Podcast
Cardionerds: A Cardiology Podcast
Hosted by CardioNerds · EN
Welcome to CardioNerds, where we bring you in-depth discussions with leading experts, case reports, and updates on the latest advancements in the world of cardiology. Tune in to expand your knowledge, sharpen your skills, and become a true CardioNerd!
27episodes
Episodes
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448. The Braunwald Chronicles: The Complete Series — A CardioNerds Tribute to Dr. Eugene Braunwald
3w ago00:41:43Tap to summarizeCardioNerds (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!
Transcribe →447. Pulmonary Embolism: Approach to Systemic Thrombolysis in Acute Pulmonary Embolism with Dr. Allison Burnett
4w ago00:42:43Tap to summarizeCardioNerds 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? <ul class="wp-block-l...
Transcribe →446. The SGLT2i Effect – Protection Against Cancer Therapy-Related Cardiac Dysfunction with Dr. Manu Mysore
Apr 1600:32:38Tap to summarizeCardioNerds (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. <a href="https://pubmed.ncbi.nlm.nih.gov/4090...
Transcribe →445. Heart Failure: The Essential Role of Palliative Care in Advanced Therapies with Dr. Sarah Chuzi
Apr 1000:54:56Tap to summarizeDr. 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.</l...
Transcribe →444. Heart Failure: LVAD Part 2 with Dr. Mark Belkin and Dr. Chris Salerno
Mar 2200:26:44Tap to summarizeCardioNerds (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.
Transcribe →443. Pulmonary Embolism: The Modern Approach to Pulmonary Embolism Care with Dr. Kenneth Rosenfield
Mar 500:25:56Tap to summarizeThis 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 Center...
Transcribe →442. Heart Failure: LVAD Part 1 with Dr. Jeff Teuteberg and Dr. Mani Daneshmand
Feb 2700:41:37Tap to summarizeCardioNerds (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 plac...
Transcribe →441. Atrial Fibrillation: Ablation of Atrial Fibrillation with Dr. Jon Piccini
Feb 1300:53:39Tap to summarizeCardioNerds (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.</li...
Transcribe →440. Heart Failure: Post-Heart Transplant Management with Dr. Shelly Hall and Dr. MaryJane Farr
Feb 400:26:16Tap to summarizeCardioNerds (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...
Transcribe →439. Atrial Fibrillation: Anti-Arrhythmic Drugs in the Management of Atrial Arrhythmias with Dr. Andrew Epstein
Dec 2500:47:13Tap to summarizeCardioNerds (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? <ul clas...
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