Cardionerds: A Cardiology Podcast

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• 452. Risk stratification in Acute Pulmonary Embolism with Dr. Stavros Konstantinides 01.06.2026 25min

  CardioNerds (Dr. Billy-Joe Mullinax, Dr. Dinu Balanescu, and Dr. Jane Ehret) discuss risk stratification in acute pulmonary embolism with Dr. Stavros Konstantinides, Chair of the 2019 ESC Pulmonary Embolism Guidelines. Using a real-world case, this episode explores how modern PE care has moved beyond “massive” and “submassive” labels toward a dynamic, physiology-based approach. The discussion highlights the limitations of static risk scores, the importance of right ventricular dysfunction and biomarkers, and why normotension does not imply stability. Special emphasis is placed on intermediate-high risk PE, early identification of impending hemodynamic collapse, and the role of lactate, serial reassessment, and PERT teams in guiding escalation of care. Audio editing by CardioNerds intern, Joshua Khorsandi.The 2026 American multi-society PE guidelines were published after this episode was recorded. Dr. Dinu Balanescu and Dr. Billy-Joe Mullinax are Co-chairs for the CardioNerds PE Series, developed in collaboration with the PERT Consortium.   Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. CardioNerds Pulmonary Embolism PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls Stable blood pressure does not mean low risk in PEHypotension is a late finding. Patients may have severe RV failure, hypoxia, and tissue hypoperfusion while remaining normotensive — a key concept behind “normotensive shock.” Risk stratification in PE must be dynamic, not staticLegacy scores like PESI and Bova provide a snapshot and predict 30-day mortality, but they do not capture short-term trajectory or impending hemodynamic collapse. Intermediate-high risk PE is a dangerous and heterogeneous groupPatients with RV dysfunction, positive biomarkers, tachycardia, hypoxemia, and elevated lactate may have in-hospital mortality approaching 15%, rivaling STEMI. Lactate is a critical but underutilized marker in PEElevated lactate reflects tissue hypoxia and early circulatory failure and may identify patients at risk for collapse before blood pressure declines. PERT enables physiology-driven, patient-centered PE carePERT teams operationalize continuous reassessment, integrate imaging, labs, and clinical trajectory, and allow timely escalation — shifting PE management from rigid categories to real-time decision-making. Notes Drafted by Dr. Jane Ehret. 1. What is the contemporary framework for risk stratification in acute pulmonary embolism? Modern PE risk stratification prioritizes hemodynamics and right ventricular (RV) function rather than clot burden. The 2019 ESC Guidelines classify PE into high risk, intermediate risk (low vs high), and low risk, based on: Hemodynamic status, RV dysfunction on imaging, and Cardiac biomarkers. This framework emphasizes early mortality risk but requires clinical context to guide escalation decisions. 2. Why is normotension insufficient to define “stability” in PE? Blood pressure is a late marker of circulatory failure in PE. Patients can maintain normal BP through Tachycardia, Increased sympathetic tone, and RV compensation. Many patients with preserved BP may already have shock physiology, including hypoxemia, elevated lactate, and RV failure — sometimes referred to as “normotensive shock.” 3. How should intermediate-risk PE be conceptualized clinically? Intermediate-risk PE is heterogeneous, ranging from patients who do well on anticoagulation to those who deteriorate rapidly. Intermediate-high risk PE is defined by RV dysfunction on imaging and positive cardiac biomarkers. Clinical features such as tachycardia, increasing oxygen requirement, and elevated lactate identify patients at highest risk within this group. 4. What are the strengths and limitations of commonly used PE risk scores? Legacy scores are useful for initial risk categorization but are static and limited in predicting short-term deterioration. Most scores were developed to predict mortality or complications at fixed time points rather than dynamic clinical trajectory. 5. What are the commonly used risk scores and clinical tools in PE, and what is each designed to predict? ESC Risk Stratification Algorithm: Identifies high-risk PE by hemodynamics. Uses PESI or sPESI in normotensive patients to distinguish low-risk from non–low-risk PE. Uses RV dysfunction and biomarkers to differentiate intermediate-low from intermediate-high risk. Forms the basis of many institutional PE pathways. PESI and sPESI: Validated to predict 30-day mortality. Widely used to identify low-risk patients appropriate for outpatient management. Heavily influenced by age and comorbidities. Bova Score: Predicts 30-day PE-related complications in normotensive patients. Composite PE Shock Score (CPES): Predicts normotensive shock in hemodynamically stable PE patients. Pulmonary Embolism Progression (PEP) Score: Predicts progression from intermediate-risk to high-risk PE within 72 hours of diagnosis. PE Short-term Clinical Outcomes Risk Estimation (PE-SCORE): Predicts clinical deterioration or death within 5 days of PE diagnosis. Hestia Criteria: Identifies low-risk PE patients safe for outpatient treatment. Wells’ Criteria and Revised Geneva Score: Determine pretest probability for diagnostic triage. PERC Score: Rules out PE in very low-risk patients. 6. What is the role of biomarkers in PE risk stratification? Troponin and natriuretic peptides reflect RV myocardial injury and strain. Current guidelines treat biomarkers as binary (positive vs negative), despite risk being continuous. Biomarkers are most helpful for: Initial risk classification. They are less useful for: Short-interval monitoring and Detecting rapid clinical deterioration. 7. Why is lactate an important physiologic marker in PE? Lactate reflects global tissue hypoxia and impaired perfusion. Elevated lactate may identify patients with: Early circulatory failure and Increased risk of imminent hemodynamic collapse. Lactate is not currently included in ESC risk algorithms but may add important prognostic information in intermediate-risk patients. 8. How does trajectory influence decision-making in PE management? Risk stratification should be viewed as a dynamic process, not a one-time label. Worsening clinical trajectory may include: Rising heart rate, Increasing oxygen needs, Rising lactate, and Progressive RV dysfunction. Serial reassessment is essential for timely escalation of care. 9. What role do Pulmonary Embolism Response Teams (PERT) play in risk stratification? PERT facilitates: Multidisciplinary decision-making and Integration of imaging, biomarkers, and clinical physiology. PERT is most valuable for: Intermediate-risk and high-risk PE and Patients with complex comorbidities or uncertain trajectory. PERT enables a shift from category-based to physiology-driven PE care. References 1. 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): The Task Force for the diagnosis and management of acute pulmonary embolism of the European Society of Cardiology (ESC). Eur Respir J. 2019;54(3):1901647. Published 2019 Oct 9. doi:10.1183/13993003.01647-2019 2. Leidi A, Bex S, Righini M, Berner A, Grosgurin O, Marti C. Risk Stratification in Patients with Acute Pulmonary Embolism: Current Evidence and Perspectives. J Clin Med. 2022;11(9):2533. Published 2022 Apr 30. doi:10.3390/jcm11092533 3. Choi WH, Kwon SU, Jwa YJ, et al. The pulmonary embolism severity index in predicting the prognosis of patients with pulmonary embolism. Korean J Intern Med. 2009;24(2):123-127. doi:10.3904/kjim.2009.24.2.123 4. Jiménez D, Aujesky D, Moores L, et al. Simplification of the pulmonary embolism severity index for prognostication in patients with acute symptomatic pulmonary embolism. Arch Intern Med. 2010;170(15):1383-1389. doi:10.1001/archinternmed.2010.199 5. Chen X, Shao X, Zhang Y, et al. Assessment of the Bova score for risk stratification of acute normotensive pulmonary embolism: A systematic review and meta-analysis. Thromb Res. 2020;193:99-106. doi:10.1016/j.thromres.2020.05.047 6. Zhang RS, Yuriditsky E, Zhang P, et al. Composite Pulmonary Embolism Shock Score and Risk of Adverse Outcomes in Patients With Pulmonary Embolism. Circ Cardiovasc Interv. 2024;17(8):e014088. doi:10.1161/CIRCINTERVENTIONS.124.014088 7. Zhang RS, Alam U, Sharp ASP, et al. Validating the Composite Pulmonary Embolism Shock Score for Predicting Normotensive Shock in Intermediate-Risk Pulmonary Embolism. Circ Cardiovasc Interv. 2024;17(2):e013399. doi:10.1161/CIRCINTERVENTIONS.123.013399 8. Ehret J, Wakefield D, Badlam J, Antkowiak M, Erdreich B. Development of the Pulmonary Embolism Progression (PEP) score for predicting short-term clinical deterioration in intermediate-risk pulmonary embolism: a single-center retrospective study. J Thromb Thrombolysis. 2025;58(2):243-253. doi:10.1007/s11239-024-03051-5 9. Weekes AJ, Raper JD, Lupez K, et al. Development and validation of a prognostic tool: Pulmonary embolism short-term clinical outcomes risk estimation (PE-SCORE). PLoS One. 2021;16(11):e0260036. Published 2021 Nov 18. doi:10.1371/journal.pone.0260036 10. Zondag W, Hiddinga BI, Crobach MJ, et al. Hestia criteria can discriminate high- from low-risk patients with pulmonary embolism. Eur Respir J. 2013;41(3):588-592. doi:10.1183/09031936.00030412 11. Wells PS, Anderson DR, Rodger M, et al. Excluding pulmonary embolism at the bedside without diagnostic imaging: management of patients with suspected pulmonary embolism presenting to the emergency department by using a simple clinical model and d-dimer. Ann Intern Med. 2001;135(2):98-107. doi:10.7326/0003-4819-135-2-200107170-00010 12. Wolf SJ, McCubbin TR, Feldhaus KM, Faragher JP, Adcock DM. Prospective validation of Wells Criteria in the evaluation of patients with suspected pulmonary embolism. Ann Emerg Med. 2004;44(5):503-510. doi:10.1016/j.annemergmed.2004.04.002 13. Le Gal G, Righini M, Roy PM, et al. Prediction of pulmonary embolism in the emergency department: the revised Geneva score. Ann Intern Med. 2006;144(3):165-171. doi:10.7326/0003-4819-144-3-200602070-00004 14. Kline JA, Mitchell AM, Kabrhel C, Richman PB, Courtney DM. Clinical criteria to prevent unnecessary diagnostic testing in emergency department patients with suspected pulmonary embolism. J Thromb Haemost. 2004;2(8):1247-1255. doi:10.1111/j.1538-7836.2004.00790.x 15. Kline JA, Courtney DM, Kabrhel C, et al. Prospective multicenter evaluation of the pulmonary embolism rule-out criteria. J Thromb Haemost. 2008;6(5):772-780. doi:10.1111/j.1538-7836.2008.02944.x
• 451: CCTA, CT-FFR, and AI Plaque Analysis to Personalize CAD Detection, Prevention, and Management with Dr. Michael Gallagher 27.05.2026 46min

