffuse. Intravascular ultrasound (IVUS) significantly improves sensitivity and the early the detection of disease. The timing and method of screening will be center-specific. As the patient is farther removed from their transplant date, dobutamine stress echo may be a reasonable method to screen for CAV. Myocardial perfusion imaging, specifically with PET Rest/Stress with absolute myocardial blood flow quantification, and coronary CTA may also be effective methods to diagnose CAV. The ISHLT grading of CAV by angiography is as follows: CAV0 (Nonsignificant): No detectable angiographic lesion CAV1 (mild): Angiographic LM lesion <50%; or primary vessel with maximum lesion of <70%; or any branch vessel stenosis <70% without allograft dysfunction CAV2 (moderate): Angiographic LM <50%; or a single primary vessel ≥70% stenosis; or isolated branch stenosis in 2 systems ≥ 70% without allograft dysfunction CAV3 (Severe): Angiographic LM ≥50%; or ≥2 primary vessel ≥70% stenosis; or isolated branch stenosis in all 3 systems ≥70%; CAV1 or CAV2 with allograft dysfunction or evidence of significant restrictive physiology 5. How Do we Treat CAV? Primary prevention remains key. Statins have been shown prospectively to reduce cardiac allograft vasculopathy and improve survival. Chronic immunosuppression is the foundation of post-transplant care. The mTOR inhibitors, everolimus and sirolimus, harbor antiproliferative properties that may prevent allograft vasculopathy. However, these are generally not first-line immunosuppressive medications in the United States, given the potential for multiple side effects including impaired wound healing in new transplant patients. In patients with documented or progressive CAV, escalation of immunosuppression to sirolimus may be considered. Revascularization for patients may be considered, given the morbidity associated with CAV, though no survival advantage has been shown. In patients with severe CAV, re-transplantation should be considered. References Mehra, M. R., Crespo-Leiro, M. G., Dipchand, A., et. al (2010). International Society for Heart and Lung Transplantation working formulation of a standardized nomenclature for cardiac allograft vasculopathy—2010. Chih, S., Chong, A. Y., Mielniczuk, L. M. et. al. (2016). Allograft vasculopathy: the Achilles’ heel of heart transplantation. Journal of the American College of Cardiology, 68(1), 80-91. Schmauss, D., & Weis, M. (2008). Cardiac allograft vasculopathy: recent developments. Circulation, 117(16), 2131-2141. CardioNerds Case Reports: Recruitment Edition Series Production Team Bibin Varghese, MDRick Ferraro, MDTommy Das, MDEunice Dugan, MDEvelyn Song, MDColin Blumenthal, MDKaran Desai, MDAmit Goyal, MDDaniel Ambinder, MD

Oct 9, 2020

CardioNerds (Amit Goyal & Daniel Ambinder) join Virginia Commonwealth University (VCU) cardiology fellows (Ajay Pillai, Amar Doshi, and Anna Tomdio) for a delicious skillet breakfast and amazing day in Richmond, VA! They discuss a fascinating case of a patient with Wolff-Parkinson-White (WPW) and hypertrophic cardiomyopathy (HCM). Dr. Keyur Shah provides the E-CPR and program director Dr. Gautham Kalahasty provides a message for applicants. Episode notes were developed by Johns Hopkins internal medicine resident Colin Blumenthal with mentorship from University of Maryland cardiology fellow Karan Desai. Jump to: Patient summary - Case media - Case teaching - References Episode graphic by Dr. Carine Hamo The CardioNerds Cardiology Case Reports series shines light on the hidden curriculum of medical storytelling. We learn together while discussing fascinating cases in this fun, engaging, and educational format. Each episode ends with an “Expert CardioNerd Perspectives & Review” (E-CPR) for a nuanced teaching from a content expert. We truly believe that hearing about a patient is the singular theme that unifies everyone at every level, from the student to the professor emeritus. We are teaming up with the ACC FIT Section to use the #CNCR episodes to showcase CV education across the country in the era of virtual recruitment. As part of the recruitment series, each episode features fellows from a given program discussing and teaching about an interesting case as well as sharing what makes their hearts flutter about their fellowship training. The case discussion is followed by both an E-CPR segment and a message from the program director. CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademySubscribe to our newsletter- The HeartbeatSupport our educational mission by becoming a Patron!Cardiology Programs Twitter Group created by Dr. Nosheen Reza Patient Summary A man in his mid-60s presented to the ED after an episode of unwitnessed syncope while drinking. Patient had suddenly passed out from a seated position with no prodrome or post-ictal state. He had episodes like this in the past, which were thought to be seizures, but otherwise PMHx only notable for alcohol use disorder. He denied any FH of SCD or syncope. In the ED, exam was unremarkable. Labs notable for mild thrombocytopenia, mild hyponatremia with AKI, 2:1 AST/ALT ratio, elevated NT-proBNP, and a very high lactate that rapidly corrected with fluids. EKG was notable for sinus tachycardia, short PR interval, wide QRS, and delta waves consistent with Wolff-Parkinson-White (WPW) pattern. Echo showed preserved LVEF, thickened LV septum (1.6 cm) and posterior wall (1.3 cm) concerning for hypertrophic cardiomyopathy (HCM). No outflow tract gradient was noted at rest or with stress, and the strain pattern demonstrated apical sparing. Evaluation for cardiac amyloid, including plasma cell dyscrasia and PYP scan, was negative. Cardiac MRI confirmed severely thickened LV inferior and inferolateral walls at 1.7 cm with no LVOT obstruction. 25% of the myocardium demonstrated patchy LGE. Due to concern for WPW syndrome, the patient underwent an EP study. This revealed a malignant septal accessory pathway that was successfully ablated with resolution of the WPW EKG features. Given large LGE burden in setting of HCM, patient underwent placement of primary prevention ICD. Genetic testing for PRKAG2 mutation is pending given comorbid WPW and HCM. Case Media AECDBFClick to Enlarge A. CXR: Slightly increased interstitial markings in the lung bases, an elevated right hemidiaphragm. No acute airspace disease or pulmonary edemaB. ECG: Sinus tachycardia rate 120bpm, PR interval 80ms, QRS 130ms, WPW pattern. Arruda algorithm localizes to posterior septum.C. CMR: Myocardium nulls before blood pool.D. CMR: Delayed gadolinium enhancementE. Follow up ECG: NSR 78, repolarization abnormalities. T wave memory inferior leads.F. CXR status post dual chamber ICD implantation TTE: Apical 4 chamber TTE: Apical 2 chamber TTE: Apical 3 chamber TTE: Strain imaging CMR: 4 chamber cine CMR: 2 chamber cine CMR: 3 chamber cine CMR: Short axis cine at base level CMR: Short axis cine at mid-papillary level CMR: Short axis cine at apical level Episode Schematics & Teaching Hypertrophic Cardiomyopathy InfographicClick to enlarge! The CardioNerds 5! – 5 major takeaways from the #CNCR case Our patient was found to have Wolff-Parkinson-White (WPW) pattern. What are the diagnostic criteria for WPW pattern and how does it differ from WPW syndrome? How can you localize the accessory pathway using the EKG? WPW pattern refers to the presence of the below criteria on a patient's surface EKG in the absence of symptomatic arrhythmias. If symptomatic arrhythmias related to the accessory pathway occur, then it is WPW syndrome. Symptoms may include palpitations, shortness of breath, presyncope, syncope, and sudden cardiac death (SCD). Not all patients with accessory pathways have EKG findings as only 60-75% of accessory pathways are "manifest" (meaning they conduct antegrade from atria to ventricles or are bidirectional). Conversely, a "concealed" accessory pathway only conducts retrograde (from ventricles to atria) and would not be apparent on resting sinus EKG; these patients can have WPW diagnosed after a ventricular premature beat, ventricular pacing, or an EP study that shows retrograde conduction through the accessory pathway. The WPW pattern is diagnosed by the following EKG criteria: Short PR interval 120 ms. The degree of pre-excitation on EKG depends on the position (how much of the ventricular myocardium is depolarized by the accessory pathway) and depolarization speed of the accessory pathway (more rapid conduction leading to earlier ventricular depolarization and wider delta wave). We can use EKG findings to localize accessory pathways using the Arruda Criteria, which has an overall sensitivity of 90% and specificity of 99%. Note, patients who have a left-lateral bypass tract as the antegrade limb may not have delta waves on surface EKG, as the atrial impulse can take longer to reach the bypass tract than the AV node. What are the major mechanisms for WPW and how do they lead to early activation of the ventricles? How can this precipitate arrhythmias? Accessory pathways are abnormal congenital connections between the atria and ventricles when there is incomplete atrio-ventricular isolation during fetal development. They can be associated with congenital cardiac malformations like Ebstein anomaly. Depolarization of the ventricles occurs via the AV node and the accessory pathway simultaneously, leading to early depolarization of a portion of the ventricles and the characteristic delta wave. Depolarization through the His Purkinje system reaches the apex first and travels back up the ventricle, meeting the slower cell to cell conduction from the accessory pathway and causing termination of the impulses. The resulting QRS complex is essentially a "fusion beat" between the two sources. Accessory pathways often have more rapid conduction, but longer refractory periods than the AV node. If a PAC occurs when the accessory pathway is refractory, there will be antegrade conduction solely through the AV node. As the impulse travels through the ventricles it can conduct retrograde through the accessory pathway from V to A. This creates a reentrant pathway that results in atrioventricular reentrant tachycardia (AVRT), which accounts for up to 80% of SVT in WPW. Orthodromic AVRT (antegrade through AV node, retrograde through accessory pathway) accounts for 90-95% of AVRT in WPW. Other tachycardias can occur where the accessory pathway is a bystander and not required for initiation and maintenance of the arrhythmia like in AVRT. This includes atrial arrhythmias (e.g., atrial fibrillation, atrial flutter), ventricular tachycardia, and ventricular fibrillation. Atrial fibrillation is relatively common (~20%) in WPW syndrome patients. Atrial fibrillation with an accessory pathway can produce rapid ventricular rates due to unencumbered conduction via the accessory pathway. In these situations, QRS width and morphology may vary due to variable conduction via the AV node vs accessory pathway. Depending on the rate of conduction, the patient can degenerate into VF. A shorter refractory period places patients at the highest risk for VF. How do we risk stratify patients with WPW pattern? When would an EP study (EPS) be beneficial? What features are high risk on EPS and would warrant treatment? Patients who are asymptomatic are typically at low risk of sudden cardiac death. Those who do have SCD typically have symptoms at some point prior to arrest. Patients with intermittent loss of the delta wave on a beat-to-beat basis are likely at lower risk, as it suggests the accessory pathway lacks the ability for rapid AV conduction. However, persistent delta wave in asymptomatic patients may still be at low risk. The risk for SCD is thought to be due to rapid conduction of Afib down the accessory pathway leading to VF. Accessory pathways with shorter refractory periods are able to conduct at higher rates (shorter R to R intervals). Delta waves disappear when R to R interval is less than the refractory period, at which point the atrial impulse only conducts through AV node. Thus, the lower the HR that delta waves become intermittent, the lower the risk of SCD. We can start risk stratification in most patients noninvasively with a resting EKG and exercise EKG stress test, unless we clearly demonstrate intermittent delta wave at rest. If preexcitation persists even with maximal sinus heart rates, then an EPS is recommended.

Oct 9, 2020

CardioNerds (Amit Goyal & Daniel Ambinder) join Baylor College of Medicine cardiology fellows (Khurrum Khan, John Suffredini, and Aliza Hussain) during restaurant week in Houston! They discuss an interesting case of STEMI in a patient with a recent diagnosis of e-cigarette or vaping product use-associated lung injury (EVALI). Dr. Vijay Nambi provides the E-CPR and APD Dr. Arunima Misra provides a message for applicants. Episode notes were developed by Johns Hopkins internal medicine resident Bibin Varghese with mentorship from University of Maryland cardiology fellow Karan Desai. Jump to: Patient summary - Case media - Case teaching - References Episode graphic by Dr. Carine Hamo The CardioNerds Cardiology Case Reports series shines light on the hidden curriculum of medical storytelling. We learn together while discussing fascinating cases in this fun, engaging, and educational format. Each episode ends with an “Expert CardioNerd Perspectives & Review” (E-CPR) for a nuanced teaching from a content expert. We truly believe that hearing about a patient is the singular theme that unifies everyone at every level, from the student to the professor emeritus. We are teaming up with the ACC FIT Section to use the #CNCR episodes to showcase CV education across the country in the era of virtual recruitment. As part of the recruitment series, each episode features fellows from a given program discussing and teaching about an interesting case as well as sharing what makes their hearts flutter about their fellowship training. The case discussion is followed by both an E-CPR segment and a message from the program director. CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademySubscribe to our newsletter- The HeartbeatSupport our educational mission by becoming a Patron!Cardiology Programs Twitter Group created by Dr. Nosheen Reza Patient Summary A male in his mid 40s with a 30 pack year smoking history, EVALI (e-cigarette and vaping associated lung injury), and asthma presented with dyspnea and persistent chest pain. He had been vaping for the past year. One month prior , CT chest showed bilateral patchy infiltrates and he was diagnosed with EVALI and started on a steroid taper with resolution of his CT abnormalities. A nuclear stress test at that time was negative for ischemia. On arrival, he was in sinus tachycardia, normotensive, and not on oxygen supplementation. Physical exam was negative for volume overload or heart murmurs. EKG showed new Q waves with STE in V2-V4, with associated Q waves and TWI in the lateral leads and troponin returned moderately elevated. He was emergently taken to the cath lab which showed an abrupt cutoff of flow to the LAD. He received a single DES with resolution of coronary flow. A post-cath TTE showed an LVEF of 40-45% with apical anterior and anteroseptal WMA. He was monitored in the CCU the next day and he was treated with aspirin, ticagrelor, ACEi, metoprolol succinate and high intensity statin and subsequently discharged in stable condition with cardiac rehab follow-up. Case Media ABClick to Enlarge A. Presentation ECG (Anterior STEMI) B. Baseline ECG LAD occlusion Post PCI RCA TTE 1 TTE 2 TTE 3 Episode Schematics & Teaching Click to enlarge! The CardioNerds 5! – 5 major takeaways from the #CNCR case 1. The patient presented with a STEMI following a diagnosis of EVALI. What is known about the cardiovascular risks of vaping and e-cigarette use? The overall cardiovascular risks of e-cigarette use remains to be elucidated In preclinical studies, e-cigarettes use have been linked to increased sympathetic activity, oxidative stress, endothelial dysfunction, vascular injury, and altered platelet activity One observational study has suggested that daily e-cigarette users were 1.79 times more likely to experience MI than individuals who had never used e-cigarettes. Additional high-quality randomized controlled trials are needed to conclusively establish the safety and efficacy of e-cigarettes. 2. So the data is still emerging regarding the overall cardiovascular risks of e-cigarette use. Of note, the patient had a negative stress test a month prior. Should that not translate into low likelihood of cardiovascular events? Remember that stress testing for the diagnosis of obstructive coronary disease is most helpful in patients with an intermediate pretest probability for coronary artery disease. Further myocardial ischemia can occur not only secondary to obstructive epicardial disease (which may be new and acute from plaque rupture/erosion), but also from microvascular disease, vasospastic disease, and so forth. Stress testing with radionuclide myocardial perfusion imaging (e.g., SPECT, PET) is a well-established method for assessing coronary disease, but it is not an anatomic assessment. With nuclear stress tests, the causes of a false-negative result could include submaximal exercise (if doing exercise stress), collateral or overlapping epicardial circulation, suboptimal images (including artifact and poorly timed stress images), inaccurate interpretation, and balanced ischemia. Nonetheless, sensitivity for obstructive CAD in SPECT approaches 85-90% with specificity around 70-75%. As SPECT imaging is not an anatomic assessment, a recent negative nuclear stress test does not necessarily mean very low risk for future major adverse cardiovascular events. Even with a normal nuclear stress test, there is a 0.65% - 1.78% annual event rate of death or non-fatal MI. 3. Can non-obstructive and potentially "vulnerable" plaque be detected before an event? Remember ECG, echocardiographic and radionuclide stress testing are different modalities to assess for obstructive CAD after inducing ischemia via exercise or medications. These modalities typically assess for flow-limiting lesions (e.g., typically greater than 50%). However, acute coronary syndrome can occur subsequently from lesions that were not initially obstructive. In the PROSPECT study looking at patients who presented with ACS and underwent PCI to the culprit lesion and were followed afterward for ~ 3 years for adverse events, recurrent major adverse plaque rupture events were noted equally at the culprit lesion and at non-culprit lesions. Non-culprit lesions that were responsible for unanticipated events were angiographically mild on initial evaluation, had thin-cap fibroatheromas, or had large plaque burden as determined by gray-scale and radiofrequency intravascular ultrasound. This is where coronary CTA has an increasingly larger role. A study looking at coronary CTA determined that plaques with positive remodeling and low attenuation features were at higher risk of ACS developing over time. Those individuals with neither of those features had high NPV in ruling out future ACS events. Typically, as a lesion increases in size, it can compromise luminal blood flow when 50% or greater narrowing of the lumen is observed (remember this is slightly different than labeling a lesion as "obstructive" to the point of potentially necessitating intervention). However, when there is an absence of luminal loss regardless of lesion size in early lesions, this is called "positive coronary artery remodeling" and there is compensatory enlargement of the epicardial vessel. Post-mortem studies have found that vessels with positive remodeling have been associated with increased lipid content, as well as features associated with unstable plaque (e.g., thin-cap fibroatheroma). 4. The patient had an MI at age 45! Apart from e-cigarette use, what other evaluation is warranted in a young patient with ACS or STEMI? Traditional risk factors such as dyslipidemia, T2DM, HTN, and family history of premature CAD must be evaluated as plaque rupture events are still the most common cause of MI in young patients (age < 45 years). Furthermore, the differential for young individuals presenting with acute myocardial infarction should include non-atherosclerotic causes such as: anomalous coronary artery, spontaneous coronary artery dissection, coronary embolus, coronary vasculitis, coronary aneurysm (all of which have been discussed in the @cardionerds #CNCR episodes!). If thrombus is present on angiography without traditional risk factors, workup should include evaluation for hypercoagulable states (e.g., Protein C and S deficiency, Factor V Leiden, APLS) or evaluating for a source of embolism (e.g., Afib, valvular lesion, LV thrombus, or even PFO [Enjoy Ep #51 - ACS & PFO]). Coronary thrombus may arise in situ from plaque rupture/erosion or as an embolus; recall that coronary emboli may be categorized as: direct, paradoxical, or iatrogenic. Angiographic and multi-modal imaging findings may reveal the underlying etiology, including SCAD (Enjoy Ep #65 - SCAD), or one of the other non-atherosclerotic coronary processes listed above. If no obvious lesion is present, one should evaluate for Myocardial Infarction with non-obstructive coronaries (MINOCA) such as coronary vasospasm, and coronary microvascular dysfunction Other considerations in young patients should include drug use, such as cocaine and methamphetamine use. Furthermore, oral contraceptives combined with another pro-thrombotic risk factor (e.g., tobacco use) may lead to acute myocardial infarction. 5. Sounds like the patient improved symptomatically after PCI placement. Going back to the basics, why do we obtain a TTE after STEMI and monitor in the CCU? Assessment of resting LV function helps us risk stratify patients, as it is one of the strongest predictors of survival. Furthermore, it will help us guide our medical therapy after STEMI. Echocardiographic evaluation can also help us characterize any suspected mechanical complications of STEMI. Beyond just survival,

Oct 6, 2020

CardioNerds (Amit Goyal & Daniel Ambinder) join University of Pittsburgh Medical Center cardiology fellows (Agnes Koczo, Natalie Stokes, and Kayle Shapero) for a boat cruise down the Allegheny river as we tour all over beautiful Pittsburgh! They discuss an important case of severe pre-eclampsia, and explore some of the exciting dimensions of cardio-obstetrics. Dr. Malamo Eleni Countouris provides the E-CPR and program director Dr. Katie Berlacher provides a message for applicants. Episode notes were developed by Johns Hopkins internal medicine resident Tommy Das with mentorship from University of Maryland cardiology fellow Karan Desai. Jump to: Patient summary - Case media - Case teaching - References Episode graphic by Dr. Carine Hamo The CardioNerds Cardiology Case Reports series shines light on the hidden curriculum of medical storytelling. We learn together while discussing fascinating cases in this fun, engaging, and educational format. Each episode ends with an “Expert CardioNerd Perspectives & Review” (E-CPR) for a nuanced teaching from a content expert. We truly believe that hearing about a patient is the singular theme that unifies everyone at every level, from the student to the professor emeritus. We are teaming up with the ACC FIT Section to use the #CNCR episodes to showcase CV education across the country in the era of virtual recruitment. As part of the recruitment series, each episode features fellows from a given program discussing and teaching about an interesting case as well as sharing what makes their hearts flutter about their fellowship training. The case discussion is followed by both an E-CPR segment and a message from the program director. CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademySubscribe to our newsletter- The HeartbeatSupport our educational mission by becoming a Patron!Cardiology Programs Twitter Group created by Dr. Nosheen Reza Patient Summary A G12P7 woman in her mid 30s in the third trimester of pregnancy presented with two months of progressive shortness of breath, orthopnea, and abdominal distension. She has a history of chronic HTN, untreated OSA, and obesity. Evaluation revealed a BP of 147/76 and spot urine protein:creatinine ratio elevated to 0.6, which in the context of her presentation was concerning for preeclampsia superimposed on chronic hypertension. TTE showed preserved ejection fraction, flattened interventricular septum during systole consistent with RV pressure overload, and moderate pulmonary HTN. She was diuresed with IV furosemide with improvement in symptoms and kept on ASA 81mg. The etiology of her elevated PA pressures was thought to be multifactorial, including untreated OSA for which she was started on CPAP. She was ultimately discharged on oral diuretics, and underwent an uncomplicated spontaneous vaginal delivery at 37 weeks. After delivery, follow-up in a clinic specializing in improving cardiovascular health in women with history of hypertensive disorders of pregnancy was arranged. Case Media ABCClick to Enlarge A. ECG: Sinus tachycardia otherwise unremarkableB. CXR: Within limitations of respiratory motion, no focal airspace consolidation; no pleural effusionsC. TTE: EF 55-60%, flattened IVS c/w RV pressure overload; normal RV size and function; mod TR; moderate pulmonary HTN (PASP 52mmHG); normal diastolic function Episode Schematics & Teaching Click to enlarge! The CardioNerds 5! – 5 major takeaways from the #CNCR case 1. Cardionerds, we all should be familiar with #CardioObstetrics. What are the hypertensive disorders of pregnancy? There are four major categories for hypertensive disorders in pregnancy: (1) chronic hypertension (2) gestational hypertension; (3) preeclampsia (along with eclampsia and HELLP syndrome); (4) chronic hypertension with superimposed preeclampsia. Chronic Hypertension: Note, the definition of chronic hypertension was updated in the 2017 ACC/AHA guidelines as SBP ≥ 130 or DBP ≥ 90, but the diagnostic criteria for gestational hypertension, pre-eclampsia and chronic hypertension with super-imposed pre-eclampsia have not changed at this time. Gestational Hypertension (per ACOG guidelines): defined as SBP ≥ 140 mmHg or DBP ≥ 90 mmHg at least 4 hours apart diagnosed after 20 weeks of gestation without proteinuria or severe features of pre-eclampsia (e.g., renal insufficiency, elevated liver enzymes, thrombocytopenia, hemolysis, pulmonary edema, or CNS symptoms) Preeclampsia: diagnosis requires (1) SBP ≥ 140 mmHg or DBP ≥ 90 mmHg at least 4 hours apart after 20 weeks gestation or SBP ≥ 160 mmHg or DBP ≥ 110 mmHg once and (2) end organ damage. This includes proteinuria (≥ 300 mg/24hr urine collection, protein/creatinine ratio of ≥ 3 mg/dL, or dipstick reading of 2+ protein if other methods are not available), thrombocytopenia ( 1.1 mg/dL), elevated liver enzymes (at least 2x upper limit of normal), pulmonary edema, or neurological symptoms (e.g., new onset headache not responding to medications or visual disturbances not attributable to another diagnosis). Eclampsia: diagnosed when new-onset, grand mal seizure occurs in patients with pre-eclampsia. HELLP Syndrome: diagnosed when Hemolysis, Elevated Liver enzymes, and Low Platelets are the predominant features. HELLP is likely a subset of preeclampsia. Note, not all patients will have hypertension. Chronic hypertension with superimposed preeclampsia: (1) characterized by sudden increase in blood pressure that was previously controlled or recent up-titration of antihypertensives to manage blood pressure and/or (2) new onset proteinuria or increase in pre-existing proteinuria 2. This case featured a patient with super-imposed pre-eclampsia; what is pathophysiology behind this disorder? The pathophysiology of preeclampsia is complex and includes multi-organ manifestations. The initial insult is thought to be secondary to abnormal trophoblast (the outer cell layer of the blastocyst which eventually gives rise to the embryo) invasion of the endometrium. Normally, as trophoblasts implant in the endometrium, the small myometrial spiral arteries remodel with loss of smooth muscle and elastic lamina from the vessel wall. This allows increased blood flow to the placenta. In preeclampsia, there is incomplete spiral artery remodeling which can lead to placental ischemia. The incomplete arterial transformation is thought to be mediated by a number of factors, including soluble fms-like tyrosine kinase-1 (sFlt-1). sFlt-1, which circulates in the maternal bloodstream, has been implicated as an underlying culprit to the multi-system endothelial dysfunction we see in pre-eclampsia (e.g., CNS, renal dysfunction). There are other factors involved as well that ultimately lead to widespread oxidative stress, abnormal vascular reactivity, microemboli, and the clinical features of preeclampsia. There are additionally immunologic and genetic factors that lead to a preeclampsia phenotype by leading to a pro-inflammatory state and reduced trophoblast invasion. 3. Clearly, pre-eclampsia can have severe adverse effects on mother and child. Which patients are at increased risk of pre-eclampsia, and what can be done to lower their risk? High risk factors for developing preeclampsia include: diabetes, chronic hypertension, chronic kidney disease, multifetal gestation, autoimmune disorders (particularly systemic lupus erythematosus and antiphospholipid syndrome), and previous pregnancy with preeclampsia. Other risk factor include obesity, maternal age over 35 years, and nulliparity. There is no consensus guideline on what defines moderate to high risk. Following the USPSTF recommendations, any pregnant woman with a high risk factor or several moderate risk factors should be advised to start low-dose aspirin after 12 weeks of gestation to reduce the risk of preeclampsia. A recent Cochrane review that included trial data from nearly 37,000 women found aspirin prophylaxis reduced risk of preeclampsia by 18%. Calcium supplementation may be of benefit to prevent preeclampsia in women with low-baseline calcium intake. The proposed mechanism is that hypocalcemia may stimulate PTH or renin release, increasing intracellular calcium including in vascular smooth muscle. This may result in vasoconstriction and higher blood pressure and calcium supplementation may attenuate this process. There is an ongoing clinical trial to investigate the role of Pravastatin in the prevention of preeclampsia. 4. What if my patient has chronic HTN or gestational HTN? How do I approach the hypertensive pregnant patient? An ounce of prevention is worth a pound of cure! In hypertensive women who may become pregnant, nifedipine, labetalol, hydralazine, or methyldopa are preferred over teratogens like ACE inhibitors, ARBs, or direct renin inhibitors. Severe HTN (SBP ≥160, DBP ≥110) should always be treated to avoid pulmonary edema, stroke or placental abruption. A more conservative approach can be taken in mild to moderate HTN, as aggressive blood pressure lowering can compromise fetal circulation. However, the optimal blood pressure to initiate treatment below this threshold is less well defined and should be individualized to the patient including factors like underlying cardiovascular disease and baseline blood pressure. The timing of delivery is a critical aspect of managing a patient's hypertension. For a detailed discussion, review the ACOG practice bulletin. 5. How does a hypertensive disorder of pregnancy change a patient's cardiovascular risk? A history of a hypertensive disorder of pregnancy is an important risk factor for future cardiovascular disease. These patients are more likely to experience hypertension, ischemic heart disease, heart failure,