  CardioNerds Dr. Joseph Kassab, Dr. Mariana Garcia-Arango, and Dr. Christopher Mason explore the technological revolution of Coronary CT Angiography (CCTA) with expert faculty Dr. Michael Gallagher. The discussion details how CCTA has evolved into a frontline diagnostic and preventive tool, moving beyond simple anatomy to incorporate physiology via CT-FFR and biology through AI-driven plaque quantification. The episode reviews landmark evidence like the SCOT-HEART and PROMISE trials, the nuances of CAD-RADS 2.0 reporting, and the emerging role of AI in monitoring treatment response and personalizing cardiovascular care. Critically, they also discuss some of the assumptions and limitations of these techniques. Stay tuned for a matching review article to be submitted to US Cardiology Review, the official Journal of CardioNerds. This episode was supported by an independent medical education grant from HeartFlow. All CardioNerds education is planned, produced, and reviewed solely by CardioNerds.  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 Multimodality Cardiovascular Imaging PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll Pearls Shift in Paradigm: CCTA is no longer just an anatomic test; with some key limitations, it can provide anatomy, physiology (CT-FFR), and plaque biology (AI-CPA) in a single non-invasive scan. The “Power of Zero” vs. Plaque: While a normal CCTA has a >95% negative predictive value, future MIs often arise from non-obstructive plaque that traditional stress tests might miss. CAD-RADS 2.0 Utility: The addition of plaque burden modifiers (P1–P4) is a “game changer,” allowing clinicians to identify high-risk patients who need aggressive lipid-lowering despite having only mild stenosis. CT-FFR as a Virtual Stress Test: CT-FFR uses computational fluid dynamics to simulate blood flow, potentially reducing unnecessary invasive catheterizations by approximately 61% without sacrificing safety. Seeing the Invisible: AI-based quantitative plaque analysis (QCPA) can identify “subvisual” plaque and low-attenuation (lipid-rich) components that are the primary drivers of acute coronary syndromes. Show Notes How has the role of CCTA changed compared to traditional functional testing? Historically, stress testing answered “is there ischemia today?”, which often reflects late-stage disease. CCTA identifies disease across the entire spectrum, asking “is there atherosclerosis and how much plaque is present?”. Landmark evidence: SCOT-HEART showed a 41% relative risk reduction in MI at 5 years attributed to intensified preventive therapies, and PROMISE showed CCTA was better at selecting patients who truly needed invasive angiography. Diagnostic CCTA imaging depends on the protocol, contrast timing, heart rate, heart rhythm, breathholding, scanner quality, and several patient factors (obesity, prior stents, heavy calcification, complex bypass anatomy, and motion artifact all may limit imaging). “CCTA is exceptional for the right patient, with the right scanner, and the right team.” What are the key modifiers introduced in CAD-RADS 2.0, and why do they matter? CAD-RADS 2.0 moved beyond stenosis severity to include plaque burden (P0 to P4), high-risk plaque (HRP) features, and the presence of ischemia based on CT-FFR. It serves as a clinical decision support tool: a patient with mild (25-49%) stenosis but “extensive” (P4) plaque burden is considered high risk and warrants aggressive risk factor modification. How is CT-FFR calculated, and when is it most useful in clinical practice? CT-FFR uses resting CCTA data and computational fluid dynamics to create a 3D model of coronary flow during simulated maximal hyperemia. It is often used for intermediate lesions (40–90% stenosis) to predict if they are  ischemia-producing, guiding the decision whether to proceed with invasive angiography.  The assumptions necessary for this computational modeling may not apply well to patients with microvascular dysfunction, significant myocardial scar or prior infarction, or ventricular hypertrophy. Still, data indicate that CT-FFR performs similarly to PET in predicting hemodynamically significant lesions.  CT-FFR performs well at the extremes (either clearly normal or clearly abnormal). Accuracy dips, however, in the intermediate range (~0.75-0.80), where decision-making is most critical. In this grey zone, additional factors can help guide the approach, including the amount of myocardium supplied, translesional gradient, and plaque features.   CT-FFR has not been validated in distal segments, stented segments, heavily calcified coronary arteries, or in patients with severe aortic stenosis. Caution with CT-FFR should be utilized in very calcified coronary segments.  What is AI-based quantitative plaque analysis (QCPA), and what metrics are ready for clinical use? This is potentially a paradigm shift, moving away from stenosis-centric thinking to a more disease burden and plaque biology focus. QCPA uses deep learning algorithms to automatically segment the vessel wall and quantify plaque volume in mm³. Ready for “prime time” metrics include: Total Plaque Volume (TPV), non-calcified plaque volume, and Low-Attenuation Plaque (LAP) burden. Can serial CCTA be used to monitor the effectiveness of medical therapies like statins? While not yet a routine guideline-driven practice, trials like PARADIGM and EVAPORATE show that therapies can stabilize plaque; notably, CCTA is better for monitoring than CAC scores, which can be misleading as statins often increase plaque calcification as part of the stabilization process. There are no randomized trials that serial CCTAs improve outcomes. Cost and radiation exposure will be notable limitations. Serial scan timing, scan acquisition and interpretation standardization would be key. Dr. Gallagher notes that we are moving toward a world in which plaque burden may become a “treatment biomarker,” similar to tumor burden in oncology.  References 1. Coronary Computed Tomography Angiography From Clinical Uses to Emerging Technologies: JACC State-of-the-Art Review. Abdelrahman KM, Chen MY, Dey AK, et al. Journal of the American College of Cardiology. 2020;76(10):1226-1243. doi:10.1016/j.jacc.2020.06.076. 2. Non-Invasive Imaging in Coronary Syndromes: Recommendations of the European Association of Cardiovascular Imaging and the American Society of Echocardiography, in Collaboration With the American Society of Nuclear Cardiology, Society of Cardiovascular Computed Tomography, and Society for Cardiovascular Magnetic Resonance. Edvardsen T, Asch FM, Davidson B, et al. Journal of the American Society of Echocardiography : Official Publication of the American Society of Echocardiography. 2022;35(4):329-354. doi:10.1016/j.echo.2021.12.012. 3. 2021 AHA/ACC/ASE/CHEST/SAEM/SCCT/SCMR Guideline for the Evaluation and Diagnosis of Chest Pain: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. Gulati M, Levy PD, Mukherjee D, et al. Journal of the American College of Cardiology. 2021;78(22):e187-e285. doi:10.1016/j.jacc.2021.07.053. 4. Contemporary, Non-Invasive Imaging Diagnosis of Chronic Coronary Artery Disease. van der Bijl P, Gulati M, Saraste A, et al. Lancet (London, England). 2025;406(10519):2577-2587. doi:10.1016/S0140-6736(25)01586-7. 5. State of the Art: Evaluation and Medical Management of Nonobstructive Coronary Artery Disease in Patients With Chest Pain: A Scientific Statement From the American Heart Association. Slipczuk L, Blankstein R, Bucciarelli-Ducci C, et al. Circulation. 2025;152(23):e443-e466. doi:10.1161/CIR.0000000000001394. 6. Diagnostic Performance of Fractional Flow Reserve Derived From Coronary CT Angiography: The ACCURATE-CT Study. Li C, Hu Y, Jiang J, et al. JACC. Cardiovascular Interventions. 2024;17(17):1980-1992. doi:10.1016/j.jcin.2024.06.027. 7. Clinical Outcomes Based on Coronary Computed Tomography-Derived Fractional Flow Reserve and Plaque Characterization. Sato Y, Motoyama S, Miyajima K, et al. JACC. Cardiovascular Imaging. 2024;17(3):284-297. doi:10.1016/j.jcmg.2023.07.013. 8. Clinical Use of Coronary Computed Tomography Angiography-Derived Fractional Flow Reserve: Expert Consensus by an International Working Group. Tang CX, Leipsic JA, Nørgaard BL, et al. European Radiology. 2026;:10.1007/s00330-025-12313-6. doi:10.1007/s00330-025-12313-6. 9. Diagnostic accuracy of computed tomography–derived fractional flow reserve: a systematic review. Cook CM, Petraco R, Shun-Shin MJ, et al. JAMA Cardiol. 2017;2(7):803-810. Doi:10.1001/jamacardio.2017.1314 10. Diagnostic performance of noninvasive fractional flow reserve derived from coronary computed tomography angiography in suspected coronary artery disease: the NXT trial (Analysis of Coronary Blood Flow Using CT Angiography: Next Steps). Nørgaard BL, Leipsic J, Gaur S, et al. J Am Coll Cardiol. 2014;63(12):1145-1155. Doi:10.1016/j.jacc.2013.11.043 11. Comparison of coronary computed tomography angiography, fractional flow reserve, and perfusion imaging for ischemia diagnosis. Driessen RS, Danad I, Stuijfzand WJ, et al. J Am Coll Cardiol. 2019;73(2):161-173. Doi:10.1016/j.jacc.2018.10.056. 12. 1-year outcomes of FFRCT-guided care in patients with suspected coronary disease: the PLATFORM study. Douglas PS, De Bruyne B, Pontone G, et al. J Am Coll Cardiol. 2016;68(5):435-445. Doi:10.1016/j.jacc.2016.05.057. 13. Comparison of an initial risk-based testing strategy vs usual testing in stable symptomatic patients with suspected coronary artery disease: the PRECISE randomized clinical trial. Douglas PS, Nanna MG, Kelsey MD, et al; PRECISE Investigators. JAMA Cardiol. 2023;8(10):904-914. Doi:10.1001/jamacardio.2023.2595. 14. Diagnostic and clinical value of FFRCT in stable chest pain patients with extensive coronary calcification: the FACC study. Mickley H, Veien KT, Gerke O, et al. JACC Cardiovasc Imaging. 2022;15(6):1046-1058. doi:10.1016/j.jcmg.2021.12.010. 15. Low-Attenuation Noncalcified Plaque on Coronary Computed Tomography Angiography Predicts Myocardial Infarction: Results From the Multicenter SCOT-HEART Trial (Scottish Computed Tomography of the HEART). Williams MC, Kwiecinski J, Doris M, et al. Circulation. 2020;141(18):1452-1462. doi:10.1161/CIRCULATIONAHA.119.044720. 16. AI-Guided Quantitative Plaque Staging Predicts Long-Term Cardiovascular Outcomes in Patients at Risk for Atherosclerotic CVD. Nurmohamed NS, Bom MJ, Jukema RA, et al. JACC. Cardiovascular Imaging. 2024;17(3):269-280. doi:10.1016/j.jcmg.2023.05.020. 17. Interaction of AI-Enabled Quantitative Coronary Plaque Volumes on Coronary CT Angiography, FFRCT, and Clinical Outcomes: A Retrospective Analysis of the ADVANCE Registry. Dundas J, Leipsic J, Fairbairn T, et al. Circulation. Cardiovascular Imaging. 2024;17(3):e016143. doi:10.1161/CIRCIMAGING.123.016143. 18. Prognostic Value of AI-Based Quantitative Coronary CTA vs Human Reader-Based Visual Assessment: Results From the CONFIRM2 Registry. van Rosendael A, Nakanishi R, Bax JJ, et al. JACC. Cardiovascular Imaging. 2026;19(3):345-359. doi:10.1016/j.jcmg.2025.09.021.13. Pericoronary Adipose Tissue as a Marker of Cardiovascular Risk: JACC Review Topic of the Week. Tan N, Dey D, Marwick TH, Nerlekar N. Journal of the American College of Cardiology. 2023;81(9):913-923. doi:10.1016/j.jacc.2022.12.021. 19. Effect of Icosapent Ethyl on Progression of Coronary Atherosclerosis in Patients With Elevated Triglycerides on Statin Therapy: Final Results of the EVAPORATE Trial. Budoff MJ, Bhatt DL, Kinninger A, et al. European Heart Journal. 2020;41(40):3925-3932. doi:10.1093/eurheartj/ehaa652. 20. Coronary CT Angiography Evaluation With Artificial Intelligence for Individualized Medical Treatment of Atherosclerosis: A Consensus Statement From the QCI Study Group. Schulze K, Stantien AM, Williams MC, et al. Nature Reviews. Cardiology. 2026;23(2):100-115. doi:10.1038/s41569-025-01191-6.
• 450. Journal Club: The I-CLASS Registry with Dr. Theofanie Mela and Dr. Pugazhendhi Vijayraman 25.05.2026 19min

  Join CardioNerds EP Council Chair Dr. Naima Maqsood and Episode Lead Dr. Sukriti Banthiya as they discuss the results of the International Collaborative LBBAP Study (I-CLAS) with expert faculty Dr. Theofanie Mela and Dr. Pugazhendhi Vijayraman. Audio editing by CardioNerds academy intern, Grace Qiu. The International Collaborative LBBAP Study (I-CLAS) evaluated clinical outcomes between biventricular pacing (BVP) and left bundle branch area pacing (LBBAP) in patients with left ventricular ejection fraction (LVEF) ≤50% undergoing cardiac resynchronization therapy. Between January 2018 and June 2023, 2,579 patients were enrolled across 18 centers. The primary composite outcome was defined as all-cause mortality or heart failure hospitalization. LBBAP demonstrated a shorter paced QRS duration and was associated with a lower risk of primary composite outcome and heart failure hospitalization. No significant difference was observed in all-cause mortality. Additionally, procedural complications were lower with LBBAP. This episode was planned in collaboration with  Heart Rhythm TV with mentorship from Dr. Daniel Alyesh and Dr. Mehak Dhande.  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 Journal Club PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron!
• 449. Atrial Fibrillation: Challenging Scenarios in Atrial Fibrillation Management with Dr. Bradley Knight 21.05.2026 37min

  In this episode, CardioNerds Dr. Colin Blumenthal, Dr. Kelly Arps, and Dr. Yong Hao Yeo are joined by electrophysiology expert Dr. Bradley Knight to discuss atrial fibrillation (AF) management in challenging clinical scenarios. We explore arrhythmias in patients with pre-excitation syndromes, particularly Wolff-Parkinson-White (WPW) syndrome, and strategies for rhythm control. We also discuss AF management in pregnancy, adult congenital heart disease, and patients with tachycardia-bradycardia (tach-brady) syndrome. This episode provides essential insights into nuanced decision-making for the care of patients with complex arrhythmia profiles. Audio editing by CardioNerds academy intern, Grace Qiu. Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. 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 AF in WPW is a true emergency—AV nodal blocking agents can be deadly. In patients with WPW syndrome, AF can rapidly conduct through the accessory pathway, risking ventricular fibrillation and sudden death. Avoid AV nodal blockers like beta-blockers and calcium channel blockers. Catheter ablation is the first-line rhythm control strategy in WPW. Catheter ablation carries a Class I recommendation and offers >90% success. If antiarrhythmic drugs are needed, sodium channel blockers like flecainide or propafenone are preferred in patients without structural heart disease. In pregnancy, protecting the mother is protecting the fetus. An unstable mother means an unstable fetus. Rate control is the first step in AF with rapid ventricular responses and electrical cardioversion is safe when needed. Multidisciplinary care is essential. AF in congenital heart disease is often outside the pulmonary veins. Surgical scars and chamber remodeling in ACHD patients often lead to AF from non-pulmonary vein foci. Electrogram-based mapping and targeted ablation strategies are essential to increase success rate of durable rhythm control. Tachy-brady syndrome may require pacing to unlock therapy. AF may cause atrial myopathy and sinus node dysfunction. These patients often require permanent pacing to allow safe use of rate-controlling medications like beta-blockers and to prevent syncope or chronotropic incompetence. Notes: Notes drafted by Dr. Yong Hao Yeo Why is atrial tachycardia in patients with WPW syndrome dangerous? Patients with WPW commonly present with supraventricular tachycardia (SVT) due to atrioventricular reentrant circuits, either orthodromic or antidromic. This SVT can degenerate into AF. In the absence of AV nodal as the governor between the atrium and ventricles, the accessory pathway may conduct impulses rapidly and frequently. This can lead to dangerously high ventricular rates, predisposing patients to ventricular fibrillation and sudden cardiac arrest. What are some strategies for rhythm control in patients with WPW and atrial tachycardia? Catheter ablation is the first-line therapy (Class I recommendation), with a success rate of over 90%. Ablation reduces the risk of sudden cardiac arrest, though some patients may remain prone to AF. If ablation is not feasible/ contraindicated, sodium channel blockers such as flecainide and propafenone are good options in patients without ischemia or structural heart disease (Class IIa recommendation). Amiodarone should be avoided because it has a long half-life, can accumulate in the system, and may delay definitive treatment with catheter ablation. AV nodal blocking agents like beta blockers and calcium channel blockers should be avoided, as they are less effective at controlling ventricular rate in WPW and can increase conduction over the accessory pathway. These agents can also exacerbate the risk of rapid ventricular rates during AF and worsen left ventricular function. What are some special considerations in managing AF in pregnant patients? The primary goal in managing cardiovascular disease during pregnancy is to protect the mother, as fetal outcomes depend on maternal well-being. Therefore, while caution is necessary, we should avoid undertreating pregnant patients with AF. In cases of AF with rapid ventricular response (RVR), rate control is usually the first-line strategy, with beta blockers preferred over digoxin or non-dihydropyridine calcium channel blockers. It is then reasonable to initially observe for spontaneous conversion in stable patients. Antiarrhythmic drugs (AADs) are generally avoided during the first trimester, but clinical judgment on a case-by-case basis is essential. Evidence for the safety of AADs in pregnancy is limited, often derived from their use in other conditions such as fetal SVT. Flecainide and sotalol are reasonable options for rhythm control (Class IIa recommendation). Electrical cardioversion is considered safe in pregnancy and should be utilized when indicated (Do not forget!). There is no pregnancy-specific thromboembolic risk stratification tool. CHA₂DS₂-VASc scoring and the presence of risk factors like mitral stenosis can help guide anticoagulation decisions, though the magnitude of thromboembolic risk during pregnancy remains unclear. Rate control agents are typically continued during delivery due to the increased physiologic stress of labor and delivery. Multidisciplinary care is crucial and should involve obstetrics, maternal-fetal medicine, cardiology, and electrophysiology specialists. What are some key considerations for AF management in patients with adult congenital heart disease (ACHD)? Patients with repaired congenital heart disease are at increased risk for arrhythmias due to two main factors: surgical scars that create arrhythmogenic foci and mechanical remodeling of the atria or ventricles resulting from the underlying disease. In these patients with structural heart disease, sodium channel blockers may not be ideal antiarrhythmic options. When selecting an antiarrhythmic drug, clinicians must consider the nature of structural or surgical impairments, such as right bundle branch block or prolonged QT interval. It is also essential to assess renal and hepatic function (often impaired in patients with ACHD) to ensure appropriate metabolism and clearance of antiarrhythmic medications. Electrogram-based ablation strategies (those leveraging artificial intelligence are developing!) may help identify effective ablation targets, which are often outside the pulmonary veins in patients with ACHD. These individualized approaches can improve ablation success rates in this complex patient population. What makes tachycardia-bradycardia (tach-brady) syndrome a unique challenge in arrhythmia management? Patients who present with both AF and bradycardia, especially with syncope, require a thoughtful diagnostic approach to identify the underlying rhythm disturbance. Extended cardiac monitoring, including event monitors or implantable loop recorders, can help capture intermittent arrhythmias and correlate them with symptoms. AF may lead to atrial myopathy, and since the sinus node resides within the atrium, this can result in sinus node dysfunction—a hallmark of tachy-brady syndrome. Following spontaneous conversion from AF to sinus rhythm, sinus node dysfunction may persist, leading to prolonged pauses or chronotropic incompetence. Management becomes more complex when beta-blockers are needed for AF with RVR, as they can exacerbate bradycardia. Permanent pacemaker implantation is often the next step to consider. Permanent pacemaker implantation is often considered to facilitate safe rate control in these cases. In younger patients, aggressive AF burden reduction may prevent atrial remodeling and the development of true atrial myopathy, potentially avoiding pacemaker implantation. References Joglar JA, Chung MK, Armbruster AL, et al. 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. 2023;149(1). doi:https://doi.org/10.1161/CIR.0000000000001193 ‌ Van IC, Rienstra M, Bunting KV, et al. 2024 ESC Guidelines for the management of atrial fibrillation developed in collaboration with the European Association for Cardio-Thoracic Surgery (EACTS). European Heart Journal. 2024;45(36). doi:https://doi.org/10.1093/eurheartj/ehae176 ‌ Joglar JA, Kapa S, Saarel EV, et al. 2023 HRS expert consensus statement on the management of arrhythmias during pregnancy. Heart Rhythm. Published online May 1, 2023. doi:https://doi.org/10.1016/j.hrthm.2023.05.017 ‌ Stout KK, Daniels CJ, Aboulhosn JA, et al. 2018 AHA/ACC Guideline for the Management of Adults With Congenital Heart Disease: Executive Summary. Journal of the American College of Cardiology. 2019;73(12):1494-1563. doi:https://doi.org/10.1016/j.jacc.2018.08.1028 ‌
• 448. The Braunwald Chronicles: The Complete Series — A CardioNerds Tribute to Dr. Eugene Braunwald 30.04.2026 41min