Oct 5, 2020

CardioNerds (Amit Goyal & Daniel Ambinder) join join UCLA cardiology fellows (Jay Patel, Hillary Shapiro, and Ruth Hsiao) for some beach bonfire in Santa Monica! They discuss a challenging case of Spontaneous Coronary Artery Dissection (SCAD) requiring heart transplantation. Dr. Jonathan Tobis provides the E-CPR and program director Dr. Karol Watson provides a message for applicants. Episode notes were developed by Johns Hopkins internal medicine resident Evelyn Song with mentorship from University of Maryland cardiology fellow Karan Desai. Jump to: Patient summary - Case media - Case teaching - References Episode graphic by Dr. Carine Hamo The CardioNerds Cardiology Case Reports series shines light on the hidden curriculum of medical storytelling. We learn together while discussing fascinating cases in this fun, engaging, and educational format. Each episode ends with an “Expert CardioNerd Perspectives & Review” (E-CPR) for a nuanced teaching from a content expert. We truly believe that hearing about a patient is the singular theme that unifies everyone at every level, from the student to the professor emeritus. We are teaming up with the ACC FIT Section to use the #CNCR episodes to showcase CV education across the country in the era of virtual recruitment. As part of the recruitment series, each episode features fellows from a given program discussing and teaching about an interesting case as well as sharing what makes their hearts flutter about their fellowship training. The case discussion is followed by both an E-CPR segment and a message from the program director. CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademySubscribe to our newsletter- The HeartbeatSupport our educational mission by becoming a Patron!Cardiology Programs Twitter Group created by Dr. Nosheen Reza Patient Summary A woman in her late 40s presented with a one day history of intermittent chest pain. EKG showed anteroseptal and lateral STE with reciprocal ST depressions in the inferior leads. High-sensitivity troponin was elevated at 333 ng/mL. Emergent LHC showed a long and narrow left main with areas of additional contrast filling into a false lumen with no flow in the LAD. RCA and LCx were normal appearing (make sure you check out the angiogram videos below!). IVUS showed dissection and heavy thrombus burden in the left main artery. Shortly after the diagnostic angiogram, the patient went into V-fib arrest and received one shock with ROSC. Amiodarone was started and an Impella CP was placed for additional left ventricular support. ECMO and emergent CABG were not readily available at this time so the interventional team attempted revascularization with PCI to the left main given patient's hemodynamic instability from ongoing ischemia. However, even after PCI to left main, flow to LAD remained poor and the LCx now also appeared occluded. The decision was made to cease further attempts at revascularization. Unfortunately, post-procedure TTE showed a reduced EF of 22% with anterior and anterolateral hypokinesis. She was transferred to CCU on maximal Impella support. Patient eventually developed acute renal and liver failure secondary to cardiogenic shock and suffered an additional V-fib arrest with ROSC. Eventually, Ronald Reagan UCLA was contacted for transfer and the mobile ECMO team was dispatched. They placed the patient on VA-ECMO in the outside facility and transferred her to Ronald Reagan UCLA. At Ronald Reagan, revascularization was attempted given persistent cardiogenic shock and 3 stents were successfully deployed in the LAD. She was eventually weaned off of both Impella and ECMO after successful PCIs to LAD. However, TTE showed persistently low EF and patient eventually underwent successful heart-kidney transplantation. Case Media ABCDClick to Enlarge A. ECG: Anterior STE, STE in I/aVL but depressedions in V4-V6, inferior reciprocal ST depressionB. X-ray of explanted heart shows stents extending from LM -> dLADC. Cross-section of explanted heart from apex to base showing infarct in the anteroseptal areaD. Histological cross section of the explanted LAD. This film shows slit like LM with no LAD. High OM/RI and LCx look ok. BMW wire used to cross distal LM into high OM/RIArrested after diagnostic, got ROSC and then Impella CP inserted L femoral Attempting wiring the true lumen, stuck in mLAD after 1st septal comes off IVUS from RI to LM. Shows dissection plane and lots of thrombusLM IVUS details: 4.57 x 5.0mm proximally, 4.52mm distally Unable to pass a wire into mid LAD PCI of LM: Synergy 4.0 x 16mm DES deployed in LM and post-dilated with Emerge NC 4.5 x 8mm balloon Flow remained poor at mLAD even after PCI to LM LCx system closed after LM PCI, so no further attempts TTE: Apical 4 Chamber TTE: Apical 2 Chamber TTE: Apical 3 Chamber LCx occluded with large OM1/Ramus still patent Post PCI of the LAD Episode Schematics & Teaching Click to enlarge! The CardioNerds 5! – 5 major takeaways from the #CNCR case What is SCAD and what population is most at risk? SCAD stands for spontaneous coronary artery dissection. It is an acute coronary event and is defined as a spontaneous separation of the coronary artery wall that is not iatrogenic or related to trauma. It is an important cause of acute myocardial infarction. Women comprise 87%-95% of SCAD patients with a mean age of presentation between 44-53 years, just like the patient in this case. The "typical" SCAD patient is a middle-aged female with few traditional cardiovascular risk factors such as hypertension, hyperlipidemia, and tobacco use. However, our understanding of a "typical" SCAD patient is limited as the majority of patients in large series have been white and it is likely that patients of different ethnic and racial backgrounds have been under-represented in most current registries. In some studies, the prevalence of SCAD appears around 4% of all patients presenting with ACS and up to 35% in women 50 years or under presenting with ACS. Pregnancy associated SCAD is an important subset of patients. It can occur at any time during the pregnancy or post-partum, with the majority of cases occurring postpartum. SCAD associated with pregnancy tends to have a more severe clinical presentation, including left main involvement, multi-vessel dissection and cardiogenic shock. Both pregnancy and non-pregnancy associated SCAD tend to occur more frequently in multiparous women and those that report a higher prevalence of pre-eclampsia. What are the two hypotheses that have been proposed to explain the pathophysiology of SCAD? Before reviewing the pathophysiology, let's briefly review the coronary arterial wall structure. The intima is the inner layer in contact with the intraluminal space. In normal vasculature, the intima is only a few cell layers thick and is separated from the media by the internal elastic lamina. The media is the middle layer and is made up of layers of smooth muscle cells which help regulate vascular tone. The media is separated from the adventitia by the external elastic lamina. Finally, the adventitia surrounds the media and through fibrous connective tissue provides support for the epicardial vessel. In SCAD, a hematoma forms within the tunica media separating the intima or intima/media from the vessel and compressing the true lumen leading to ischemia. There are several proposed hypotheses for how this occurs: "Inside-out" hypothesis: an endothelial-intimal disruption or "flap" develops first and then blood enters the sub-intimal space from the true lumen via this "flap" "Outside-in" hypothesis: a hematoma forms within the media, possibly from disruption of traversing micro-vessels, and compresses and occludes the true lumen as the hematoma expands. In both hypotheses, the end result is separation of the layers of coronary artery wall, creating a false vs. true lumen. Currently, the evidence favors the "outside-in" theory because in most SCAD cases, there are no communication between the true and false lumens observed. What are the angiographic appearances of SCAD? Left anterior descending artery is the most commonly affected vessel in SCAD. There are three classifications of SCAD based on angiographic appearance (the Yip-Saw classification). Type 1: Contrast dye staining of the arterial wall demonstrates double or multiple radiolucent lumens separated by a radiolucent flap. There may be dye "hang-up" or slow contrast clearing. Type 2: This is the most common subtype. It is characterized by long, diffuse, and smooth narrowing that can vary from mild stenosis to complete occlusion, often with abrupt changes in lumen diameter. Type 2a SCAD demonstrates normal arterial segments proximal and distal to a dissection and does not extend into a distal vessel. Type 2b does extend into the distal tip of a vessel. Type 3: The angiographic appearance mimics a focal stenosis of atherosclerotic disease and typically requires intracoronary imaging to make a definitive diagnosis. There are other angiographic findings that may clue the cardiology team into a diagnosis of SCAD. SCAD tends to affect more distal segments than atherosclerotic disease. Furthermore, the left anterior descending (LAD) artery is the most commonly affected vessel in SCAD. Patients with SCAD tend to have more tortuous vessels and atherosclerotic lesions are usually absent from vessels not affected by the SCAD. Some reports have indicated the external luminal compression by the intramural hematoma (IMH) gives the appearance of a stick insect. What is the management of SCAD in the acute setting? As Dr. Hayes et al. note in their JACC review,

Oct 2, 2020

CardioNerds (Amit Goyal & Daniel Ambinder) join Houston Methodist cardiology fellows (Isaac Tea, Stephanie Fuentes, Peter Rothstein) for a trip to Hermann Park! They discuss a challenging case of right ventricular (RV) infarction leading to acute RV failure treated with right ventricular assist device (RVAD) support. Dr. Mahwash Kassi provides the E-CPR and program director Dr. Stephen Little provides a message for applicants. Episode notes were developed by Johns Hopkins internal medicine resident Tommy Das with mentorship from University of Maryland cardiology fellow Karan Desai. Jump to: Patient summary - Case media - Case teaching - References Episode graphic by Dr. Carine Hamo The CardioNerds Cardiology Case Reports series shines light on the hidden curriculum of medical storytelling. We learn together while discussing fascinating cases in this fun, engaging, and educational format. Each episode ends with an “Expert CardioNerd Perspectives & Review” (E-CPR) for a nuanced teaching from a content expert. We truly believe that hearing about a patient is the singular theme that unifies everyone at every level, from the student to the professor emeritus. We are teaming up with the ACC FIT Section to use the #CNCR episodes to showcase CV education across the country in the era of virtual recruitment. As part of the recruitment series, each episode features fellows from a given program discussing and teaching about an interesting case as well as sharing what makes their hearts flutter about their fellowship training. The case discussion is followed by both an E-CPR segment and a message from the program director. CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademySubscribe to our newsletter- The HeartbeatSupport our educational mission by becoming a Patron!Cardiology Programs Twitter Group created by Dr. Nosheen Reza Patient Summary A man in his early 70s with ASCVD risk factors and known CAD (PCI to proximal LAD 4 years prior) presented with typical angina refractory to maximal medical therapy. A nuclear stress test showed a reversible perfusion defect in the RCA territory, and he was referred for PCI. Coronary angiogram showed severe stenosis of the proximal RCA and a DES was successfully deployed with TIMI 3 flow, though several large acute marginal branches were jailed. The night following PCI, the patient developed bradycardia, hypotension, and tachypnea. Physical exam showed newly elevated JVP, lower extremity edema, and bibasilar crackles without a new cardiac murmur. ECG showed ST elevation in V1-V4, and bedside echocardiogram showed a severely dilated RV with decreased systolic function. With concern for acute RV failure, the patient was fluid resuscitated, started on dopamine for chronotropy, and was admitted to the CCU. A Swan-Ganz catheter was placed, showing a CVP 12, RV 41/15, PA 36/20 (25), PCWP 18, CI 1.6 (by Fick method). The calculated PAPi was 0.84. The patient was transitioned to dobutamine to improve RV inotropy, epinephrine in the setting of hypotension, and inhaled nitric oxide in an attempt to decrease RV afterload. Despite these interventions, the patient had worsening shock, anuric renal failure requiring CVVH, and respiratory failure requiring intubation. A centrifugal RA to PA pump was placed (Protek Duo) for right-sided mechanical circulatory support, with improvement in RV hemodynamics and cardiogenic shock. Notably, a repeat angiogram was done, which showed a patent left coronary circulation as well as a right coronary artery without flow in the acute marginal branches. After 6 days of mechanical circulatory support, the patient was ultimately able to be weaned from vasoactive agents, and the Protek Duo was removed. He continued to have junctional bradycardia, and a permanent pacemaker was placed. After a nearly month-long admission, the patient was discharged to rehab; at 4 months follow-up, the patient's RV function had improved on TTE, and he was not limited from heart failure symptoms. Case Media ABCDEFGClick to Enlarge A: ECG, initialB: ECG: 8 hours post PCI he was noted to have junctional bradycardia with ST-segment elevations in V1-V4.C: Pre and post RCA PCI D: TTE: EF 50-55%, Severely enlarged RV with severely reduced systolic function, TAPSE 1.4 cm, Myocardial systolic excursion velocity (S’): 5.9E: CXR- shock F: Swan, Protek Duo Cannula, Temporary pacer G: CXR and TTE images demonstrating Protek Duo cannula placement Left Coronary System -1 Left Coronary System - 2 Severe eccentric serial stenoses in the proximal to mid RCA - 1 RCA - 2 RCA PCI - 1 RCA PCI - 2 RCA PCI - 3 RCA PCI - 4 RCA - Final TTE -1 TTE -2 Repeat angiogram: Patent stents, sluggish flow Protek Duo Placement Episode Schematics & Teaching Click to enlarge! The CardioNerds 5! – 5 major takeaways from the #CNCR case 1) Don’t forget about the RV, because it sure won't forget about you! Cardionerds, how do you break down the pathophysiology of acute RV failure? Understanding the pathophysiology of RV failure requires a basic understanding of RV physiology. Normal RV function depends on systemic venous return, RV afterload, pericardial compliance/constraint, and native RV contractility. Remember, the thin-walled RV requires much less energy to generate output compared to the LV as the RV is pumping into the highly compliant, low-resistance pulmonary circulation. Overall, the RV is highly sensitive to changes in RV afterload. Thus, when we think of acute RV failure, our primary considerations are factors that rapidly increase RV afterload (e.g., pulmonary embolus), as well as conditions with decreased RV contractility (e.g., RV ischemia). The RV is more adept to tolerating changes in volume rather than pressure (since it is coupled to the low-resistance, high compliance pulmonary circulation). Contrast this with the LV, which tolerates changes in pressure more than volume. An acute increase in RV afterload can abruptly precipitate a fall in RV cardiac output! With an acute decreased in RV contractility (e.g., RV infarct), the RV can dilate leading to functional TR; this can further exacerbate RV dilation, leading to impaired LV filling due to ventricular interdependence. As the septum shifts leftward, this can impair LV filling by increasing LVEDP and lead to hypotension. Direct RV injury can promote more RV injury/ischemia, as elevated right heart pressures can cause coronary sinus congestion reducing coronary blood flow and leading to more RV ischemia. For more detailed explanation of Right-Sided Heart Failure, see this fantastic Scientific Statement from the AHA! 2) Lets focus on ischemic RV disease: what is the coronary supply to the RV, and how does coronary blood flow to the RV differ than that of the LV? Compared to the LV, the RV is more resistant to irreversible ischemia. Coronary blood flow to the RV occurs both in systole and diastole, RV myocardial oxygen demand at rest is lower than that of the LV with smaller muscle mass, and there is often extensive collateral circulation from the left coronary system. However, RV coronary perfusion pressure can decrease rapidly in the setting of systemic hypotension and increased RV intracavitary pressure. In most patients, the RV is supplied by the RCA via RV acute marginal branches largely supplying the anterior RV free wall. Significant RV involvement in an RCA culprit acute myocardial infarction tends to only occur if the occlusion is proximal to the acute marginal branch. Furthermore, the extent of RV involvement may be attenuated by the amount of left to right collateralization. Note, the LAD supplies the RV apex, as well as a portion of the RV anterior wall that is contiguous with the anterior septum. Notably, in patients with a left dominant coronary system or in patients with a chronically occluded RCA with extensive left to right collateral flow, more than half of the RV free wall may be supplied by the left system. 3) Now that we know what causes acute RV failure, what can we do to assess for acute RV failure, both at the bedside and with advanced diagnostics? Physical exam: In acute RV failure, we will likely see elevated neck veins +/- Kussmaul's sign, hypotension, possibly clear lungs depending on etiology, and tricuspid regurgitation murmur. Enjoy Ep #58 - Constrictive Pericarditis CN5 for more details on right-sided exam findings! ECG: Unfortunately, the standard 12-lead ECG provides limited definitive information on RV failure. However, we should evaluate for acute occlusive myocardial infarction (MI) involving the RV, including ST elevation in the inferior leads (classically with III > II), V1 > V2, and/or V1 +/- ST depression in V2. Right-sided leads can further confirm acute occlusive MI, with STE > 1mm in lead V4R sensitive and specific for RV infarct. With a large RV infarct, we may see brady-arrhythmias. Other signs of acute RV failure may include RV strain pattern (e.g., ST depression and T wave inversions in V1-V3). Enjoy Ep #60 - Massive PE for more on ECG changes in acute PE and RV failure! CT: While usually not obtained in the setting of acute RV failure unless evaluating for acute PE or parenchymal lung disease, RV:LV ratio >1.0, pulmonary trunk enlargement, and contrast reflux into the inferior vena cava and hepatic veins suggest right heart failure. A gated cardiac contrast-enhanced CT can provide more information about chamber size/function and valvular pathology. TTE: Echo is crucial in the diagnosis of RV failure! One of the first things to pay attention to is RV size, with RV dilation being a poor prognostic sign; RV:LV ratio > 1 is associated with increased in-hospital mortality in some studies of acute PE patients. Evaluate the position of the interventricular septum,

Sep 30, 2020

CardioNerds (Amit Goyal & Daniel Ambinder) join University of Florida cardiology fellows (Ashley Mohadjer, Hussain Khalid, and Morgan Randall) for an authentic Gainesville-style tailgate! They discuss a fascinating case of severe peripheral artery disease (PAD) and cerebral hyperperfusion syndrome. Dr. Khanjan Shah provides the E-CPR and a message for applicants. Episode notes were developed by Johns Hopkins internal medicine resident Richard Ferraro with mentorship from University of Maryland cardiology fellow Karan Desai. Jump to: Patient summary - Case media - Case teaching - References Episode graphic by Dr. Carine Hamo The CardioNerds Cardiology Case Reports series shines light on the hidden curriculum of medical storytelling. We learn together while discussing fascinating cases in this fun, engaging, and educational format. Each episode ends with an “Expert CardioNerd Perspectives & Review” (E-CPR) for a nuanced teaching from a content expert. We truly believe that hearing about a patient is the singular theme that unifies everyone at every level, from the student to the professor emeritus. We are teaming up with the ACC FIT Section to use the #CNCR episodes to showcase CV education across the country in the era of virtual recruitment. As part of the recruitment series, each episode features fellows from a given program discussing and teaching about an interesting case as well as sharing what makes their hearts flutter about their fellowship training. The case discussion is followed by both an E-CPR segment and a message from the program director. CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademySubscribe to our newsletter- The HeartbeatSupport our educational mission by becoming a Patron!Cardiology Programs Twitter Group created by Dr. Nosheen Reza Patient Summary A woman in her 60s with a past medical history of type 2 diabetes, hypertension, and hypothyroidism presented to the University of Florida with a chief complaint of "Someone told me my neck artery was blocked." Someone call 227-346-6373. What does that spell? CardioNerd! She noted exertional pain in both legs with limited exertion. Has a family history of CAD and MI in her father in his 20s. Her only medications were baby aspirin, atorvastatin 80mg, and thyroid replacement. Her blood pressures were noted to be dropping and so her regimen was being titrated off as a result. Physical exam was notable only for poorly palpable pulses in all extremities. To further work this up, a myocardial perfusion scan, CTA head/neck/abdomen, and ABIs were ordered. ABI on the right was 0.86 and on the left was 0.76 with monophasic doppler waveforms throughout. CT abdomen exhibited an occlusion of the abdominal aorta from just below the renal arteries extending to the common iliac arteries with distal reconstitution. CT head/neck showed occlusion of the right carotid artery, complete occlusion of the right innominate artery, near complete occlusion of the right vertebral artery, and delayed flow in the right posterior cerebral artery. On the left side, she had high-grade subclavian stenosis. Myocardial perfusion imaging exhibited no defects. On subsequent visits her exercise tolerance improved with an exercise regimen, but blood pressures were more and more difficult to obtain. As a result, revascularization was pursued with stenting of the left subclavian artery. She was discharged, but returned a few hours later with severe left sided pulsatile headache and nausea/vomiting. She was admitted for monitoring, but fortunately improved and discharged with close outpatient follow-up. She continued to improve in the outpatient setting. After MRI brain and extensive work-up, she was deemed to have cerebral hyperperfusion syndrome following revascularization. She had no further complications and was monitored thereafter. Final diagnosis: severe peripheral artery disease (PAD) and cerebral hyperperfusion syndrome. Case Media ABCDEFClick to Enlarge A: ECG B: ABIsC: CT Angiogram D: CT Angiogram - head and neck E: Pre and post subclavian stentinng F: CT head and neck - follow up Subclavian via L radial Aortic Root Cine 1 Aortic Root Cine 2 Stent Post Stent Post Stent 2 Post Stent 3 Episode Schematics & Teaching Click to enlarge! The CardioNerds 5! – 5 major takeaways from the #CNCR case What are the risk factors and prevalence of PAD? PAD refers to atherosclerotic peripheral artery disease, and is the accumulation of plaque in various peripheral arterial beds akin to CAD involving coronary arteries. 6% of adults over the age of 40 have PAD, and 30% of American adults over the age of 70. This all leads to an annual healthcare expenditure in the US of ~$4 billion! PAD is associated with a 3-4x increased risk of cardiovascular events. Furthermore, mortality overall is 15-20% at 5 years in patients with PAD. Risk factors for PAD include all the risk factors for ASCVD we consider for CAD, including diabetes, hypertension, and hyperlipidemia. What Should We Look for on Physical Exam with PAD? Get a brachial blood pressure (Class Ib AHA/ACC Recommendation), listen for bruits (areas of turbulent flow), and look at the extremities for: skin color changes, temperatures changes, loss of hair, or ulcerations (typically at the tips of digits). In patients with claudication and/or risk factors for PAD, these can all be signs of PAD. In particular, palpate the dorsalis pedis and tibialis pulses. In office maneuvers can also include Buerger's test where the affected limb is elevated from a supine position till pallor is observed. In a normal limb, even elevating to 90 degrees should not elicit pallor; however, in an ischemic limb, especially severe ischemia, elevation to even 20 degrees for 30 to 60 seconds can lead to pallor. Then when returning the limb to resting position, the pink color will return slowly (I.e., >20 seconds) and may demonstrate rubor as there is reactive hyperemia (dilation of the arterioles) in attempt to remove metabolic waste and restore circulation. At the bedside, we should also test for diseases commonly associated with PAD, particularly diabetes. Testing for diabetic neuropathy is critical in patients with PAD, as it is a modifiable risk factor and can make patients prone to developing diabetic foot ulcers. Remember, that there are classic locations for arterial ulcers but often patients have a mixed picture given concomitant venous insufficiency and/or diabetes. These arterial ulcers tend to occur where arteries terminate, including between the digits and tips of the toes. Furthermore, they can occur at areas of increased pressure, including the lateral malleolus. How do we obtain and interpret ABIs in chronic limb ischemia? ABI stands for Ankle-Branchial Index. This means taking the ankle blood pressure and indexing it against the brachial blood pressure. The ABI is an easily done test. To ensure we have an accurate ABI, we typically ask the patient to rest for at least 5-10 minutes prior to measuring ankle pressure. We also want to make sure we have the appropriate cuff size, and thus in the limbs the cuff width should be at least 40% of the limb circumference. We can start by taking the brachial pressure in one arm. After obtaining our initial brachial SBP, we then proceed with taking a blood pressure from either the dorsalis pedis or posterior tibial artery on the same side, with the cuff just above the ankle. We utilize a continuous wave doppler signal to identify the pulse and insufflate the cuff to just above where the Doppler signal disappears. We then slowly release the pressure in the cuff and record where the systolic pressure returns and repeat the process for the artery (e.g., DP or PT) that was not tested and then move onto to the contralateral limb. We then finally obtain the SBP in the brachial on the side opposite from where we started. The ABI for a specific extremity is then the highest pressure in a lower extremity limb (DP or PT) divided by the highest systolic brachial pressure in either limb. As discussed above, we usually calculate the ABI at bedside using a continuous-wave doppler probe, but when blood pressures are low or if there is significant venous congestion leading to pulsatile flow (e.g., congestive heart failure), the venous signal can be difficult to distinguish from the arterial signal. Briefly, a normal ABI is considered 1.0 to 1.4; 0.91 to 0.99 is considered borderline; and 1.4 are considered abnormal. In patients with symptoms of PAD (e.g., claudication), ABI has a sensitivity of ~ 95% and specificity of 100% of diagnosing lesions with >50% stenosis in one or major lower extremity vessels. An ABI > 1.4 suggests the presence of calcified vessels and we need additional vascular studies, such as measurement of the toe brachial index (TBI) or pulse volume recordings (PVR) to assess for significant PAD. The vessels in the toe have been shown to be less prone to medial calcification. Finally, segmental brachial index measurements are also considered abnormal if there is a decrease in 20 mmHg or more between adjacent levels in the lower extremity, a decrease in segmental brachial index of 0.15 or more over time, or a difference in systolic pressure more than 30 mmHg between contralateral limbs. How Do We Treat Symptomatic PAD? Exercise! First and foremost, supervised treadmill exercise training is a Class Ia recommendation from the AHA/ACC guidelines. Multiple studies have shown exercise to be beneficial in improving time and distance to developing claudication symptoms and increasing pain-free walking distance up to 180%. Notably, an exercise trial is recommended prior to any attempted revascularization. As with CAD, lifestyle measures to mitigate ASCVD risk factors are vital, including diet, weight loss,

Sep 27, 2020

CardioNerds (Amit Goyal & Daniel Ambinder) join Johns Hopkins Hospital cardiology fellows (Rick Vakil, Pranoti Hiremath, and Vasanth Sathiyakumar) for some gelato by the bay in Baltimore, Maryland! They discuss a challenging case of RV failure & shock after placement of an AV graft. Dr. Monica Mukherjee provides the E-CPR and program director Dr. Steven Schulman provides a message for applicants. Episode notes were developed by Johns Hopkins internal medicine resident Colin Blumenthal with mentorship from University of Maryland cardiology fellow Karan Desai. Jump to: Patient summary - Case media - Case teaching - References Episode graphic by Dr. Carine Hamo The CardioNerds Cardiology Case Reports series shines light on the hidden curriculum of medical storytelling. We learn together while discussing fascinating cases in this fun, engaging, and educational format. Each episode ends with an “Expert CardioNerd Perspectives & Review” (E-CPR) for a nuanced teaching from a content expert. We truly believe that hearing about a patient is the singular theme that unifies everyone at every level, from the student to the professor emeritus. We are teaming up with the ACC FIT Section to use the #CNCR episodes to showcase CV education across the country in the era of virtual recruitment. As part of the recruitment series, each episode features fellows from a given program discussing and teaching about an interesting case as well as sharing what makes their hearts flutter about their fellowship training. The case discussion is followed by both an E-CPR segment and a message from the program director. CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademySubscribe to our newsletter- The HeartbeatSupport our educational mission by becoming a Patron!Cardiology Programs Twitter Group created by Dr. Nosheen Reza Patient Summary A man in his early 40s, with a history of type 1 diabetes and prior failed renal and pancreatic transplants currently on iHD, was referred to Johns Hopkins Hospital for dialysis access. A left groin AV loop graft was pursued due to multiple access point failures in the past secondary to severe peripheral artery disease. Pre-op evaluation included risk stratification with RHC which was consistent with WHO Group 2 pulmonary HTN and diffuse atherosclerosis in the RCA on LHC. Intra-op, patient had an episode of significant hypotension after administration of protamine that required phenylephrine and ephedrine. In the PACU, his BPs continued to be low (70s/40s mmHg), requiring admission to the SICU where cardiology was consulted. In the SICU, patient had ongoing hypotension despite pressors and fluids. Exam demonstrated a systolic murmur consistent with TR and elevated JVP. Labs were notable for a mild elevation in liver enzymes, elevated troponin, high NT-proBNP and elevated lactate. TTE demonstrated a moderately dilated and hypokinetic RV, elevated RVSP and evidence of pressure/volume overload. CTA abdomen/pelvis demonstrated extensive mesenteric atherosclerosis and signs of gastric ischemia. Patient was treated for RV failure with norepinephrine, inhaled epoprostenol, and CVVHD for volume removal. He became febrile and was treated empirically with broad spectrum antibiotics. Due to concern for the new loop graft causing high output heart failure vs RV failure, it was temporarily occluded for testing and then permanently ligated by vascular surgery with significant improvement in his BPs and RV function on repeat TTE. Case Media ABCDEClick to Enlarge A. Plato's allegory of the cave by Jan Saenredam, according to Cornelis van Haarlem, 1604, Albertina, ViennaB-C. Anesthesia flow sheets D. CXR: Pulmonary vascular congestion, bibasilar atelectasisE. ECG: Sinus tachycardia to 110, RAD, RBBB, similar to prior TTE: LVEF 60-65%, mild to moderate concentric hypertrophy, trace effusion TTE: Flattened septum in systole and diastole c/f RV pressure and volume overload. RV moderately dilated and hypokinetic. RVSP 63 mmHg. CT Abdomen and Pelvis: Negative for PE, gastric pneumatosis, air within the gastroepiploic veins, and portal venous gas, most concerning for gastric ischemia, extensive atherosclerotic calcifications throughout the mesenteric vessels TTE follow up: Mild/moderate concentric hypertrophy, EF 60%, G2DD TTE follow up: RV mildly dilated and mild global hypokinesis of the RV. TAPSE 1.54. RV S’ was 9.6 cm/s (normal > 9.5) Episode Schematics & Teaching Click to enlarge! The CardioNerds 5! – 5 major takeaways from the #CNCR case 1. In this case the patient became hypotensive shortly after administration of protamine. What are the risk factors for a protamine reaction and the proposed mechanisms? Protamine is a protein commonly used in cardiovascular procedures to reverse the effects of heparin. Although rare, it can cause severe reactions that have multiple different proposed mechanisms. They include hypotension mediated by histamine release from mast cells and IgE-mediated anaphylaxis. Other proposed mechanisms include acute severe pulmonary hypertension with or without RV failure mediated by complement and thromboxane A2 and fulminant noncardiogenic pulmonary edema likely through a thromboxane-mediated process. Risk factors for protamine reactions have been difficult to rigorously prove, but might include patients with a true fish allergy (Protamine is produced from the sperm of salmon or similar species), men s/p vasectomy (disruption of blood-testes barrier and sensitization against sperm), insulin dependent diabetic patients taking NPH insulin (protamine is used in NPH), and previous exposure to protamine 2. Our patient had signs of RV failure clinically and on TTE following AV graft creation. How common is this, what is the mechanism, and when might one consider avoiding fistula or graft creation in a patient with CHF? AV fistulas (AVF) are the preferred chronic iHD access due to reductions in infections, morbidity, and mortality compared to central venous access. However, this data is based on observational studies. Remember, changes in hemodynamics occur in phases following creation of AV hemodialysis access. Acutely, an AVF or prosthetic graft (AVG) decreases systemic vascular resistance (SVR) through a surgical arterial to venous shunt. This acute decrease in SVR leads to increased stroke volume and a decrease in blood pressure. The decrease in SVR activates the sympathetic nervous system and leads to increased HR and combined with the increased SV, an increase in cardiac output. The increased cardiac output leads to increased right sided venous return and sub-acutely can lead to progressively increasing left and right sided filling pressures. Eventually, there can be worsening RV dilation and systolic dysfunction, elevated pulmonary artery pressures, and myocardial remodeling. Retrospective analyses have shown that creation of an AVF/AVG can increase the prevalence of RV dilation and dysfunction by 2-3 fold in patients with ESRD. The risk of worsening heart failure in patients with pre-existing cardiac disease is generally related to the flow in the AV access. Some small studies have suggested there is increased risk of developing heart failure in patients with an upper-arm AV fistula compared with a forearm fistula Although there are not clear guidelines that dictate when a patient should not receive an AVF/AVG, a permanent dialysis catheter should be considered as an alternative option in patients with pre-existing heart failure or pulmonary hypertension due to increased risk of right heart failure. 3. AV vascular access can lead to high output heart failure. What is high output heart failure and what are the major mechanisms? Most CHF occurs in the setting normal or low CO. However, certain conditions can precipitate high output heart failure (HoHF). The underlying pathophysiologic change in HoHF seems to be disproportionately low SVR +/- increased oxygen consumption. The low SVR leads to decreased afterload, increased LV emptying and thus increased stroke volume and cardiac output. Furthermore, this leads to increased cardiac preload. Increased oxygen demand also requires increased cardiac output. The persistently low SVR causes low renal perfusion pressure (renal hypoperfusion) which leads to RAAS activation and volume expansion. Combined with the increased preload, this can lead to heart failure in susceptible individuals. Obesity (the most common etiology), AV fistulas (congenital or acquired), cirrhosis, and Paget's disease lead to HoHF predominantly due to systemic vasodilation. Lung disease, myeloproliferative disorders, and hyperthyroidism can cause HoHF and have a proportionally larger contribution from increased metabolic demand and therefore increased oxygen consumption. Lower SVR has been associated with higher mortality. 4. How might someone differentiate high output heart failure from low output heart failure or RV failure? RHC is the gold standard to diagnose high output heart failure. Characteristic features include an elevated CO or CI (CI ≥4 L/min/m2) and a low SVR in the setting of clinical signs of heart failure. In a Mayo Clinic study of patients with CI > 4 L/min/m2 with or without signs of heart failure, a CI ≥3.54 L/min/m2 estimated by TTE identified HoHF patients with 62% sensitivity and 96% specificity. Furthermore, patients with HoHF frequently demonstrated doppler-estimated RV systolic pressure ≥ 42 mmHg (92% sensitivity and 100% specificity). 5. After temporary occlusion of his loop graft, our patient had improvement of his blood pressure and a decrease in his HR. What does this indicate and how is it mediated?