  CardioNerds (Amit Goyal, Daniel Ambinder, Carine Hamo, and Karan Desai) are honored to bring you The Braunwald Chronicles — a special tribute to the life and legacy of Dr. Eugene Braunwald. Originally released as a 6-part series, we are now bringing these chapters together as one complete experience. These are stories of discovery, innovation, accidents, perseverance, and more… truly, these are the stories of cardiology itself — told firsthand by the father of modern cardiology. Dr. Braunwald’s life and work form the very foundation of contemporary cardiovascular medicine, and his story is, in many ways, the story of our field. Join us as we journey through the history of cardiology across six extraordinary chapters — from the early days of physiologic discovery, to the development of transseptal access, to defining the natural history of valvular disease, to shaping modern therapies for myocardial infarction, and beyond. Through it all, Dr. Braunwald reflects on the principles that guided his career — curiosity, perseverance, mentorship, and the importance of being in the right place, at the right time, with the right people.We hope this collection serves not only as an educational experience, but as a tribute to one of the greatest minds in the history of medicine. We thank Dr. Karan Desai, Editorial APD with the CardioNerds Academy and fellow at the 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!
• 447. Pulmonary Embolism: Approach to Systemic Thrombolysis in Acute Pulmonary Embolism with Dr. Allison Burnett 24.04.2026 42min

  CardioNerds Drs. Dinu Balanescu, Billy-Joe Mullinax, and Mariana Garcia discuss systemic thrombolysis in pulmonary embolism with expert Dr. Allison Burnett. Audio editing by CardioNerds Academy intern, student doctor, Pace Wetstein. Pulmonary embolism is the third leading cause of cardiovascular death in the US, and high-risk PE carries a 30-day mortality risk as high as 30-50%. In this episode, we discuss the indications for systemic thrombolysis, including high-risk PE and cardiac arrest. We addressed how to appropriately select candidates for systemic thrombolysis, balancing the high risk of bleeding. Additionally, we discussed anticoagulation management and timing concurrent with lytic therapy, as well as the importance of multidisciplinary PERT teams.  The 2026 American multi-society PE guidelines were published after this episode was recorded. Dr. Dinu Balanescu and Dr. Billy-Joe Mullinax are Co-chairs for the CardioNerds PE Series, developed in collaboration with the PERT Consortium.   Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. CardioNerds Pulmonary Embolism PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls Risk stratification is crucial in acute pulmonary embolism care. Based on the ESC 2019 guidelines, low-risk PE patients are those who are normotensive with no evidence of right ventricular dysfunction. Intermediate risk includes two categories: intermediate-low, with normotensive patients who have a high PE score with negative biomarkers, and intermediate-high risk, which has elevated biomarkers or signs of RV strain. High-risk PE includes hemodynamically unstable patients (SBP<90) who have end-organ dysfunction, shock, or cardiac arrest. The 2026 American multi-society PE guidelines presented a new clinical classification scheme is presented, entitled “Acute Pulmonary Embolism Clinical Categories,” with 5 categories (A-E) and subcategories, ranging from low to high risk for adverse outcomes. Systemic lysis has been studied in patients at high and intermediate risk. Overall, the reduction in mortality has been seen in patients with high-risk PE.  Systemic thrombolysis is associated with high rates of bleeding, 2% fatal or high-risk intracranial hemorrhage per the PEITHO trial; therefore, selecting the appropriate population is critical to improve outcomes and balance the risks and benefits.  Multidisciplinary PERT teams are crucial for making high-quality decisions, and stewardship is necessary to optimize the care of patients with PE.  Notes Notes: Notes drafted by Dr. Mariana Garcia-Arango What is the role of systemic thrombolysis in the current era of available catheter-directed therapies? Thrombolytic therapy reduces mortality, PE recurrence, and PE-related mortality in patients with acute PE.  The evidence supports use during high-risk PE and cardiac arrest.  The clinical presentation is often severe, with high stakes and limited time to mobilize to the cath lab on time for catheter therapies, especially in rural populations.  How to approach the use of systemic thrombolysis during CPR? Cardiac arrest from PE carries a very poor outlook, with survival rates under 10%. Rapid, targeted interventions to restore circulation are critical. Systemic thrombolysis may be considered for patients in cardiac arrest due to confirmed or strongly suspected pulmonary embolism, especially when standard ACLS interventions have not been successful.  What is the best anticoagulation approach while using lytics?  Most of the time, we should opt for low-molecular-weight heparin over unfractionated heparin, which has been shown to lead to less major bleeding and reduction of recurrent PE.  Exceptions to the rule include renal dysfunction or if there is consideration of cannulation for ECMO or other invasive procedures.  There is variation in practice regarding timing and initiation of anticoagulation while using lytics. There are different protocols given the variety of how studies were conducted. If they are going to get mechanical catheter-based therapy, the trend is to prefer LMWH. When lytics are included, either systemic or catheter-directed lytics, there is flexibility and room to discuss with the multidisciplinary PERT team which strategy to use. Future studies and trials are needed to standardize the best therapies.  What are the pharmacologic properties of available thrombolytics? Thrombolytics catalyze the conversion of plasminogen to plasmin, leading to fibrin degradation and thrombus dissolution. Alteplase is a recombinant tissue plasminogen activator, administered intravenously at a dose of IV 100 mg infusion over 2 hours. In cardiac arrest, the initial: 50 mg bolus over 2 minutes and continue CPR; after 15 minutes, if return of spontaneous circulation is not achieved and the medical team decides to continue CPR, repeat 50 mg bolus. Tenecteplase is a modified variant of alteplase with increased fibrin specificity. The usual dose is weight-based and delivered via IV bolus, which facilitates rapid delivery in emergency settings. Dose per weight: ≥60 to <70 kg: 35 mg, ≥70 to <80 kg: 40 mg, ≥80 to <90 kg: 45 mg, ≥90 kg: 50 mg Are there any ongoing clinical trials and emerging therapies investigating novel thrombolytics and strategies to optimize efficacy while minimizing bleeding risk? PEITHO-3 is a large, randomized, double-blind, multinational study comparing reduced-dose intravenous alteplase with standard heparin in patients with intermediate-high-risk PE.  References Sedhom R, Megaly M, Elbadawi A, et al. Contemporary national trends and outcomes of pulmonary embolism in the United States. Am J Cardiol. 2022;176:132-138. doi:10.1016/j.amjcard.2022.03.060 Marti C, John G, Konstantinides S, Combescure C, Sanchez O, Lankeit M, Meyer G, Perrier A. Systemic thrombolytic therapy for acute pulmonary embolism: a systematic review and meta-analysis. Eur Heart J. 2015 Mar 7;36(10):605-14. Epub 2014 Jun 10. Zuo Z, Yue J, Dong BR, Wu T, Liu GJ, Hao Q. Thrombolytic therapy for pulmonary embolism. Cochrane Database Syst Rev. 2021;CD004437. Feltes J, Popova M, Hussein Y, Pierce A, Yamane D. Thrombolytics in cardiac arrest from pulmonary embolism: a systematic review and meta-analysis. J Intensive Care Med. 2023;39(5):477-483. Javaudin F, Lascarrou JB, Le Bastard Q, Bourry Q, Latour C, De Carvalho H, Le Conte P, Escutnaire J, Hubert H, Montassier E, Leclère B; Research Group of the French National Out-of-Hospital Cardiac Arrest Registry (GR-RéAC). Thrombolysis during resuscitation for out-of-hospital cardiac arrest caused by pulmonary embolism increases 30-day survival: findings from the French National Cardiac Arrest Registry. Chest. 2019 Dec;156(6):1167-1175. Epub 2019 Aug 2. Bonnard T, Tennant Z, Niego B, Kanojia R, Alt K, Jagdale S, Law LS, Rigby S, Medcalf RL, Peter K, Hagemeyer CE. Novel thrombolytic drug based on thrombin cleavable microplasminogen coupled to a single-chain antibody specific for activated GPIIb/IIIa. J Am Heart Assoc. 2017 Feb 3;6(2):e004535. Kearon C, Akl EA, Comerota AJ, Prandoni P, Bounameaux H, Goldhaber SZ, Nelson ME, Wells PS, Gould MK, Dentali F, Crowther M, Kahn SR. Antithrombotic therapy for VTE disease: Antithrombotic Therapy and Prevention of Thrombosis, 9th ed: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines. Chest. 2012 Feb;141(2 Suppl):e419S-e496S. Erratum in: Chest. 2012 Dec;142(6):1698-1704. Levine M, Hirsh J, Weitz J, Cruickshank M, Neemeh J, Turpie AG, Gent M. A randomized trial of a single bolus dosage regimen of recombinant tissue plasminogen activator in patients with acute pulmonary embolism. Chest. 1990 Dec;98(6):1473-1479. Rivera-Lebron B, Weinberg AS. Acute pulmonary embolism in adults: Reperfusion therapy in intermediate- and high-risk patients. In: Connor RF, ed. UpToDate. Waltham, MA: UpToDate Inc. Accessed August 28, 2025.
• 446. The SGLT2i Effect – Protection Against Cancer Therapy-Related Cardiac Dysfunction with Dr. Manu Mysore 16.04.2026 32min

  CardioNerds (Drs. Natalie Marrero, Shivani Reddy, and Rebecca S. Steinberg), discuss the role of SGLT2i in cancer therapy-related cardiac dysfunction (CTRCD) with Dr. Manu Murali Mysore. This episode was produced as part of the CardioNerds Academy curriculum by House Taussig under the guidance of House Chief, Dr. Natalie Marrero, and Academy Program Director, Dr. Gurleen Kaur. A matching review article will be published in US Cardiology Review, the official journal of CardioNerds. Audio editing for this episode was performed by CardioNerds Intern, Dr. Julia Marques Fernandes. Summary: Cancer therapy-related cardiac dysfunction (CTRCD) spans a spectrum from subclinical biomarker elevation to overt heart failure, with risk amplified by preexisting cardiovascular disease, diabetes, hypertension, obesity, and exposure to therapies, such as anthracyclines, HER2-targeted therapies, or radiation. This episode explores the emerging and promising role of SGLT2 inhibitors as a cardioprotective adjunct in cardio-oncology — examining mechanisms, clinical evidence, ongoing trials, and critical knowledge gaps — while affirming that guideline-directed medical therapy remains the cornerstone of prevention and treatment. 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 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 CTRCD is a spectrum — catch it early. CTRCD ranges from subclinical injury detected by imaging and biomarkers to overt heart failure. Early identification in high-risk patients (preexisting CVD, diabetes, HTN, obesity, anthracycline/HER2/radiation exposure) is essential, and early initiation of guideline-directed medical therapy — including ACE inhibitors/ARBs/ARNIs, mineralocorticoid receptor antagonists, and beta-blockers — remains the backbone of prevention and treatment to preserve LVEF and allow safe continuation of cancer therapy. SGLT2 inhibitors are a promising new pillar of cardioprotection in cardio-oncology. They act through a unique combination of mechanisms: renal effects, metabolic reprogramming of the myocardium, anti-inflammatory and antioxidant pathways, and vascular fibrosis modulation — making them a compelling complement to standard therapies rather than a replacement. Early clinical data is encouraging but not yet definitive. The 2024 EMPACARD-PILOT trial demonstrated preserved LVEF and reduced CTRCD in higher-risk patients with diabetes or kidney disease. Ongoing trials — EMPACT and PROTECT — are actively exploring SGLT2 inhibitors for primary prevention during anthracycline and HER2-targeted therapy. SGLT2 inhibitors are NOT yet indicated for ICI-related myocarditis. Immune checkpoint inhibitor (ICI)-related myocarditis is mechanistically immune-driven. While SGLT2 inhibitors have theoretically anti-inflammatory benefits, there is currently no clinical evidence to support their use in this specific setting. The use of SGLT2 inhibitors should be guided by patient risk, existing indications, and ongoing research. Large prospective trials, clarity on timing and patient selection, long-term safety data, and deeper mechanistic understanding in humans remain the most urgent gaps in the field before broader adoption can be recommended. References Theofilis P, Vlachakis PK, Oikonomou E, et al. Cancer therapy-related cardiac dysfunction: A review of current trends in epidemiology, diagnosis, and treatment. Biomedicines. 2024;12(12):2914. doi:10.3390/biomedicines12122914. https://pubmed.ncbi.nlm.nih.gov/39767820/ 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 Cardio-Oncology Study Group of the Heart Failure Association of the European Society of Cardiology in collaboration with the International Cardio-Oncology Society. Eur J Heart Fail. 2020;22(11):1945-1960. doi:10.1002/ejhf.1920. https://pmc.ncbi.nlm.nih.gov/articles/PMC8019326/ Li X, Li Y, Zhang T, et al. Role of cardioprotective agents on chemotherapy-induced heart failure: A systematic review and network meta-analysis of randomized controlled trials. Pharmacol Res. 2020;151(104577):104577. doi:10.1016/j.phrs.2019.104577. https://pubmed.ncbi.nlm.nih.gov/31790821/ Lee YH, Lim S, Davies MJ. Cardiometabolic and renal benefits of sodium-glucose cotransporter 2 inhibitors. Nat Rev Endocrinol. 2025;21(12):783-798. doi:10.1038/s41574-025-01170-4. https://pubmed.ncbi.nlm.nih.gov/40935880/ Dabour MS, George MY, Daniel MR, Blaes AH, Zordoky BN. The cardioprotective and anticancer effects of SGLT2 inhibitors: JACC: CardioOncology state-of-the-art review. JACC CardioOncol. 2024;6(2):159-182. doi:10.1016/j.jaccao.2024.01.007. https://pubmed.ncbi.nlm.nih.gov/38774006/ Armillotta M, Angeli F, Paolisso P, et al. Cardiovascular therapeutic targets of sodium-glucose co-transporter 2 (SGLT2) inhibitors beyond heart failure. Pharmacol Ther. 2025;270(108861):108861. doi:10.1016/j.pharmthera.2025.10886. https://pubmed.ncbi.nlm.nih.gov/40245989/ Góes-Santos BR, Castro PC, Girardi ACC, Antunes-Correa LM, Davel AP. Vascular effects of SGLT2 inhibitors: evidence and mechanisms. Am J Physiol Cell Physiol. 2025;329(4):C1150-C1160. doi:10.1152/ajpcell.00569.2025. https://pubmed.ncbi.nlm.nih.gov/40908107/ Daniele AJ, Gregorietti V, Costa D, López-Fernández T. Use of EMPAgliflozin in the prevention of CARDiotoxicity: the EMPACARD – PILOT trial. CardioOncology. 2024;10(1):58. doi:10.1186/s40959-024-00260-y. https://pubmed.ncbi.nlm.nih.gov/39237985/ Clinicaltrials.gov. Clinicaltrials.gov. Accessed April 16, 2026. https://clinicaltrials.gov/study/NCT05271162 Greco A, Quagliariello V, Rizzo G, et al. SGLT2i Dapagliflozin in primary prevention of chemotherapy induced cardiotoxicity in breast cancer patients treated with neo-adjuvant anthracycline-based chemotherapy +/- trastuzumab: rationale and design of the multicenter PROTECT trial. CardioOncology. 2025;11(1):79. doi:10.1186/s40959-025-00368-9. https://pmc.ncbi.nlm.nih.gov/articles/PMC12400668/ Key Guideline Reference: Lyon AR, López-Fernández T, Couch LS, et al. 2022 ESC guidelines on cardio-oncology developed in collaboration with the European hematology association (EHA), the European society for therapeutic radiology and oncology (ESTRO) and the international cardio-oncology society (IC-OS). Eur Heart J Cardiovasc Imaging. 2022;23(10):e333-e465. doi:10.1093/ehjci/jeac106. https://pubmed.ncbi.nlm.nih.gov/36017575/ Be sure to check out the corresponding review article on the cardioprotective role of SGLT2 inhibitors in CTRCD that will be published in US Cardiology Review, the official journal of CardioNerds. Additionally, please reference CardioNerds Cardio-Oncology Episodes 261 and 274 for related content.
• 445. Heart Failure: The Essential Role of Palliative Care in Advanced Therapies with Dr. Sarah Chuzi 10.04.2026 54min

  Dr. Jenna Skowronski, Dr. Shazli Khan, and Dr. Alix Barnes discuss the involvement of palliative care throughout the heart failure spectrum with Dr. Sarah Chuzi. Audio editing for this episode was performed by CardioNerds Intern, Dr. Julia Marques Fernandes. In this episode, we discuss utilizing palliative care principles while caring for patients with heart failure, particularly those being considered for advanced therapies. We emphasize utilization of communication frameworks when discussing prognosis and making decisions on pursuing therapies such as palliative inotropes, left ventricular assist devices (LVADs), and heart transplant. Additionally, we discuss when to involve specialty palliative care services. Finally, we highlight the difference between palliative care and hospice and how to help patients navigate the transition from life-prolonging care to hospice. Dr. Jenna Skowronski is the Chair for the CardioNerds Heart Failure Council. Dr. Jenna Skowronski and Dr. Shazli Khan are the Co-chairs for the CardioNerds Advanced Heart Failure Therapies Series. Dr. Alix Barnes is the CardioNerds FIT Ambassador at UPMC and member of the CardioNerds Critical Care Cardiology Council. 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 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 Primary palliative care is care provided by a clinician that is not a palliative care specialist, such as a heart failure clinician having a conversation with a patient about their goals and values in clinic.  Taking time to get to know a patient as an individual and learning their goals and values prior to diving into conversations about prognosis and change in treatment plan facilitates more effective goals of care discussions.   Utilizing and practicing a communication framework can improve our skills at goals of care discussions.   Palliative inotropes should be reserved for patients experiencing symptomatic benefit from the therapy that outweighs the associated risks including arrhythmias and infections. The burden of managing these therapies at home should also be considered. Partnerships between cardiologists and hospice agencies can improve the experience for patients with heart failure who enroll in hospice. Cardiologists can continue to see their patients even after hospice enrollment and help with symptom management.   Notes Notes: Notes drafted by Dr. Barnes. 1. What is the difference between primary palliative care and specialty palliative care? Primary palliative care is the delivery of palliative care services that any clinician can deliver. This includes aligning treatment with a patient’s goals and basic symptom management. For heart failure patients, symptom management can include cardiac symptoms such as dyspnea and chest pain as well as managing comorbid mood disorders such as adjustment disorder, depression, and anxiety. Advanced palliative care skills take additional training and time to develop. These include leading a difficult family meeting, managing symptoms that are not controlled with standard therapies and responding to emotional and spiritual distress. When these situations are encountered, referral to a specialty palliative care service should be considered. 1 2. How is palliative care integrated throughout the disease trajectory of a patient with heart failure? Heart failure clinicians deliver primary palliative care when assessing a patient’s preferences, goals and values or managing symptoms. As a patient’s disease progresses, the heart failure team also engages in primary palliative care when delivering news about prognosis. When advanced therapies are being considered, utilization of shared decision-making (SDM) should be employed (see question 3 for further discussion on SDM). For patients being considered for LVAD, the Centers for Medicare and Medicaid Services (CMS) mandates that patients are seen by a palliative care specialist prior to implantation. 2 Despite this, there remains variability in how institutions involve specialty palliative care in this decision-making process. Thoughtful consideration of what palliative care resources are available at your institution should guide how best to integrate specialty palliative care teams into the LVAD decision tree. One example of a model for meeting this mandate is having a small team of heart failure clinicians with additional palliative care training meet all patient’s being evaluate for LVAD. 3. What is shared decision-making (SDM) and how is it utilized when evaluating a patient for advanced therapies? SDM is a collaborative process where patients and clinicians work together to make medical decisions that are aligned with a patient’s goals and values.3 There are a variety of communication frameworks that can be used to engage in effective SDM. One framework is the Serious Illness Conversation guide. This is an evidenced based framework that can be used to deliver the news about a patient’s current condition and then assess their goals, values and preferences for next steps in their treatment plan.4  This framework can be helpful when discussing prognosis prior to introducing the idea of an evaluation for advanced therapies. REMAP is a second commonly used framework which stands for Reframe, Expect Emotion, Map What’s Important, Align, and Plan.5 This framework is similarly helpful when starting a discussion about advanced therapies with a patient. Both frameworks prioritize learning about a patient’s goals, values, and preferences prior to making a recommendation for a treatment plan. Listening more than speaking and accepting that a patient and their family may choose a path that is different than what you personally might choose for yourself or your loved ones are vital pillars to engaging in these conversations effectively. When discussing LVAD, it is important to avoid framing the decision as “LVAD or no LVAD,” rather LVAD versus best supportive care. The “Best Case, Worst Case” framework is an effective way to create choice awareness for patients when they are faced with making this decision. This is a way to discuss both the best outcomes after LVAD implantation as well as the potential complications so a patient is better able to understand the full spectrum of possible outcomes. 6 4. How do you select which patients would benefit from home inotrope therapy? There is no data demonstrating a survival benefit with use of palliative inotropes. There may be subsets of patients who derive a survival benefit, such as patients whose renal function worsens when the agent is withdrawn, however there is no concrete data proving this. 7 Therefore, the benefit of home inotrope therapy should be based on if the patient derives symptomatic benefit from these agents. Additionally, risks of the therapy such as arrhythmias and infection as well as the burden of managing these therapies at home should also be weighed in the decision.8 Life expectancy for patients being initiated on palliative inotropes likely ranges from 6 to 9 months. Given this prognosis, concordant palliative care efforts should be intensified when starting patients on these agents. This can either be through involvement in specialty palliative care or increasing primary palliative care interventions. 9 5. How do you determine if a patient would be a candidate for hospice and how do you discuss hospice with patients and their families? Hospice is a comprehensive program that provides supportive care to patients at end of life. This includes a team of physicians, nurses, aids, social workers and chaplains that can deliver care in the home, at a nursing facility, or in an inpatient hospice facility. 10 Patients with a prognosis of 6 months or less can qualify for hospice services. Even if a patient qualifies for hospice based on their prognosis, it is important to assess if a patient’s goals and values align with hospice. Introducing hospice to patients who still desire life prolonging care can cause mistrust between the patient and their health care team. When introducing hospice, it is helpful to describe the services hospice offers in addition to naming the service as some patients may have a negative connotation with the word “hospice.” 6. How can cardiologists partner with hospice agencies to provide better care for these patients? Heart failure specialists can continue to see their patients even after they enroll in hospice. Partnering in hospice agencies in this way can help improve symptom management for patients while also allowing them to continue meaningful relationships with providers with whom they’ve developed a longitudinal relationship with. Guideline directed medical therapy (GDMT) and diuretics can be continued while enrolled in hospice as long as they are offering symptomatic benefit. Heart failure specialists can help with adjusting GDMT to cheaper formulations, such as exchanging angiotensin receptor-neprilysin inhibitors (ANRIs) for angiotensin receptor blockers (ARBs). Many hospice agencies cannot accept patients receiving palliative inotropes due to the resources and training required to safely care for these patients. Understanding what hospice agencies in your area can and cannot support allows heart failure specialists to have informed discussions with patients and make appropriate referrals. References Quill TE, Abernethy AP. Generalist plus Specialist Palliative Care — Creating a More Sustainable Model. N Engl J Med. 2013;368(13):1173-1175. doi:10.1056/NEJMp1215620. https://www.nejm.org/doi/full/10.1056/NEJMp1215620 Ventricular Assist Devices for Bridge-to-Transplant and Destination Therapy. Published online August 1, 2013. https://www.cms.gov/medicare-coverage-database/view/ncacal-decision-memo.aspx?proposed=Y&NCAId=268 Godfrey S, Barnes A, Gao J, Katz JN, Chuzi S. Shared Decision-making in Palliative and End‑of‑life Care in the Cardiac Intensive Care Unit. US Cardiol Rev. 2024;18:e13. doi:10.15420/usc.2024.03. https://pubmed.ncbi.nlm.nih.gov/39494405/ Baxter R, Pusa S, Andersson S, Fromme EK, Paladino J, Sandgren A. Core elements of serious illness conversations: an integrative systematic review. BMJ Support Palliat Care. 2024;14(e3):e2268-e2279. doi:10.1136/spcare-2023-004163. https://pmc.ncbi.nlm.nih.gov/articles/PMC11671901/ Childers JW, Back AL, Tulsky JA, Arnold RM. REMAP: A Framework for Goals of Care Conversations. J Oncol Pract. 2017;13(10):e844-e850. doi:10.1200/JOP.2016.018796. https://ascopubs.org/doi/10.1200/JOP.2016.018796 Kruser JM, Nabozny MJ, Steffens NM, et al. “Best Case/Worst Case”: Qualitative Evaluation of a Novel Communication Tool for Difficult in-the-Moment Surgical Decisions. J Am Geriatr Soc. 2015;63(9):1805-1811. doi:10.1111/jgs.13615. https://pmc.ncbi.nlm.nih.gov/articles/PMC4747100/ Tolia S, Khan M, Khan S, et al. Mortality and long-term outcomes of palliative inotropes in ischemic and non-ischemic cardiomyopathy. Eur Heart J.  2021;42(Supplement_1):ehab724.0915. doi:10.1093/eurheartj/ehab724.0915. https://academic.oup.com/eurheartj/article/42/Supplement_1/ehab724.0915/6392681 Chuzi S, Allen LA, Dunlay SM, Warraich HJ. Palliative Inotrope Therapy: A Narrative Review. JAMA Cardiol. 2019;4(8):815. doi:10.1001/jamacardio.2019.2081. https://jamanetwork.com/journals/jamacardiology/article-abstract/2737414#google_vignette Chuzi S, Gao J, Thariath J, et al. Characteristics and Outcomes of Palliative Continuous Intravenous Inotrope Support Among Medicare Beneficiaries With Heart Failure. J Am Heart Assoc. 2025;14(14):e039397. doi:10.1161/JAHA.124.039397. https://www.ahajournals.org/doi/10.1161/JAHA.124.039397 What is hospice? Published online September 24, 2024. https://hospicefoundation.org/what-is-hospice/
• 444. Heart Failure: LVAD Part 2 with Dr. Mark Belkin and Dr. Chris Salerno 22.03.2026 26min