Sep 25, 2020

CardioNerds (Amit Goyal & Daniel Ambinder) join Medical College of Wisconsin cardiology fellows (Katie Cohen, Div Mohananey, and Dave Lewandowski) for some cold brews by Lake Michigan in Cream City aka Milwaukee, WI! They discuss a case of a pregnant woman presenting cardiac arrest due to peripartum cardiomyopathy. Dr. Sarah Thordsen provides the E-CPR and program director, Dr. Nunzio Gaglianello, provides a message for applicants. Episode notes were developed by Johns Hopkins internal medicine resident, Eunice Dugan, with mentorship from University of Maryland cardiology fellow Karan Desai. Jump to: Patient summary - Case media - Case teaching - References Episode graphic by Dr. Carine Hamo The CardioNerds Cardiology Case Reports series shines light on the hidden curriculum of medical storytelling. We learn together while discussing fascinating cases in this fun, engaging, and educational format. Each episode ends with an “Expert CardioNerd Perspectives & Review” (E-CPR) for a nuanced teaching from a content expert. We truly believe that hearing about a patient is the singular theme that unifies everyone at every level, from the student to the professor emeritus. We are teaming up with the ACC FIT Section to use the #CNCR episodes to showcase CV education across the country in the era of virtual recruitment. As part of the recruitment series, each episode features fellows from a given program discussing and teaching about an interesting case as well as sharing what makes their hearts flutter about their fellowship training. The case discussion is followed by both an E-CPR segment and a message from the program director. CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademySubscribe to our newsletter- The HeartbeatSupport our educational mission by becoming a Patron!Cardiology Programs Twitter Group created by Dr. Nosheen Reza Patient Summary A G2P1 woman in her early 30s with a history palpitations presented after a witnessed out-of-hospital cardiac arrest while at work. She received 6 rounds of CPR and 2 shocks before ROSC was achieved. She was intubated and given fluids but continued to remain hypoxic and hypotensive. Exam demonstrated sinus tachycardia, no murmurs, gravid abdomen and cool extremities. Initial labs demonstrated leukocytosis to 14k, lactic acid at 4.3 mmol/L, troponin-I peak at 0.07 ng/dL and elevated NT-proBNP. CXR demonstrated bilateral effusions and pulmonary congestion, and post-arrest EKG showed a wide complex tachycardia, leading to suspicion of VT arrest. In sinus, there were no ST segment elevations and TTE showed LVEF 10-20%, global hypokinesis and no valvular disease. Given the severity of her shock, she was placed on central VA-ECMO with Impella support as an LV vent. During ECMO cannulation, she underwent emergent cesarean section due to fetal distress. Coronary angiography showed non-obstructive coronaries, but with sluggish flow in the setting of her cardiogenic shock and possible coronary spasm in setting of multiple vasoactive medications. Endomyocardial biopsy was negative for giant cell myocarditis. Within 4-5 days, she was weaned off all vasoactive agents and ECMO was decannulated; repeat echocardiogram showed LV functional recovery. GDMT was slowly titrated and a subcutaneous ICD was eventually placed before discharge. She and her child have done well over the course of a year! Case Media ABClick to Enlarge A: ECG: Initially in sustained wide complex irregular tachycardiaB: CXR: Extensive consolidative changes throughout the lungs TTE: Parasternal Long Axis TTE: Apical 4 Chamber Episode Schematics & Teaching Click to enlarge! The CardioNerds 5! – 5 major takeaways from the #CNCR case 1. What is the differential for cardiac arrest in pregnant patients? When thinking about a cardiac etiology of arrest, the differential should include pregnancy-induced hypertension, peripartum cardiomyopathy, myocardial infarction from acute coronary syndrome or spontaneous coronary artery dissection, pulmonary embolism, amniotic fluid embolism and aortic dissection. Non-cardiac etiologies include hemorrhagic shock, sepsis, stroke, trauma and anesthetic complications. In addition to these unique considerations, pregnant patients are also susceptible to the usual culprits! As noted in the 2015 AHA Scientific Statement, cardiac arrest in pregnancy is not common, occurring in 1:12,000 admissions for delivery. As of 2016, per the CDC the pregnancy-related mortality rate was ~17 deaths per every 100,000 live births. However, mortality data does not fully capture critical illness in pregnancy, and thus the AHA recommends considering maternal "near-miss" data. Knowledge gaps, provider unfamiliarity, and lack of medical ward or medical/cardiac ICU preparation for cardiac arrest in pregnancy may contribute to morbidity and mortality. Finally, as many of the early warnings signs of impending cardiac arrest may overlap with symptoms of pregnancy (e.g., progressive dyspnea), early interventions may be delayed. Thus, the AHA recommends using a validated obstetric early warning score to risk stratify ill pregnant patients. 2. Remind us of some important physiologic changes in pregnancy that can affect cardiopulmonary resuscitation Hormonal and physiologic changes during pregnancy make pregnant patients more prone to hypoxia, hypotension, pulmonary edema, and difficult airway intubation. Systemic vascular resistance typically decreases due to the production of endogenous vasodilators, though there are important differences in patients with pre-eclampsia. The enlarging uterus can reduce preload by compressing the IVC and increase afterload by compressing the aorta. In the supine position, which is preferable for resuscitation, this compression can be exacerbated. Furthermore, as the uterus enlarges and limits diaphragmatic movement, functional residual capacity can decrease by 10-25%. At the same time, there is increased oxygen consumption due to metabolic and fetal demands. With limited reserve and increased oxygen demands, hypoventilation or apnea can rapidly precipitate hypoxemia. Cardiac output increases by 30-50% via increased stroke volume, and lesser extent HR, leading to increased circulating volume, making patients prone to pulmonary edema. Finally, pregnancy hormones can lead to airway edema and more friable tissue making intubation more difficult with increased risk of bleeding. For more on pregnancy physiology, enjoy: Ep #48 - Critical Bicuspid Aortic Valve Stenosis Complicating Pregnancy Ep # 57 - Peripartum Cardiomyopathy with Cardiogenic Shock 3. What are some aspects unique to advanced cardiac life support (ACLS) in pregnant patients? Cardiac arrest is inherently different than other cardiac arrest that we typically encounter as there are two patients: mother and the fetus. Chest compressions, delivery of shocks and medications can continue per standard adult ACLS algorithm. Importantly, while chest compressions are ongoing and patient is in the supine position, there should be continuous manual left uterine displacement (LUD) to relieve aortocaval compression. Furthermore, IVs should be established above the diaphragm so that intravenous infusions and medications are not impeded by caval compression of the uterus. Teams should be prepared for perimortem caesarean delivery (PMCD) and this should occur at the site of arrest. PMCD may facilitate return of spontaneous circulation (ROSC) after the gravid uterus is emptied. PMCD should occur within four minutes due to a rapid decline in fetal survival with longer delays to delivery. 4. What are the considerations for post-arrest care for pregnant patients? Targeted temperature management (TTM) is not contraindicated in pregnancy, and no necessary intervention should be withheld for fear of fetal damage. The primary focus should be maternal outcomes since that best serves fetal outcomes. If TTM is pursued, there should be continuous fetal monitoring. The patient should continue to be in the left lateral decubitus position if it does not compromise other management. Routine cardiac catheterization is certainly not recommended unless post-arrest EKG demonstrates clear signs of ischemia. Remember that embryogenesis is mostly complete by 12 weeks of gestation. Thus, the AHA recommends providing all necessary medications, even teratogenic medications (e.g., corticosteroids, phenytoin) especially if the cardiac arrest occurs after the first trimester. 5. What is the data for extra-corporeal life support (ECLS) during pregnancy and postpartum There are no consensus guidelines, however, ECLS is not contraindicated in pregnancy and should be considered for life-threatening conditions. There is lack of long-term data for maternal and fetal outcomes. Although survival varied depending on indication, one systematic review of ECLS in peripartum patients showed overall 30-day survival of 75% for mother and 64% for fetus. Interestingly, survival in the immediate post-partum group was the highest. Complications includes bleeding, deep vein thrombosis, and vascular complications similar to the non-pregnant population. References Arany Zolt, and Elkayam Uri. “Peripartum Cardiomyopathy.” Circulation 133, no. 14 (April 5, 2016): 1397–1409. Campbell, Tabitha A, and Tracy G Sanson. “Cardiac Arrest and Pregnancy.” Journal of Emergencies, Trauma and Shock2, no. 1 (2009): 34–42. Jeejeebhoy Farida M., Zelop Carolyn M., Lipman Steve, Carvalho Brendan, Joglar Jose, Mhyre Jill M., Katz Vern L., et al. “Cardiac Arrest in Pregnancy.” Circulation 132, no. 18 (November 3, 2015): 1747–73. Gilotra, Nisha A, and Gerin R Stevens. “Temporary Mechanical Circulatory Support: A Review of the Options, Indications, and Outcomes.” Clinical Medicine Insights. Cardiology 8, no. Suppl 1 (February 3,

Sep 23, 2020

CardioNerds (Amit Goyal & Daniel Ambinder) join Cedars-Sinai cardiology fellows (Natasha Cuk, Ronit Zadikany, Neal Yuan) for some drinks at the local pub 3rd Stop after a walk down Hollywood boulevard! They discuss a fascinating case of a massive pulmonary embolus presenting as STEMI. Dr. Babak Azarbal provides the E-CPR and program director Dr. Joshua Goldhaber provides a message for applicants. Episode notes were developed by Johns Hopkins internal medicine resident Bibin Varghese with mentorship from University of Maryland cardiology fellow Karan Desai. Jump to: Patient summary - Case figures & media - Case teaching - References - Production team Episode graphic by Dr. Carine Hamo The CardioNerds Cardiology Case Reports series shines light on the hidden curriculum of medical storytelling. We learn together while discussing fascinating cases in this fun, engaging, and educational format. Each episode ends with an “Expert CardioNerd Perspectives & Review” (E-CPR) for a nuanced teaching from a content expert. We truly believe that hearing about a patient is the singular theme that unifies everyone at every level, from the student to the professor emeritus. We are teaming up with the ACC FIT Section to use the #CNCR episodes to showcase CV education across the country in the era of virtual recruitment. As part of the recruitment series, each episode features fellows from a given program discussing and teaching about an interesting case as well as sharing what makes their hearts flutter about their fellowship training. The case discussion is followed by both an E-CPR segment and a message from the program director. CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademySubscribe to our newsletter- The HeartbeatSupport our educational mission by becoming a Patron!Cardiology Programs Twitter Group created by Dr. Nosheen Reza Patient Summary A man in his mid-40s with no known past medical history presented to the ER in PEA arrest with ongoing cardiopulmonary resuscitation (CPR). Prior to his arrest, his coworkers reported that he was complaining of lightheadedness, dizziness and that he was found slumped over at his desk. His EKG in the ambulance showed STE in aVR and V1 - V4 with TWI in III and aVF initially concerning for an anterior STEMI. He was cannulated with VA-ECMO for extracorporeal cardiopulmonary resuscitation (E-CPR) and was taken to the catheterization lab emergently. In the catheterization lab, his coronary angiogram did not show obstructive coronary disease. The interventionalists decided to perform a pulmonary artery (PA) angiogram which revealed a large amount of thrombus bilaterally in the proximal PAs. He underwent surgical embolectomy with removal of almost all his clot burden. The patient was thereafter cooled for neurological protection. Unfortunately, the patient had a very poor neurological exam with lack of brainstem reflexes upon rewarming. There was loss of gray-white differentiation on CT, and EEG and evoked potential testing were consistent with severe anoxic brain injury. After discussions with the patient's family, the patient was transitioned to comfort care and subsequently passed away peacefully. Case Media Click to Enlarge Right Coronary Artery Left Coronary System - 1 Left Coronary System - 2 Left Pulmonary Artery Right Pulmonary Artery Episode Schematics & Teaching Click to enlarge! The CardioNerds 5! – 5 major takeaways from the #CNCR case The patient presented initially with STE in aVR as well as the septal and anterior leads. What is the differential for an ST elevation in lead aVR? STE in aVR with diffuse ST depression can be a potential finding of LM or LAD stenosis. However, there have been several studies that have shown that the combination of STE and multi-lead STD was not associated with complete occlusion of a culprit vessel. Thus, the differential for STE in aVR more commonly includes significant LM or LAD stenosis, severe three-vessel disease with diffuse sub-endocardial ischemia (e.g., CAD in the setting of sepsis, anemia, shock), as well as pulmonary embolism with right ventricular injury (see below)! Remember that lead aVR is opposite I, aVL, II and V5-6 and thus elevation in aVR may represent reciprocal changes of diffuse sub-endocardial ischemia. Furthermore, aVR doesn't directly overlie myocardium but reflects electrical activity from the RV outflow tract and basal septum. Thus, in the context of an anterior STEMI, STE in aVR (> 1mm) strongly predicts LAD occlusion proximal to the first septal perforator, which supplies the basal septum. The patient was found to have non-obstructed coronaries and was ultimately diagnosed with a PE. Could we have suspected that from the initial EKG? What are the EKG changes that have been noted in patients with a PE? Generally, an EKG does not make the diagnosis of PE, as most findings have low sensitivity and specificity. Rather, an EKG can be helpful in evaluating other causes of a patient's cardiopulmonary symptoms and provide supporting evidence of acute PE. The EKG findings in acute PE can be thought to be secondary to three primary mechanisms: (1) increased adrenergic drive, (2) RV and/or RA dilation, and/or (3) RV myocardial ischemia and injury. The most common EKG fining is sinus tachycardia. Atrial arrhythmia (e.g., atrial fibrillation or flutter) can be seen and is predominantly a result of RA/RV dilation with increased adrenergic drive. Complete or incomplete RBBB may occur as the RBB is vulnerable to stretch, especially early in its course. Due to acute RV dilation with accompanying rotation of the heart in relation to the ECG leads (more commonly in sub-massive or massive PE), we can see right axis deviation, a dominant R-wave in V1, and the R to S transition point in the precordial leads shifting towards V5. As a result of ischemia and/or RV injury, we may see the classic S1Q3T3 pattern, but this is not a sensitive finding and thus its absence should not change decision-making. We can also see an RV strain pattern with T-wave inversions (TWI) in the right precordial leads (V1-V3) as well as the inferior leads. Non-specific ST-T changes are relatively common and along with sinus tachycardia, may be the most frequent finding. ST elevation in aVR with accompanying elevation in V1-V3 may be seen in PE (especially if complicated by obstructive shock). The injury current in the limb leads is directed towards aVR in this circumstance. In the precordial leads the injury current is more variable. A differentiating point between proximal LAD or LM acute MI and acute PE could be the presence of prominent reciprocal STD and the distribution of TWI. This patient presented in cardiac arrest and obstructive shock from a massive PE. What is the treatment for patients with a massive PE and cardiac arrest? In patients with cardiac arrest or circulatory collapse, VA-ECMO in combination with surgical embolectomy or catheter-directed treatment is given a Class IIb recommendation in patients with massive PE per 2019 ESC guidelines. In general, the decision to proceed with active thrombus removal, whether it be with thrombolytic-based, catheter-based, or surgical embolectomy, is driven by first the severity of the PE and secondarily by patient-specific factors for bleeding and co-morbidities. However, if VA-ECMO is pursued, it should not be a stand-alone strategy In patients with massive (AHA) or high risk (ESC) PE – defined as systolic blood pressure 40 mmHg for at least 15 minutes – systemic thrombolytic therapy carries a Class IB recommendation. Trial data has demonstrated earlier hemodynamic improvement with systemic thrombolysis compared to anticoagulation alone, especially if treatment is initiated within 48 hours of symptom onset Catheter directed therapy may have a role in massive PE – whether it be through mechanical, saline or ultrasound lysis – in patients who have persistent hemodynamic instability despite systemic thrombolysis and patients with moderate to high bleeding risk. Embolectomy is indicated in hemodynamically unstable patients with massive PE in whom thrombolytic therapy is contraindicated or patients who fail thrombolytic therapy. Furthermore, it may be considered early in patients with extensive clot burden where there is surgical expertise.Although the patient presented with refractory cardiac arrest, he was able to be stabilized with E-CPR before diagnostic evaluation was performed. What does ECPR stand for? Has it been proven to improve clinical outcomes? As defined by the AHA guidelines, extracorporeal cardiopulmonary resuscitation or ECPR is the use of VA-ECMO during the resuscitation of a patient in cardiac arrest, with the goal of providing end-organ perfusion while reversible causes of arrest are identified and treated. There have been several studies regarding the use of ECPR in out of hospital and in hospital cardiac arrest (OHCA and IHCA), respectively. It remains unclear whether ECPR is of consistent benefit with regards to morbidity and mortality as studies have lacked a uniform definition of EPCR, consisten inclusion criteria for ECPR, and many studies have been single-center introducing the potential for bias. Thus, in the 2019 AHA Focused Updated on ACLS guidelines, ECPR is given a Class 2b indication (with level of evidence C-LD), where it can be considered in select patients as rescue therapy when conventional CPR efforts are failing in clinical settings in which it can be quickly implemented and supported by trained providers. It sounds like the benefits of E-CPR remain to be further elucidated. Are there any specific features that help predict who would benefit from ECPR? While we do not have high quality randomized data, observational data in EPCR has shown that shorter no flow times (i.

Sep 21, 2020

CardioNerds (Amit Goyal & Daniel Ambinder) join join Mayo Clinic cardiology fellows (Mays Ali, Charlie Jain, Korosh Sharain) for a scenic walk through gorgeous Rochester, Minnesota! They discuss a fascinating case of constrictive pericarditis and severe mitral regurgitation. Dr. Rick Nishimura provides the E-CPR and program director Dr. Frank Brozovich provides a message for applicants. Episode notes were developed by Johns Hopkins internal medicine resident Bibin Varghese with mentorship from University of Maryland cardiology fellow Karan Desai. Jump to: Patient summary - Case figures & media - Case teaching - References - Production team Episode graphic by Dr. Carine Hamo The CardioNerds Cardiology Case Reports series shines light on the hidden curriculum of medical storytelling. We learn together while discussing fascinating cases in this fun, engaging, and educational format. Each episode ends with an “Expert CardioNerd Perspectives & Review” (E-CPR) for a nuanced teaching from a content expert. We truly believe that hearing about a patient is the singular theme that unifies everyone at every level, from the student to the professor emeritus. We are teaming up with the ACC FIT Section to use the #CNCR episodes to showcase CV education across the country in the era of virtual recruitment. As part of the recruitment series, each episode features fellows from a given program discussing and teaching about an interesting case as well as sharing what makes their hearts flutter about their fellowship training. The case discussion is followed by both an E-CPR segment and a message from the program director. CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademySubscribe to our newsletter- The HeartbeatSupport our educational mission by becoming a Patron!Cardiology Programs Twitter Group created by Dr. Nosheen Reza Constrictive Pericarditis & Severe Mitral Regurgitation - Patient Summary A woman in her late 40s with a history of lupus and hypertension presented with worsening dyspnea on exertion and orthopnea over a year. She reported intermittent pleuritic chest discomfort that had persisted since an episode of acute pericarditis years prior. A TTE suggested severe mitral regurgitation, and she was referred to the Mayo Clinic for mitral valve intervention. The official TTE report from the OSH suggested non-dilated LV, EF 55-60%, normal RV function, severe MR with thickened leaflets and sub-valvular apparatus, moderate to severe TR and a dilated IVC. Furthermore, the CXR showed pericardial calcifications. Upon evaluation by the Mayo Clinic fellows, the JVP was elevated to about 10-12 cm with rapid x and y descents, a positive Kussmaul’s sign, and the murmurs of MR and TR. Her lungs were clear to auscultation and extremities did not demonstrate edema. Re-review of the TTE images revealed posterior pericardial thickening, no septal shift on respiration, but suggestion of annulus reversus where medial mitral annulus tissue doppler (9 cm/s) was greater than lateral (8 cm/s). Further, there was evidence of expiratory hepatic vein diastolic flow reversal. For the team, there was discordance between the apparent severity of her MR reported by echocardiogram and her clinical symptoms. In addition, the echocardiogram was suggestive of specific signs of constrictive pericarditis. Thus, simultaneous RHC/LHC was obtained. There was equalization of RV/LV pressures during diastole, demonstration of a “square root sign” and importantly discordance between LV and RV pressures with respiration. Thus, discordant clinical findings led to a suspicion for constrictive pericarditis and was corroborated by discordance on invasive hemodynamics! Further, the V-waves were not prominent on wedge pressure tracing and to investigate the mitral regurgitation further, an LV ventriculogram was done. This demonstrated 3+ to 4+ MR. Based on all the findings, the patient was diagnosed with constrictive pericarditis, severe MR and moderate to severe TR. She underwent pericardiectomy, mitral valve replacement (given that repair was not feasible due to the sub-valvular thickening) and given that TR has been shown to worsen after pericardiectomy and is a poor prognostic factor, she additionally underwent tricuspid valve repair. Her symptoms improved markedly following intervention. Case Media ABCDEFGHClick to Enlarge A. CXR: Heart size was borderline enlarged with biatrial enlargement. LV does not appear very enlarged. B. Mitral Regurgitation by CW Doppler C. Tricuspid regurgitation by CW Doppler. TR Max 2.43D. Tissue Doppler of the mitral valve annulus: Medial e' = 9 cm/s, Lateral e' 8 cm/sE. Hepatic Vein PW Doppler F. Right atrial pressure tracingG. RV and LV simultaneous pressure tracings H. Wedge pressure and LV simultaneous pressure tracings Neck Vein Exam TTE TTE: Color Doppler across mitral valve TTE: Short Axis TTE: Short Axis, TV TTE: Hepatic Vein Doppler Left ventriculogram with severe mitral regurgitation Episode Schematics & Teaching Click to enlarge! The CardioNerds 5! – 5 major takeaways from the #CNCR case- Constrictive Pericarditis & Severe Mitral Regurgitation One of the early clues to the etiology of this patient’s dyspnea was a positive Kussmaul's sign. What is the mechanism and differential of Kussmaul’s Sign? Typically the JVP decreases with inspiration as the negative intrathoracic pressure "sucks in" blood from the vena cavae. When there is a lack of decrease or an increase in JVP with inspiration, this finding is called Kussmaul’s sign. Kussmaul’s sign reflects conditions where there is right ventricular dysfunction, impaired RV filling and elevated right atrial pressure Kussmaul’s sign is classically associated with constrictive pericarditis. Remember, during normal inspiration, the diaphragm contracts and increases abdominal pressure with variable effect on venous return. However, in constriction, the rise in abdominal pressure increases venous return from the congested hepato-splanchnic vasculature. And since RV filling is constrained by a non-compliant pericardium, there is a rise in JVP during inspiration. Other conditions where we may see a positive Kussmaul’s sign include restrictive cardiomyopathy, RV predominant infarction, massive pulmonary embolism, tricuspid stenosis, and severe tricuspid regurgitation. 2. A decision was made to pursue invasive hemodynamic evaluation to differentiate between restrictive and constrictive physiology. How do we differentiate between the two on echocardiogram? Differentiating between the two diagnoses requires an understanding of the pathophysiologic differences between constriction and restriction. Enjoy Ep #58 and CN5 for understanding constrictive physiology and echocardiographic findings! In restriction we do not have intrathoracic-intracardiac disassociation as intrathoracic pressures are transmitted normally to the cardiac chambers during respiration. Further, there is no exaggerated interventricular dependence. We may see increased myocardial thickness in restriction (secondary to infiltrative or storage disorders - enjoy Ep #50 - restrictive cardiomyopathy) and increased pericardial thickness/calcification in constriction. Unlike constrictive pericarditis, restrictive cardiomyopathies should not demonstrate respirophasic septal shift or variation across the atrioventricular valves. Both conditions will demonstrate hepatic vein diastolic flow reversal. However, in constriction, the exaggerated ventricular interdependence and greater LV filling during expiration causes septal bowing into the RV and results in greater hepatic vein diastolic flow reversal during expiration. In restriction, hepatic vein flow reversal is more prominent in inspiration as the stiff myocardium is unable to tolerate the increased RV preload that occurs during inspiration. The estimated pulmonary artery systolic pressures tend to be elevated (>55-60 mmHg) in restrictive cardiomyopathy and are often normal in constriction. In constriction, the annular tissue velocity is preserved except at the lateral annulus, where tethering of the lateral wall results in decreased velocities and annulus reversus (See Ep#58 and CN5). Meanwhile, annular tissue velocity (e’) is significantly reduced in restrictive cardiomyopathy. Enjoy Ep #58 and CN5 for differences on invasive hemodynamics! 3. Given that the patient had subvavlular thickening, the patient was not a candidate for mitral valve repair and the patient underwent mitral valve replacement. What are the indications for mitral valve surgery in patients with severe chronic MR? Why is mitral valve repair preferred for primary MR? Class I indications for mitral valve surgery include (1) symptomatic patients in the absence of severe LV dysfunction (defined as EF 60% and LVESD 95% and expected mortality is 50 mmHg) and preserved LVEF. For primary mitral regurgitation involving an abnormality of the valve apparatus (e.g., leaflets, chordae, annulus, papillary muscles) – MV repair is preferred over MV replacement in most patients as it is associated with lower operative mortality and improved long term survival. Feasibility of valve repair will generally depend on valve anatomy and surgical experience.

Sep 18, 2020

CardioNerds (Amit Goyal & Daniel Ambinder) join join University of Tennessee cardiology fellows (Rachel Goodwin, Emmanuel Isang, and William Black) for some chocolate cake and hikes in the Smoky Mountains! They discuss a fascinating case of constrictive pericarditis. Dr. Tjuan Overly provides the E-CPR and a message for applicants. Episode notes were developed by Johns Hopkins internal medicine resident Evelyn Song with mentorship from University of Maryland cardiology fellow Karan Desai. Jump to: Patient summary - Case figures & media - Case teaching - References - Production team Episode graphic by Dr. Carine Hamo The CardioNerds Cardiology Case Reports series shines light on the hidden curriculum of medical storytelling. We learn together while discussing fascinating cases in this fun, engaging, and educational format. Each episode ends with an “Expert CardioNerd Perspectives & Review” (E-CPR) for a nuanced teaching from a content expert. We truly believe that hearing about a patient is the singular theme that unifies everyone at every level, from the student to the professor emeritus. We are teaming up with the ACC FIT Section to use the #CNCR episodes to showcase CV education across the country in the era of virtual recruitment. As part of the recruitment series, each episode features fellows from a given program discussing and teaching about an interesting case as well as sharing what makes their hearts flutter about their fellowship training. The case discussion is followed by both an E-CPR segment and a message from the program director. CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademySubscribe to our newsletter- The HeartbeatSupport our educational mission by becoming a Patron!Cardiology Programs Twitter Group created by Dr. Nosheen Reza Patient Summary A man in his late 40s with a history of renal failure secondary to IgA nephropathy and now status post a kidney transplant 10-15 years ago was referred by hepatology for evaluation of recurrent ascites and LE edema. He appeared grossly volume overloaded on exam with JVP elevated past the mandible, RV heave, and 2+ pitting edema. TTE demonstrated LVEF of 55-60%, RVSP 40mmHg, abnormal septal motion with respiration, and respirophasic variation in mitral inflow across the mitral valve raising the suspicion for constrictive pericarditis. RHC pressures demonstrated a mean RA pressure of 20mmHg, RV 40/25mmHg, PA 38/30mmHg (mean 32 mmHg) and PCWP mean of 26 with V-waves at 28 mmHg. Simultaneous LV and RV pressure tracings showed ventricular discordance with respirophasic variation, consistent with constrictive physiology. Patient underwent pericardiectomy with markedly improved heart failure symptoms. Repeat TTE showed no evidence of constriction. Case Media ABCClick to Enlarge! A. ECGB. Pulsed-wave Doppler spectrum of tricuspid inflow velocities demonstrates a marked respiratory variation (In irregular rhythms, such as the atrial fibrillation seen here, respirophasic changes may still be seen but are confounded by the varying R-R interval)C. Simultaneous LV and RV pressure tracings showing discordance with respirophasic variation Apical 4-chamber view demonstrating abnormal septal motion due to interventricular dependence – dissociation of thoracic and cardiac chamber pressures leads to increased RV filling during inspiration Short axis view of the LV demonstrating a D-shaped interventricular septum during inspiration. Note the presence of a pericardial effusion as well. Episode Schematics & Teaching Click to enlarge! The CardioNerds 5! – 5 major takeaways from the #CNCR case The initial presentation clinically seemed to be right greater than left heart failure. What are the signs and common causes of right heart failure? The signs and symptoms of RHF are often similar to left-sided CHF, but may describe more severe dyspnea on exertion, significant abdominal distension, and early satiety due to ascites or gut edema. Symptoms of pulmonary edema from elevated left-sided filling pressures (orthopnea, paroxysmal nocturnal dyspnea) may be absent. On examination, there will be elevated JVP with likely prominent v-waves, possibly Kussmaul’s sign (inspiratory rise in JVP rather than fall) depending on the pathology, abdominal ascites, pulsatile hepatomegaly, and lower extremity edema. An RV heave may be discernible along with a loud P2 component and murmur of TR. Broadly, RV failure may be caused by pressure overload (ex: pulmonary hypertension, pulmonic stenosis), volume overload (ex: intracardiac shunt, tricuspid regurgitation), or myocardial disease (ex: cardiomyopathies, ischemia/infarct). The most common cause of chronic right heart failure is LV failure (causing post-capillary pulmonary hypertension). Other causes of RV failure include pre-capillary pulmonary hypertension, congenital heart disease (e.g., ASD, residual RVOT obstruction in Tetralogy of Fallot patients), ARVC, RV ischemia, myocarditis, right sided valvular disease, constrictive pericarditis, and restrictive cardiomyopathy. The patient in this case was diagnosed with constrictive pericarditis (CP). What are the causes of CP? Remember that the etiology of CP can vary considerably depending on the patient’s demographics. In developed countries, the majority of cases are idiopathic or viral, post-operative, or post-radiation therapy. In developing countries, infectious etiologies are more common, with tuberculosis the most common cause. Amongst the causes, remember that acute bacterial and tuberculosis pericarditis have the highest chances of progressing into constriction. With post-radiation constrictive pericarditis, remember there can be significant delay (even up to 20 years) between radiation therapy and development of constriction and often accompanies concomitant myocardial fibrosis with restrictive physiology as well. Other etiologies include immunologic disorders (e.g., rheumatoid arthritis, lupus, sarcoidosis), malignancy (e.g., breast and lung cancers, lymphoma, mesothelioma), and myocardial infarction. 3. What are the TTE findings suggestive of constrictive pericarditis? To understand the basic TTE findings, we need a basic understanding of the pathophysiology. Constriction leads to a noncompliant pericardium that encases the heart. Heart failure occurs because there is impaired diastolic ventricular filling. The ventricles fill almost entirely in early diastole, because once they can no longer expand because of the non-distensible pericardium, diastolic filling abruptly stops. This pathophysiology reflects one of the key findings in CP: equalization of the end-diastolic pressures. At the same time, the thickened/fibrotic/calcified pericardium prevents the normal transmission of intrathoracic pressures to the cardiac chambers. However, structures “outside” the pericardium – such as the pulmonary vasculature – still “see” the normal changes in intrathoracic pressure. Normally, when we take a breath in: the intrathoracic pressure falls and this is transmitted equally to the pulmonary capillaries (e.g., the wedge pressure) and the cardiac chambers. The gradient for mitral valve inflow reflects the difference in wedge pressure and intra-cardiac chamber (LV) pressure. In CP, the drop in intrathoracic pressure with inspiration is transmitted to the pulmonary capillaries but not the cardiac chambers. Thus, there is now a decreased gradient for mitral valve inflow during inspiration. This is called intrathoracic-intracardiac pressure disassociation. At the same time, with inspiration right heart preload increases and to accommodate this volume the RV expands. However, RV expansion is limited by the encasing noncompliant pericardium, and thus to accommodate the volume the interventricular septum shifts to the left. This, further decreases the gradient for mitral valve inflow and the physiology is termed enhanced ventricular interdependence. The opposite occurs on expiration. Thus, on echocardiogram we may see abnormal respirophasic septal shift, reflecting enhanced ventricular interdependence. The septum moves to the left in early diastole with inspiration and then back to the right on expiration. This is one of the most sensitive echocardiographic findings for CP. Reflecting compromised diastolic filling, markedly elevated filling pressures, and equalization of end-diastolic pressures, there will be a high E-wave velocity with a decreased A-wave velocity (E/A > 1) across the mitral valve. Due to pericardial restraint, this early rapid diastolic filling (high velocity with a tall E wave) stops abruptly and so the E wave has a short deceleration time. The latter is analogous to the pericardial knock heard on physical exam and the ventricular early diastolic "square root" sign (dip and plateau) on the RHC. Reflecting intrathoracic-intracardiac pressure disassociation and enhanced ventricular interdependence, there will be increased respirophasic variation in mitral and tricuspid valve inflow. This typically is best demonstrated with the first few beats of inspiration and expiration. Specific cut-offs include a decrease in peak mitral E-wave velocity > 25% and increase in peak tricuspid E-wave velocity > 40% during inspiration (opposite during expiration). In other words, as you inspire there is increased filling of the RV with decreased filling of the LV. Expiratory hepatic vein diastolic flow reversal is one of the most specific findings of CP. Reflecting intrathoracic-intracardiac pressure disassociation and enhanced ventricular interdependence, during expiration RV filling is compromised (as the LV is filling with septal shift to the right) and thus there is “back-flow” from the right heart and we see more prominent flow reversal in the hepatic veins during expiration. In contrast,