  CardioNerds (Dr. Hamza Patel, Dr. Jenna Skowronski, and Dr. Apoorva Gangavelli) discuss advanced heart failure and LVAD management with Dr. Mark Belkin, Advanced Heart Failure & Transplant Cardiologist, and Dr. Chris Salerno, Cardiothoracic Surgeon. They explore the nuances of right ventricular (RV) physiology, perioperative hemodynamic optimization, long-term complications, sensitization and transplant considerations, and the evolving role of GDMT in LVAD patients.  This episode highlights the delicate interplay between surgical and medical management in achieving optimal outcomes for patients living with durable mechanical circulatory support.Audio editing by CardioNerds Academy intern, student doctor, 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 “The right ventricle sets the stage.” — LVAD success hinges on RV performance; a struggling RV can turn a perfect LVAD surgery into a perfect storm.  “Watch the ratios.” — A PAPi < 2 and RA:PCWP >0.6 signal high risk for RV failure post-implant; trends and response to optimization matter more than static numbers.  “From hemocompatibility to hemodynamics.” — The LVAD field has moved from fighting pump thrombosis to mastering long-term RV failure and aortic insufficiency.  “Not all antibodies are created equal.” — LVAD-related sensitization often resolves post-transplant, reminding clinicians to interpret PRA trends in context.  “Recovery is possible.” — The RESTAGE-HF trial and emerging SGLT2 data hint at a new era: not just sustaining life with LVADs but restoring native heart function.  Notes Notes drafted by Dr. Hamza Patel. 1. Hemodynamic & Vasoactive Management of the RV  Use norepinephrine and vasopressin for pressor support; consider dobutamine as inotrope of choice.  Consider avoiding early milrinone due to hypotension and reduced coronary perfusion.  Use inhaled NO or epoprostenol selectively; institutional variation depends on cost and supply.  Key hemodynamic markers:  PAPi = (PA systolic – PA diastolic) / RA pressure.  PAPi < 2 → increased RV failure risk.  RA:PCWP ratio ≈ 0.6 normal; ≈ 1 → severe RV dysfunction.  RV reserve—the ability to improve these indices with optimization—is a stronger predictor of outcomes than baseline numbers alone.  NOTE: there is no robust data to guide vasoactive medical decision-making and there is substantial institutional variability in practive.  2. Long-Term LVAD Complications  MOMENTUM 3 trial: HeartMate 3 reduced pump thrombosis (10 → 1 %), stroke (14 → 5%), and GI bleed (77 → 43 %).  Persistent issues: driveline infections, RV failure, and aortic insufficiency.  Driveline care: silver sulfadiazine (Silvadene) cream linked to lower infection rates (Cowher & Kenmore 2025).  Field now focuses on hemodynamic-related adverse events—the next frontier in LVAD outcomes.  Innovation ahead: smaller drivelines and fully implantable LVADs to eliminate infection risk.  3. Sensitization and Transplant Candidacy  LVADs may induce de novo HLA antibodies, complicating transplant matching.  These antibodies tend to be transient and less cytotoxic, often resolving post-transplant.  Sensitization degree varies by device and patient; management strategies are center-dependent.  The field is redefining which antibodies are truly LVAD-induced versus incidental.  4. GDMT & Myocardial Recovery  GDMT data in LVAD patients limited—excluded from major HFrEF trials.  RESTAGE-HF: aggressive GDMT post-LVAD yielded 52% explant rate within 18 months.  SGLT2 inhibitors: emerging evidence of reverse remodeling and reduced LV size (Belkin et al., THT 2025).  GDMT promotes recovery but requires cautious titration to avoid hypotension and RV strain.  5. Future of LVAD Therapy  The fully implantable LVAD remains the goal—wireless energy, no driveline, and fewer infections.  Short-term focus: device miniaturization, improved energy efficiency, and better hemocompatibility.  HeartMate 3 remains gold standard until next-generation systems mature.  References Mehra MR et al. NEJM 2018 — MOMENTUM 3 Final Report.  Takeda K et al. JHLT 2020 — Predictors of RV Failure After LVAD.  Imamura T et al. Circ Heart Fail 2017 — Hemodynamics and RV Adaptation Post-LVAD.  RESTAGE-HF Trial, JHLT 2019.  Cowher J, Kenmore C et al. 2025 — Driveline Care & Infection Outcomes.  Belkin M et al. THT 2025 — SGLT2 Inhibition and Reverse Remodeling Post-LVAD. 
• 443. Pulmonary Embolism: The Modern Approach to Pulmonary Embolism Care with Dr. Kenneth Rosenfield 05.03.2026 25min

  This inaugural episode of the CardioNerds Pulmonary Embolism (PE) Series explores the evolution of acute PE care. Dr. Ibrahim Zahid, Dr. Dinu Balanescu, and Dr. Billy Joe Mullinax join guest expert Dr. Kenneth Rosenfield to discuss the shifting landscape of PE management. Pulmonary embolism (PE) remains a leading cause of cardiovascular mortality and a frequent diagnostic challenge, often masquerading as myocardial infarction or a benign illness. Over the past decade, PE care has evolved from anticoagulation-only strategies to nuanced, risk-stratified, multidisciplinary management. Modern approaches integrate hemodynamics, biomarkers, and advanced imaging to guide therapy, including catheter-directed interventions and large-bore thrombectomy. The Pulmonary Embolism Response Team (PERT) model addresses historical gaps by coordinating rapid, multispecialty decision-making and standardizing care pathways. The PERT Consortium further advances PE care through education, research, and the world’s largest PE registry, while fostering leadership and research opportunities for trainees. Despite advances, long-term outcomes and post-PE syndromes remain important areas for future investigation. Audio editing by CardioNerds Academy intern, student doctor, Pace Wetstein. Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. CardioNerds Pulmonary Embolism PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls PE is a “master masquerader”—maintain suspicion for atypical presentations like myocardial infarction, heart failure, flu, or anxiety. Multidisciplinary management mediated through pulmonary embolism response teams improves outcomes and standardizes care. Risk stratification integrates hemodynamics, biomarkers, and imaging. Advanced therapies have expanded beyond anticoagulation. Long‑term follow‑up and post‑PE syndrome need more research. Notes Notes: Notes drafted by Dr. Ibrahim Zahid. 1. How has the clinical approach to PE changed over the past decade? PE is the third leading cause of cardiovascular death and historically under‑recognized. Symptoms mimic MI, HF, asthma, syncope, and more.PE is a silent killer, and it should be recognized more as a cause of spontaneous cardiac arrest. Where life threatening disease like stroke which is owned by neurological specialists and MI is primarily managed by cardiac specialists, PE is an entity without a professional home. The PERT Consortium brings the specialties together for PE care. 2. Ten years ago, a 58-year-old patient with a large bilateral PE, RV dilation, and positive biomarkers might have been managed with anticoagulation and close observation alone. Today, with evolving—but still uneven—data on advanced therapies, PE care feels far more nuanced and highly dependent on where you practice. What are the major gaps in traditional PE management that clinicians should recognize, and what care pathways should they be aware of across different hospital systems? Care has shifted from anticoagulation‑only to multidisciplinary approaches like catheter directed thrombectomy. Risk‑based pathways and the use of CT angiogram has improved early recognition. Risk stratification tools must be used as tools for early recognition of intermediate risk PE. Untreated PE leads to chronic complications like chronic thromboembolic disease and chronic thromboembolic pulmonary hypertension, which requires long term clinic follow up. 3. What is the role of risk stratification tools such as PeSI, sPeSI scores, cardiac biomarkers, and imaging findings in PE, and how do they guide treatment decisions in real world practice? Integrate vitals (blood pressure and heart rate), biomarkers (troponin, pro-BNP), RV/LV ratio assessment, acid‑base status, and scores. Tools include PESI, sPESI, BOVA, HESTIA, FAST, Geneva, NEWS, shock index. Vitals, lactate, acid-base status, and tools like NEWS or shock index track clinical evolution. PESI/sPESI estimate 30-day mortality and help identify low-risk patients who may be candidates for early discharge or outpatient therapy. Clinical judgment matters—scores don’t fully capture clot burden, trajectory, or bleeding risk. 4. How was the pulmonary embolism response team created, and since its creation, what evidence or outcome data became available to support the PERT model? Originated after a sentinel case at MGH: A young, pregnant woman in her 30s, who collapsed at home, underwent thrombectomy, and had to be on ECMO for a few days. The case brought cardiology, cardiac surgeons and critical care physicians together for planning and improvement in her health, which was rewarding. Thereby, it was decided to bring specialties involved in PE care together to create a response team. The name of the team, Pulmonary Embolism Response Team (PERT), was coined by Richard Channick in the first meeting. Posters were set up all over the hospital to call a centralized line when an acute PE is recognized A meeting was held to present the concept of putting together a consortium, with development of action items and a PERT database. Enabled rapid multidisciplinary input using early teleconferencing tools. 5. Given concerns about having too many ‘cooks in the kitchen’ during the initial PE call—especially with rotating teams—how can institutions reconcile workflow complexity with standardized pathways in a way that meaningfully supports and justifies the added burden on frontline clinicians? Every hospital’s PERT is different, catering to their needs and workflow At least two disciplines are needed to make a PERTData is currently being collected to guide further on how the workflow can be standardized Most importantly, the team brings in resources that were not available prior to PERT formation. 6. What are the main goals of the PERT consortium, and how does it support clinicians and institutions involved? To improve care and improve outcomes for patients with PE Expand education, refine algorithms, standardize care with Centers of Excellence. Maintain the largest PE registry for research and outcomes improvement. 7. Beyond global networking, shared learning from successful systems, and the pathway toward Center of Excellence designation, what additional benefits can clinicians and health systems gain by participating in the PERT Consortium? The ability to learn from other systems, the ability to share experiences. Allow people to develop their professional careers like leadership experience, becoming a member of the trainee council Initiate projects and receive funding for your ideas 8. For trainees interested in pulmonary embolism care, how can a trainee be a champion at their institution? Does PERT provide assistance and how can they really contribute meaningfully even before becoming a fellow/attending? Medical students and residents interested in PE should reach out to the consortium and the consortium will hook you up with the correct mentors who can nurture you along. Listen to the podcasts. Participate with your local PERT team PERT wants involvement of people who are social media savvy to help spread the word on PE. Top three take-away points from this episode Acute PE care has advanced and multiple treatment modalities for acute PE including catheter directed therapy, large bore thrombectomy, are becoming standard of care. Multidisciplinary models like PERT improve coordination and outcomes. Trainees play a vital role in advancing PE care through involvement, research, and education References Konstantinides SV, Meyer G, Becattini C, Bueno H, Geersing GJ, Harjola VP, Huisman MV, Humbert M, Jennings CS, Jiménez D, Kucher N, Lang IM, Lankeit M, Lorusso R, Mazzolai L, Meneveau N, Ní Áinle F, Prandoni P, Pruszczyk P, Righini M, Torbicki A, Van Belle E, Zamorano JL; ESC Scientific Document Group. 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 Jan 21;41(4):543-603. doi: 10.1093/eurheartj/ehz405. PMID: 31504429. https://pubmed.ncbi.nlm.nih.gov/31504429/ Rosovsky R, Zhao K, Sista A, Rivera-Lebron B, Kabrhel C. Pulmonary embolism response teams: Purpose, evidence for efficacy, and future research directions. Res Pract Thromb Haemost. 2019 Jun 9;3(3):315-330. doi: 10.1002/rth2.12216. PMID: 31294318; PMCID: PMC6611377. https://pmc.ncbi.nlm.nih.gov/articles/PMC6611377/ Rosenfield K, Bowers TR, Barnett CF, Davis GA, Giri J, Horowitz JM, Huisman MV, Hunt BJ, Keeling B, Kline JA, Klok FA, Konstantinides SV, Lanno MT, Lookstein R, Moriarty JM, Ní Áinle F, Reed JL, Rosovsky RP, Royce SM, Secemsky EA, Sharp ASP, Sista AK, Smith RE, Wells P, Yang J, Whatley EM; Pulmonary Embolism Research Collaborative (PERC) Attendees. Standardized Data Elements for Patients With Acute Pulmonary Embolism: A Consensus Report From the Pulmonary Embolism Research Collaborative. Circulation. 2024 Oct;150(14):1140-1150. doi: 10.1161/CIRCULATIONAHA.124.067482. Epub 2024 Sep 12. PMID: 39263752; PMCID: PMC11698503. https://pubmed.ncbi.nlm.nih.gov/39263752/ Sharifi M, Awdisho A, Schroeder B, Jiménez J, Iyer P, Bay C. Retrospective comparison of ultrasound facilitated catheter-directed thrombolysis and systemically administered half-dose thrombolysis in treatment of pulmonary embolism. Vasc Med. 2019 Apr;24(2):103-109. doi: 10.1177/1358863X18824159. Epub 2019 Mar 5. PMID: 30834822. https://pubmed.ncbi.nlm.nih.gov/30834822/ Pandya V, Chandra AA, Scotti A, Assafin M, Schenone AL, Latib A, Slipczuk L, Khaliq A. Evolution of Pulmonary Embolism Response Teams in the United States: A Review of the Literature. J Clin Med. 2024 Jul 8;13(13):3984. doi: 10.3390/jcm13133984. PMID: 38999548; PMCID: PMC11242386. https://pubmed.ncbi.nlm.nih.gov/38999548/ Rivera-Lebron B., McDaniel M., Ahrar K., Alrifai A., Dudzinski D.M., Fanola C., Blais D., Janicke D., Melamed R., Mohrien K., et al. Diagnosis, Treatment and Follow Up of Acute Pulmonary Embolism: Consensus Practice from the PERT Consortium. Clin. Appl. Thromb. Hemost. 2019;25:1076029619853037. doi: 10.1177/1076029619853037.https://pubmed.ncbi.nlm.nih.gov/31185730/
• 442. Heart Failure: LVAD Part 1 with Dr. Jeff Teuteberg and Dr. Mani Daneshmand 27.02.2026 41min

  CardioNerds (Dr. Jenna Skowronski [Heart Failure Council Chair], Dr. Shazli Khan, and Dr. Josh Longinow) are joined by renowned leaders in the field of AHFTC (Advanced Heart Failure and Transplant Cardiology) and mechanical circulatory support, Dr. Jeff Teuteberg and Dr. Mani Daneshmand to continue the discussion of advanced heart failure therapies by taking a deep dive into the world of durable LVADs (Left Ventricular Assist Devices). In this episode, we will review the history of ventricular assist devices, the basics of LVAD function, selection criteria for LVAD therapy, and surgical nuances of LVAD implantation. Audio Editing by CardioNerds intern, Joshua Khorsandi. 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 There have been significant advances in the field of MCS/LVAD therapy since the first implanted LVAD in the 1960s, to the first FDA approved device in the early 2000’s, to now the HM3 LVAD, with the most important change being a centrifugal flow/magnetically levitated design that led to minimized hemocompatibility-related adverse events (HRAE’s) (MOMENTUM 3 trial comparing HM2 and HM3).  The REMATCH trial in 2001 was a pivotal trial for LVAD therapy, demonstrating that in a population of patients with advanced HF (70% IV inotrope dependent), LVAD therapy significantly improved survival at both 1 and 2 years as compared to medical therapy alone.    MOMENTUM 3 trial was a landmark trial for the HM3 device, showing that in a population of end stage HF patients (86% inotrope dependent, 32% INTERMACS 1-2, and 60% DT strategy), 5-year survival with HM3 was 58% and HM3 had lower HRAE’s compared with HM2.  There are both patient-specific factors and surgical considerations when it comes to candidacy for LVAD therapy.  RV function prior to LVAD is a key determinant for success post-LVAD  Many patients being considered for LVAD may not have robust RV function, however, predicting RV failure after LVAD is exceedingly difficult.   In general, it doesn’t matter how bad the RV may look on imaging; we care more about the pre-LVAD hemodynamics (look at the PAPi and RA/wedge ratio).   What happens in the OR may be the most important determinant of how the RV will do with the LVAD!  Notes Notes drafted by Dr. Josh Longinow.  1. Historical background of heart pumps and LVADs  LVAD Evolution   FDA approval year  2001  2008  2012  2017  Pump  HeartMate XVE   HeartMate II  Heartware HVAD  HeartMate III  Flow/Design Features  Pulsatile Technology   Continuous flow Axial design  Continuous flow  Centrifugal design  Continuous flow   Full MagLev + Centrifugal design  The 1960’s ushered in the first ‘LVADs’, when the first air-powered ‘LVAD’ was implanted. It kept the patient alive for four days before the patient expired.   The first generation of LVADs were pulsatile pumps   The first nationally recognized, FDA approved LVAD was the HeartMate XVE (late 1990s to early 2000s, REMATCH trial). The XVE pump used compressed air (pneumatically driven) to power the pump.   Prior to the XVE, OHT was the standard of care for patients with advanced, end-stage heart failure.   The second and third generations of LVADs were non-pulsatile, continuous flow devices and included the HVAD, HM2, and HM3 devices.   MOMENTUM 3 was a landmark trial for the HM3 device, showing that in a population of sick patients with end stage HF (86% inotrope dependent, 32% INTERMACS 1-2, and 60% DT strategy), 5-year survival with HM3 was 58% and HM3 had lower HRAE’s compared with HM2.   The only pump that is currently FDA approved for implant is the HM3, although other pumps are in clinical trials (BrioVAD system, INNOVATE Trial).  2. What are LVADs, and how do they work?   In simplest terms, the LVAD is a heart pump comprised of several key mechanistic components:   Inflow cannula  Mechanical pump   Outflow cannula  Driveline  Controller/Power source  The HM3 differs from its predecessors (HM2 and HVAD) in several key ways;   HM3 is placed intrapericardial whereas the HM2 was placed pre-peritoneal.   Perhaps most importantly, the HM3 is a fully magnetically levitated, centrifugal flow pump, whereas the HM2 is an axial flow device.  Axial flow pumps are not magnetically levitated, leading to more friction produced between the ruby bearing’s contact with the pump rotors, and higher rates of hemocompatibility related adverse events (HRAEs, i.e. pump thrombosis) and the HM2 was ultimately discontinued in favor of the HM3 (MOMENTUM 3 trial).  3. What do the terms ‘Destination Therapy’ (DT) or ‘Bridge to Transplant’ (BTT) mean when it comes to LVADs?   When LVADs first came on the stage, EVERYONE was a BTT; these early pumps weren’t designed for long term use (I.e. REMATCH Trial, Heartmate XVE)  Destination therapy means the LVAD was placed in leu of transplant because there are contraindications to transplant   REMATCH trial brought about the concept of “Destination therapy”, comparing outcomes in patients (with contraindications for transplant) who received an LVAD vs optimal medical therapy  Bridge to transplant means we are placing the LVAD in a patient who may not be a transplant candidate at this moment in time (is too sick, or conversely, not sick enough), but may be down the line   Bridge to recovery is another term used when the LVAD is being placed for a patient we think may have a recoverable cardiomyopathy  4. What are some factors we should consider when assessing a patient’s candidacy for LVAD, in general, and from a surgical perspective?   Patient factors   Older age might push us towards thinking LVAD rather than transplant  In general, age > 70 is the cutoff for transplant, but this is not a hard cut off and varies institution to institution    In general, think about things that help predict recovery after a major surgery; Frailty and Nutritional status are important, we try to optimize these prior to LVAD implant   Right ventricular function remains the Achilles heel of LV support  We know that needing temporary RV support post LVAD puts you on a different survival curve than patients who don’t need RVAD support  Studies have not been able to successfully predict who will develop RV failure after LVAD implantation  What happens in the time between when the patient goes to the OR and when they get back to the ICU is an important determinant who might develop RV failure post LVAD   Surgical techniques such as implanting the HM3 in the intra-thoracic cavity, rather than intra-pericardial may help maintain LV/RV geometry to help optimize the RV post LVAD   Surgical considerations for LVAD candidacy  Small, hypertrophied LV: HM3 inflow cannula is small, but small hypertrophied ventricles tend towards chamber collapse during systole causing suction, needing to run slower with lower flow rates  Chest size/diameter: pumps have gotten so small now, that for adults, these have become less of a consideration  BMI: low BMI used to be more of a concern with the older pumps due to where they were placed, and the relative size of the pump itself, not so much now with the smaller HM 3 pumps  Calcified LV apex: would increase risk of stroke, bleeding   Driveline tunneling becomes a concern in the super obese population, higher risk for driveline infections (might tunnel these driveline’s shorter, and to a less fatty region of the abdomen, could even tunnel out the thoracic cavity in the super obese to limit skin motion)    5. Is there a role for MCS (i.e. temporary LVAD such as Impella) in pre-habilitation of patients prior to LVAD surgery?   The theory of being able to improve systemic perfusion, decongest the organs, and make the patient feel better prior to surgery makes sense, but becomes problematic due to the lack of a hard end point/time for prehabilitation which might risk delays in surgery   More likely that it can lead to delay in the surgery, with less-than-optimal benefit; you don’t want to prolong the wait for surgery and increase the risk for complications prior to surgery    An Impella 5.5 is currently FDA approved for 2 weeks of support, not 2 months so timing is important to keep in mind  It’s unlikely that you will take a patient and convert them from a malnourished, cachectic person in 2 weeks’ time   6. Is there a role for LVAD therapy in the younger patient population? Should we be thinking of LVAD up front for these patients, with the goal of transplanting down the line?   Recovery may be more likely in certain populations, particularly younger females with smaller LV’s; in those populations, perhaps bridge to recovery should be the focus, optimizing them on GDMT etc.   The replacement of transplant, with MCS (LVAD) in young patients has become a topic of discussion, because these pumps have become better and better, with the thinking that an LVAD could bridge a patient for 10 years or so, and they could get a transplant later   It is still a big unknown, but several concerns exist  Patients who get LVADs might end up with complications that become contraindication to transplant down the line (stroke, sensitization etc)   Patients and providers are more hesitant because of the more recent iteration for the UNOS criteria for OHT listing which no longer gives patients with an uncomplicated LVAD higher priority, and therefore they could end up waiting a longer time for a heart after undergoing LVAD  References Rose EA, Gelijns AC, Moskowitz AJ, et al. Long-term use of a left ventricular assist device for end-stage heart failure. N Engl J Med. 2001;345(20):1435-1443. doi:10.1056/NEJMoa012175  Mehra MR, Uriel N, Naka Y, et al. A Fully Magnetically Levitated Left Ventricular Assist Device – Final Report. N Engl J Med. 2019;380(17):1618-1627. doi:10.1056/NEJMoa1900486  Mancini D, Colombo PC. Left Ventricular Assist Devices: A Rapidly Evolving Alternative to Transplant. J Am Coll Cardiol. 2015;65(23):2542-2555. doi:10.1016/j.jacc.2015.04.039  Mehra MR, Goldstein DJ, Cleveland JC, et al. Five-Year Outcomes in Patients With Fully Magnetically Levitated vs Axial-Flow Left Ventricular Assist Devices in the MOMENTUM 3 Randomized Trial. JAMA. 2022;328(12):1233-1242. doi:10.1001/jama.2022.16197  Rose EA, Moskowitz AJ, Packer M, et al. The REMATCH trial: rationale, design, and end points. Randomized Evaluation of Mechanical Assistance for the Treatment of Congestive Heart Failure. Ann Thorac Surg. 1999;67(3):723-730. doi:10.1016/s0003-4975(99)00042-9  Kittleson MM, Shah P, Lala A, et al. INTERMACS profiles and outcomes of ambulatory advanced heart failure patients: A report from the REVIVAL Registry. J Heart Lung Transplant. 2020;39(1):16-26. doi:10.1016/j.healun.2019.08.017  Mehra MR, Netuka I, Uriel N, et al. Aspirin and Hemocompatibility Events With a Left Ventricular Assist Device in Advanced Heart Failure: The ARIES-HM3 Randomized Clinical Trial. JAMA. 2023;330(22):2171-2181. doi:10.1001/jama.2023.23204  Mehra MR, Nayak A, Morris AA, et al. Prediction of Survival After Implantation of a Fully Magnetically Levitated Left Ventricular Assist Device. JACC Heart Fail. 2022;10(12):948-959. doi:10.1016/j.jchf.2022.08.002  Bhardwaj A, Salas de Armas IA, Bergeron A, et al. Prehabilitation Maximizing Functional Mobility in Patients With Cardiogenic Shock Supported on Axillary Impella. ASAIO J. 2024;70(8):661-666. doi:10.1097/MAT.0000000000002170 
• 441. Atrial Fibrillation: Ablation of Atrial Fibrillation with Dr. Jon Piccini 13.02.2026 53min

  CardioNerds (Dr. Ramy Doss, Dr. Kelly Arps, and Dr. Naima Maqsood) dive into the nuances of atrial fibrillation (AF) ablation with Dr. Jon Piccini. They provide a high-yield overview of AF ablation, guiding listeners from patient selection through post-procedural management. We review appropriate candidacy for catheter ablation across AF phenotypes, key elements of pre-procedural evaluation including imaging and anticoagulation strategy, and the fundamental procedural steps with pulmonary vein isolation as the cornerstone. The discussion compares lesion set strategies in de novo ablation and reviews currently used energy sources—including radiofrequency, cryoablation, and pulsed-field ablation—highlighting differences in safety and efficacy. They also examine surgical and hybrid approaches for selected patients and outline essential components of post-ablation care, including rhythm monitoring, anticoagulation decisions, and management of complications. This episode integrates contemporary evidence with practical insights to support clinicians delivering comprehensive AF ablation care. Audio editing for this episode was performed by CardioNerds intern Dr. Bhavya Shah. NOTE: This episode was recorded in March 2025. Since then, the OCEAN trial showed that among patients who had had successful catheter ablation for atrial fibrillation at least 1 year earlier and had risk factors for stroke, treatment with rivaroxaban did not result in a significantly lower incidence of a composite of stroke, systemic embolism, or new covert embolic stroke than treatment with aspirin.  Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. 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  Pulmonary veins (PVs) are the dominant triggers in early AF due to their unique myocardial sleeve electrophysiology.   Pulmonary vein isolation (PVI) remains the cornerstone of AF ablation by blocking PV triggers from reaching the left atrium. Posterior wall isolation is sometimes performed in persistent AFib, but large RCTs found no significant benefit over PVI alone.  Paroxysmal AF has the highest ablation success rates.  Left atrial health remains the major determinant of outcome.  Ablation modalities include pulsed field ablation, radiofrequency ablation, and cryo-balloon ablation. PFA offers advantage of relative myocardial selectivity with near zero risk of atrio-esophageal fistula.  Long-term anticoagulation decisions after ablation currently depend on CHA₂DS₂-VASc score. Recent evidence suggests the safety of stopping anticoagulation in low-risk patients after ablation.  Early atrial arrhythmia recurrence during a blanking period after ablation (≤3 months) often reflects inflammation — not procedural failure. Late recurrence suggests PV reconnection or residual substrate and often requires repeat ablation.   Hybrid surgical and catheter Afib ablation represent an aggressive strategy for rhythm control in patients with persistent or long-standing persistent AF with extensive substrate and/or patients who have had multiple failed catheter ablations.  Notes 1. What is the mechanism behind AF initiation? Atrial fibrillation (AF) is a progressive condition. Early AF is primarily trigger-driven, most commonly from the pulmonary veins. Pulmonary vein myocardial sleeves have unique electrophysiologic properties that promote premature beats and afterdepolarizations. As AF progresses, atrial remodeling (fibrosis and scar) leads to a more substrate-driven arrhythmia. 2. How does early catheter ablation for atrial fibrillation work? Electrical Isolation of pulmonary veins, blocking PV triggers from reaching the left atrium. By reducing burden of atrial fibrillation, this may slow adverse atrial remodeling. 3. Which patients are good candidates for Afib ablation? Functional Status: ambulatory, active patients derive the greatest benefit. Advanced frailty or severe end-stage cardiovascular disease reduces expected benefit. Comorbidity Burden: CHA₂DS₂-VASc score helps risk-stratify not only stroke risk but also rhythm-control outcomes. Type and Duration of AF Paroxysmal AF → highest likelihood of success (burden reduction often 95–99%). Long-standing persistent AF → lower suppression rates (often 50–80%). Left Atrial Health: a major determinant of outcomes. LA diameter >5.5 cm associated with significantly worse outcomes. LA volume index (normal ≤34 mL/m²) is preferred over diameter for assessment. 4. What are the predictors of complications from AFib ablation procedures? Low and high body mass index (BMI) Chronic corticosteroid use Severe enlargement of other cardiac chambers Female gender is associated with a numerically higher risk of complications. 5. Role of preprocedural imaging with cardiac CT or MRI Cardiac CT Faster and convenient Help define LA geometry and Pulmonary vein anatomy Anatomic Variants as Right middle pulmonary vein, accessory pulmonary veins common pulmonary vein ostium, Atrial diverticula or Accessory left atrial appendage Consider Cardiac MRI when: Strong family history of atrial fibrillation or cardiomyopathy Suspicion of occult structural heart disease 6. Key Procedural Steps in AF Ablation There is significant variation across centers in anesthesia, mapping, and ablation strategies. The following outline reflects a common contemporary approach. Anesthesia & Monitoring Most commonly performed under general anesthesia. Benefits include improved catheter stability, enhanced patient comfort, and controlled ventilation (e.g., low-volume, high-frequency). Invasive arterial line (A-line) is preferred for rapid detection of hypotension. Vascular Access Ultrasound-guided femoral venous access with multiple sheaths. Micropuncture technique is ideal to minimize complications. Intracardiac Echocardiography (ICE) ICE catheter insertion. Reduces complications, guides transseptal puncture, assesses catheter contact, and monitors for pericardial effusion. Anticoagulation Systemic heparin initiated before or immediately after transseptal access. Activated clotting time (ACT) maintained in therapeutic range (typically >300 seconds). Transseptal Puncture Access to the left atrium via transseptal sheath. Often uses electrocautery-assisted wire, with ICE guidance to improve safety. Left Atrial Mapping Creation of electroanatomic map (common in many centers). Ideally performed in sinus rhythm. Assesses left atrial geometry, voltage (for scar/substrate), and activation timing. Ablation Strategy Core component is pulmonary vein isolation (PVI). Technology options include pulse field ablation (PFA), radiofrequency ablation, and cryoballoon ablation. Additional ablation (case-dependent): Posterior wall isolation Targeting non-pulmonary vein triggers Linear lesions Ablation of organized atrial tachycardias/flutters Emerging approaches include AI-guided strategies. Post-Ablation Assessment Confirm pulmonary vein entrance and exit block. Remap left atrium (in many practices) to evaluate lesion completeness. Check for complications (e.g., ICE assessment for pericardial effusion). 7. What is Electroanatomic Mapping? Combines 3D geometry (anatomic reconstruction of cardiac chamber) with electrophysiology (electrical signals from tissue). How it works: Mapping catheter is moved along the atrial wall Records electrograms System generates: 3D chamber model Voltage map (tissue health/scar) Activation map (depolarization timing) Key information provided Voltage map (substrate assessment): High voltage = healthy tissue Low voltage = scar/fibrosis Identifies areas needing additional ablation (e.g., posterior wall scar) Activation map: Visualizes wavefront propagation Essential for diagnosing and ablating macroreentrant atrial flutters and organized atrial tachycardias 8. What is the current role of Afib ablaton outside pulmonary vein isolation? While Pulmonary Vein Isolation (PVI) remains the cornerstone of atrial fibrillation (AF) ablation, adjunctive strategies are increasingly used for persistent AF, with varying levels of supporting data. Non-PVI Triggers: Arrhythmogenic foci found outside the pulmonary veins in 10% to 20% of patients. Common sites include SVC, LAA, CS, and Crista Terminalis. Identifying and ablating these inducible triggers—often provoked by isoproterenol—can reduce recurrence in persistent AF. Posterior Wall Isolation (PWI): The posterior wall is a driver for persistent AF. Randomized evidence for routine PWI is conflicting. Large RCTs found no significant benefit over PVI alone for first-time ablations. Remains a primary adjunctive target for redo procedures. AI-Guided Ablation: Uses AI to identify “spatio-temporal dispersion” areas. Recent TAILORED-AF trial demonstrate increased freedom from AF at 12 months compared to conventional PVI. 9. Comparison of ablation techniques Pulsed Field Ablation (PFA) – Non-Thermal Mechanism: irreversible electroporation Key advantages: Shorter procedural time Comparable efficacy to thermal ablation Higher myocardial tissue selectivity No known risk of esophageal fistula or pulmonary vein stenosis Low risk of phrenic nerve (usually transient) Disadvantages: Less flexibility for complex substrate Hemolysis with possible AKI Early and delayed coronary spasms Skeletal muscle stimulation during energy delivery Loss of all electrograms even with reversible injury can be misleading Limited long term data Radiofrequency Ablation (RFA) – Thermal (Heat) Mechanism: resistive heating Key advantages: Highly versatile Can tailor lesions Long term experience Disadvantages: More procedural time (less with ultrahigh power RFA) Very small risk of esophageal fistula (1/2000 but 50% mortality!) Pulmonary vein stenosis Rare Phrenic nerve palsy Stem pops Cryoballoon Ablation (CBA) – Thermal (Cold) Mechanism: Uses extreme cold Key Advantages: Short learning curve Single shot balloon Highly reproducible Good catheter stability (adhesion during freeze) Low risk of thrombus Disadvantages: Similar to RFA More phrenic nerve palsy Less esophageal fistula and pulmonary vein stenosis 10. Other Complications of AF Catheter Ablation common to all modalities Pericardial effusion/tamponade: 0.4–2.2% Stroke/TIA: ~0.2–1.8% In-hospital mortality: Very low (0.05–0.46%) Often overstated in studies based on National Inpatient Sample (NIS) due to selection bias Vascular access complications: Hematoma 11. Expert approach to Antiarrhythmic Drug (AAD) Therapy After AF Ablation Continue AAD for the 3-month blanking period after catheter ablation. Supported by multiple trials to reduce early AF recurrences. Decreases hospitalizations during the healing phase by suppressing inflammation-related arrhythmias. AADs do not clearly improve long-term freedom from AF. At the 3-month follow-up: If the patient is asymptomatic with no documented recurrence → discontinue AAD. If recurrent AF occurs or high substrate burden persists → consider continuing AAD. 12. Expert approach to Anticoagulation After AF Ablation All patients require anticoagulation for at least 3 months post–ablation. Current guidelines recommend long-term anticoagulation decisions guided solely by CHA₂DS₂-VASc score. Decisions should not be based on ablation success or arrhythmia burden. New data support discontinuation in low-risk patients after careful shared decision-making. In high-risk patients: Observational data indicate ~2.5-fold increased stroke risk when anticoagulation is stopped. OCEAN trial: Generally low risk patients (mean CHA2DS2-VASc score 2.2). Rivaroxaban did not significantly reduce composite stroke outcomes compared with aspirin. 13. Approach to recurrent Atrial Arrhythmias After AF Ablation Early (≤3 months – blanking period): True blanking probably less (6 weeks to 2 months) Likely less with PFA Often due to inflammation or lesion maturation Should not be considered procedural failure Management: Continue or restart AAD Electrical cardioversion for persistent symptomatic episodes Avoid early repeat ablation Late (>3 months) recurrences: More likely due to pulmonary vein reconnection or residual atrial substrate Arrhythmias include: Recurrent atrial fibrillation Atypical (macroreentrant) atrial flutter Typical atrial flutter (cavotricuspid isthmus–dependent) Focal atrial tachycardia Management is often challenging and may include AAD, cardioversion, or repeat ablation. 14. When to Consider Hybrid Surgical and Catheter Ablation for Atrial Fibrillation? Aggressive rhythm control strategy when standard endocardial approaches are insufficient. Typically for persistent or long-standing persistent AF (>12 months). Often used in patients with extensive substrate or multiple failed catheter ablations. Can be performed during concomitant cardiac surgery or as a stand-alone hybrid procedure. Benefits of surgical approach: Epicardial posterior wall/dome ablation PVI Ligation of the ligament of Marshall Left atrial appendage closure (e.g., AtriClip) Approach: Subxiphoid/minimally invasive surgical access Endocardial EP confirmation Additional PVI ablation and gap closure Evidence suggests increased freedom from atrial arrhythmias at the expense of higher major adverse event risk.
• 440. Heart Failure: Post-Heart Transplant Management with Dr. Shelly Hall and Dr. MaryJane Farr 04.02.2026 26min