Sep 16, 2020

CardioNerds (Amit Goyal & Daniel Ambinder) join Penn cardiology fellows (Brian McCauley, Norrisa Haynes, and Mahesh Vidula) for a rooftop picnic in sunny Philadelphia! They discuss an informative case of peripartum cardiomyopathy with cardiogenic shock. Program director Dr. Frank Silvestry provides the E-CPR segment and a message to applicants. Johns Hopkins internal medicine resident Colin Blumenthal with mentorship from University of Maryland cardiology fellow Karan Desai. Jump to: Patient summary - Case figures & media - Case teaching - References - Production team Episode graphic by Dr. Carine Hamo The CardioNerds Cardiology Case Reports series shines light on the hidden curriculum of medical storytelling. We learn together while discussing fascinating cases in this fun, engaging, and educational format. Each episode ends with an “Expert CardioNerd Perspectives & Review” (E-CPR) for a nuanced teaching from a content expert. We truly believe that hearing about a patient is the singular theme that unifies everyone at every level, from the student to the professor emeritus. We are teaming up with the ACC FIT Section to use the #CNCR episodes to showcase CV education across the country in the era of virtual recruitment. As part of the recruitment series, each episode features fellows from a given program discussing and teaching about an interesting case as well as sharing what makes their hearts flutter about their fellowship training. The case discussion is followed by both an E-CPR segment and a message from the program director. CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademySubscribe to our newsletter- The HeartbeatSupport our educational mission by becoming a Patron!Cardiology Programs Twitter Group created by Dr. Nosheen Reza Patient Summary Two weeks postpartum, a woman in her mid 20s, G1P1, with no past medical history presented following a tonic-clonic seizure. Prior to this, she had been experiencing 1 week of worsening dyspnea and lower extremity edema. Initial work-up revealed a left MCA stroke and she underwent thrombectomy. Limited TTE found LVEF R-side filling pressures with low cardiac index despite inotropes. Cardiac power output (CPO) was severely decreased with borderline pulmonary artery pulsatility index (PAPI), corroborating left > right heart failure. Patient ultimately required a durable left ventricular assist device (LVAD). Over the course of 9 months her guideline directed medical therapy (GDMT) was titrated and her intrinsic cardiac function and symptoms improved. Her EF improved to 35-40% and she tolerated an LVAD weaning protocol, so her LVAD was ultimately explanted! She is currently doing well on GDMT alone! Case Media CXR: Mild interstitial edema, +ET tubeST (131), LAD, nonspec T wave flattening, nl intervalsClick to Enlarge TTE 1 TTE 2 Episode Schematics & Teaching Click to enlarge! The CardioNerds 5! – 5 major takeaways from the #CNCR case 1. How do we define Peripartum Cardiomyopathy? Diagnosis is made by the development of heart failure towards the end of pregnancy or in the months following delivery (~5 months postpartum), no other identifiable cause of HF, and demonstration of LV systolic dysfunction with LVEF typically less than 45% with or without dilation. Risk factors include history of pre-eclampsia, hypertension, cocaine use, multifetal pregnancies, older maternal age, and African descent. Keep a broad differential diagnosis for new onset heart failure in the peripartum period. The differential includes pre-existing cardiomyopathy, valvular disease or congenital cardiomyopathy unmasked by the hemodynamic changes of pregnancy (see CNCR episode 48 for more on the hemodynamic changes of pregnancy!). Other differentials should include ischemia/spontaneous coronary artery dissection (SCAD), stress-induced cardiomyopathy, CM due to systemic disease (e.g. sepsis, rheumatologic disease), myocarditis and tachycardia-induced CM. 2. The team used invasive hemodynamics to guide shock management. Why is a PAC helpful? Despite data from the ESCAPE trial, a pulmonary artery catheter (PAC) can be very useful in the diagnosis and management of cardiogenic shock. Remember, the ESCAPE trial included chronic HF patients in whom there was clinical uncertainty on whether a PAC may be useful. Further, any patient on milrinone was excluded. Cardiac power output (CPO) and pulmonary artery pulsatility index (PAPi) are some of the parameters obtained from a PAC that can guide cardiogenic shock therapy and need for mechanical circulatory support (MCS). Resting CPO = CO x MAP / 451. CPO measures the "pumping power" of the LV and correlates with end-organ perfusion. In the SHOCK registry, CPO 50%) as they are at higher risk of future recurrence. The 2018 ESC guidelines advise against pregnancy if EF has not recovered to >50-55%. Contraception counseling should be done early: before discharge or at the time of diagnosis. Patients should avoid estrogen-containing methods especially in the early postpartum period as thromboembolism risk is high. If a patient plans on another pregnancy, teratogenic HF medications, like ACE/ARB/ARNI and spironolactone, must be stopped prior to stopping contraception. Following cessation of these GDMT medication, follow-up echocardiography to ensure LV functional stability should be performed after at least 3 months off therapy.

Sep 14, 2020

CardioNerds (Amit Goyal & Daniel Ambinder) join Northwestern University cardiology fellows (Sarah Hale, Sarah Chuzi, and Graham Lohrmann) for burgers and a great case by the Chicago River! They discuss a fascinating case of arrhythmogenic desmoplakin cardiomyopathy. Dr. Lisa Wilsbacher provides the E-CPR and program director Dr. Benjamin Freed provides a message for applicants. Episode notes were developed by Johns Hopkins internal medicine resident Richard Ferraro with mentorship from University of Maryland cardiology fellow Karan Desai. Jump to: Patient summary - Case figures & media - Case teaching - References - Production team Episode graphic by Dr. Carine Hamo The CardioNerds Cardiology Case Reports series shines light on the hidden curriculum of medical storytelling. We learn together while discussing fascinating cases in this fun, engaging, and educational format. Each episode ends with an “Expert CardioNerd Perspectives & Review” (E-CPR) for a nuanced teaching from a content expert. We truly believe that hearing about a patient is the singular theme that unifies everyone at every level, from the student to the professor emeritus. We are teaming up with the ACC FIT Section to use the #CNCR episodes to showcase CV education across the country in the era of virtual recruitment. As part of the recruitment series, each episode features fellows from a given program discussing and teaching about an interesting case as well as sharing what makes their hearts flutter about their fellowship training. The case discussion is followed by both an E-CPR segment and a message from the program director. CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademySubscribe to our newsletter- The HeartbeatSupport our educational mission by becoming a Patron!Cardiology Programs Twitter Group created by Dr. Nosheen Reza Patient Summary A male in his early 40s presented for second opinion regarding multiple ICD shocks. 10 years prior he was diagnosed with a "weak heart," thought secondary to a viral illness and a dual-chamber ICD was placed at that time. He noted shocks occurring for the first time 5 years prior, at which time amiodarone was started. They recurred two years prior, when he was diagnosed with paroxysmal atrial fibrillation. Finally, he was hospitalized one month before presentation with multiple ICD shocks and was found to have high defibrillation thresholds (DFTs) and amiodarone was stopped. He then presented for a second opinion from the Northwestern CardioNerds! The patient had been doing well on GDMT and had NYHA Class I symptoms (Enjoy Ep #13 - Approach to GDMT). He did note a family history of a cousin with "cardiac issues" and did not know his father's family history. Physical exam demonstrated bradycardia and ECG demonstrated an a-paced, v-sensed rhythm at 50 bpm. TTE demonstrated a moderately dilated LV with LVEF 30%, globally reduced LV function and multiple wall motion abnormalities without a vascular distribution. PET-CT was performed which showed diffuse uptake and high-intensity signal at the inferolateral and basal anterior walls. Cardiac MRI showed diffuse circumferential epicardial delayed enhancement with associated diffuse, enhancing thickening of the pericardium favoring inflammatory versus fibrotic process. Patient was initially diagnosed with cardiac sarcoid and started on prednisone and weekly methotrexate. On return of genetic testing, patient found to have a pathogenic variant for desmoplakin gene, and it was felt his cardiomyopathy was secondary to desmoplakin Left Dominant Arrhythmogenic Cardiomyopathy (LDAC, or left-dominant ARVC) presenting with inflammatory myocardial injury. On follow up the patient remained listed for transplant, and DFTs improved off amiodarone. Case Media CXRECGCardiac MRIPET CT (Cardiac Sarcoid Protocol)Click to Enlarge Episode Schematics & Teaching Created by Dr. Karan DesaiClick to enlarge! The CardioNerds 5! – 5 major takeaways from the #CNCR case We started the case talking about DFTs. What are DFTs?! Defibrillation Thresholds (DFTs) are the minimal amount of energy required to return a patient to sinus rhythm that is in a cardiac dysrhythmia. Most modern ICD leads have thresholds less than 15 joules and typically less than 10 joules with biphasic shocks. High DFT thresholds tend to be defined as >25J or a safety margin of <10J. DFT testing is not routinely recommended during implantation of left-sided transvenous devices; however, in patients undergoing right-sided transvenous ICD or ICD pulse generator changes, DFT testing is a reasonable approach. Patients undergoing subcutaneous ICD placement should generally have DFT testing. Contraindications to DFT testing include acute LV thrombus, atrial fibrillation/flutter without adequate anticoagulation, severe aortic stenosis, recent stroke or TIA, or hemodynamic compromise as DFT itself can cause hypotension and/or CVA. What are the major causes of high DFTs? First there are myocardial factors. This includes pathology that affects the current density through the myocardium. Conditions like hypertrophic cardiomyopathy, inflammatory cardiomyopathy, or significant LV dilation can lead to high DFTs. The second set of factors are extra-cardiac causes that lead to increased impedance or resistance in the counter coil, such as high BMI or medications that lead to electrical imbalances such as amiodarone, which is a common cause of increased DFTs. However, the increase in DFT caused by amiodarone can be small and routine DFT testing in patients is not recommended. The last cause is a device factor, such as a lead fracture or a mal-positioned lead. In the case, we used MRI and PET. What are their role in Cardiomyopathy? Cardiac MRI (CMR) has transformed our ability to assess cardiomyopathies, specifically by accurately defining chamber size & function, characterizing myocardial tissue, and determining ischemia & viability. The specific pattern of late gadolinium enhancement (LGE) can help us differentiate between ischemic and non-ischemic etiologies and specific cardiomyopathies have characteristic patterns on MRI. Further, MRI can reliably identify edema, inflammation, and fatty replacement. CMR can provide a wealth of information in a variety of disease processes. Enjoy Ep #33 - CMR!When evaluating an unexplained cardiomyopathy, FDG-PET can be useful in identifying active myocardial inflammation. 18F-FDG is a glucose analogue that can differentiate activated macrophages in areas of inflammation from normal myocytes if there is appropriate suppression of normal physiologic myocardial glucose uptake (I.e., Ketogenic Diet). This can be especially useful in Cardiac Sarcoidosis. Note, if there is global myocardial uptake, without diffuse perfusion defects, it may be a false positive scan in the setting of inadequate prep! For more on evaluation of heart failure, enjoy Ep #12 - Eval of New Onset HF & CPS Ep #48 - HFrEF. When should we consider a genetic cause to cardiomyopathy? If a family history suggests a genetic predisposition to cardiomyopathy, a cardiomyopathy seems out of proportion to an identified ischemic or non-ischemic cause, a patients presents with a cardiomyopathy at a young age, or if multi-modal imaging has not revealed a clear cause of a cardiomyopathy, genetic testing would be appropriate. Various studies have indicated that 30 to 50% of unexplained cases of (DCM) may have a genetic component. A detailed, at least three-generation family history should be obtained when initially evaluating a dilated CM, as most genetic cardiomyopathies are autosomal dominant with variable penetrance. Genetic counseling is key prior to genetic testing given complexities including interpretation of potentially confounding results and contextualizing results for relatives. Our patient's final diagnosis was "Arrhythmogenic Desmoplakin Cardiomyopathy"…what's that?! Arrhythmogenic RV Cardiomyopathy is a familial cardiomyopathy which usually affects the RV via fibrous or fibro-fatty replacement of normal myocardium. This predisposes patients to sudden cardiac death (SCD), ventricular arrhythmias, and heart failure. ARVC classically displays autosomal dominant inheritance from mutations in genes encoding desmosomal proteins affecting the cell-to-cell junction: desmoplakin (DSP), plakophilin 2 (PKP2), desmoglein 2 (DSG2), and desmocollin 2 (DSC2). Rarely, genes unrelated to cell-to-cell junction may be involved. Clinically we have noted a "Left-Dominant Arrhythmogenic Cardiomyopathy" (LDAC), with similarities to classic ARVC, but affecting predominantly the LV. Genotype-phenotype studies are shedding light on these "Arrhythmogenic Cardiomyopathies". DSP mutations affect predominantly the LV (causing LDAC) whereas PKP2 mutations affect predominantly the RV (causing ARVC); these are distinct entities with key differences in presentation, progression, and markers of SCD risk (see Smith et al., Circulation 2020 reference for more!). Pertinent to our case, a subset of patients with DSP cardiomyopathy will have evidence of myocardial inflammation on FDG-PET and will are initially misdiagnosed as a myocarditis or sarcoidosis. References Smith, E. D., Lakdawala, N. K., Papoutsidakis, N. et. al. (2020). Desmoplakin Cardiomyopathy, a Fibrotic and Inflammatory Form of Cardiomyopathy Distinct from Typical Dilated or Arrhythmogenic Right Ventricular Cardiomyopathy. Circulation. 141(23), 1872-1884 Crawford, T.C (2020). Desmoplakin Cardiomyopathy. https://www.acc.org/latest-in-cardiology/journal-scans/2020/06/11/15/43/desmoplakin-cardiomyopathy Shulka, H. H., Flaker, G. C., Jayam, V. et. al. (2003). High defibrillation thresholds in transvenous biphasic implantable defibrillators: clinical predictors and prognostic implications. Pacing and clinical electrophysiology, 26(1p1), 44-48. Russo, A. M., Sauer, W.,

Sep 11, 2020

CardioNerds (Amit Goyal & Daniel Ambinder) join UT-Austin cardiology fellows (Priya Kothapali, Sergio Montano, Travis Benzing, and Michael Grzeskowiak) for a speedboat adventure on Lake Travis! They discuss a fascinating case of Suicide LV post-TAVR. Dr. Mark Pirwitz provides the E-CPR and program director Dr. Clay Cauthen provides a message for applicants. Episode notes were developed by Johns Hopkins internal medicine resident Evelyn Song with mentorship from University of Maryland cardiology fellow Karan Desai. Jump to: Patient summary - Case figures & media - Case teaching - References - Production team Episode graphic by Dr. Carine Hamo The CardioNerds Cardiology Case Reports series shines light on the hidden curriculum of medical storytelling. We learn together while discussing fascinating cases in this fun, engaging, and educational format. Each episode ends with an “Expert CardioNerd Perspectives & Review” (E-CPR) for a nuanced teaching from a content expert. We truly believe that hearing about a patient is the singular theme that unifies everyone at every level, from the student to the professor emeritus. We are teaming up with the ACC FIT Section to use the #CNCR episodes to showcase CV education across the country in the era of virtual recruitment. As part of the recruitment series, each episode features fellows from a given program discussing and teaching about an interesting case as well as sharing what makes their hearts flutter about their fellowship training. The case discussion is followed by both an E-CPR segment and a message from the program director. CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademySubscribe to our newsletter- The HeartbeatSupport our educational mission by becoming a Patron!Cardiology Programs Twitter Group created by Dr. Nosheen Reza Patient Summary A woman in her early 70s, with a history of CAD s/p PCI to LAD & RCA with DES six months prior, to presentation, paroxysmal atrial fibrillation s/p ablation, type 2 diabetes mellitus, hypertension, prior TIA, and severe symptomatic AS was admitted for elective TAVR. She underwent successful implantation of a 29mm Medtronic Evolut Pro valve via left common femoral artery access. Post-valve deployment and following protamine administration for heparin reversal, course was complicated by hypotension with PEA arrest requiring CPR for 4 minutes. Intra-op TEE and angiogram showed a well-seated prosthetic valve with trace paravalvular leak and no evidence of acute aortic regurgitation, significant paravalvular leak, pericardial effusion, coronary obstruction, aortic dissection, or access site complications. She was treated for suspected Protamine reaction with high dose steroids & epinephrine. However, she remained hypotensive with MAP in the 50s on high dose Epinephrine, Norepinephrine, and Vasopressin. Hemodynamics by pulmonary artery catheter demonstrated CVP 7, mPA 26, PCWP 18 mmHg and CO/CI 2.8 L/min and 1.3 L/min/m2. Her lactate was elevated at 5.92 mmol/L and EKG demonstrated normal sinus rhythm. Bedside TTE in the ICU showed hyperdynamic LV function with LVEF 70% and near-complete mid to distal cavity obliteration with significant intracavitary gradient. She was diagnosed with post-TAVR suicide LV and managed with aggressive volume resuscitation and rapid wean of Epinephrine/Norepinephrine with improvement in her hemodynamics. She was eventually extubated and discharged on beta-blocker therapy. Case Media A. ECGB. CXRClick to Enlarge A. ECG: Normal sinus rhythm, no evidence of AV block, no ST segment elevation or depression.B. CXR: Pulmonary vascular congestion, no pneumothorax, ETT at level of carina, PAC in appropriate position Pre-Aortogram Implantation Post-Dilation Post-Aortogram TEE: Mid-Esophageal Three-Chamber View TEE: Mid-Esophageal Short Axis View Abdominal aortography showed no evidence of vascular access site complication or contrast extravasation. Aortic root angiography showed no evidence of AI, coronary obstruction, or dissection. TTE: PLAX and A4C Episode Schematics & Teaching Created by Dr. Karan DesaiGraphic by Dr. Carine HamoClick to enlarge! The CardioNerds 5! – 5 major takeaways from the #CNCR case Remind all CardioNerds – how do we define Severe Aortic Stenosis? By TTE, severe AS is defined as a mean gradient >40 mmHg, a peak velocity >4 m/s, an aortic valve area <1 cm2 and dimensionless index < 0.25. But remember, in HF patients decreased trans-aortic valve flow secondary to LV disease can make the diagnosis challenging! In HFrEF, patients with severe AS by aortic valve area (AVA) may not meet velocity or gradient criteria in one of four contexts: AVA measurement error, pseudo-severe AS, poor contractile reserve, or true severe Low Flow, Low Gradient AS (LFLG AS). Similarly, in HFpEF patients, disproportionately low flow or gradient AS may occur due to AVA measurement error or from true severe “paradoxical” LFLG due to decrease stroke volume (stroke volume index <35 mL/m2). Low gradient AS is a critical subset of patients with generally with a comparatively worse clinical trajectory marked by increased heart failure hospitalizations and mortality compared with high gradient AS. Enjoy the aortic stenosis series (Ep #1-2) and related figure for a deeper dive! 2. This patient received a TAVR for her severe AS. What are the major complications? Generally there are five relatively important post-TAVR complications – termed the “Big 5” – that contribute to long-term morbidity. These include disabling stroke, acute kidney injury, moderate/severe paravalvular leak, vascular and bleeding complications, and conduction abnormalities with possible need for PPM. Modern TAVR valves include mechanisms to reduce paravalvular leak (i.e., an outer skirt or a porcine pericardial tissue wrap or cuff), but may lead to more conduction abnormalities 3. This case covered Suicide LV. What is the pathophysiology behind this? Severe AS leads to LV hypertrophy and chronic pressure overload. When the fixed obstruction is relieved, the increased contractility of the LV is "unmasked" and can lead to dynamic LV cavity obstruction or obliteration. When this compromises cardiac output, these labile hemodynamics are termed "suicide LV". 4. What are risk factors for developing Suicide LV post-AVR? The major risk factors for Suicide LV with dynamic intracavitary gradient include small LVOT and LV size, hyperdynamic and elevated LVEF, asymmetric septal hypertrophy with an elevated interventricular septal to posterior wall thickness ratio, high valve gradients prior to AVR and small LV wall mass. 5. What should be my basic approach to Suicide LV management? The management of suicide LV is similar to that of Hypertrophic Obstructive Cardiomyopathy (see Ep#3) and related figure for a refresher! The basics include increasing preload with intravenous fluids, increasing afterload to reduce intra-cavitary gradients (phenylephrine tends to be the vasoactive of choice), avoiding inotropes (e.g., digoxin or beta-agonist infusions) while considering negative inotropes (e.g., beta blockers), and maintaining AV synchrony to ensure adequate LV preload References Evaluation of Shock Following TAVR - ACC Big 5 Complications post-TAVR - JACC IC 2019 Suh 2010 - Suicide LV following TAVI CardioNerds Case Reports: Recruitment Edition Series Production Team Bibin Varghese, MDRick Ferraro, MDTommy Das, MDEunice Dugan, MDEvelyn Song, MDColin Blumenthal, MDKaran Desai, MDAmit Goyal, MDDaniel Ambinder, MD

Sep 9, 2020

CardioNerd (Amit Goyal) join Washington University in St. Louis cardiology fellows (Adam Lick, Manny Rivera Maza, and Sam Lindner) for some amazing local St. Louis craft brews! They discuss a fascinating case of wild-type aTTR cardiac amyloid. Prior to meeting up with the group, Amit bumps into Rachita Navara: a Wash U #FIT, aspiring electrophysiologist, & a rock star of the band "The Pacemakers" (be sure to check out their performance at the end of the episode!) who shares thoughts about the program and her cutting edge contributions to the field of EP. Dr. Katie Zhang provides the E-CPR and program director Dr. Andy Kates provides a message for applicants. Episode notes were developed by Johns Hopkins internal medicine resident Colin Blumenthal with mentorship from University of Maryland cardiology fellow Karan Desai. Jump to: Patient summary - Case figures & media - Case teaching - References - Production team Episode graphic by Dr. Carine Hamo The CardioNerds Cardiology Case Reports series shines light on the hidden curriculum of medical storytelling. We learn together while discussing fascinating cases in this fun, engaging, and educational format. Each episode ends with an “Expert CardioNerd Perspectives & Review” (E-CPR) for a nuanced teaching from a content expert. We truly believe that hearing about a patient is the singular theme that unifies everyone at every level, from the student to the professor emeritus. We are teaming up with the ACC FIT Section to use the #CNCR episodes to showcase CV education across the country in the era of virtual recruitment. As part of the recruitment series, each episode features fellows from a given program discussing and teaching about an interesting case as well as sharing what makes their hearts flutter about their fellowship training. The case discussion is followed by both an E-CPR segment and a message from the program director. CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademySubscribe to our newsletter- The HeartbeatSupport our educational mission by becoming a Patron!Cardiology Programs Twitter Group created by Dr. Nosheen Reza Patient Summary A man in his early 70s, with a history of hypertension, a bicuspid aortic valve, chronic kidney disease and carpal tunnel syndrome presents with two weeks of worsening dyspnea on exertion. At baseline, he is an avid cyclist and noticed he can now only bike ½ mile when before he could bike extended distances. In addition, he noted abdominal swelling and palpitations. Vitals signs showed mild tachycardia, irregularly irregular rhythm, and no clear evidence of volume overload. Labs demonstrated acute on chronic kidney disease, an elevated NT-proBNP and elevated troponin. ECG demonstrated atrial flutter with variable conduction block. TTE demonstrated marked concentric left ventricular hypertrophy with preserved ejection fraction, biatrial enlargement, reduced global longitudinal strain with apical sparing, and bicuspid aortic valve with moderate aortic stenosis. Further diagnostics revealed normal serum kappa/lambda light chains and PYP scan was positive. Patient underwent EMB which demonstrated ATTR amyloid deposition and genetic screening did not show mutations commonly associated with hereditary ATTR. Case Media ABCD A. CXR: Stable mild enlargement of the cardiac silhouette; mildly tortuous aorta. Lung fields are clear, no pneumonia, pleural effusions, or pneumothorax.B. AV continuous wave DopplerC. Strain ImageD. Tc-99 PYP Scan TTE 1 TTE 4 TTE 2 TTE 5 TTE 3 TC-99 PYP Scan Strain video 1 Strain video 2 Strain video 3 Episode Schematics & Teaching Created by Dr. Karan DesaiCreated by Dr. Carine Hamo (updated 9.2020)Click to enlarge! The CardioNerds 5! – 5 major takeaways from the #CNCR case Cardiac amyloidosis can have a range of cardiac and extra-cardiac findings as amyloid fibrils can deposit in many different tissues, depending on the amyloid protein involved. The first step in diagnosis is maintaining a high index of suspicion. The presence of prominent right-sided HF symptoms, low voltage on ECG, biatrial enlargement, ventricular hypertrophy, conduction disease, and pericardial effusion should prompt a high suspicion for cardiac amyloid. These are typical features of infiltrative or storage restrictive cardiomyopathies. PEARL: ATTR CM can cause asymmetric LVH and is an important HCM phenocopy! Remember, amyloidosis is a systemic disease and extra-cardiac findings are common. ATTR amyloid has a predilection for the musculoskeletal system (including bilateral carpal tunnel syndrome, lumbar spinal stenosis, and biceps tendon rupture) and peripheral nerves. Conversely, AL amyloid is widely deposited outside the CNS an can result in protean manifestations, including periorbital ecchymoses from vascular fragility, macroglossia, and visceral organ involvement (including nephrotic syndrome, hepatic infiltration, and gut amyloid). When considering cardiac amyloid, there are four primary etiologies: Wild-Type (non-hereditary) ATTR amyloidosis is caused by deposition of misfolded transthyretin proteins. It is an under-recognized cause of HFpEF, with incidence increasing with age. Hereditary ATTR is caused by a genetic mutation that leads to instability of the transthyretin tetramer. The most common mutation is the Val30Met variant. Specific mutations tend to have templated organ manifestations, natural history, and prognosis. AL amyloidosis is caused by deposition of light-chains from a clonal plasma cell dyscrasia. AA amyloidosis is a rare form of cardiac amyloid caused by deposition of the acute phase reactant serum amyloid A protein due to a chronic inflammatory process. Evaluating for AL amyloid with appropriate lab workup is crucial. "Missing AL amyloid is like missing a STEMI" - Dr. Paul Cremer (Episode #8)! Workup should include SPEP, UPEP, serum/urine immunofixation, and serum kappa/lambda free light chains to maximize sensitivity. Note: SPEP and UPEP alone are insensitive and inadequate! Like many cardiac diseases, multimodal diagnostics are key in the diagnosis of cardiac amyloid ECG: Low voltage, pseudoinfarct pattern, variable conduction disease, atrial arrhythmias. PEARL: 10% of patients with cardiac amyloid may have high voltages on ECG. LVH on imaging out of proportion to EKG voltages is a red flag! TTE: We have discussed typical features of an infiltrative or storage restrictive cardiomyopathy previously , including marked LVH with normal LV volumes and bi-atrial enlargement. Other features include: RV hypertrophy, thickened valve leaflets, thick interatrial septum, speckled appearance of the myocardium, and small pericardial effusion. Bi-atrial enlargement may lead to functional MR and TR as well as atrial arrhythmias. Mitral inflow pattern and tissue doppler will show varying degrees of diastolic dysfunction depending on stage. Systolic function may be borderline and progressively decline in "burned-out" disease. Reduced global longitudinal strain with apical sparing may help differentiate cardiac amyloid from hypertensive heart disease. There is an overlap with aortic stenosis which will frequently manifest as a low flow and/or low gradient phenotype due to reduce stroke volumes. Cardiac MRI: There are characteristic findings of early subendocardial late gadolinium enhancement (LGE) and later transmural LGE with abnormal blood-pool-to-myocardial nulling (an MRI technique to accentuate pathology). PYP scan: >99% sensitivity for cardiac ATTR amyloid. If monoclonal gammopathy is excluded, the positive predictive value is 100%. RHC +/- EMBx: the hemodynamic profile is that of restrictive cardiomyopathy with elevated filling pressures, blunted x descent, and steep y descent. There may be diastolic pressure equalization. If EMBx is pursued, pathology will reveal amyloid protein as a salmon-pink color when congo red stain is applied and when placed under polarized light the amyloid proteins have an apple-green birefringence. Amyloid fibrils are seen with electron microscopic study. Mass spec for protein identification. Cardiac amyloid can be very difficult to treat with typical HF regimens, as beta blockers and ACE-I/ARB can lead to excessive hypotension in the setting of autonomic neuropathy and restrictive hemodynamics. For TTR amyloid, there are treatment options like tafamidis (a transthyretin protein stabilizer) which can reduce mortality considerably in selected patients. Investigational RNA-targeted therapies (i.e., patisiran) are increasing the options for treating TTR, but cost remains a major barrier to care. For AL amyloid, a multidisciplinary cardio-oncology team is vital to coordinate chemotherapy and cardiovascular care. Heart transplant +/- bone marrow transplant may be options in advanced stages of disease. The challenges of managing advanced disease highlight the importance of early recognition. References TTR Ca Review - JACC 2019 Amyloid CM Case - JACC Case Reports 2019 CardioNerds Amyloid Page Strain Imaging Echocardiography: What Imaging Cardiologists Should Know Tafamidis Treatment for Patients with Transthyretin Amyloid Cardiomyopathy CardioNerds Case Reports: Recruitment Edition Series Production Team Bibin Varghese, MDRick Ferraro, MDTommy Das, MDEunice Dugan, MDEvelyn Song, MDColin Blumenthal, MDKaran Desai, MDAmit Goyal, MDDaniel Ambinder, MD