  CardioNerds (Dr. Shazli Khan, Dr. Jenna Skowronski, and Dr. Shiva Patlolla) discuss the management of patients post‑heart transplantation with Dr. Shelley Hall from Baylor University Medical Center and Dr. MaryJane Farr from UTSW. In this comprehensive review, we cover the physiology of the transplanted heart, immunosuppression strategies, rejection surveillance, and long-term complications including cardiac allograft vasculopathy (CAV) and malignancy. Audio editing for this episode was performed by CardioNerds intern Dr. Bhavya Shah. 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 Denervated Heart: The donor heart is surgically severed from the autonomic nervous system, leading to a higher resting heart rate (90-110 bpm) due to loss of vagal tone. Because the heart relies on circulating catecholamines rather than neural input to increase heart rate, patients experience a delayed chronotropic response to exercise and stress. Importantly, because afferent pain fibers are severed, ischemia is often painless. Rejection Surveillance: Rejection is classified into Acute Cellular Rejection (ACR), which is T-cell mediated, and Antibody-Mediated Rejection (AMR), which is B-cell mediated. While endomyocardial biopsy remains the gold standard for diagnosis, non-invasive surveillance using gene-expression profiling (e.g., AlloMap) and donor-derived cell-free DNA (dd-cfDNA) is increasingly utilized to reduce the burden of invasive procedures. The Infection Timeline: The risk of infection follows a predictable timeline based on the intensity of immunosuppression. The first month is dominated by nosocomial infections. Months one through six are the peak for opportunistic infections (Cytomegalovirus, Pneumocystis, Toxoplasmosis) requiring prophylaxis. After six months, patients are primarily at risk for community-acquired pathogens, though late viral reactivation can occur. Cardiac Allograft Vasculopathy (CAV): Unlike native coronary artery disease, CAV presents as diffuse, concentric intimal thickening that affects the entire length of the vessel, including the microvasculature. Due to denervation, patients rarely present with angina; instead, CAV manifests as unexplained heart failure, fatigue, or sudden cardiac death. Malignancy Risk: Long-term immunosuppression significantly increases the risk of malignancy. Skin cancers (squamous and basal cell) are the most common, followed by Post-Transplant Lymphoproliferative Disorder (PTLD), which is often driven by Epstein-Barr Virus (EBV) reactivation. Notes Notes: Notes drafted by Dr. Patlolla 1. What are the unique physiological features of the transplanted heart? The hallmark of the transplanted heart is denervation. Because the autonomic nerve fibers are severed during harvest, the heart loses parasympathetic or vagal tone, resulting in a resting tachycardia (typically 90-110 bpm). The heart also loses the ability to mount a reflex tachycardia; thus, the heart rate response to exercise or hypovolemia relies on circulating catecholamines, which results in a slower “warm-up” and “cool-down” period during exertion. 2. What are the pillars of maintenance immunosuppression regimen? The triple drug maintenance regimen typically consists of: Calcineurin Inhibitor (CNI): Tacrolimus is preferred over cyclosporine. Key side effects include nephrotoxicity, hypertension, tremor, hyperkalemia, and hypomagnesemia. Antimetabolite: Mycophenolate mofetil (MMF) inhibits lymphocyte proliferation. Key side effects include leukopenia and GI distress. Corticosteroids: Prednisone is used for maintenance but is often weaned to low doses or discontinued after the first year to mitigate metabolic side effects (diabetes, osteoporosis, weight gain). 3. How is rejection classified and diagnosed? Rejection is the immune system’s response to the foreign graft and is categorized by the arm of the immune system involved: Acute Cellular Rejection (ACR): Mediated by T-lymphocytes infiltrating the myocardium. It is graded from 1R (mild) to 3R (severe) based on the extent of infiltration and myocyte damage. Antibody-Mediated Rejection (AMR): Mediated by B-cells producing donor-specific antibodies (DSAs) that attack the graft endothelium. It is diagnosed via histology (capillary swelling) and immunofluorescence (C4d staining). Diagnosis has historically relied on endomyocardial biopsy. However, non-invasive tools are gaining traction. Gene Expression Profiling (GEP) assesses the expression of genes associated with immune activation to rule out rejection in low-risk patients. Donor-Derived Cell-Free DNA (dd-cfDNA) measures the fraction of donor DNA in the recipient’s blood. Elevated levels suggest graft injury which can occur in both ACR and AMR. 4. What is the timeline of infectious risk and how does it guide prophylaxis? Infectious risk correlates with the net state of immunosuppression. < 1 Month (Nosocomial): Risks include surgical site infections, catheter-associated infections, and aspiration pneumonia. 1 – 6 Months (Opportunistic): This is the period of peak immunosuppression. Patients are at risk for PJP, CMV, Toxoplasma, and fungal infections. Prophylaxis typically includes Trimethoprim-Sulfamethoxazole (for PJP/Toxo) and Valganciclovir (for CMV, dependent on donor/recipient serostatus). > 6 Months (Community-Acquired): As immunosuppression is weaned, the risk profile shifts toward community-acquired respiratory viruses (Influenza, RSV) and pneumonias. However, patients with recurrent rejection requiring boosted immunosuppression remain at risk for opportunistic pathogens. 5. How does Cardiac Allograft Vasculopathy (CAV) differ from native CAD? CAV is the leading cause of late graft failure. Unlike the focal, eccentric plaques seen in native atherosclerosis, CAV is an immunologically driven process causing diffuse, concentric intimal hyperplasia. It affects both epicardial vessels and the microvasculature. Because of this diffuse nature, percutaneous coronary intervention (PCI) is often technically difficult and provides only temporary palliation. The only definitive treatment for severe CAV is re-transplantation. Surveillance is critical and is typically performed via annual coronary angiography, often using intravascular ultrasound (IVUS) to detect early intimal thickening before it is visible on the angiogram. References Costanzo MR, Dipchand A, Starling R, et al. The International Society of Heart and Lung Transplantation Guidelines for the care of heart transplant recipients. J Heart Lung Transplant. 2010;29(8):914-956. doi:10.1016/j.healun.2010.05.034. https://www.jhltonline.org/article/S1053-2498(10)00358-X/fulltext Kittleson MM, Kobashigawa JA. Cardiac Allograft Vasculopathy: Current Understanding and Treatment. JACC Heart Fail. 2017;5(12):857-868. doi:10.1016/j.jchf.2017.07.003. https://www.jacc.org/doi/10.1016/j.jchf.2017.07.003 Velleca A, Shullo MA, Dhital K, et al. The International Society for Heart and Lung Transplantation (ISHLT) guidelines for the care of heart transplant recipients. J Heart Lung Transplant. 2023;42(5):e1-e141. doi:10.1016/j.healun.2022.10.015. https://www.jhltonline.org/article/S1053-2498(22)02187-5/fulltext
• 439. Atrial Fibrillation: Anti-Arrhythmic Drugs in the Management of Atrial Arrhythmias with Dr. Andrew Epstein 25.12.2025 47min