Sep 7, 2020

CardioNerds (Amit Goyal & Daniel Ambinder) join Temple Cardiology Fellows (Anika Vaidy and Anne- Sophie LaCharite-Roberge) in Philadelphia, PA! They discuss a fascinating case of pulmonary hypertension secondary to Chronic Thromboembolic Pulmonary Hypertension (CTEPH) associated with May Thurner syndrome and large uterine fibroids. Dr. Vaidya provides the E-CPR and message to applicants. Episode notes were developed by Johns Hopkins internal medicine resident, Eunice Dugan, with mentorship from University of Maryland cardiology fellow Karan Desai. Jump to: Patient summary - Case figures & media - Case teaching - Educational video - References - Production team Episode graphic by Dr. Carine Hamo The CardioNerds Cardiology Case Reports series shines light on the hidden curriculum of medical storytelling. We learn together while discussing fascinating cases in this fun, engaging, and educational format. Each episode ends with an “Expert CardioNerd Perspectives & Review” (E-CPR) for a nuanced teaching from a content expert. We truly believe that hearing about a patient is the singular theme that unifies everyone at every level, from the student to the professor emeritus. We are teaming up with the ACC FIT Section to use the #CNCR episodes to showcase CV education across the country in the era of virtual recruitment. As part of the recruitment series, each episode features fellows from a given program discussing and teaching about an interesting case as well as sharing what makes their hearts flutter about their fellowship training. The case discussion is followed by both an E-CPR segment and a message from the program director. CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademySubscribe to our newsletter- The HeartbeatSupport our educational mission by becoming a Patron!Cardiology Programs Twitter Group created by Dr. Nosheen Reza Patient Summary A woman in her late 40s with history of iron deficiency anemia, uterine fibroids, and recurrent DVTs/PEs for the past 6 years despite different anticoagulation regimens, presented with syncope and progressive dyspnea on exertion. Family history was negative for DVT/PE or hypercoagulable states. On exam, she was euvolemic. Labs were significant for anemia, a normal pro-BNP, and a negative extensive hypercoagulable workup. TTE showed interventricular systolic septal flattening, right ventricular outflow tract pulse wave doppler with mid-systolic notch, and shortened acceleration time consistent with elevated pulmonary artery pressure. A VQ scan showed bilateral right greater than left mis-matched perfusion defects. CT angiogram showed right greater than left chronic mural thrombus, correlating with pulmonary angiogram which showed severe proximal and mid-vessel disease on the right and distal disease on the left. RHC corroborated the diagnosis of chronic thromboembolic pulmonary hypertension (CTEPH) with mean pulmonary artery pressure of 41 and PVR of 5.2 Woods Units (WU). To determine the etiology of her recurrent clots, a lower extremity venogram was performed and showed 80% stenosis of her left common iliac vein by the overlying right common iliac artery confirming May-Thurner syndrome. Lower extremity venogram also showed severe proximal stenosis of right iliac vein thought to be due to large uterine fibroids. Given her severe proximal and mid-vessel clot burden, she underwent pulmonary thromboendarterectomy with a subsequent drop in pulmonary vascular resistance to 1 WU. The etiology of DVTs and CTEPH was determined to be external compression related to both May-Thurner syndrome and uterine fibroids. To prevent future thromboembolic events, she underwent stenting of her left common iliac vein and hysterectomy. With these interventions, RV function returned to normal, and her symptoms completely resolved! Case Media A B C D E F G H I J Click to enlarge ??? Figue Legend: A. CXRB. ECGC. TTE: Interventricular systolic septal flattening, RVOT pulse wave Doppler with mid-systolic notch and shortened acceleration time, consistent with elevated PVR, RV:LV ratio 1.3, consistent with moderate RV enlargement, The RV is apex-sharing with an open apical angleD. VQ Scan: Multiple b/l perfusion defects, R > L, V scan normalE. CT Angiogram: 1) Enlarged R main PA2) large proximal chronic mural thrombus with minimal vessel count throughout R side, 3) Segmental LLL lining thrombusF. Pulmonary angiogram significant for severe proximal and mid-vessel disease in the right segmental arteries. Patient also had severe distal disease in the left sub segmental disease (not shown).G. Pulmonary Thromboendarterectomy (PTE)H. LE Venogram: LEFT CIV > 80% stenosis as a result of compression from an overlying right common iliac artery. This is consistent with May-Thurner syndrome. RIGHT EIV (not shown)– Significant proximal stenosisI. Status Post left iliac vein stentJ. ECG: New typical atrial flutter Episode Schematics & Teaching Click to enlarge ??? The CardioNerds 5! – 5 major takeaways from the #CNCR case In patients with progressive dyspnea, exercise intolerance, and persistence of symptoms of PE despite adequate anticoagulation, there should be an evaluation for Chronic Thromboembolic Pulmonary Hypertension (CTEPH). CTEPH is a form of pre-capillary pulmonary hypertension (PH) from incomplete resolution of pulmonary thromboemboli causing chronic, fibrotic, flow limiting changes to the pulmonary vascular bed. Risk factors include recurrent PE, hypercoagulable states, and medical conditions such as splenectomy, ventriculo-atrial shunts, infected intravenous catheters/devices, malignancy, and external venous compression. NOTE: many patients will not have a documented history of DVT/PE and so a high index of suspicion is important. The following echocardiographic findings suggest pulmonary hypertension: interventricular systolic septal flattening indicating RV pressure overload, RV outflow tract (RVOT) pulse wave doppler with mid-systolic notch, decreased RVOT acceleration time, right atrial enlargement, right ventricular dilation and hypertrophy +/- functional tricuspid regurgitation, and an elevated estimated RV systolic pressure (RVSP). CTEPH is rare and carries a high rate of morbidity and mortality; therefore, a high index of suspicion is necessary. There are two components to diagnosis: Diagnose CTEPH: Multiple imaging modalities are involved to confirm and assess severity. V/Q scan is highly sensitive and is the initial screening modality to detect perfusion abnormalities. Chest CT with IV contrast may identify parenchymal and mediastinal pathology not otherwise seen; although not sensitive, CT may show: PA dilation, eccentric filling defects with variable degrees of occlusion, vascular webs or bands, mosaic perfusion pattern of the lung parenchyma, and RV enlargement. RHC can confirm the diagnosis of pulmonary hypertension, differentiate pre-capillary from post-capillary PH, quantify vascular resistance and cardiac output, and can be a comparative marker post-intervention. Conventional PA angiography is useful for pre-operative planning. Diagnose the underlying predisposition/etiology: Think about Virchow's Triad: Hypercoagulability, Stasis, and Endothelial injury. Apart from ruling out hypercoagulable states, evaluating for lower extremity vascular compression can be important in select patients with imaging such as venography. May-Thurner syndrome is a condition of extrinsic venous compression of the left common iliac vein by the common iliac artery. Evidence of any compression should be addressed to prevent future venous thrombi and subsequent emboli. Treatment for CTEPH starts with lifelong anticoagulation. Pulmonary angiography aids in surgical planning as proximal disease is more likely to be operable than distal disease. Based on severity and other comorbidities, pulmonary endarterectomy (PEA) can be a favorable option. PEA improves symptoms, survival, hemodynamics parameters, and RV remodeling. Other treatment strategies include medical management, balloon pulmonary angioplasty, and lung transplant. Pulmonary artery denervation is being considered as an experimental modality. Supraventricular tachycardia (SVT) is common in patients with pulmonary artery hypertension and CTEPH and often indicate progression of right-sided dysfunction. PH patients rely more on active than passive RV filling, and are highly sensitive to changes in RV afterload. Supraventricular tachycardias may further precipitate decompensation given (1) the loss of atrial kick which compromises diastolic filling, and (2) tachycardias which increase RV wall tension increasing RV afterload. Therefore, restoration of sinus rhythm is strongly encouraged. Educational Video Produced by Dr. Karan Desai References JACC 2018 - CTEPH Review ACC Expert Analysis 2019 - Rx of CTEPH May-Thurner Updodate Pulmonary Circulation 2019 - Pathophysiology, incidence, management, and consequences of cardiac arrhythmia in PAH and CTEPH Pulmonary Circulation 2012 - Evaluation of patients with CTEPH for PTE ESC/ERC Dx and Eval PH CardioNerds Case Reports: Recruitment Edition Series Production Team Bibin Varghese, MD Rick Ferraro, MD Tommy Das, MD Eunice Dugan, MD Evelyn Song, MD Colin Blumenthal, MD Karan Desai, MD Amit Goyal, MD Daniel Ambinder, MD

Sep 3, 2020

CardioNerds (Amit Goyal & Carine Hamo) discuss the past, present, and future of Women's Heart Health & Women in Cardiology with Dr. Nanette Wenger, Professor of Medicine in the Division of Cardiology at the Emory University School of Medicine. Dr. Wenger is a true leader in the field of women’s heart health and a strong proponent for women in cardiology and medicine. Her passion, dedication, and advocacy have inspired countless trainees to carry this torch and continue to build on her truly impactful work. Special introduction by Dr. Martha Gulati and birthday wishes to Dr. Wenger by the entire CardioNerds Team! Special thanks to Dr. Kimberly Manning for her invaluable mentorship. Episode graphic by Dr. Carine Hamo The Cardionerds CV prevention series includes in-depth deep dives on so many prevention topics including the ABCs of prevention, approach to obesity, hypertension, diabetes mellitus and anti-diabetes agents, personalized risk and genetic risk assessments, hyperlipidemia, women’s cardiovascular prevention, coronary calcium scoring and so much more! CardioNerds Episode PageCardioNerds Prevention PageCardioNerds Women's Cardiovascular Health PageCardioNerds Academy - Apply now! Subscribe to our newsletter- The HeartbeatSupport our educational mission by becoming a Patron! We are truly honored to be producing the Cardionerds CVD Prevention Series in collaboration with the American Society for Preventive Cardiology! The ASPC is an incredible resource for learning, networking, and promoting the ideals of cardiovascular prevention! This series is kicked off by a message from Dr. Amit Khera, President of the American Society for Preventive Cardiology and President of the SouthWest Affiliate of the American Heart Association. Cardionerds Cardiovascular Prevention Series References and Links 1. Wenger NK (2005) Women in cardiology: The US experience. Heart. 2. Douglas PS, Rzeszut AK, Noel Bairey Merz C, Duvernoy CS, Lewis SJ, Walsh MN, Gillam L (2018) Career preferences and perceptions of cardiology among us internal medicine trainees factors influencing cardiology career choice. JAMA Cardiol. 3. Wenger NK, Speroff L, Packard B (1993) Cardiovascular Health and Disease in Women. N Engl J Med. 4. Burgess S, Shaw E, Zaman S (2019) Women in Cardiology. Circulation. Meet Dr. Wenger! Dr. Nanette Wenger is Professor of Medicine in the Division of Cardiology at the Emory University School of Medicine. Dr. Wenger received her medical degree from Harvard Medical School in 1954 as one of their first female graduates followed by training at Mount Sinai Hospital where she was the first female to be chief resident in the cardiology department. She is among the first physicians to focus on heart disease in women with an expertise in cardiac rehabilitation and geriatric medicine. Dr. Wenger has received numerous awards including the Distinguished Achievement Award from the Scientific Councils of the American Heart Association and its Women in Cardiology Mentoring Award, the James D. Bruce Memorial Award of the American College of Physicians for distinguished contributions in preventive medicine, the Gold Heart Award, the highest award of the American Heart Association, a Lifetime Achievement Award in 2009 and the Inaugural Bernadine Healy Leadership in Women’s CV Disease Distinguished Award, American College of Cardiology. She chaired the U.S. National Heart, Lung, and Blood Institute Conference on Cardiovascular Health and Disease in Women, is a Past President of the Society of Geriatric Cardiology and is past Chair, Board of Directors of the Society for Women’s Health Research. Dr. Wenger serves on the editorial boards of numerous professional journals and is a sought-after lecturer for issues related to heart disease in women, heart disease in the elderly, cardiac rehabilitation, coronary prevention, and contemporary cardiac care. She is listed in Best Doctors in America. Carine Hamo, MDAmit Goyal, MD

Aug 28, 2020

CardioNerds (Amit Goyal & Dan Ambinder) join Lankenau Medical Center cardiology fellows (Gwen McNeill and Shaung Ooi) for some Philly cheesesteaks! They discuss a fascinating case of Embolic Acute Coronary Syndrome from PFO and Pulmonary Hypertension. Dr. John Clark provides the E-CPR and program director Dr. Jeanine Romanelli provides a message for applicants. Episode notes were developed by Johns Hopkins internal medicine resident Tommy Das with mentorship from University of Maryland cardiology fellow Karan Desai. Jump to: Patient summary - Case figures & media - Case teaching - Educational video - References - Production team Episode graphic by Dr. Carine Hamo The CardioNerds Cardiology Case Reports series shines light on the hidden curriculum of medical storytelling. We learn together while discussing fascinating cases in this fun, engaging, and educational format. Each episode ends with an “Expert CardioNerd Perspectives & Review” (E-CPR) for a nuanced teaching from a content expert. We truly believe that hearing about a patient is the singular theme that unifies everyone at every level, from the student to the professor emeritus. We are teaming up with the ACC FIT Section to use the #CNCR episodes to showcase CV education across the country in the era of virtual recruitment. As part of the recruitment series, each episode features fellows from a given program discussing and teaching about an interesting case as well as sharing what makes their hearts flutter about their fellowship training. The case discussion is followed by both an E-CPR segment and a message from the program director. CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademySubscribe to our newsletter- The HeartbeatSupport our educational mission by becoming a Patron!Cardiology Programs Twitter Group created by Dr. Nosheen Reza Patient Summary A woman in her early 40s with history of tobacco and prior methamphetamine use presented with acute onset chest pain. She was found to have an elevated troponin, anterior T wave inversions, and apical akinesis on TTE. Coronary angiography showed a coronary embolism in the mid-distal LAD. Attempts to wire the lesion led to distal embolization of the clot, and IVUS showed no underlying arteriosclerosis. To investigate the etiology of the coronary embolus, a repeat TTE with agitated saline was done that suggested a PFO with right to left flow, as well as decreased RV function with an estimated RVSP of 70 mmHg. The clinical picture was that of a paradoxical coronary embolus, arising from the right (venous) side traveling to the left (arterial) side via a PFO. PFO closure was discussed but not performed given severe pulmonary hypertension with Right to Left shunt. In this circumstance, the PFO functions as a "pop-off valve" for the overloaded RV; closing it risks precipitating acute RV overload and failure. A RHC showed a PA pressure of 70/24 mmHg with mPAP of 40 mmHg, PCWP 5 mmHg, and PVR of 11 woods units. Given concern for idiopathic PH, a vasodilator challenge was done which did not show reactivity, and she was started on ambrisentan and sildenafil. Ultimately, the etiology of her pulmonary hypertension was felt to be due to PAH from prior methamphetamine use vs. idiopathic PAH. On follow-up, her PA pressures and RV function had greatly approved, allowing for safe and successful PFO closure in an attempt to prevent future emboli. Final diagnosis: Embolic Acute Coronary Syndrome from PFO & Pulmonary Hypertension. Case Media Before treatment: short axisBefore treatment: apical 4Before treatment: RVSPAfter treatment: Short axisAfter treatment: Apical 4After treatment: RVSPClick to enlarge ??? https://youtu.be/XpnJKZuNVrM 1. Coronary angio of embolism2. PFO on TEE with R to L shunt by Doppler3. TTE bubble after PFO closure Episode Schematics & Teaching Click to enlarge ??? The CardioNerds 5! – 5 major takeaways from the #CNCR case Coronary emboli are an uncommon cause of myocardial infarction. We can think of the etiology of coronary emboli in three major categories: Direct, Paradoxical, or Iatrogenic. Direct emboli originate from the left side of the heart: sources include clot (from atrial appendage, apical thrombus), valvular lesion (vegetation, thrombus, fibroelastoma), or left sided cardiac mass (atrial myxoma, rhabdomyosarcoma). Paradoxical emboli originate from the right side or systemic venous circulation, and pass from right to left through an atrial septal defect, patent foramen ovale, or pulmonary arteriovenous malformation. Iatrogenic emboli occur following procedures such as valve replacement or PCI. Note that iatrogenic is the most common etiology! PFOs are present in up to 25% of adults, but are usually clinically insignificant. However, there is increasing evidence that PFO closure is moderately beneficial compared to antiplatelet therapy alone in patients less than 60 years old with cryptogenic, non-lacunar ischemic stroke. PFO closure may particularly benefit those with a large right-to-left shunt or an associated atrial septal aneurysm.Remember closing an ASD in the setting of significant pulmonary hypertension can lead to decompensation, as the interatrial connection may be serving as a "pop-off" valve to decompress the RV and maintain cardiac output in the setting of high PA pressures! Specifically, ASD closure is generally contraindicated if the PA systolic pressure is > 2/3 systolic blood pressure, pulmonary vascular resistance > 2/3 systemic vascular resistance, or if a net right-to-left shunt is present. Recall that the hemodynamic definitions of pulmonary hypertension changed in 2019. A mean pulmonary artery pressure of 20 or greater confirms a diagnosis of pulmonary hypertension. A PCWP ≤15 mmHg with pulmonary vascular resistance ≥3 woods units suggests pre-capillary pulmonary hypertension, while a PCWP >15 with pulmonary vascular resistance 10 mmHg, with unchanged or increased cardiac output. These patients can be started on amlodipine or nifedipine, but should be followed closely as they may not always remain vasoreactive and clinical deterioration is possible! Educational Video https://youtu.be/IidG4gUijm8 Produced by Dr. Karan Desai References P Raphael, C. E., Heit, J. A., Reeder, G. S. et al. (2018). Coronary Embolus: An Underappreciated Cause of Acute Coronary Syndromes. JACC. Cardiovascular interventions, 11(2), 172–180. Mojadidi, M. K., Zaman, M. O., Elgendy, I. Y. et al. (2018). Cryptogenic Stroke and Patent Foramen Ovale. Journal of the American College of Cardiology, 71(9), 1035–1043. Silvestry, F. E., Cohen, M. S., Armsby, L. B. et al. (2015). Guidelines for the Echocardiographic Assessment of Atrial Septal Defect and Patent Foramen Ovale: From the American Society of Echocardiography and Society for Cardiac Angiography and Interventions. Journal of the American Society of Echocardiography : official publication of the American Society of Echocardiography, 28(8), 910–958. Simonneau, G., Montani, D., Celermajer, D. S. et al. (2019). Haemodynamic definitions and updated clinical classification of pulmonary hypertension. The European respiratory journal, 53(1), 1801913. Stout, K. K., Daniels, C. J., Aboulhosn, J. A. et al. (2019). 2018 AHA/ACC Guideline for the Management of Adults With Congenital Heart Disease: Executive Summary: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines. Circulation, 139(14), e637–e697. CardioNerds Case Reports: Recruitment Edition Series Production Team Bibin Varghese, MDRick Ferraro, MDTommy Das, MDEunice Dugan, MDEvelyn Song, MDColin Blumenthal, MDKaran Desai, MDAmit Goyal, MDDaniel Ambinder, MD

Aug 26, 2020

CardioNerds (Amit Goyal & Dan Ambinder) discuss a case of hereditary restrictive cardiomyopathy with Duke University cardiology fellows Navid Nafissi and Sipa Yankey, and Marat Fudim, an advanced heart failure attending. E-CPR is provided by Dr. Richa Agarwal, fellowship program director of advanced heart failure and cardiac transplantation at Duke University with a final message by fellowship director Dr. Anna Lisa Crowley. Episode notes were developed by Johns Hopkins internal medicine resident Colin Blumenthal with mentorship from University of Maryland cardiology fellow Karan Desai. Jump to: Patient summary - Case figures & media - Case teaching - Educational video - References - Production team Episode graphic by Dr. Carine Hamo The CardioNerds Cardiology Case Reports series shines light on the hidden curriculum of medical storytelling. We learn together while discussing fascinating cases in this fun, engaging, and educational format. Each episode ends with an “Expert CardioNerd Perspectives & Review” (E-CPR) for a nuanced teaching from a content expert. We truly believe that hearing about a patient is the singular theme that unifies everyone at every level, from the student to the professor emeritus. We are teaming up with the ACC FIT Section to use the #CNCR episodes to showcase CV education across the country in the era of virtual recruitment. As part of the recruitment series, each episode features fellows from a given program discussing and teaching about an interesting case as well as sharing what makes their hearts flutter about their fellowship training. The case discussion is followed by both an E-CPR segment and a message from the program director. CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademySubscribe to our newsletter- The HeartbeatSupport our educational mission by becoming a Patron!Cardiology Programs Twitter Group created by Dr. Nosheen Reza Patient Summary A 69 yo M with history of atrial fibrillation presents with 5 months of progressive HF symptoms, now NYHA class IV. He was found to be grossly volume overloaded, tachycardic in atrial fibrillation, and hypoxic. CXR demonstrated significant cardiomegaly, and labs indicated new normocytic anemia with evidence of hepatic dysfunction and an elevated NT proBNP. TTE demonstrated massive bi-atrial enlargement, preserved ejection fraction, filling pattern consistent with grade III diastolic dysfunction, and torrential TR. The echocardiogram did not have evidence of constrictive pericarditis and agitated saline study showed Right to Left shunt through a likely PFO. MRI to evaluate for infiltrative cardiomyopathy did not show late gadolinium enhancement (LGE). RHC demonstrated findings consistent with restrictive cardiomyopathy including equalization of diastolic pressures, square root sign, and concordance of RV and LV pressures. PYP scan evaluating for TTR amyloid was negative and laboratory workup did not suggest AL amyloid, Fabry's, Hemochromatosis, or storage disease. Patient's symptoms remained refractory and thus eventually underwent successful OHT. Genetic testing eventually revealed missense mutation in MYBPC3 – revealing an inherited cause of restrictive CM for the patient! Case Media Chest X-ray-Rate-controlled A fib with frequent PVCs, LPFB, non-specific ST changes https://youtu.be/LTUaLd2R7js Episode Schematics & Teaching Click to enlarge ??? The CardioNerds 5! – 5 major takeaways from the #CNCR case When thinking about the etiology of a restrictive cardiomyopathy, we can organize the causes into four major categories: Infiltrative (e.g., amyloidosis, sarcoidosis) Storage diseases (e.g., hemochromatosis, Fabry's) Non-infiltrative (e.g., idiopathic, diabetic cardiomyopathy, genetic causes) Endomyocardial (e.g., endomyocardial fibrosis, hypereosinophilic syndrome) On examination, patients with restrictive cardiomyopathy may have prominent right-sided symptoms, including hepatomegaly, ascites, and significant peripheral edema. On exam, neck veins may demonstrate a steep y descent, and cardiac auscultation may have a +S4, and murmurs of tricuspid and mitral regurgitation.A multimodal imaging workup is recommended for evaluating RCM. TTE: Typically demonstrates normal LVEF, normal chamber volumes, biatrial enlargement, and restrictive diastolic filling patterns (.e.g, E/A > 2, E/e' > 14, decreased mitral deceleration time 99% sensitivity for cardiac ATTR amyloid. If monoclonal gammopathy excluded, PPV 100%. Invasive hemodynamics can show physiology consistent with RCM. This includes square root sign, equalization of diastolic pressures, and concordance during respiration of LV/RV pressure changes. In contrast, constrictive physiology will yield discordant respirophasic LV/RV pressure changes. Endomyocardial biopsy may be necessary to identify etiology but the yield for patchy diseases, like sarcoid, can be low. Patients with end-stage RCM can be difficult to manage medically, especially as they become refractory to diuretics. They poorly tolerate antihypertensive agents (due to inability to augment limited stroke volume), heart rate lowering medication (due to low SV, they are dependent on HR to maintain CO which is HR x SV), and have a very limited optimal preload window (need high filling pressures to fill the stiff ventricles but also have symptoms of fluid overload). Due to anatomic considerations, patients are rarely candidates for durable left ventricular assist devices and often require orthotopic heart transplant. However, patients with RCM have higher waitlist mortality and longer wait times, in part due to lower utilization of MCS. Educational Video https://youtu.be/LDgP_3Cv49w Produced by Dr. Karan Desai https://twitter.com/CBlumenthal2/status/1299288171981598722?s=20 References Spectrum of Restrictive & Infiltrative CM - Part 1 article Spectrum of Restrictive & Infiltrative CM - Part 2 article Spectrum of Restrictive & Infiltrative CM - Part 1 notes Spectrum of Restrictive & Infiltrative CM - Part 2 notes Restrictive CM - Circ Res 2017 Echocardiography Diagnostic Criteria for Constriction Differentiation of Constriction and Restriction: Complex Cardiovascular Hemodynamics Constrictive Pericarditis Versus Restrictive Cardiomyopathy? Does Survival on the Heart Transplant Waiting List Depend on the Underlying Heart Disease? Genetic Counseling in Inherited Cardiomyopathies 2016 ASE Echo Guidelines CardioNerds Case Reports: Recruitment Edition Series Production Team Bibin Varghese, MDRick Ferraro, MDTommy Das, MDEunice Dugan, MDEvelyn Song, MDColin Blumenthal, MDKaran Desai, MDAmit Goyal, MDDaniel Ambinder, MD

Aug 24, 2020

CardioNerds (Amit Goyal & Daniel Ambinder) join Allegheny Health Network cardiology fellows (Adnan Khalif, Mahathi Indaram, Kushani Gajjar, and Michael Nestasie) for a lovely Pittsburgh hike and discuss a fascinating case of platypnea-orthodeoxia secondary to a PFO. Dr. Farhan Katchi provides the E-CPR and Program director Dr. Craig Alpert provides a message for applicants. Episode notes were developed by Johns Hopkins internal medicine resident Richard Ferraro with mentorship from University of Maryland cardiology fellow Karan Desai. Jump to: Patient summary - Case figures & media - Case teaching - Educational video - References - Production team Episode graphic by Dr. Carine Hamo The CardioNerds Cardiology Case Reports series shines light on the hidden curriculum of medical storytelling. We learn together while discussing fascinating cases in this fun, engaging, and educational format. Each episode ends with an “Expert CardioNerd Perspectives & Review” (E-CPR) for a nuanced teaching from a content expert. We truly believe that hearing about a patient is the singular theme that unifies everyone at every level, from the student to the professor emeritus. We are teaming up with the ACC FIT Section to use the #CNCR episodes to showcase CV education across the country in the era of virtual recruitment. As part of the recruitment series, each episode features fellows from a given program discussing and teaching about an interesting case as well as sharing what makes their hearts flutter about their fellowship training. The case discussion is followed by both an E-CPR segment and a message from the program director. CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademySubscribe to our newsletter- The HeartbeatSupport our educational mission by becoming a Patron!Cardiology Programs Twitter Group created by Dr. Nosheen Reza Patient Summary A 64 y/o female with a history of venous and arterial embolism on anticoagulation, known PFO, and obesity presented after a fall. There was no loss consciousness, pre-syncopal symptoms, chest pain, aura, weakness, or palpitations. She had no recent preceding illness. When she arrived in the ED she was hypoxic to 87% on ambulation on room air and required 4L of nasal cannula O2 supplementation. The AGH CardioNerds were consulted! On examination, the team noted that upon sitting up the patient would desaturate to the mid 80% but when lying down oxygen saturation would improve to 95%! Her ECG demonstrated a RBBB and no acute ST-T changes. TTE was obtained and showed normal LV and RV function and size, no valvular disease, and a likely PFO on an agitated saline study. Cardiac MRI revealed mild RV hypertrophy and Qp:Qs of 0.8 (right/pulm cardiac output 5 to 6 beats) occurs when the bubbles slowly build in the LV with each successive beat as they circulate to the LV and suggests extra-cardiac shunt. Cardiac MRI is helpful in quantifying the shunt fraction (Qp:Qs). This is the ratio of pulmonary flow (Qp) to systemic flow (Qs), where hemodynamically significant Left-to-Right shunt is > 1.5, especially when we see RA/RV dilation. Qp/Qs < 1.1 indicates net R to L shunt. Other ways to measure a Qp:Qs are echocardiogram (less accurate) and right heart catheterization. If there remains clinical concern for PFO with right to left shunting without evidence of a clear functional cause clinically or by catheterization (I.e., no evidence of high PA pressures, pericardial effusion, constrictive pericarditis), consider a right femoral vein bubble study. Upper extremity agitated saline enters the RA via the SVC; however, patients with prominent eustachian valve at the IVC can have blood flow directed towards the interatrial septum. This will be demonstrated on femoral vein bubble study! Educational Video https://youtu.be/sBEcMebmv6Q Produced by Dr. Karan Desai https://twitter.com/RichardAFerraro/status/1298310254766235648?s=20 References Cheng, T. O. (2002). Mechanisms of platypnea-orthodeoxia: what causes water to flow uphill. Circulation, 105(6), e47. Tobis, J. M., & Abudayyeh, I. (2016). Platypnea-orthodeoxia syndrome: an overlooked cause of hypoxemia. Sanikommu, V., Lasorda, D., & Poornima, I. (2009). Anatomical factors triggering platypnea‐orthodeoxia in adults. Clinical Cardiology: An International Indexed and Peer‐Reviewed Journal for Advances in the Treatment of Cardiovascular Disease, 32(11), E55-E57. CardioNerds Case Reports: Recruitment Edition Series Production Team Bibin Varghese, MDRick Ferraro, MDTommy Das, MDEunice Dugan, MDEvelyn Song, MDColin Blumenthal, MDKaran Desai, MDAmit Goyal, MDDaniel Ambinder, MD