  CardioNerds (Dr. Colin Blumenthal, Dr. Kelly Arps, and Dr. Natalie Marrero) discuss anti-arrhythmic drugs in the management of atrial fibrillation and atrial flutter with electrophysiologist Dr. Andrew Epstein. We discuss two major classes of anti-arrhythmic drugs, class IC and class III, as well as digoxin. Dr. Epstein explains their mechanisms of action, indications and specific patient populations in which they would be particularly helpful, efficacy, adverse side effects, contraindications, and key drug-drug interactions. We also elaborate on defining clinical trials and their clinical implications. Given the large burden of atrial fibrillation and atrial flutter in our patient population and the high prevalence of anti-arrhythmic drug use, this episode is sure to be applicable to many practicing physicians and trainees. Audio editing by CardioNerds academy intern, Grace Qiu.  Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. 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 Anti-arrhythmic drugs should not be thought of as an alternative to ablation but, instead, should be considered an adjunct to catheter ablation.   Class IC anti-arrhythmic drugs, flecainide and propafenone, are highly efficacious for acute cardioversion and a great option for patients with infrequent episodes of AF who do not have a history of ischemic heart disease.    Class III anti-arrhythmic drugs like ibutilide, sotalol, and dofetilide, are highly effective for acute conversion; however, they require hospitalization for close monitoring during initiation and dose titration given the risk of prolonged QT.   Amiodarone should not be used as a first line agent given its toxicities, prolonged half-life, large volume of distribution, and drug-drug interactions.   Dr. Epstein notes that, “All drugs are poisons with a few beneficial side effects,” when highlighting the many adverse side effects of anti-arrhythmic drugs, particularly amiodarone, and the importance of balancing their benefit in rhythm control with their side effect profile.   Notes Notes: Notes drafted by Dr. Natalie Marrero.  What are the Class IC anti-arrhythmic drugs and what indications exist for their use?   Class IC anti-arrhythmic drugs are anti-arrhythmic drugs that work by blocking sodium channels and, thereby, prolonging depolarizing.   Class IC anti-arrhythmic drugs include flecainide and propafenone.   Class IC anti-arrhythmic drugs are good agents to use in patients that have infrequent episodes of AF and do not want daily dosing as these agents can be used by patients when they feel palpitations and desire acute conversion back to sinus rhythm (“pill in the pocket” approach).    What are the adverse consequences and/or contraindications to using a class IC agent?  Class IC anti-arrhythmic agents are contraindicated in patients with a history of ischemic heart disease based on increased mortality associated with their use in these patients in the CAST trial.   Given the results of the CAST trial, providers should screen annually for ischemia via a functional stress test in patients on these drugs at risk for coronary disease.   These drugs can increase 1:1 conduction of atrial flutter and, therefore, require concomitant use of a beta blocker.   These agents are generally well-tolerated without any organ toxicities; however, they can precipitate heart failure in patients with cardiomyopathies, cause sinus node depression, and unmask genetic arrythmias such as a Brugada pattern.   What are the class III agents and what are indications for their use?   Class III agents are drugs that block the potassium channel, prolonging the QT, and include Ibutilide, Sotalol, and Dofetilide.    Class III agents can be considered in patients with or without a history of ischemic heart disease that desire effective acute chemical cardioversion and are willing to go to the hospital for close monitoring during dose initiation and titration.   Other specific circumstances in which one can use these agents, specifically Ibutilide, are in patients with recurrent atrial fibrillation and Wolf Parkinson White (due to slowed conduction via the accessory pathway).  What are the adverse consequences and/or contraindications to using a class III agent?  Ibutilide, Sotalol, and Dofetilide prolong the QT and increase the risk of torsade de pointes, which is why they require ECG monitoring in-patient during drug initiation and dose titration.    These agents are generally well-tolerated.   Sotalol should be avoided or used cautiously in patients with left ventricular dysfunction, while dofetilide can be used and has dose-response beneficial effects in patients with left ventricular dysfunction.   Both sotalol and dofetilide are renally cleared with specific creatinine clearance cutoffs (CrCl < 20 for dofetilide and CrCl <40 for sotalol) and their dose should be adjusted based on the patient’s creatinine clearance (not eGFR).  What is the mechanism of action and indications for using amiodarone?   Amiodarone is a class III anti-arrhythmic agent, so it blocks the potassium channel prolonging the QT. Amiodarone is a “dirty drug” as it also has Class I (sodium channel blockade), Class II (antisympathetic action), and Class IV (calcium channel blockade) actions.    Amiodarone should be used as a second line agent.   Amiodarone can be considered in young, stable outpatients who are already in sinus rhythm especially greater than 60 beats per minute for outpatient loading.   What are the drawbacks of amiodarone?   Amiodarone, given its large volume of distribution and need to reach ~10 g for efficacy in conversion, takes a longer time to load and, therefore, a longer time to cardiovert.   Amiodarone is associated with multiple organ toxicities including pulmonary fibrosis, thyroid toxicity (both hypothyroidism and hyperthyroidism), peripheral neuropathy, sinus bradycardia, QT prolongation, corneal deposits, retinitis and vision loss.   Given the organ toxicities, patients on amiodarone should have their LFTs and TSH, a chest X-ray, and electrocardiogram checked at least every 6 months.   Amiodarone sensitizes patients to warfarin and increases digoxin levels, so if patients are on amiodarone with warfarin or digoxin, lower levels of warfarin or digoxin should be used.   What is dronedarone? How does it differ from amiodarone?   Dronedarone is a class III antiarrhythmic, which means it works by blocking the potassium channel and prolonging the QT.   Dronedarone differs from amiodarone in that it lacks iodine moiety and, therefore, does not have the associated thyroid toxicities. It also has a shorter half-life and smaller volume of distribution.   What are the contraindications to using dronedarone?   In the PALACE trial, dronedarone was associated with increased mortality in patients with heart failure, so it should be avoided in patients with clinical heart failure within the last six months.   What is the mechanism of action and indication for using digoxin?   Digoxin has several mechanisms of action including increasing vagal tone, inhibiting the sodium potassium ATPase, and acting as a positive inotrope.  Digoxin is indicated as a second line drug when better rate control is needed.   Digoxin improves rate control by increasing vagal tone and so may have an impact on resting rates. However, exertional rates may remain unctonrolled since these are mediated by sympathetic tone.   Digoxin is a good option in patients that are not particularly active given that it decreases ventricular rate at rest, but not with exercise.  Digoxin may be particularly beneficial in patients with heart failure given its positive ionotropic effects.   What are the adverse side effects of digoxin and special monitoring required for patients on digoxin?   Typically, digoxin levels are monitored, however they are usually not helpful as the levels are often drawn randomly. To be informative, the levels need to be a trough levels drawn right before the drug is given.   The literature contains conflicting results on the mortality associated with digoxin levels.   In general, the consensus in the field is that lower levels are better.   Digoxin is renally cleared, so levels should be closely monitored in patients with renal failure.   References 1. Mar PL, Horbal P, Chung MK, et al. Drug interactions affecting antiarrhythmic drug use. Circulation: Arrhythmia and Electrophysiology. 2022;15(5):e007955. https://doi.org/10.1161/CIRCEP.121.007955. doi: 10.1161/CIRCEP.121.007955.  2. Gianfranchi L, Luzi M, Solano A, et al. Outpatient treatment of recent-onset atrial fibrillation with the “pill-in-the-pocket” approach. N Engl J Med. 2004;351(23):2384–2391. https://doi.org/10.1056/NEJMoa041233. doi: 10.1056/NEJMoa041233.  3. Barker AH, Echt DS, Arensberg D, et al. Mortality and morbidity in patients receiving encainide, flecainide, or placebo. N Engl J Med. 1991;324(12):781–788. https://doi.org/10.1056/NEJM199103213241201. doi: 10.1056/NEJM199103213241201.  4. Markman Timothy M., Jarrah Andrew A., Ye T, et al. Safety of pill-in-the-pocket class 1C antiarrhythmic drugs for atrial fibrillation. JACC: Clinical Electrophysiology. 2022;8(12):1515–1520. https://doi.org/10.1016/j.jacep.2022.07.010. doi: 10.1016/j.jacep.2022.07.010.  5. Joglar JA, Chung MK, Armbruster AL, et al. 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):e1–e156. https://doi.org/10.1161/CIR.0000000000001193. doi: 10.1161/CIR.0000000000001193.  6. Ferrari F, Santander IRMF, Stein R. Digoxin in Atrial Fibrillation: An Old Topic Revisited. Curr Cardiol Rev. 2020;16(2):141-146. doi:10.2174/1573403X15666190618110941  7. Van Gelder I,C., Rienstra M, Bunting KV, et al. 2024 ESC guidelines for the management of atrial fibrillation developed in collaboration with the european association for cardio-thoracic surgery (EACTS): Developed by the task force for the management of atrial fibrillation of the european society of cardiology (ESC), with the special contribution of the european heart rhythm association (EHRA) of the ESC. endorsed by the european stroke organisation (ESO). Eur Heart J. 2024;45(36):3314–3414. https://doi.org/10.1093/eurheartj/ehae176. doi: 10.1093/eurheartj/ehae176.  8. Copaescu AM, Vogrin S, James F, et al. Efficacy of a Clinical Decision Rule to Enable Direct Oral Challenge in Patients With Low-Risk Penicillin Allergy: The PALACE Randomized Clinical Trial. JAMA Intern Med. 2023;183(9):944-952. doi:10.1001/jamainternmed.2023.2986  9. Kirchhof P, Camm AJ, Goette A, et al. Early Rhythm-Control Therapy in Patients with Atrial Fibrillation. N Engl J Med. 2020;383(14):1305-1316. doi:10.1056/NEJMoa2019422  10. Anderson JL, Platia EV, Hallstrom A, et al. Interaction of baseline characteristics with the hazard of encainide, flecainide, and moricizine therapy in patients with myocardial infarction. A possible explanation for increased mortality in the Cardiac Arrhythmia Suppression Trial (CAST). Circulation. 1994;90(6):2843-2852. doi:10.1161/01.cir.90.6.2843  11.Akiyama T, Pawitan Y, Greenberg H, Kuo C, Reynolds-Haertle R, The CI. Increased risk of death and cardiac arrest from encainide and flecainide in patients after non-Q-wave acute myocardial infarction in the cardiac arrhythmia suppression trial. Am J Cardiol. 1991;68(17):1551–1555. https://doi.org/10.1016/0002-9149(91)90308-8. doi: 10.1016/0002-9149(91)90308-8.  12. Parkash R, Wells GA, Rouleau J, et al. Randomized Ablation-Based Rhythm-Control Versus Rate-Control Trial in Patients With Heart Failure and Atrial Fibrillation: Results from the RAFT-AF trial. Circulation. 2022;145(23):1693-1704. doi:10.1161/CIRCULATIONAHA.121.057095 
• 438. Heart Failure: Perioperative Heart Transplant Management with Dr. Dave Kaczorowski and Dr. Jason Katz 16.12.2025 33min

  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. doi:10.1016/j.healun.2020.03.020  Velleca A, Shullo MA, Dhital K, et al. The International Society for Heart and Lung Transplantation (ISHLT) guidelines for the care of heart transplant recipients. J Heart Lung Transplant. 2023;42(5):e1-e141. doi:10.1016/j.healun.2022.10.015  Sicim H, Tam WSV, Tang PC. Primary graft dysfunction in heart transplantation: the challenge to survival. J Cardiothorac Surg. 2024;19(1):313. doi:10.1186/s13019-024-02816-6 
• 437. Atrial Fibrillation: The Diagnosis and Management of Atrial Flutter with Dr. Joshua Cooper 05.12.2025 30min

  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.  Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. 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.
• 436. Heart Failure: Pre-Heart Transplant Evaluation and Management with Dr. Kelly Schlendorf 24.11.2025 32min

  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 
• 435. Atrial Fibrillation: Chronic Management of Atrial Fibrillation with Dr. Edmond Cronin 20.11.2025 47min

  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. Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. 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, patients become dependent on pacing and lifelong pacemaker implantation, and the potential for device complications  AVNA does not prevent progression or recurrence of AF  The type of device is dependent on patient comorbidities but the advent of conduction system pacing may improve outcomes in these patients compared with RV pacing.   What are some recommendations for managing atrial fibrillation in the perioperative period?  In patients with AF (excluding those with recent stroke or TIA, or a mechanical valve) and on oral anticoagulation with either warfarin or DOAC who are scheduled to undergo an invasive procedure or surgery, temporary cessation of oral anticoagulation without bridging anticoagulation is recommended (COR-LOE 1-B)  In patients with AF on DOAC that has been interrupted for an invasive procedure or surgery, in general, resumption of anticoagulation the day after low bleeding risk surgery and between the evening of the second day and the evening of the third day after high bleeding risk surgery is reasonable, as long as hemostasis has been achieved and further bleeding is not anticipated (COR-LOE 2a-B)  Preop prophylaxis to prevent AF after cardiac surgery with either beta blocker or amiodarone shows mixed benefit and carries a 2a-B recommendation; however, beta blocker is a class 1-A recommendation in patients who do develop AF in the postop period  It should be noted that patients who develop AF in the setting of an acute illness or surgery are at risk of recurrence   References Joglar, J, Chung, M. et al. 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. JACC. 2024 Jan, 83 (1) 109–279. https://doi.org/10.1016/j.jacc.2023.08.017  Fuster F, Rydén L, et al. ACC/AHA/ESC Guidelines for the Management of Patients With Atrial Fibrillation: Executive Summary A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and the European Society of Cardiology Committee for Practice Guidelines and Policy Conferences (Committee to Develop Guidelines for the Management of Patients With Atrial Fibrillation) Developed in Collaboration With the North American Society of Pacing and Electrophysiology. Circulation. 2001 Oct, 104 (17). https://doi.org/10.1161/circ.104.17.2118  Kirchhof P, Camm A, et al. Early Rhythm-Control Therapy in Patients with Atrial Fibrillation. N Engl J Med. 2020 Aug, 383 (14) 1305-1416. DOI: 10.1056/NEJMoa2019422  Olshansky, B, Rosenfeld, L, Warner, A. et al. The Atrial Fibrillation Follow-up Investigation of Rhythm Management (AFFIRM) study: Approaches to control rate in atrial fibrillation. JACC. 2004 Apr, 43 (7) 1201–1208.https://doi.org/10.1016/j.jacc.2003.11.032  Whitlock R, Belley-Cote E, et al. Left Atrial Appendage Occlusion during Cardiac Surgery to Prevent Stroke. N Engl J Med. 2021 May, 384 (22) 2081-2091. DOI: 10.1056/NEJMoa2101897  Kirchhof P, Toennis T, et al. Anticoagulation with Edoxaban in Patients with Atrial High-Rate Episodes. N Engl J Med. 2023 Aug, 389 (13) 1167-1179. DOI: 10.1056/NEJMoa2303062  Healey J, Lopes R, et al. Apixaban for Stroke Prevention in Subclinical Atrial Fibrillation. N Engl J Med. 2023 Nov, 390 (2) 107-117. DOI: 10.1056/NEJMoa2310234  Roy D, Talajic M, et al. Rhythm Control versus Rate Control for Atrial Fibrillation and Heart Failure. N Engl J Med. 2008 Jun, 358 (25) 2667-2677. DOI: 10.1056/NEJMoa0708789  Gillinov A, Bagiella E, et al. Rate Control versus Rhythm Control for Atrial Fibrillation after Cardiac Surgery. N Engl J Med. 2016 Mar, 374 (20) 1911-1921. DOI: 10.1056/NEJMoa1602002 
• 434. Heart Failure: Advanced Therapies Evaluation with Dr. Michelle Kittleson 07.11.2025 14min

  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. We Were Thrilled to Join the American Heart Association’s Scientific Sessions 2025! AHA Scientific Sessions 2025 took place November 7–10 in New Orleans, LA — one of the premier annual gatherings in cardiovascular science and education. It was an incredible opportunity to connect with colleagues, hear cutting-edge research, and contribute to the ongoing conversations shaping the future of cardiovascular care. We’re grateful to everyone who joined us in New Orleans and made this year’s meeting so impactful. 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 
• 433. The Evolution and Future of Cardio-Obstetrics with Dr. Afshan Hameed, Dr. Doreen DeFaria Yeh, Dr. Garima Sharma, and Dr. Rina Mauricio 05.11.2025 31min

  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.  We Were Thrilled to Join the American Heart Association’s Scientific Sessions 2025! AHA Scientific Sessions 2025 took place November 7–10 in New Orleans, LA — one of the premier annual gatherings in cardiovascular science and education. It was an incredible opportunity to connect with colleagues, hear cutting-edge research, and contribute to the ongoing conversations shaping the future of cardiovascular care. We’re grateful to everyone who joined us in New Orleans and made this year’s meeting so impactful. Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. 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!