Aug 21, 2020

CardioNerds (Amit & Dan) join Vanderbilt University cardiology fellows (Tara Holder, Majd El-Harasis, and Amar Parikh) for a Sunday morning brunch, Nashville style! They discuss an enthralling case of bicuspid aortic valve with critical aortic stenosis complicating pregnancy. Program director Dr. Julie Damp provides the E-CPR and a message for applicants. Episode notes were developed by Johns Hopkins internal medicine resident Tommy Das with mentorship from University of Maryland cardiology fellow Karan Desai. Jump to: Patient summary - Case figures & media - Case teaching - Educational video - References - Production team Episode graphic by Dr. Carine Hamo The CardioNerds Cardiology Case Reports series shines light on the hidden curriculum of medical storytelling. We learn together while discussing fascinating cases in this fun, engaging, and educational format. Each episode ends with an “Expert CardioNerd Perspectives & Review” (E-CPR) for a nuanced teaching from a content expert. We truly believe that hearing about a patient is the singular theme that unifies everyone at every level, from the student to the professor emeritus. We are teaming up with the ACC FIT Section to use the #CNCR episodes to showcase CV education across the country in the era of virtual recruitment. As part of the recruitment series, each episode features fellows from a given program discussing and teaching about an interesting case as well as sharing what makes their hearts flutter about their fellowship training. The case discussion is followed by both an E-CPR segment and a message from the program director. CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademySubscribe to our newsletter- The HeartbeatSupport our educational mission by becoming a Patron!Cardiology Programs Twitter Group created by Dr. Nosheen Reza Patient Summary A 22yo transgender F2M man (G1P0000) at 32w5d was found to have a late-peaking systolic ejection murmur on a regularly scheduled OB visit. He reported recent left-sided exertional chest pain and intermittent lightheadedness, as well as a history of a childhood heart murmur. TTE showed a bicuspid aortic valve (LCC-NCC fusion) with severe aortic stenosis (peak velocity 4.83 m/s, mean gradient of 56 mmHg, AVA at 0.5 cm2 and Dimensionless Index at 0.15). Furthermore, there was preserved ejection fraction and no associated aortopathy. Following a syncopal episode, the patient was admitted for cardiac optimization prior to delivery. With shared decision making, he ultimately delivered via cesarean section prior to valvular intervention. Post-partum, he underwent balloon aortic valvuloplasty with improvement in mean aortic gradient to 27 mmHg and trace aortic insufficiency. He was asymptomatic at 5 months post-procedure with similar gradients across the aortic valve on TTE. Case Media Chest - X ray Final gradients: Peak velocity 4.83 m/s Mean >50 (56) mmHg AVA 0.5 (AVAi=0.27) DOI=0.15 https://youtu.be/YF8TrNmsGh4 Episode Schematics & Teaching Click to enlarge ??? The CardioNerds 5! – 5 major takeaways from the #CNCR case Hemodynamics change dramatically during pregnancy. Cardiac output increases by 30-50% during pregnancy due to: ↑ SV, ↑HR, ↓SVR. Immediately post-partum, patients with existing valvular lesions are at high risk of heart failure! Hemodynamic changes peripartum are unpredictable. ↑Preload: relief of IVC compression, auto-transfusion of 300-500mL blood from placenta with each uterine contraction, and intravenous fluids and/or blood products. ↓Preload: hemorrhage ↑Afterload: SBP & DBP increase with each uterine contraction ↓Afterload: systemic vasodilation from epidural and spinal analgesia ↑CO: by up to 30% in the first stage of labor and up to 80% in the immediate post-partum period. 2/2 ↑SV. Most pregnant patients with symptomatic AS can be managed medically, with balloon aortic valvuloplasty reserved for patients with refractory symptoms. TAVR and SAVR may be considered, ideally reserved for the 2nd trimester. Spontaneous vaginal delivery carries a lower risk than c-section due to smaller shifts in blood volume, decreased bleeding, and avoidance of preload-shifting anesthetic agents. In a woman of child-bearing age with severe symptomatic AS who is planned for AVR, shared decision making is key in choice of valve! A mechanical valve is more durable than a bioprosthetic valve, but requires anticoagulation that could complicate a future pregnancy. Alternatives include a Ross procedure (replacing the aortic valve using the patient's own pulmonic valve - "pulmonary autograft" - and a cadaveric pulmonic valve is placed in the pulmonic position - "pulmonary allograft"), Ozaki procedure (recreating a new aortic valve from the patient's pericardium), performing a bioprosthetic AVR with risk of earlier degeneration, and performing a TAVR with plans for a surgical AVR later. Decision making is complex and warrants a multidisciplinary team accounting for patient preferences. The modified World Health Organization (WHO) classification stratifies the risk of pregnancy in women with cardiovascular disease. Pregnancy is contraindicated in women with WHO group IV lesions: Pulmonary artery hypertension Severe systemic ventricular dysfunction (EF 45mm in Marfan, >50mm a/w bicuspid aortic valve) Severe (re)coarctation Vascular Ehlers-Danlos syndrome Fontan with any complication Educational Video https://youtu.be/GzqFaNJseDc Produced by Dr. Karan Desai https://twitter.com/ThomasMDas/status/1297266319650435078?s=20 References Nishimura, R. A., Otto, C. M., Bonow, R. O. et al. (2017). 2017 AHA/ACC Focused Update of the 2014 AHA/ACC Guideline for the Management of Patients With Valvular Heart Disease: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines. Circulation, 135(25), e1159–e1195. Sharma, G., Lindley, K., & Grodzinsky, A. (2020). Cardio-Obstetrics: Developing a Niche in Maternal Cardiovascular Health. Journal of the American College of Cardiology, 75(11), 1355–1359. Elkayam, U., Goland, S., Pieper, P. G. et al. (2016). High-Risk Cardiac Disease in Pregnancy: Part I. Journal of the American College of Cardiology, 68(4), 396–410. Orwat, S., Diller, G. P., van Hagen, I. M. et al (2016). Risk of Pregnancy in Moderate and Severe Aortic Stenosis: From the Multinational ROPAC Registry. Journal of the American College of Cardiology, 68(16), 1727–1737. Mazine, A., El-Hamamsy, I., Verma, S. et al. (2018). Ross Procedure in Adults for Cardiologists and Cardiac Surgeons: JACC State-of-the-Art Review. Journal of the American College of Cardiology, 72(22), 2761–2777. European Society of Gynecology (ESG), Association for European Paediatric Cardiology (AEPC), German Society for Gender Medicine (DGesGM), Regitz-Zagrosek, V., Blomstrom Lundqvist, C., Borghi, C. et al. (2011). ESC Guidelines on the management of cardiovascular diseases during pregnancy: the Task Force on the Management of Cardiovascular Diseases during Pregnancy of the European Society of Cardiology (ESC). European heart journal, 32(24), 3147–3197. CardioNerds Case Reports: Recruitment Edition Series Production Team Bibin Varghese, MDRick Ferraro, MDTommy Das, MDEunice Dugan, MDEvelyn Song, MDColin Blumenthal, MDKaran Desai, MDAmit Goyal, MDDaniel Ambinder, MD

Aug 19, 2020

CardioNerds (Amit & Dan) join UT Southwestern cardiology fellows (Shreya Rao, Sonia Shah, and Nick Hendren) for some delicious Dallas Tacos! They discuss a fascinating case of syphilitic aortitis with severe aortic regurgitation presenting as cardiogenic shock. Program director Dr. Gail Peterson provides the E-CPR and a message for applicants. Episode notes were developed by Johns Hopkins internal medicine resident Evelyn Song with mentorship from University of Maryland cardiology fellow Karan Desai. Jump to: Patient summary - Case figures & media - Case teaching - Educational video - References - Production team Episode graphic by Dr. Carine Hamo The CardioNerds Cardiology Case Reports series shines light on the hidden curriculum of medical storytelling. We learn together while discussing fascinating cases in this fun, engaging, and educational format. Each episode ends with an “Expert CardioNerd Perspectives & Review” (E-CPR) for a nuanced teaching from a content expert. We truly believe that hearing about a patient is the singular theme that unifies everyone at every level, from the student to the professor emeritus. We are teaming up with the ACC FIT Section to use the #CNCR episodes to showcase CV education across the country in the era of virtual recruitment. As part of the recruitment series, each episode features fellows from a given program discussing and teaching about an interesting case as well as sharing what makes their hearts flutter about their fellowship training. The case discussion is followed by both an E-CPR segment and a message from the program director. CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademySubscribe to our newsletter- The HeartbeatSupport our educational mission by becoming a Patron!Cardiology Programs Twitter Group created by Dr. Nosheen Reza Patient Summary A 57 year old male presents with 3 months of progressive dyspnea on exertion, orthopnea and lower extremity edema. However, his symptoms suddenly worsened over the past few days. He has no other known medical history or prior surgeries. Further, he denies tobacco, alcohol or illicit drug use and reports a preference for male sexual partners. On presentation to the hospital, he had a markedly wide pulse pressure, a decrescendo diastolic murmur at the left upper sternal border and a water hammer pulse readily identifiable. TTE confirmed the clinical findings of severe aortic regurgitation with holodiastolic flow reversal in the thoracic, as well as the thoraco-abdominal aorta. Right heart catheterization was performed and showed equalization of the LVEDP and aortic diastolic pressure at 40 mmHg with Cardiac Output of 1.73 L/min. RPR was positive at a high titer (1:512). He was ultimately diagnosed with syphilitic aortitis with severe aortic regurgitation. He progressed to cardiogenic shock and was managed with nitroprusside, dobutamine, and furosemide infusion as well as IV penicillin for syphilitic aortitis and presumed neurosyphilis. The patient was stabilized and eventually underwent an uncomplicated prosthetic aortic valve replacement and aortic root resection and reconstruction and has done well post-operatively! Pathology was consistent with syphilitic aortitis: "lymphoplasmacytic inflammation, large foci of necrosis, and neovascularization" Case Media CXR: Cardiomegaly, bilateral pleural effusions, evidence of pulmonary congestionNormal sinus rhythm, left atrial enlargement, LVH and possible septal infarct.LV tracing (black), Aortic tracing (red)Apical long view with color Doppler noting marked flow through aortic valve during diastole.Continuous Doppler through trileaflet aortic valve consistent with severe AI (P1/2 92 msec).Pulse wave Doppler of abdominal aorta demonstrating holodiastolic flow reversal consistent with severe AI.Click to enlarge ??? Episode Schematics & Teaching The CardioNerds FiveSevere Aortic RegurgitationPathophysiology of Aortic RegurgitationClick to enlarge ??? The CardioNerds 5! – 5 major takeaways from the #CNCR case When suspecting severe AR, first characterize the AR as either acute or chronic based on clinical evaluation and hemodynamics. From there, AR can further be characterized as primary (valve disorder) or secondary (disorder of the aortic root/aorta). Chronic AR exposes the LV to volume overload (leading to increased LVEDV), afterload, and increased wall stress. Chronic severe AR has two phases: Compensated Phase: Responding to increased wall stress, eccentric hypertrophy occurs. LVEF is maintained during this stage, though LV dilation may begin to occur. Patients are typically asymptomatic. Decompensated Phase: Eventually, compensatory mechanisms are insufficient and significant LV dilation occurs and LVEF decreases. Patients will develop exertional dyspnea and CHF symptoms. The physical exam of patients with chronic AR is full of classic findings and eponyms! Specifically, regarding murmurs of AR, there is the classic diastolic, blowing, decrescendo murmur heard in the LUSB. Typically, the severity of AR correlates with the duration of the murmur more than the intensity. Some 2D echo findings of chronic, severe AR include pressure half-time less than 200 ms, holo-diastolic flow reversal in the proximal descending aorta and/or abdominal aorta, and a dilated LV due to remodeling. Other criteria include vena contracta > 0.6 cm, flail valve, regurgitant volume > 60 mL/beat, regurgitant fraction > 50%, and LVESD > 50 mm. The goal of management of acute AR is temporary stabilization before proceeding with surgical intervention. This includes vasodilators to reduce afterload and potentially inotropy to support cardiac output. Avoid excessive negative chronotropy as it can prolong diastole and worsen acute AR. If patient is bradycardiac, can increase HR with beta agonists or temporary pacing to decrease time spent in diastole. Produced by Dr. Karan Desai, MD References AR Review 2019 Syphilitic Aortitis, Roberts 2009 ACCSAP - AI CardioNerds Case Reports: Recruitment Edition Series Production Team Bibin Varghese, MDRick Ferraro, MDTommy Das, MDEunice Dugan, MDEvelyn Song, MDColin Blumenthal, MDKaran Desai, MDAmit Goyal, MDDaniel Ambinder, MD

Aug 17, 2020

CardioNerds Amit and Dan are joined by Dr. Nosheen Reza, chair of the ACC FIT section, to announce the launch of the CardioNerds Case Reports: Recruitment Edition Series! In this exciting project, the CardioNerds collaborated with the ACC FIT section to invite every fellowship program to co-produce a case-based episode. Fellows from the program present and discuss a fascinating case and an expert provides the E-CPR editorial, followed by a message to applicants from the program director. We've asked every program to help us promote diversity in their fellow ambassadors to the CardioNerds show. We also discuss the value of podcasts and innovations in medical education, Dr. Reza's perspectives and advice for the upcoming virtual recruitment, getting involved with the ACC as fellows-in-training (#FIT!), promoting diversity and inclusion within cardiology, and Dr. Reza's advice for thriving during fellowship. We also introduce the brand new CardioNerds Academy! We will be growing the platform by offering a uniquely tailored and mentored experience to several future CardioNerds Fellows. Our goal is to teach our CardioNerds Fellows the ropes of med-ed podcasting through a comprehensive curriculum with dedicated mentorship. We are honored to have recruited Dr. Justin Berk as program director and Dr. Heather Kagan as associate program director. Episode graphic by Dr. Carine Hamo CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademySubscribe to our newsletter- The HeartbeatSupport our educational mission by becoming a Patron!Cardiology Programs Twitter Group created by Dr. Nosheen Reza Key Reference: Reza N, Krishnan S, Adusumalli S. A Model for the Career Advancement of Women Fellows and Cardiologists. J Am Coll Cardiol. 2020;76(8):996 LP - 1000. Nosheen Reza, MD Dr. Nosheen Reza is a cardiologist and translational researcher at the University of Pennsylvania focusing on advanced heart failure and transplant cardiology and cardiovascular genetics, genomics, and phenomics. She obtained her medical degree from the University of Virginia School of Medicine in 2012 and completed her internal medicine residency training at the Massachusetts General Hospital in 2015. She then completed her Cardiovascular Disease fellowship at the University of Pennsylvania in 2018 and served as 2017-2018 Chief Fellow. At Penn, Dr. Reza pursued additional scholarship in genomic medicine as an NIH T32-funded postdoctoral fellow and in healthcare quality as a Penn Benjamin & Mary Siddons Measey Fellow in Quality Improvement and Patient Safety. She completed her final year of clinical training at Penn in Advanced Heart Failure and Transplant Cardiology and joined the faculty at the University of Pennsylvania in July 2020. Dr. Reza is passionate about medical education and has won many distinctions in the field throughout her training. She serves as an editorial board member for JACC: Case Reports, JACC: CardioOncology, and Current Cardiovascular Risk Reports. Dr. Reza is an active leader in the Heart Failure Society of America, American Heart Association, and American College of Cardiology at the local and national levels and volunteers on multiple leadership councils and steering committees within these organizations. CardioNerds Case Reports: Recruitment Edition Series Production Team Daniel Ambinder, MDAmit Goyal, MDHeather Kagan, MDJustin Berk, MD MPH MBA

Aug 14, 2020

CardioNerds (Amit Goyal & Daniel Ambinder) discuss a case report of COVID myocarditis and cardiogenic shock with Dr. Travis Howard and Dr. Zach Il'Giovine, cardiology fellows at the Cleveland Clinic. Dr. Nir Uriel, Professor of Medicine at Columbia University and Director of Advanced Heart Failure and Transplant at NewYork-Presbyterian Hospital Network in New York joins to discuss COVID-19 myocarditis and management of cardiogenic shock. The CardioNerds Cardiology Case Reports series shines light on the hidden curriculum of medical storytelling. We learn together while discussing fascinating cases in this fun, engaging, and educational format. Each episode ends with an “Expert CardioNerd Perspectives & Review” (E-CPR) for a nuanced teaching from a content expert. We truly believe that hearing about a patient is the singular theme that unifies everyone at every level, from the student to the professor emeritus. Check out the Cardionerds Cardiology Case Reports Topic Page Check out the Cardionerds Topics and Episode page for all podcast episodesSupport our educational mission by becoming a Patron! Case Summary Healthy and physically fit incarcerated 49M who presents with 2 weeks of fevers, myalgias, and SOB. His past medical history includes GSW to abdomen, psoriasis not currently on medications, prior tobacco and alcohol abuse. Transferred for undifferentiated shock on norepinephrine, and was found to be in sinus tachycardia to 110 bpm, hypotensive despite vasopressor infusions with labs showing a hyperinflammatory state, multi-organ failure, and eventually found to be COVID+. The patient quickly progressed into refractory cardiogenic shock requiring VA-EMCO, as well as Impella placement for LV unloading. The patient underwent endomyocardial biopsy with electron microscopy which was notable for COVID virions in the myocardium and was diagnosed with COVID myocarditis. Interestingly, his chest CT showed normal lung parenchyma and therefore presented as isolated cardiac involvement of COVID-19. The patient improved with tocilizumab, IVIG, and steroids. Episode Producer: Colin Blumenthal, MDMedical Education Mentor: Karan Desai, MD Episode graphic by Dr. Carine Hamo The CardioNerds 5! - 5 major takeaways from the #CNCR case Diagnose Cardiogenic Shock at the Bedside! Exam: Narrow Pulse Pressure, Labored Breathing, Cheyne-Stokes Respirations, Abdominal Bloating/Nausea, Cool Extremities, Oliguria, Altered Mental Status If PAC available, low central (PA) mixed venous saturation (<55-60%) suggestive* of cardiogenic shock COVID-19 can cause myocardial injury through several mechanisms Ischemic - Supply/Demand Mismatch, Acute Plaque Rupture Nonischemic - Stress Cardiomyopathy, Lymphocytic Infiltration, Direct Viral Cardiomyocyte Injury, Bystander Injury from Systemic Inflammation Different forms of mechanical support give varying levels of cardiac output and pulmonary support Consider VA-ECMO in refractory cardiogenic shock, especially if there is evidence of biventricular failure +/- pulmonary compromise VA-ECMO may require "LV unloading" when there is high afterload leading to pulmonary congestion and/or stasis of blood flow in the LV Myocarditis Infographic https://twitter.com/CBlumenthal2/status/1295043817855475715?s=20 References Dexamethasone in Hospitalized Patients with COVID-19 Non-invasive imaging in the diagnosis of acute viral myocarditis Evaluation Study of Congestive Heart Failure and Pulmonary Artery Catheterization Effectiveness: The ESCAPE Trial Mechanical Circulatory Support Devices for Cardiogenic Shock: State of the Art Left ventricular distension and venting strategies for patients on venoarterial extracorporeal membrane oxygenation Remdesivir for the Treatment of Covid-19 - Preliminary Report Effect of Convalescent Plasma Therapy on Time to Clinical Improvement in Patients With Severe and Life-threatening COVID-19: A Randomized Clinical Trial Resources: CardioNerds Myocarditis page https://www.cardionerds.com/episodes/myocarditis/ Talking Tall Rounds Epsiode https://my.clevelandclinic.org/podcasts/cardiac-consult/talking-tall-rounds-covid-19-related-myocarditis Tall Rounds Conference http://consultqdlive.mediaspace.kaltura.com/media/0_7llcuh5t Colin Blumenthal, MDKaran Desai, MDAmit Goyal, MDDaniel Ambinder, MD

Aug 10, 2020

The CardioNerds discuss Coronary Artery Calcium Scoring with Dr. Michael Blaha, Director of Clinical Research for the Johns Hopkins Ciccarone Center for the Prevention of Cardiovascular Disease. Joining the discussion is Dr. Gabriel Shaya, cardiology fellow at the Johns Hopkins Hospital and prevention researcher. Carine Hamo, Heather Kagan and Dan Ambinder take a deep dive into the crunchy and calcified world of coronary artery disease discussing the evidence and utility of coronary artery calcium scoring as a powerful tool for individualized risk stratification of cardiovascular disease prevention. Cardionerds Cardiovascular Prevention PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! The Cardionerds CV prevention series includes in-depth deep dives on so many prevention topics including the ABCs of prevention, approach to obesity, hypertension, diabetes mellitus and anti-diabetes agents, personalized risk and genetic risk assessments, hyperlipidemia, women’s cardiovascular prevention, coronary calcium scoring and so much more! We are truly honored to be producing the Cardionerds CVD Prevention Series in collaboration with the American Society for Preventive Cardiology! The ASPC is an incredible resource for learning, networking, and promoting the ideals of cardiovascular prevention! This series is kicked off by a message from Dr. Amit Khera, President of the American Society for Preventive Cardiology and President of the SouthWest Affiliate of the American Heart Association. Cardionerds Cardiovascular Prevention Series References and Links https://www.mesa-nhlbi.org/CAC-Tools.aspxBlaha MJ, Blankstein R, Nasir K. Coronary Artery Calcium Scores of Zero and Establishing the Concept of Negative Risk Factors. J Am Coll Cardiol. 2019;74(1):12-14. Peng AW, Mirbolouk M, Orimoloye OA, et al. Long-Term All-Cause and Cause-Specific Mortality in Asymptomatic Patients With CAC ≥1,000: Results From the CAC Consortium. JACC Cardiovasc Imaging. 2020;13(1 Pt 1):83-93. Shaya GE, Al-Mallah MH, Hung RK, et al. High Exercise Capacity Attenuates the Risk of Early Mortality After a First Myocardial Infarction: The Henry Ford Exercise Testing (FIT) Project. Mayo Clin Proc. 2016;91(2):129-139. Dr. Michael Blaha is an Associate Professor of Cardiology and Epidemiology and presently serves as the Director of Clinical Research for the Johns Hopkins Ciccarone Center for the Prevention of Cardiovascular Disease. Dr. Blaha completed both his MD and MPH and Vanderbilt University. He then completed his Internal Medicine residency in the Osler Medical Housestaff Training Program at Johns Hopkins where he also completed fellowship training. He is an Associate Editor for the Journal of Cardiovascular Computed Tomography, Associate Editor for the Diabetes and Cardiometabolic Clinical Community on acc.org and is a standing member of the Endocrinologic and Metabolic Drug Advisory Committee (EMDAC) for the FDA. He is Principal Investigator for the Coronary Artery Calcium Consortium, co-chair of the Cross-Cohort Collaboration, and a Principle Investigator for the American Heart Association (AHA) Tobacco Regulation and Addiction Center. Dr. Gabriel Shaya earned both his Medical Degree and Masters of Public Health at the University of Miami Miller School of Medicine. He went on to complete his residency in Internal Medicine at the New York Presbyterian – Weill Cornell Medical Center. He has returned to his hometown of Baltimore for Cardiology fellowship with the intent of pursuing a career as an academic cardiologist. His clinical and research interests center on the refinement of cardiovascular risk assessment with the goal of tailoring preventive therapies to avert adverse cardiovascular events before they happen. Michael Joseph Blaha, M.D., M.P.H.Gabe Shaya, MD, MPHCarine Hamo, MDHeather Kagan, MDDaniel Ambinder, MD

Aug 6, 2020

JACC: Case Reports Editor-in-Chief, Dr. Julia Grapsa joins Cardionerds, Amit and Dan, to introduce a new episode series: CardioNerds Case Reports (#CNCR)! We discuss the value of learning through cases, podcasts and other innovations in education, importance of promoting wellness in medicine, the editorial review process for case reports, and being an editor-in-chief as a woman in medicine. The CardioNerds Case Reports series will shine light on the hidden curriculum of medical storytelling. We learn together while discussing fascinating cases in this fun, engaging, and educational format. Each episode ends with an "Expert CardioNerd Perspectives & Review" (E-CPR) for a nuanced teaching from a content expert. We truly believe that hearing about a patient is the singular theme that unifies everyone at every level, from the student to the professor emeritus. Take me to the Cardionerds Case Report (CNCR) Series PageTake me to the Cardionerds Episode Topics Page Episode graphic created by Dr. Carine Hamo References Grapsa J (2019) Voices in Cardiology. JACC Case Reports. Grapsa J, Fuster V (2019) JACC: Case Reports: New Era of Clinical Cases, Bridging Patients With Guidelines. J Am Coll Cardiol. Grapsa J, Fuster V (2020) JACC: Case Reports: Moving to a Multimedia Educational Vehicle. J Am Coll Cardiol. (2006) Mindset: the new psychology of success. Choice Rev Online. Balasubramanian S, Saberi S, Yu S, Duvernoy CS, Day SM, Agarwal PP (2020) Women representation among cardiology journal editorial boards. Circulation. Dr. Julia Grapsa serves as the Editor-in-Chief of JACC: Case Reports. Dr. Grapsa worked for Cleveland Clinic Abu Dhabi and then she moved to UK as a a consultant cardiologist for Barts Heart Center. In March 2020, Dr. Grapsa started working as consultant cardiologist at Guys and St Thomas NHS Trust. Within the UK’s leading structural valve disease group, Dr. Grapsa is responsible for the valvular heart disease network and echocardiography, a position previously held by Professor John Chambers. Dr. Grapsa has served as chair of the young community for multimodality imaging for the European Association of Cardiovascular Imaging and as a member of the European Society of Cardiology (ESC) education committee, leading the ESC clinical case gallery. She was responsible for ESC social media, since its birth and she has been a member of imaging and online education committees of Heart Failure Association. Prior to her role as JACC: Case Reports editor-in-chief, Dr. Grapsa served as an editorial consultant for JACC: Cardiovascular Imaging. She is a fellow of the ACC, the American Heart Association, the American Society of Echocardiography and the European Society of Cardiology. Julia Grapsa, MD, PhD, FACC Amit Goyal, MD Daniel Ambinder, MD

Aug 2, 2020

The CardioNerds discuss Lipid Management with Dr. Ann Marie Navar and Dr. Nishant Shah from Duke Medical Center, Division of Cardiology. Amit, Carine and Dan take a deep dive into the greasy world of lipids and cholesterol, covering lipid metabolism, therapeutic targets, approach across the entire spectrum of predicted risk, and key common management scenarios (statin intolerance, hypertriglyceridemia, elevated LP(a)), and more. Episode 42. Lipids and Cholesterol with Drs. Drs. Ann Marie Navar and Nishant Shah Take me to the Cardionerds Cardiovascular Prevention PageTake me to episode topics page The Cardionerds CV prevention series will include in-depth deep dives on so many topics related to prevention starting with this case discussion. Stay tuned for upcoming episodes on the ABCs of prevention, obesity, hypertension, diabetes mellitus and anti-diabetes agents, personalized risk and genetic risk assessments, hyperlipidemia, women’s cardiovascular prevention, coronary calcium scoring and so much more! Key references: Toth, P. P. (2020). Familial Hypercholesterolemia and Lipoprotein(a): Unraveling the Knot That Binds Them. Journal of the American College of Cardiology, 75(21), 2694–2697.Michos, E. D., McEvoy, J. W., & Blumenthal, R. S. (2019). Lipid management for the prevention of atherosclerotic cardiovascular disease. New England Journal of Medicine, 381(16), 1557–1567. AHA/ACC/AACVPR/AAPA/ABC/ACPM/ADA/AGS/APhA/ASPC/NLA/PCNA Guideline on the Management of Blood Cholesterol: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines. Journal of the American College of Cardiology, 73(24), e285–e350.Lloyd-Jones, D. M., Braun, L. T., Ndumele, C. E., Smith, S. C., Sperling, L. S., Virani, S. S., & Blumenthal, R. S. (2019). Use of Risk Assessment Tools to Guide Decision-Making in the Primary Prevention of Atherosclerotic Cardiovascular Disease: A Special Report from the American Heart Association and American College of Cardiology. Circulation, 139(25), E1162–E1177.Laufs, U., Parhofer, K. G., Ginsberg, H. N., & Hegele, R. A. (2020). Clinical review on triglycerides. European Heart Journal, 41(1), 99–109.ACC/AHA Guideline on the Primary Prevention of Cardiovascular Disease: Executive Summary: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines. Journal of the American College of Cardiology, 74(10), 1376–1414. We are truly honored to be producing the Cardionerds CVD Prevention Series in collaboration with the American Society for Preventive Cardiology! The ASPC is an incredible resource for learning, networking, and promoting the ideals of cardiovascular prevention! This series is kicked off by a message from Dr. Amit Khera, President of the American Society for Preventive Cardiology and President of the SouthWest Affiliate of the American Heart Association. Cardionerds Cardiovascular Prevention Series Dr. Ann Marie Navar is a cardiologist and epidemiologist at the Duke Clinical Research Institute focusing on cardiovascular disease prevention. She received an MD from Duke University and a PhD in Global Disease Epidemiology and Control from the Johns Hopkins School of Public Health in 2009 before completing residency in internal medicine and pediatrics and fellowship in cardiology at Duke. Dr. Navar’s research focuses on improving cardiovascular disease prevention through better identification of at-risk populations, targeted interventions to improve quality of care and patient engagement through the electronic health record, and better treatment of hypertension and cholesterol to lower CV risk. She also studies the impact of payer-imposed barriers to novel therapies. Her areas of expertise include risk prediction, patient risk communication, real world data analyses using EHR- and claims-based datasets, and registries. She is an associate editor at JAMA-Cardiology and a board member of the American Society of Preventive Cardiology. Dr. Nishant Shah obtained his medical degree from Wake Forest University School of Medicine. He completed internal medicine residency training at the Johns Hopkins Osler Program as part of the Barker Firm. He completed his cardiology fellowship training at the Cleveland Clinic. He is currently faculty at Duke Medical Center, Division of Cardiology and is an expert in preventive cardiology as well as a member of the cardiometabolic prevention program. Dr. Shah’s research revolves around the clinical manifestations of genetic lipid biomarkers and advanced dyslipidemias. He is also interested in ways to make impacts at the primary prevention level. Furthermore, Dr. Shah is involved in many epidemiologic and clinical trial based work with several leaders in the field. He also serves as an associate editor for the American Heart Journal. Dr. Shah is very passionate about clinical education and has won many distinctions in education throughout his training. Ann Marie Navar, MD, PhDNishant Shah, MDAmit Goyal, MDCarine Hamo, MDDaniel Ambinder, MD

Jul 26, 2020

The CardioNerds discuss Women's Cardiovascular Prevention with Dr. Leslie Cho, Interventional Cardiologist and Director of the Cleveland Clinic’s Women’s Cardiovascular Center. She is also Section Head of Preventive Cardiology and Rehabilitation in the Robert and Suzanne Tomsich Department of Cardiovascular Medicine at Cleveland Clinic. Amit, Dan and Carine take a deep dive into women's cardiovascular prevention and discuss the epidemiology, unique risk factors, different manifestations of CVD and treatment strategies to lower cardiovascular risk in women. Tune in as we discuss cases from the CardioNerds Women's Clinic to learn more! Take me to the Cardionerds Cardiovascular Prevention PageTake me to episode topics page Cardiac Consult PodcastTall Rounds Lectures Key Reference: Cho L, Davis M, Elgendy I, et al (2020) Summary of Updated Recommendations for Primary Prevention of Cardiovascular Disease in Women: JACC State-of-the-Art Review. J Am Coll Cardiol 75:2602–2618 We are truly honored to be producing the Cardionerds CVD Prevention Series in collaboration with the American Society for Preventive Cardiology! The ASPC is an incredible resource for learning, networking, and promoting the ideals of cardiovascular prevention! This series is kicked off by a message from Dr. Amit Khera, President of the American Society for Preventive Cardiology and President of the SouthWest Affiliate of the American Heart Association. Cardionerds Cardiovascular Prevention Series Dr. Leslie Cho is a professor of Medicine at Cleveland Clinic Lerner School of Medicine Case Western Reserve Medical School and serves as Director of the Cleveland Clinic’s Women’s Cardiovascular Center. She is also Section Head, Preventive Cardiology and Rehabilitation in the Robert and Suzanne Tomsich Department of Cardiovascular Medicine at Cleveland Clinic. Dr. Cho received her undergraduate degree in interdisciplinary studies from the University of California, Los Angeles, graduating cum laude. She received her medical degree from the University of Chicago Pritzker School of Medicine, and took her residency in internal medicine at the University of Washington Medical Center where she received the John Humphrey Award as Most Outstanding Internal Medicine Resident. Her clinical training continued when she accepted a fellowship in cardiology, followed by a fellowship in interventional cardiology and peripheral disease, both from Cleveland Clinic. Leslie Cho, MDAmit Goyal, MDCarine Hamo, MDDaniel Ambinder, MD

Jul 19, 2020

The CardioNerds discuss The 'ABC's of Cardiovascular Prevention with Dr. Roger Blumenthal, Director of the Johns Hopkins Ciccarone Center for the Prevention of Cardiovascular Disease and co-chairperson of the 2019 American College of Cardiology/American Heart Guideline on prevention of cardiovascular disease. Joining the discussion is Dr. David Feldman, Osler housestaff and first author of a beautiful State-of-the-Art review in the American Journal of Preventive Cardiology discussing a comprehensive ABCs of prevention. A: Assess Risk, Anti-Inflammatory, AspirinB: Body weight, Blood PressureC: Cigarette Cessation, CholesterolD: Dream (sleep), Diet, Digital Health, DiabetesE: Exercise F: Factors of the EnvironmentG: Genetics Take me to the Cardionerds Cardiovascular Prevention PageTake me to episode topics page Key Reference: Summarizing 2019 in Cardiovascular Prevention using the Johns Hopkins Ciccarone Center for the Prevention of Cardiovascular Disease’s ‘ABC’s Approach We are truly honored to be producing the Cardionerds CVD Prevention Series in collaboration with the American Society for Preventive Cardiology! The ASPC is an incredible resource for learning, networking, and promoting the ideals of cardiovascular prevention! This series is kicked off by a message from Dr. Amit Khera, President of the American Society for Preventive Cardiology and President of the SouthWest Affiliate of the American Heart Association. Dr. Roger Blumenthal is a Professor of Medicine and the Director of the Johns Hopkins Ciccarone Center for the Prevention of Cardiovascular Disease for which he was the principal developer. He received his medical degree from Cornell Medical College, where he was awarded the Weiss Prize for Excellence in Clinical Medicine. He completed his internal medicine and cardiology fellowship training at The Johns Hopkins Hospital before joining the Johns Hopkins cardiology faculty. Dr. Blumenthal was the most recent recipient of the Landon School Anthony Kupka Distinguished Alumnus Award. He was co-chairperson of the 2019 American College of Cardiology/American Heart Guideline on prevention of cardiovascular disease. Dr. David Feldman is a Junior Assistant Resident in the Osler Medical Residency Program at the Johns Hopkins Hospital. Prior to joining the housestaff, David received his MD and MPH degrees from the University of Miami. David first joined the Ciccarone Center as a pre-doctoral fellow in 2013 under the mentorship of Drs. Roger Blumenthal and Mike Blaha. David is passionate about cardiovascular disease prevention and hopes to pursue a career in academic cardiology, with a particular interest in preventive cardiology. Roger Scott Blumenthal, M.D.David Feldman, MDCardionerds Cardiovascular Prevention SeriesDaniel Ambinder, MDAmit Goyal, MDCarine Hamo, MD

Jul 17, 2020

CardioNerds Amit Goyal and returning guest Dr. Zach Il’Giovine explore the patient's perspective on cardiovascular prevention with the star patient of this series: Kanak Amin. to explore the patient perspective on cardiovascular prevention. Mr. Amin tells us about his perspectives on being a heart patient and offers important advice for both patients and providers on the. He gives us many pearls, but especially highlights the importance of diabetes education, cardiac rehabilitation, engaging loved ones, and getting to know the patient on a deeper level. Special messages from Dr. Wael Jaber and Dr. Nishant Shah, who both knew Mr. Amin as a colleague, friend, and patient. Take me to the Cardionerds Cardiovascular Prevention PageTake me to episode topics page We are truly honored to be producing the Cardionerds CVD Prevention Series in collaboration with the American Society for Preventive Cardiology! The ASPC is an incredible resource for learning, networking, and promoting the ideals of cardiovascular prevention! This series is kicked off by a message from Dr. Amit Khera, President of the American Society for Preventive Cardiology and President of the SouthWest Affiliate of the American Heart Association. Kanak Amin is the Program Manager of the Radiochemistry Nuclear Medicine program at Cleveland Clinic. His hobbies and interests include woodworking, learning Wall Street and the financial world as well as computer web design. We are so appreciative this phenomenal patient perspective on cardiovascular prevention! Dr. Zachary Il’Giovine is a general cardiology fellow at the Cleveland Clinic. He received his medical degree from the Wright State University Boonshoft School of Medicine before completing internal medicine training at Duke University. He has clinical interests in advanced heart failure and cardiac critical care. Outside of the hospital he loves playing soccer and spending time with his wife Clare and son Luca. Kanak AminNishant Shah, MDZachary Il’Giovine, MD Amit Goyal, MDCardionerds Cardiovascular Prevention Series

Jul 12, 2020

This is the first episode in an important series on cardiovascular prevention. It's no secret that cardiovascular disease is the #1 killer worldwide; the total impact on humanity is just staggering. A focus on preventing CVD is an impetus for every cardionerd. In this episode Dan, Amit, Carine, and Heather discuss an illustrative case discussion and review the Cardionerds 2+4 paradigm of cardiovascular prevention: 2 fundamental principles of management + 4 steps in risk stratification. The Cardionerds CV prevention series will include in-depth deep dives on so many topics related to prevention starting with this case discussion. Stay tuned for upcoming episodes on the ABCs of prevention, obesity, hypertension, diabetes mellitus and anti-diabetes agents, personalized risk and genetic risk assessments, hyperlipidemia, women's cardiovascular prevention, coronary calcium scoring and so much more! Take me to the Cardionerds Cardiovascular Prevention PageTake me to episode topics page We are truly honored to be producing the Cardionerds CVD Prevention Series in collaboration with the American Society for Preventive Cardiology! The ASPC is an incredible resource for learning, networking, and promoting the ideals of cardiovascular prevention! This series is kicked off by a message from Dr. Amit Khera, President of the American Society for Preventive Cardiology and President of the SouthWest Affiliate of the American Heart Association. TWO principles of management Emphasize healthy lifestyle for everyone regardless of riskEscalate Preventive Measures with ↑ Risk FOUR steps of risk stratification Qualitative risk approximation - identify major risk factors and start counseling and education. Quantitative risk estimation - use a validated model to quantify a patient’s future risk of CVD. Identify Risk Enhancing Factors - personalize risk if patient is in the gray zones after step 2Measure coronary artery calcium score - selectively if risk remains uncertain Cardiovascular Prevention Amit Goyal, MDDaniel Ambinder, MDCarine Hamo, MDHeather Kagan, MD

Jun 21, 2020

The role of palliative care in the management of heart failure is discussed by palliative care expert, Dr. Rab Razzak, clinical associate professor and clinical director of palliative care at University Hospital Cleveland Medical Center. CardioNerds host Amit Goyal is joined by special guest interviewer, Dr. Arsalan Derakhshan, Assistant Program director at Case Western Internal Medicine residency program and the head of the Global Health Pathway as well as co-host of the Clinical Problem Solvers podcast! Take me to the Heart Failure Topic PageTake me to episode topics page Dr. Rab Razzak went to medical school at Bangledesh Medical College and internal medicine residency at St. Joseph Regional Medical Center in Patterson, NJ. He worked initially as a hospitalist at Cedars Sinai and was grandfathered into palliative care. He moved to Maryland to work at Johns Hopkins, where he practiced for 4.5 years. He is now a clinical associate professor and clinical director of palliative care at University Hospital Cleveland Medical Center. He is also a devoted husband, dedicated father, and a stand-up comedian! We could think of no one better to discuss Palliative Care in Heart Failure than Dr. Razzak. Dr. Arsalan Derakhshan was born in Iran and moved to Atlanta, Georgia as a young child. He loves to travel and considers himself a global citizen. After graduating from Emory University, he attended the Medical College of Georgia and completed internal medicine residency at Johns Hopkins Hospital. He spends his time attending on inpatient team, staffing resident clinic, and working as the global health track director. He enjoys working with medical students and interns to help them discover their passions. His primary interests include clinical reasoning, global health, and medical innovations. He co-hosts one of the most popular medicine podcast, The Clinical Problem Solvers and has been incredibly instrumental in the launch of The CardioNerds! Rab Razzak, MDArsalan Derakhshan, MDCardioNerds Heart Failure Series

Jun 14, 2020

Dr. Robert Mentz, director of the Heart Failure section in the Duke Division of Cardiology, discusses diuretics, anti-hyperglycemic therapies including SGLT2/GLP1 agents, angiotensin receptor-neprilysin inhibitors (ARNi), iron as therapies for Heart Failure with Preserved Ejection Fraction (HFpEF). Additionally, study design and ongoing research in HFpEF is discussed. At the end of the episode Dr. Mentz provides an additional update that highlights how the COVID-19 pandemic has influenced clinical trials around the world. Special thanks to guest interviewers, Duke cardiology fellows, Dr. Kelly Arps and Dr. Rahul Loungani! On the CardioNerds Heart Failure topic page you’ll podcast episodes, references, guest experts and contributors, and so much more. Take me to the Heart Failure Topic PageTake me to episode topics pageAcute Decompensated Heart Failure Primer – Youtube Dr. Robert Mentz completed internal medicine training at Brigham and Women’s Hospital and cardiology fellowship followed by advanced heart failure and transplant cardiology training at Duke University Hospital and the Duke Clinical Research Institute. He is the new director of the Heart Failure section in the Duke Division of Cardiology. His areas of clinical and research focus include treating comorbid diseases in heart failure patients, use of biomarkers and surrogate and non-fatal outcomes in heart failure trials, and novel therapeutic approaches to heart failure. Dr. Mentz is heavily involved in many clinical trials and serves as the associate editor at Circulation: Heart Failure. In addition to his clinical and research endeavors, Dr. Mentz is heavily invested in the cardiology fellowship where he serves as associated program director and renown mentor for which he has won many fellow-nominated awards. Finally, as former director of the Duke University Cooperative Cardiovascular Society, he expanded the network of current and former Duke trainees to be a leading enroller in clinical trials. We are really excited about him joining the show to discuss Diuretics ARNi SGLT2/GLP1 therapies for HFpEF. Dr. Rahul Loungani completed medical school at the medical university of SC and then traveled to Baltimore for internal medicine training in the Osler Residency Program at the Johns Hopkins Hospital. Here he fell in love with the management and hemodynamics of critically ill patients. He is currently a third-year cardiology fellow at Duke University Medical Center where he will also be pursuing fellowship in advanced heart failure and transplant cardiology next year. His current interests are in Cardiac amyloid, in particular it's arrhythmic manifestations, early diagnosis, and novel therapeutics. He also loves teaching the housestaff and was awarded the Cassell-Saperstein award at Duke, recognizing the fellow who most demonstrates a commitment to teaching and passion for clinical education. Outside of the hospital loves being a new dad to baby Arya. Dr. Kelly Arps completed medical school at Emory University school of medicine and internal medicine training in the Osler Residency Program at the Johns Hopkins Hospital. She is currently is pursuing her cardiology fellowship at Duke University Medical Center. CardioNerds Heart Failure Series

Jun 8, 2020

We discuss Heart Failure with Preserved Ejection Fraction (HFpEF) with Dr. Kavita Sharma, director of the Heart Failure with Preserved Ejection Fraction Program and interim director of Advanced Heart Failure Transplant section at The Johns Hopkins Hospital. CardioNerds hosts Carine Hamo and Daniel Ambinder are joined by Dr. Beth Feldman (resident at The Johns Hopkins Hospital). Topics discussed include a definitions, diagnosis, phenotypic presentations, inpatient management of acute decompensated heart failure, role of dopamine, advanced therapies of HFpEF, and the Paraglide trial.References mentioned in this episode can be found here On the CardioNerds Heart Failure topic page you’ll podcast episodes, references, guest experts and contributors, and so much more. Take me to the Heart Failure Topic PageTake me to episode topics pageAcute Decompensated Heart Failure Primer – Youtube Dr. Kavita Sharma graduated from the University of Virginia School of Medicine and completed her residency and served as the assistant chief of service, cardiology fellowship and advanced heart failure fellowship at the Johns Hopkins Hospital. She is the Director of the Johns Hopkins Heart Failure with Preserved Ejection Fraction Program and is currently the interim director of Advanced Heart Failure Transplant section at Hopkins. She has a specialized interest in heart failure with preserved ejection fraction (HFpEF), and directs one of the largest programs in the country dedicated to caring for patients with this condition. She is the principal investigator of numerous clinical and translational trials in HFpEF and leads a team of nurses, research coordinators, and fellows-in-training in this multifaceted program. She is an invited speaker at national meetings in topic areas covering advanced heart failure and HFpEF. Dr. Beth Feldman graduated from Temple University School of Medicine and is currently on the Longcope Firm on the Osler Medical Service at Johns Hopkins University Hospital. Before pursuing a career in medicine, she worked in health care consulting focusing in health systems. She is passionate about health policy and health systems research. She is hoping to pursue a career in cardiology, with a particular interest in critical care. Kavita Sharma, MDBeth Feldman, MDCardioNerds Heart Failure Series

May 31, 2020

Interventional cardiology and structural interventions in heart failure are discussed by Dr. Jeffrey Moses, Director of Interventional Therapeutics at Columbia University Medical Center Director of Advanced Cardiac Interventions at St Francis Hospital and Heart Center in Roslyn, NY. CardioNerds hosts Amit Goyal and Daniel Ambinder are joined by Dr. Jackie Latina (Cardiology fellow at The Johns Hopkins Hospital). Topics discussed include percutaneous intervention and complex and high-risk coronary intervention (CHIP), treatment of functional mitral and tricuspid regurgitation, aortic stenosis, and the utility of interatrial shunt devices for the treatment congestive heart failure. On the CardioNerds Heart Failure topic page you’ll podcast episodes, references, guest experts and contributors, and so much more. Take me to the Heart Failure Topic PageTake me to episode topics pageAcute Decompensated Heart Failure Primer – Youtube Dr. Jeffrey W. Moses completed medical school at the University of Pennsylvania School of Medicine and his internship, residency and fellowship in Cardiology at the Presbyterian University of Pennsylvania Medical Center. He currently serves as Director of Interventional Cardiovascular Therapeutics at Columbia University Medical Center and as Director of Advanced Cardiac Interventions at St Francis Hospital and Heart Center in Roslyn, NY. Dr. Moses is an Associate Director of the Transcatheter Cardiovascular Therapeutics (TCT) conference. He has served as lead investigator for numerous national and international clinical studies and he has made important contributions in the areas of clinical research and educational activities in interventional vascular therapy. He is also a pioneer in developing approaches involving minimally invasive surgery, angioplasty, gene therapy, novel imaging technologies and various support devices that allow for wider application of interventional cardiovascular procedures. Dr. Jacqueline Latina was born and raised in the suburbs of Boston, MA, but fortunately escaped without a Boston accent. She is a graduate of Princeton University with an A.B. in chemistry. She earned her M.D. at Tufts University School of Medicine. Her internship and internal medicine residency were completed at Mount Sinai Hospital in New York City, where she stayed on for an American Heart Association postdoctoral research fellowship. She completed an M.S. in clinical research methods at the Columbia Mailman School of Public Health during that time. She is currently a cardiology fellow at Johns Hopkins Hospital, and plans to start interventional cardiology fellowship in June 2020. She chuckles if you ask “Are you Latina?” Jeffrey W. Moses, MDJacqueline Latina, MDCardioNerds Heart Failure Series

May 26, 2020

The Cleveland Clinic Director of Cardiac MRI, Dr. Deborah Kwon, discusses the principles and clinical applications of cardiac MRI, taking us from the protons to the bedside with a series of illustrative cases. CardioNerds hosts Amit Goyal, Daniel Ambinder, and Carine Hamo are joined by Dr. Nicole Pristera (Cleveland Clinic cardiology fellow). Flutter moment by student doctor Arooma Shahid. On the CardioNerds Myocarditis page you will find podcast episodes, infographic, youtube videos, references, tweetorials and guest experts & contributors, flutter stars and so much more. CardioNerds Myocarditis PageCardioNerds Multimodality CV Imaging PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Links in this episode: Mental Filter: Matters of the Heart: Part 1Mental Filter: Matters of the Heart: Part 2Cardiac Imaging Agorà Dr. Debbie Kwon attended medical school at the University of Michigan and internal medicine residency at the University of Pennsylvania. She completed her general cardiology and cardiovascular imaging fellowships at the Cleveland Clinic. She is the Director of Cardiac MRI At the Cleveland Clinic and serves as the Core Lab MRI director for the Pulmonary Vascular Disease Phenomics (PVDOMICS) multicenter National institution of Health (NIH) Study. Dr. Nicole Pristera is a cardiology fellow at the Cleveland Clinic. She earned her medical degree at Case Western Reserve University and completed her internal medicine residency training at Duke University. Her clinical interests include interventional cardiology and cardiac critical care. Outside of the hospital, she enjoys traveling, hiking, and learning foreign languages. Dr. Arooma Tahir completed her medical degree from Lahore Medical and Dental college in Lahore Pakistan. She went to medical school to pursue her passion and currently she is studying for USMLEs in Fresno, CA. She enjoys hiking, trying out different cuisines, and podcast by cardionerds. Interview Questions How would you give a basic intro to cardiac MRI principles to a first year cardiology fellow? What should we know about the common sequences for cardiac MRI?We all learn about the risks of NSF. How much of these risks are a reality and when should we truly avoid gadolinium exposure?What are some challenges to MRI?What types of information about the heart can we obtain with a CMR? The role for Cardiac MRI in particular cases discussed with Dr. Kwon CAD: A 45 year old G1P1 woman with prior preeclampsia and anterior STEMI s/p LAD PCI 3 years ago is being seen for chest pain. TTE shows LVEF 45% with mid-apical anterior hypokinesis and apical aneurysm. How does CMR help delineate ischemic heart disease (perfusion, viability, chambers) Pericarditis: her stress MRI shows an anteroapical perfusion defect and apical aneurysm with mural thrombus, with corresponding LGE. On further review, her chest pain is sharp, pleuritic, and worsens with recumbency. EKG on follow-up shows diffuse ST elevations and PR depressions except for in aVR which shows ST depression and PR elevation. ESR and CRP are moderately elevated. ARVC: A 35 year old female athlete who is admitted after VF arrest that occurred during a tennis match. Thankfully she received immediate bystander CPR with early defibrillation and prompt ROSC. She has had prior syncope during training and an uncle died suddenly at age 40. Resting EKG shows an incomplete right bundle, right precordial TWIs, and epsilon waves in V1-V3. On tele she’s had multiple runs of NSVT of LBBB morphology. Echocardiogram shows RV dilation. A heart failure consult is considering EMBx but requests a CMR beforehand. Role in select other cardiomyopathies: HCM, Amyloid, hemochromatosis etc (if time) Valvular Heart Disease: A 28 year old man with no PMH who presents with progressive dyspnea during his routine morning runs. On exam he has a early diastolic decrescendo murmur best heard at end expiration while leaning forward. While concentrating on the murmur you notice a subtle rhythmic head bobbing. TTE shows eccentric AI and a dilated LV, but further characterization is limited. (CMR shows bicuspid aortic valve, TAA, LV dilation) Cardiac mass: a 55 year old woman with subacute fevers, chills, and night sweats now presents with acute ischemic left leg pain. Auscultation reveals a mid-diastolic plop. TTE is limited by poor sonographic windows, but there is a nondescript echodensity in the LA. What is the role of CMR in cardiac masses? Myocarditis: Chas Miller is our patient from episodes 31 & 32 who had presented with cardiogenic shock and heart block found to have fulminant myocarditis. Now unfortunately he was too sick to undergo a cardiac mri, but how would it have helped? Deborah Kwon, MDNicole Pristera, MDArooma Tahir, MBBSCardioNerds Myocarditis, updated 1.20.21

May 17, 2020

What does it feel like to have fulminant myocarditis? How does it feel to see a loved one on ECMO? What impact do healthcare heroes have on their patients' and their families'? Tune into this remarkable firsthand patient perspective as Chas and Julie Miller recount their experience with fulminant myocarditis. In Episode 31 we discussed the science & medicine of myocarditis. Now in Episode 32 we realize the emotions and human experience on the other side through the lens of a patient and his loving wife. Special messages from CCU nursing, Megan VanName, Alyssa Noonan, and Kelly Norsworthy, as well as Dr. Dan Choi, cardiac surgeon at Johns Hopkins Hospital. On the CardioNerds Myocarditis page you will find podcast episodes, infographic, youtube videos, references, tweetorials and guest experts & contributors, flutter stars and so much more. Take me to the Myocarditis Series PageTake me to the episode topics pagesCheck out Amit Goyal’s Myocarditis Tweetorial 5 points of maximal impulse in approaching myocarditis (review from episode 31) Build the clinical suspicion for myocarditis: You need a high index of suspicion given the variable presentation, and definitely need to keep a differential so you don’t miss things like acute coronary syndromes.Decide if EMBx is necessary: Most often obtained in fulminant presentations to look for pathologic findings of giant cell myocarditis or eosinophilic myocarditis, because these findings will change management.Manage the acute cardiac injury, which can range from supportive care to treatment of shock, arrhythmias, and even tamponade.Manage the chronic cardiac sequelae: Recovering from the acute phase of myocarditis doesn’t necessarily mean smooth sailing — some develop chronic heart failure, warranting GDMT — or guideline directed management and therapy, as defined byDr. Randall Starling in Ep 13.Treat the myocarditis: Immunosuppression is often started empirically in fulminant disease, but continuation depends on what you find on pathology.

May 11, 2020

The CardioNerds discuss a case of fulminant myocarditis, teaching a comprehensive approach to myocarditis with just 5 foundational principles. Review the myocarditis infographic on the myocarditis topic page. The episode ends with a special message from the true heroes of this episode, Chas and Julie Miller. This marks our first episode after 100,000 downloads of the show - and this is a benchmark that we are celebrating together with all of you. Since launch, we have had 82 voices on the show and youtube channel. Our website which collates all the podcast episodes, youtube videos, tweetorials, and more has been accessed in 120 countries. We just cannot thank you enough! On the CardioNerds Myocarditis page you will find podcast episodes, infographic, youtube videos, references, tweetorials and guest experts & contributors, flutter stars and so much more. Take me to the Myocarditis Series PageTake me to the episode topics pagesCheck out Amit Goyal's Myocarditis Tweetorial 5 points of maximal impulse in approaching myocarditis Build the clinical suspicion for myocarditis: You need a high index of suspicion given the variable presentation, and definitely need to keep a differential so you don’t miss things like acute coronary syndromes.Decide if EMBx is necessary: Most often obtained in fulminant presentations to look for pathologic findings of giant cell myocarditis or eosinophilic myocarditis, because these findings will change management.Manage the acute cardiac injury, which can range from supportive care to treatment of shock, arrhythmias, and even tamponade.Manage the chronic cardiac sequelae: Recovering from the acute phase of myocarditis doesn’t necessarily mean smooth sailing -- some develop chronic heart failure, warranting GDMT -- or guideline directed management and therapy, as defined by Dr. Randall Starling in Ep 13.Treat the myocarditis: Immunosuppression is often started empirically in fulminant disease, but continuation depends on what you find on pathology.

May 3, 2020

Cardiovascular experts, Drs. JoAnn Lindenfeld, Javid Moslehi and Richa Gupta from Vanderbilt University Medical Center and Dr. Enrico Ammirati from Milan, Italy join Amit and Dan for a two part discussion about all things to consider for myocarditis in general (part 1) and COVID-19 myocarditis and heart transplantation in the COVID-19 era (part 2). Flutter Moment by Barrie Stanton (RN). On the CardioNerds Myocarditis page you will find podcast episodes, infographic, youtube videos, references, tweetorials and guest experts & contributors, flutter stars and so much more. Take me to the Myocarditis Series Page Take me to the COVID-19 Series Page Take me to the Episode Topics Page Dr. JoAnn Lindenfeld, is a Professor of Medicine and the Director of Heart Failure and Heart Transplantation Section at Vanderbilt Heart and Vascular Institute. She is the past president of the Heart Failure Society of America and serves on editorial boards of numerous journals including JACC, JACC Heart Failure and JHLT. She is also a member of the AHA/ACC/HFSA heart failure guideline writing committee and was previously chair of the HFSA practice guidelines for the 2006 and 2010 guidelines. In addition to this she’s been an investigator in multiple large-scale clinical trials including the COAPT trial and has served on numerous steering committees, end point committees and data and safety monitoring committees. She is the author of a more than 300 original papers, reviews, and book chapters in the field of heart failure and heart transplantation. Dr. Javid Moslehi is an associate professor of medicine at Vanderbilt University Medical Center where he is the director of the cardio-oncology program. He is a clinical cardiologist and basic/translational biologist interested in cardiovascular complications associated with novel molecular targeted cancer therapies and the implications of these on our knowledge of basic cardiovascular biology. At Vanderbilt he runs an independent basic and translational research laboratory and program with a focus on signal transduction in the myocardium and vasculature as well as establishing pre-clinical models of cardiotoxicity involving novel targeted oncologic therapies. Dr. Enrico Ammirati is an assistant professor of cardiology and advanced heart failure and transplant cardiologist in Milan, Italy at the Niguarda Hospital with a special research interest and expertise in acute myocarditis and acute heart failure. He is a fellow of the European Society of Cardiology and has won numerous awards, he has also published incredibly important work on the distinction between fulminant and nonfulminant myocarditis and the prognostic implication of histologic subtypes. His research interests also include the role of adaptive immunity in heart transplantation and atherosclerosis and he is the author of well over 100+ peer reviewed publications.

Apr 27, 2020

Cardiovascular experts, Drs. JoAnn Lindenfeld, Javid Moslehi and Richa Gupta from Vanderbilt University Medical Center and Dr. Enrico Ammirati from Milan, Italy join Amit and Dan for a two part discussion about all things to consider for myocarditis in general (part 1) and COVID-19 myocarditis and heart transplantation in the COVID-19 era (part 2). Flutter Moment/Song by Drs. Matt (Internal Medicine) and Beth Faiman (Oncology). On the CardioNerds Myocarditis page you will find podcast episodes, infographic, youtube videos, references, tweetorials and guest experts & contributors, flutter stars and so much more. Take me to the Myocarditis Series Page Take me to the COVID-19 Series PageTake me to the Episode Topics Page Interview Questions What is myocarditis?How do we classify it?How do we diagnose myocarditis?Why don’t we biopsy everyone?When do we think biopsy may change management?Do we really understand the mechanism of myocardial injury in what we call myocarditis?How do we figure mechanisms out and why is this important? Guests and Experts Dr. JoAnn Lindenfeld, is a Professor of Medicine and the Director of Heart Failure and Heart Transplantation Section at Vanderbilt Heart and Vascular Institute. She is the past president of the Heart Failure Society of America and serves on editorial boards of numerous journals including JACC, JACC Heart Failure and JHLT. She is also a member of the AHA/ACC/HFSA heart failure guideline writing committee and was previously chair of the HFSA practice guidelines for the 2006 and 2010 guidelines. In addition to this she’s been an investigator in multiple large-scale clinical trials including the COAPT trial and has served on numerous steering committees, end point committees and data and safety monitoring committees. She is the author of a more than 300 original papers, reviews, and book chapters in the field of heart failure and heart transplantation. Dr. Javid Moslehi is an associate professor of medicine at Vanderbilt University Medical Center where he is the director of the cardio-oncology program. He is a clinical cardiologist and basic/translational biologist interested in cardiovascular complications associated with novel molecular targeted cancer therapies and the implications of these on our knowledge of basic cardiovascular biology. At Vanderbilt he runs an independent basic and translational research laboratory and program with a focus on signal transduction in the myocardium and vasculature as well as establishing pre-clinical models of cardiotoxicity involving novel targeted oncologic therapies. Dr. Enrico Ammirati is an assistant professor of cardiology and advanced heart failure and transplant cardiologist in Milan, Italy at the Niguarda Hospital with a special research interest and expertise in acute myocarditis and acute heart failure. He is a fellow of the European Society of Cardiology and has won numerous awards, he has also published incredibly important work on the distinction between fulminant and nonfulminant myocarditis and the prognostic implication of histologic subtypes. His research interests also include the role of adaptive immunity in heart transplantation and atherosclerosis and he is the author of well over 100+ peer reviewed publications. JoAnn Lindenfeld, MDEnrico Ammirati, MDJavid Moslehi, MDMyocarditis Infographic

Apr 19, 2020

In the midst of the COVID-19 pandemic, we take a look at the association between influenza and myocardial infarction with Dr. Steven Schulman, director of the coronary care unit and cardiology fellowship program director at The Johns Hopkins Hospital and Dr. Rhanderson Cardoso, cardiology fellow at the Johns Hopkins Hospital. Flutter moment by Euri Perio (RN). In light of the COVID-19 pandemic, we shifted gears to meet the educational need as we all are learning more about the cardiovascular implications of SARS-CoV-2. On the CardioNerds COVID-19 series page, you will find our collection of podcast episodes, infographic, youtube videos, curated #Tweetorials, references, guest experts & contributors, flutter stars and so much more. Check out the COVID-19 series page!Take me to episode topics pageClick here for Youtube COVID-19 PlaylistClick here for our Youtube CV fundamentals playlistYoutube video on QTc measurement Dr. Steven Schulman graduated from Johns Hopkins University School of Medicine. He fulfilled his training in internal medicine and chief residency, as well as completing his cardiology fellowship at Hopkins. Dr. Schulman is the director of the Coronary Care Unit (CCU) as well as the Cardiology Fellowship Program Director at Johns Hopkins. His main research interests include acute myocardial infarction. He has won numerous teaching awards from Hopkins residents and fellows over the years. While attending the CCU, Dr. Schulman teaches and guides the next generation of residents and fellows about acute cardiac care. Dr. Rhanderson Cardoso graduated from medical school at the University of Goias in his home country Brazil. He then completed Internal Medicine residency and a chief year at the University of Miami-Jackson Memorial Hospital. Rhanderson has diverse interests in cardiovascular diseases, including electrophysiology, imaging, and prevention. He is especially passionate about teaching and hopes to have a career in academic medicine. He is currently earning a Masters degree in Cardiovascular Epidemiology at the Hopkins Bloomberg School of Public health and is planning on pursuing additional imaging training at Brigham and Women’s Hospital in the upcoming academic year.

Apr 12, 2020

Infectious disease experts from the Johns Hopkins Hospital, Drs. Natasha Chida and Saman Nematollahi join the CardioNerds for a 4 part COVID-19 infectious disease series. In this final episode, we discuss the virology and epidemiology of SARS-CoV-2 that serves as the underpinnings for the three prior episodes. Flutter Moment by Dr. Sumeet Bahl (Vascular and Interventional Radiology) We are honored to promote the incredible efforts of #GetUsPPE, a nonprofit organization working hard to make sure every healthcare worker is protected. Dr. Seth Trueger, emergency medicine physician and digital media editor @JAMA Network Open shares an earnest request. In light of the COVID-19 pandemic, we shifted gears to meet the educational need as we all are learning more about the cardiovascular implications of SARS-CoV-2. On the CardioNerds COVID-19 series page, you will find our collection of podcast episodes, infographic, youtube videos, curated #Tweetorials, references, guest experts & contributors, flutter stars and so much more. Check out the COVID-19 series page! Take me to episode topics page Click here for Youtube COVID-19 Playlist Click here for our Youtube CV fundamentals playlist Dr. Natasha Chida, an infectious disease expert at Johns Hopkins. Dr Chida received her MD from the University of Miami Miller School of Medicine, where she also earned an MSPH (masters of science in public health). She completed internal medicine residency at Jackson Memorial Hospital and infectious disease fellowship at Johns Hopkins, where we were lucky to keep her on as faculty. She is a truly incredible educator and mentor to all levels of trainees -- she serves as assistant director of the infectious disease fellowship program, co-director of the medical education pathway for residents, director of education for the Johns Hopkins Center for Global Health Education, and course director for the ‘Topics in Interdisciplinary Medicine’ course for medical students. Dr. Saman Nematollahi grew up in Tucson, Arizona. He completed his undergrad at the University of Arizona with dual degrees in Physiology and Spanish Literature. He spent some time after undergrad working in a neuroscience lab before starting med school at the University of Arizona. He then moved to NYC where he completed residency at Columbia. His clinical interests include management of immunocompromised hosts, and his research interest is in medical education. More than that he is a teacher at heart and is obtaining a Master’s of Education at the Johns Hopkins School of Education and was recently awarded a grant to develop a fungal diagnostic curriculum for residents. He loves to play soccer with his wife and son. He is master educator, appeared on and has authored many important tweetorials. He has also appeared on the hit medical podcast, The Clinical Problem Solvers.

Apr 6, 2020

Infectious disease experts from the Johns Hopkins Hospital, Drs. Natasha Chida and Saman Nematollahi join the CardioNerds for a 4 part COVID-19 infectious disease series. In this third episode, we discuss all things to consider with regards the clinical presentation & diagnosis of COVID-19. Be sure to stay tuned for the remaining part of this mini-series where we will the virology of SARS-CoV-2. Flutter Moment by Dr. Dani Dumitriu from the frontlines of the COVID-19 pandemic in NYC. We are honored to promote the incredible efforts of #GetUsPPE, a nonprofit organization working hard to make sure every healthcare worker is protected. Dr. Michelle Myles, emergency medicine physician shares her PPE story. In light of the COVID-19 pandemic, we shifted gears to meet the educational need as we all are learning more about the cardiovascular implications of SARS-CoV-2. On the CardioNerds COVID-19 series page, you will find our collection of podcast episodes, infographic, youtube videos, curated #Tweetorials, references, guest experts & contributors, flutter stars and so much more. Check out the COVID-19 series page! Take me to episode topics page Click here for Youtube COVID-19 Playlist Click here for our Youtube CV fundamentals playlist Dr. Natasha Chida, an infectious disease expert at Johns Hopkins. Dr Chida received her MD from the University of Miami Miller School of Medicine, where she also earned an MSPH (masters of science in public health). She completed internal medicine residency at Jackson Memorial Hospital and infectious disease fellowship at Johns Hopkins, where we were lucky to keep her on as faculty. She is a truly incredible educator and mentor to all levels of trainees -- she serves as assistant director of the infectious disease fellowship program, co-director of the medical education pathway for residents, director of education for the Johns Hopkins Center for Global Health Education, and course director for the ‘Topics in Interdisciplinary Medicine’ course for medical students. Dr. Saman Nematollahi grew up in Tucson, Arizona. He completed his undergrad at the University of Arizona with dual degrees in Physiology and Spanish Literature. He spent some time after undergrad working in a neuroscience lab before starting med school at the University of Arizona. He then moved to NYC where he completed residency at Columbia. His clinical interests include management of immunocompromised hosts, and his research interest is in medical education. More than that he is a teacher at heart and is obtaining a Master’s of Education at the Johns Hopkins School of Education and was recently awarded a grant to develop a fungal diagnostic curriculum for residents. He loves to play soccer with his wife and son. He is master educator, appeared on and has authored many important tweetorials. He has also appeared on the hit medical podcast, The Clinical Problem Solvers.

Apr 2, 2020

Infectious disease experts from the Johns Hopkins Hospital, Drs. Natasha Chida and Saman Nematollahi join the CardioNerds for a 4 part COVID-19 infectious disease series. In this second episode, we discuss all things to consider with regards to protecting healthcare workers in COVID-19 as well as their families as they face the pandemic. Be sure to stay tuned for the remaining 2 parts of this mini-series where we will discuss the clinical presentation and diagnosis of COVID-19, and the virology. Flutter Moment by Dr. Meredith Sloan (Internal medicine, University of Mississippi Medical Center). Check out the COVID-19 series page! Take me to episode topics page Click here for Youtube COVID-19 Playlist Dr. Natasha Chida, an infectious disease expert at Johns Hopkins. Dr Chida received her MD from the University of Miami Miller School of Medicine, where she also earned an MSPH (masters of science in public health). She completed internal medicine residency at Jackson Memorial Hospital and infectious disease fellowship at Johns Hopkins, where we were lucky to keep her on as faculty. She is a truly incredible educator and mentor to all levels of trainees -- she serves as assistant director of the infectious disease fellowship program, co-director of the medical education pathway for residents, director of education for the Johns Hopkins Center for Global Health Education, and course director for the ‘Topics in Interdisciplinary Medicine’ course for medical students. Dr. Saman Nematollahi grew up in Tucson, Arizona. He completed his undergrad at the University of Arizona with dual degrees in Physiology and Spanish Literature. He spent some time after undergrad working in a neuroscience lab before starting med school at the University of Arizona. He then moved to NYC where he completed residency at Columbia. His clinical interests include management of immunocompromised hosts, and his research interest is in medical education. More than that he is a teacher at heart and is obtaining a Master’s of Education at the Johns Hopkins School of Education and was recently awarded a grant to develop a fungal diagnostic curriculum for residents. He loves to play soccer with his wife and son. He is master educator, appeared on and has authored many important tweetorials. He has also appeared on the hit medical podcast, The Clinical Problem Solvers. Besides for discussing Protecting Healthcare Workers in COVID-19, we are thrilled to have Dr. Meridith Sloan on the Cardionerds podcast for her inspiring flutter moment! Dr. Meredith Sloan is a proud graduate of the University of Virginia (Wahoowa!) and went to the Medical University of South Carolina. She is currently a third year Internal Medicine resident at the University of Mississippi Medical Center, and is looking forward to being a Chief Resident next year.

Mar 30, 2020

Infectious disease experts from the Johns Hopkins Hospital, Drs. Natasha Chida and Saman Nematollahi join the CardioNerds for a 4 part COVID-19 infectious disease series. In this first part we discuss the emerging therapies in our armamentarium. Be sure to stay tuned for the remaining 3 parts in which we tackle advice for the health care worker, the clinical presentation & diagnosis, and the virology. Flutter Moment by Dr. Justin Berk (Medicine/Pediatrics). Check out the COVID-19 series page! Take me to episode topics page Dr. Natasha Chida, an infectious disease expert at Johns Hopkins. Dr Chida received her MD from the University of Miami Miller School of Medicine, where she also earned an MSPH (masters of science in public health). She completed internal medicine residency at Jackson Memorial Hospital and infectious disease fellowship at Johns Hopkins, where we were lucky to keep her on as faculty. She is a truly incredible educator and mentor to all levels of trainees -- she serves as assistant director of the infectious disease fellowship program, co-director of the medical education pathway for residents, director of education for the Johns Hopkins Center for Global Health Education, and course director for the ‘Topics in Interdisciplinary Medicine’ course for medical students. Dr. Saman Nematollahi grew up in Tucson, Arizona. He completed his undergrad at the University of Arizona with dual degrees in Physiology and Spanish Literature. He spent some time after undergrad working in a neuroscience lab before starting med school at the University of Arizona. He then moved to NYC where he completed residency at Columbia. His clinical interests include management of immunocompromised hosts, and his research interest is in medical education. More than that he is a teacher at heart and is obtaining a Master’s of Education at the Johns Hopkins School of Education and was recently awarded a grant to develop a fungal diagnostic curriculum for residents. He loves to play soccer with his wife and son. He is master educator, appeared on and has authored many important tweetorials. He has also appeared on the hit medical podcast, The Clinical Problem Solvers.

Mar 27, 2020

Dr. Dan Grove is a critical care physician who was diagnosed with COVID-19. Join us as we discuss Dr. Grove’s personal journey and reflections while transitioning from physician to patient, the etymology of the word quarantine, tips and tricks to keep family members safe while in self isolation, and a message to our brothers and sisters on the frontlines as well as the general public. Flutter Moment by Dr. Dani Dumitriu (Pediatrics, Neuroscientist and Pediatric environmental health science) Check out the COVID-19 series page! Take me to episode topics page Follow Dr. Grove’s personal Covid-19 Journey Dr. Daniel Grove serves as assistant director of critical care at Medstar Union Memorial Hospital. He earned his medical degree at Emory University School of Medicine where he also completed his residency and fellowship training in internal medicine and pulmonary and critical care medicine. Dr. Grove is a physician leader in his community and is involved in patient advocacy on many levels. Dan Grove, MD

Mar 25, 2020

We share with you the Iranian experience with COVID-19, a rare first hand report from ICU doctor, Dr. Reza Hashemian, covering the clinical, the societal, and the personal. Flutter Moment by Edward Nejat (Reproductive Endocrinology). Check out the COVID-19 series page! Take me to episode topics page Ventilation primer for the cardiologist (Youtube) Dr. Reza Hashemian serves as Professor of Critical care medicine at a large academic hospital in the heart of Iran. He in on the frontlines at Masih Daneshvari hospital in Tehran, the country’s top pulmonary public hospital and the main facility overseeing coronavirus patients.

Mar 22, 2020

Tune in to hear the Italian perspective from a “COVID A” cardiovascular hospital in Milan, the heart of the country’s epidemic shared by Dr. Gianluca Pontone, who serves as Director of Cardiovascular Imaging Department Centro Cardiologico Monzino IRCCS, University of Milan. We discuss management of COVID-19 patients with underlying cardiovascular disease and cardiac manifestations of COVID-19 including acute coronary syndromes, cardiogenic shock, and myocarditis. Dr. Pontone shares his personal experience in terms of how he prepares himself to take care of patients during this time and his message for all CardioNerds to hear. Flutter Moment by Nino Isakadze (Cardiology). Check out the COVID-19 series page! Take me to episode topics page Ventilation primer for the cardiologist (Youtube) Dr. Gianluca Pontone serves as Director of Cardiovascular Imaging Department Centro Cardiologico Monzino IRCCS, University of Milan, Italy. He graduated with honors in medicine in 1997 followed by post-graduate degree in cardiology and radiology at University of Milan in 2001 and 2006 respectively. He is currently in the board of directors of Society of Cardiovascular Computed Tomography (SCCT), chairman of CT certification committee of European Association of Cardiovascular Imaging (EACVI) and chairman of working group of cardiac magnetic resonance of Italian society of cardiology.

Mar 20, 2020

COVID-19 in the ICU: The CardioNerds follow the case of Sara S Covids through her journey with COVID-19 complicated by progressive respiratory failure. Learn how critical care physicians, Drs. David Furfaro and Sam Brusca approach cardiopulmonary mechanics, general ventilator settings, ventilation in patients with cardiac disease, ARDS diagnosis and management algorithms, including VV and VA ECMO support considerations. Importantly, we discuss these issues in the context of the COVID-19 era and how applies to the safety of the healthcare worker and appropriate use of personal protective equipment with a particular emphasis on COVID-19 in the ICU. Both physicians share tips and tricks on coping and staying motivated as they face this crisis. This episode is broadly applicable for anyone taking care of patients with cardiopulmonary disease. In the COVID era, this is every provider. Flutter Moment by Emily (Pediatric RN) Check out the COVID-19 series page! Take me to episode topics page Ventilation primer for the cardiologist (Youtube) Dr. Samuel Brusca received his medical degree from New York University School of Medicine. He went on to complete his internal medicine training in the Osler Residency Program at Johns Hopkins Hospital and is currently a research fellow in the Critical Care Medicine Fellowship at the National Institutes of Health. His current interests include critical care cardiology, pulmonary arterial hypertension, and right ventricular failure. He is thrilled to be joining the Cardiovascular Disease Fellowship at UCSF this coming July. Outside the hospital, Sam and his amazing wife, Becky, were recently joined by their first daughter, the adorable Madeleine. Dr. David Furfaro received a degree in chemistry with a minor in pharmacology from Duke University. After college, he volunteered with Americorps for a year working with patients with HIV. He received his MD from Harvard Medical School. From there he completed his internal medicine training in the Osler Residency at Johns Hopkins. He returned to Johns Hopkins as an Assistant Chief of Service. He is currently a Pulmonary and Critical Care Medicine Fellow at Columbia University Medical Center. He is interested in critical care, pulmonary hypertension, and lung transplantation. He is also a dedicated medical educator and a huge Cardio Nerds fan!

Mar 17, 2020

The CardioNerds explore the cardiovascular implications of COVID-19 caused by the SARS-CoV 2, in patients with and without underlying cardiovascular disease. We discuss a range of important topics such as ACE-I and ARBS and COVID-19, a 4 part ID mini-series on SARs-CoV 2, important perspectives from clinicians on the frontlines of Italy and Iran, a primer on ICU care for COVID-19 positive patients and so much more! The series kicks off with Dr. Oscar Cingolani, Director of the Hypertension Center at the Johns Hopkins Hospital is joined by Drs. Amit Goyal, Carine Hamo, and Daniel Ambinder and discuss what is known about the interplay between ACE-I and ARBS and COVID-19. We also learn tips and tricks from Dr. Cigolani's experience with telemedicine use with the hypertension clinic. Flutter Moment by Dr. Stephen Lockey (Orthopedic Surgery) Check out the COVID-19 series page! Take me to episode topics page Follow us on Twitter! Dr. Oscar Cingolani earned his medical degree from the National University of La Plata, Argentina, and completed his Internship and Internal Medicine Residency at CEMIC, Buenos Aires, Argentina, and hypertension research post-doctoral fellowship at Henry Ford Hospital, Detroit, Michigan. After completing his Internal Medicine Residency at The Reading Hospital and Medical Center in Pennsylvania, Dr. Cingolani joined The Johns Hopkins Hospital as a Cardiology fellow, where he remained on Faculty after his training. He is currently the Associate Director of The Johns Hopkins Hospital Cardiac Care Unit and the Director of the Hypertension Center. Dr. Cingolani’s research interests focus on hypertensive heart disease and its transition to heart failure. Dr. Stephen Lockey graduated from Georgetown University School of Medicine and obtained an MBA from the McDonough School of Business. He is currently a third-year resident in Orthopaedic Surgery at Georgetown University Hospital. He is interested in pursuing additional training in spine surgery.

Mar 8, 2020

Best-selling author Dr. Martha Gulati joins the CardioNerds squad, Carine Hamo, Heather Kagan, Amit Goyal, and Daniel Ambinder for an unbelievable discussion on women's cardiovascular health relevant to anyone taking care of women. Topics discussed include disparities in diagnosis, treatment, and outcomes in women vs men, sex specific risk factors for cardiovascular disease, special considerations for the evaluation of women presenting with chest pain, and cardiac conditions that have a female predominance, how to be a trailblazer in cardiovascular medicine and so much more! Check out the Women's Cardiovascular Health Topic Page Take me to episode topics page Dr. Martha Gulati completed medical school at the University of Toronto, Canada and her internship, residency and cardiology fellowship at the University of Chicago. She previously served as the Sarah Ross Soter Chair in Women’s Cardiovascular Health and the section director for Women’s Cardiovascular Health and Preventive Cardiology at Ohio State University. She currently serves as division chief of Cardiology for the UA College of Medicine – Phoenix. She is also editor-in-chief of ACC’s CardioSmart. Dr. Gulati has made incredible contributions to researching cardiovascular disease in women. She is the principal investigator of the St. James Women Take Heart Project, a co-investigator on the Women Ischemic Syndrome Evaluation (WISE); previously served as a co-investigator on the Women’s Health Initiative (WHI); a member of numerous advisory boards and societies, including the American Heart Association and the American College of Cardiology; and has published articles in The New England Journal of Medicine, Circulation and Journal of the American Medical Association (JAMA). She is also the best-selling author of Saving Women’s Hearts! References Gulati, M., & Merz, C. (2016). Advances in Lipid Therapy: The Role of Lipid Treatment in Women in Primary Prevention. Progress in Cardiovascular Diseases.Gulati, M. (2017). Improving the Cardiovascular Health of Women in the Nation: Moving beyond the Bikini Boundaries. Circulation, 135(6), 495-498. Lippincott Williams and Wilkins.Wenger NK (2005) Women in cardiology: The US experience. Heart.Douglas PS, Rzeszut AK, Noel Bairey Merz C, Duvernoy CS, Lewis SJ, Walsh MN, Gillam L (2018) Career preferences and perceptions of cardiology among us internal medicine trainees factors influencing cardiology career choice. JAMA Cardiol.Wenger NK, Speroff L, Packard B (1993) Cardiovascular Health and Disease in Women. N Engl J Med.Burgess S, Shaw E, Zaman S (2019) Women in Cardiology. Circulation.

Mar 1, 2020

Duke cardiology fellow, Rahul Loungani, interviews Dr. Jonathan Piccini, director of the Electrophysiology Clinical Trials Program and Arrhythmia Core Laboratory at Duke University, about atrial fibrillation management in patients with heart failure. They discuss rate vs rhythm control and strategies for both, new onset AF in the context of critical illness, wearable devices in AF, escalation of therapy in AF, ideal patient for catheter ablation, and AF patients with cardiac resynchronization therapy. On the CardioNerds Heart Failure topic page you’ll podcast episodes, references, guest experts and contributors, and so much more. Take me to the Heart Failure Topic Page Take me to episode topics page Acute Decompensated Heart Failure Primer – Youtube Jonathan P. Piccini, MD, MHS is a clinical cardiac electrophysiologist and Associate Professor of Medicine at Duke University Medical Center and the Duke Clinical Research Institute. His research interests include the conduct of clinical trials and the assessment of cardiovascular therapeutics for the care of patients with heart rhythm disorders. At present, he is the Director of the EP Clinical Trials Program and Arrhythmia Core Laboratory at Duke University. He also serves on the Clinical Working Group of the American Heart Association’s Get With The Guidelines – Atrial fibrillation (GWTG-Afib) registry program. He is an associate editor for the American Heart Journal and serves on the editorial board of Heart Rhythm, the European Heart Journal, and the Journal of Cardiac Electrophysiology. He is the Principal Investigator of the data and coordinating center for ORBIT AF, a 25,000 patient registry focused on quality of care and improving outcomes in patients with atrial fibrillation. He is also the PI of the GENETIC AF clinical trial, the first clinical trial to study genotype-directed rhythm control therapy for atrial fibrillation. He also serves on the steering committees of multiple international randomized trials focused on the treatment of atrial fibrillation. Dr. Piccini has more than 175 publications in the field of heart rhythm medicine. Clinically, his focus is on the care of patients with atrial fibrillation and complex arrhythmias, with particular emphasis on catheter ablation and lead extraction. Dr. Rahul Loungani completed medical school at the medical university of SC and then traveled to Baltimore for internal medicine training in the Osler Residency Program at the Johns Hopkins Hospital. Here he fell in love with the management and hemodynamics of critically ill patients. He is currently a third-year cardiology fellow at Duke University Medical Center where he will also be pursuing fellowship in advanced heart failure and transplant cardiology next year. His current interests are in Cardiac amyloid, In particular its arrhythmic manifestations, early diagnosis, and novel therapeutics. He also loves teaching the housestaff and was awarded the Cassell-Saperstein award at Duke, recognizing the fellow who most demonstrates a commitment to teaching and passion for clinical education. Outside of the hospital loves being a new dad to baby Arya

Feb 26, 2020

Vanderbilt fellows, Richa Gupta and Jessica Huston, interview past HFSA president Dr. JoAnn Lindenfeld, Director of Heart Failure and Heart Transplantation Section at Vanderbilt Heart and Vascular Institute about the nuts and bolts of cardiac transplantation. Topics discussed include organ allocation, recipient selection, high risk donors, short and long term complications, and what non-transplant physicians should know about immunosuppressive medications. On the CardioNerds Heart Failure topic page you’ll podcast episodes, references, guest experts and contributors, and so much more. Take me to the Heart Failure Topic Page Take me to episode topics page Acute Decompensated Heart Failure Primer – Youtube Dr. JoAnn Lindenfeld, is a Professor of Medicine and the Director of Heart Failure and Heart Transplantation Section at Vanderbilt Heart and Vascular Institute. She is the past president of the Heart Failure Society of America and serves on editorial boards of numerous journals including JACC, JACC Heart Failure and JHLT. She is also a member of the AHA/ACC/HFSA heart failure guideline writing committee and was previously chair of the HFSA practice guidelines for the 2006 and 2010 guidelines. In addition to this she’s been an investigator in multiple large-scale clinical trials including the COAPT trial and has served on numerous steering committees, end point committees and data and safety monitoring committees. She is the author of a more than 300 original papers, reviews, and book chapters in the field of heart failure and heart transplantation. Dr. Richa Gupta completed medical school at the Johns Hopkins School of Medicine and stayed on for internal medicine training in the Osler Residency Program at the Johns Hopkins Hospital. She is currently a third-year cardiology fellow at Vanderbilt University Medical Center where she will also be pursuing fellowship in advanced heart failure and transplant cardiology next year. Her current interests include post-transplant outcomes, the genetics of tachycardia-induced cardiomyopathy, the sequelae of mechanical circulatory support and applications of cardiac MRI. She also loves teaching the housestaff and medical students and getting them excited about all things heart failure. Outside of the hospital she loves horror movies, food, travel and good exercise. Dr. Jessica Huston is an Advanced Heart Failure and Cardiac Transplant fellow at Vanderbilt University Medical Center where she also completed her Cardiovascular Medicine fellowship and served as chief fellow. Prior to her time at Vanderbilt she completed residency at the University of Utah. Her clinical and research interests include pulmonary vascular remodeling in heart failure, pulmonary hypertension and right ventricular failure. Outside the hospital she enjoys exploring the outdoors with her son.

Feb 23, 2020

Carine and Dan delve into left ventricular assist devices (LVAD) 101 with Dr. Steven Hsu, heart failure specialist at the Johns Hopkins Hospital. We get big picture, we get detail oriented and we hit the highlights for the psycho-social-and medical management of our LVAD patient population.

Feb 19, 2020

Amit and co-fellow Dr. Kartik Telukuntla discuss advanced heart failure therapies, or salvage therapies, with Dr. Jerry Estep, section head of heart failure at the Cleveland Clinic. Show page: https://www.cardionerds.com/heart-failure-awareness-cardionerds-series/ Dr. Jerry Estep earned his bachelor of arts at the University of Texas, Austin and subsequently received his medical degree from Baylor College of Medicine. He completed internal medicine residency training at University of Texas Southwestern Medical Center and went back to Baylor for his cardiology and heart failure fellowship training. Prior to joining Cleveland Clinic in 2018 as our section head for the division of heart failure and transplant, Dr. Estep was the Section Head of Heart Failure at Methodist DeBakey in Houston, Texas. Dr. Estep has been involved in numerous clinical trials and co-authored over a 100 peer reviewed articles. He has a special interest in mechanical circulatory support devices and has published heavily on the percutaneous placement of intra-aortic balloon pump in the axillary artery as a long-term support option to bridge patients to transplant.

Feb 16, 2020

Amit and co-fellow Kartik Telukuntla talk to Dr. Randall Starling, former president of the HSFA about his approach to guideline-directed medical therapy in heart failure. Dr. Randall Starling obtained his Bachelor’s degree and Master’s in Public Health at the University of Pittsburgh and medical degree from Temple University. He went back to University of Pittsburgh for his internal medicine residency training and then went to Ohio State University for his cardiology fellowship. He stayed on as faculty at Ohio State until 2005 at which time he joined the Cleveland Clinic. He is the former section head of the Division of Heart Failure and former Vice Chairman of the Cardiovascular Medicine Department. Dr. Starling has been the principal investigator on numerous clinical trials and most recently completed his tenure as President of the Heart Failure Society of America. Show page: https://www.cardionerds.com/heart-failure-awareness-cardionerds-series/

Feb 13, 2020

Dan and Carine chat with cardiomyopathy expert Dr. Ed Kasper with regards to his approach to the new onset heart failure patient. This episode is dedicated to Dr. Kasper's mentor and friend, Dr. Kenneth L. Baughman. Dr. Edward K. Kasper, is a graduate of the Johns Hopkins University with a B.A. in Natural Sciences. He earned his M.D. at the University of Connecticut School of Medicine. His internship and residency in Internal Medicine and assistant chief of service (ACS) of the Thayer service as well as his fellowship in Cardiology, were completed at the Johns Hopkins Hospital, where he then joined the faculty in 1993. He is currently the E. Cowles Andrus Professor of Cardiology and Director of Clinical Cardiology at Johns Hopkins Medicine. Show page: https://www.cardionerds.com/heart-failure-awareness-cardionerds-series/

Feb 12, 2020

In conjunction with the 2020 Heart Failure Awareness Week, sponsored by the Heart Failure Society of America the CardioNerds are supporting the society’s efforts to promote heart failure awareness, patient education, and heart failure prevention by launching our Heart Failure Awareness CardioNerds Series. This series is a tribute to Dr. David Taylor. Dr. Taylor was a heart failure attending at the Cleveland Clinic. He died early morning of Thursday, February 5th 2020. We remember him for the legend he is. A passionate clinician, skilled educator, devoted mentor. Series page: https://www.cardionerds.com/heart-failure-awareness-cardionerds-series/

Feb 9, 2020

Dr. Ron Witteles from Standford university provides an approach to cardiac amyloid and specifically AL (Light-Chain) Cardiac Amyloidosis. The discussion is lead by Amit and Dr. Ashley Bock. This episode is the fourth and final part of our immersive journey into the jungle of beta-pleated sheets in the heart. We focus on AL amyloidosis in this episode. Flutter moment by Lois Adamski. On the CardioNerds Cardiac Amyloid Topic Page you will find podcast episodes, infographic, references, guest contributors, flutter stars, and so much more. Take me to the Amyloid Topic Page Take me to episode topics page Cardiac imaging for Amyloid - Youtube Dr. Ronald Witteles is a graduate of Northwestern University where he earned his B.A. in Biology, and of the University of Chicago Pritzker School of Medicine, where he earned his M.D. with Honors. He then moved west to Stanford University where he completed IM residency and Cardiology fellowship training, serving as both Chief Resident and Chief Fellow. He subsequently joined the faculty at Stanford, and is currently appointed as Professor of Medicine (Cardiovascular Medicine). He has served as Program Director for the Stanford University Internal Medicine Residency Training Program for more than 10 years, where he leads a residency program of approximately 140 residents. He is Co-Director of the Stanford Amyloid Center – one of the nation’s largest centers in the country which specializes in the treatment of patients with amyloidosis, and he leads an active research program in this area. He also serves as Co-Director of the Stanford Multidisciplinary Sarcoidosis Program, and he is a national leader in Cardio-Oncology, serving as Associate Editor for the country’s premier journal dedicated to the field, JACC: CardioOncology. Dr. Ashley Bock earned her medical degree at the University of Colorado and completed her internal medicine residency training at Duke University. From there she came to the Cleveland Clinic for general cardiology fellowship and advanced heart failure training. She joins our team today to discuss AL cardiac amyloidosis with Dr. Witelles.

Feb 2, 2020

Cardionerds (Daniel Ambinder and Carine Hamo) chat with Dr. Virginia Hahn about her work profiling HFpEF patients via endomyocardial biopsy only to find a significant proportion of patients with unsuspected cardiac amyloid. This is followed by a high yield discussion with Dr. Joban Vaishnav about ATTR cardiac amyloid treatment and management options. Flutter moment by David Ambinder (MS IV). On the CardioNerds Cardiac Amyloid Topic Page you will find podcast episodes, infographic, references, guest contributors, flutter stars, and so much more. Take me to the Amyloid Topic PageTake me to episode topics pageCardiac imaging for Amyloid - Youtube Dr. Virginia Shalkey Hahn is a fourth-year Cardiology fellow at Johns Hopkins in Baltimore, MD. She earned her medical degree from the Perelman School of Medicine at the University of Pennsylvania, where she stayed for residency. She moved to Johns Hopkins for Cardiology fellowship (after a 1 year hiatus as an ICU hospitalist). During fellowship, she completed 2 years on the NIH T32 Training grant and one year as chief fellow. She feels passionate about translational heart failure research and mothering her 2 young children. Dr. Joban Vaishnav completed her undergraduate and medical school training at St. Louis University. She has since been at Johns Hopkins for residency, cardiology fellowship, and advanced heart failure fellowship. Her early research pursuits were in heart failure with preserved ejection fraction. From this, and from her advanced heart failure training, she developed a strong clinical interest and research interest in early diagnosis and treatment of cardiac amyloidosis. In addition to the great discussion on Cardiac Amyloid ATTR treatment, we are excited to have Dan's brother, David, join the Cardionerds cardiology podcast to share a special flutter moment! David Ambinder is a 4th year medical student at the University of Maryland and will be starting urology residency this coming July at Westchester Medical Center. He grew up in New York and graduated from Touro College before heading to Baltimore for medical school. He enjoys spending time with his wife Samantha and 3 lovely children. Carine Hamo, MDDaniel Ambinder, MD

Jan 26, 2020

Amit and Dr. Zach Il’Giovine learn about multimodality imaging in amyloid from Dr. Paul Cremer at the Cleveland Clinic. On their way to Dr. Cremer’s office, they run into Dr. Eoin Donnellan and discuss some incredible fellow research related to cardiac amyloid from an electrophysiologic perspective. Show notes and images: https://www.cardionerds.com/cardiac-amyloid/

Jan 19, 2020

A new case of congestive heart failure due to amyloid cardiomyopathy is presented by Yuxuan Wang and discussed by Carine, Heather, Dan and Amit. Guest oncology star: Jackie Zimmerman. Flutter moment by Mark Heslin. Show notes and images: https://www.cardionerds.com/cardiac-amyloid/

Jan 12, 2020

Amit joins Dr. Laura Young to take a pulse check with experts, and learn more about the structural management of obstructive HCM. They discuss the interventional perspective with interventional cardiologist Dr. Amar Krishnaswamy and surgical perspective from cardiothoracic surgeon Dr. Per Wierup. Flutter moment by Crystal Silbak, RN. Show notes and images: https://www.cardionerds.com/hypertrophic-cardiomyopathy/

Jan 5, 2020

Dr. Edward Kasper shares a unique historical perspective on how the field evolved as medicine learned more about HCM. He shares so many life lessons and clinical pearls that apply to HCM and the practice of medicine in general. Flutter moment by Dr. Sidney Schechet (ophthalmology). Show notes and images: https://www.cardionerds.com/hypertrophic-cardiomyopathy/

Dec 29, 2019

Clinical and echo expert Dr. Jose Madrazo discusses a high yield and practical approach to diagnosis and management of hypertrophic cardiomyopathy. Show notes and images: https://www.cardionerds.com/hypertrophic-cardiomyopathy/

Dec 13, 2019

Dr. Fatimah Alkhunaizi and the CardioNerds discuss a case of hypertrophic cardiomyopathy, covering pathophysiology, diagnosis, imaging, and management of HCM. Show notes and images: https://www.cardionerds.com/hypertrophic-cardiomyopathy/

Dec 11, 2019

Amit, Carine, and Dan interview imaging expert Dr. Sneha Vakamudi and structural heart disease expert Dr. Rani Hasan about nuances regarding the diagnosis and treatment of aortic stenosis. Show notes and images: https://www.cardionerds.com/episodes/aortic-stenosis/

Dec 11, 2019

Dr. Heather Kagan and the CardioNerds discuss a case of aortic stenosis, covering diagnosis, surveillance, imaging, management and followup. ​ Show notes and images: https://www.cardionerds.com/episodes/aortic-stenosis/

Dec 9, 2019

Amit, Dan, and Clinical Problem Solver host Reza Manesh introduce The CardioNerds podcast and the CardioNerd mission.