Episodes Archives - Cardionerds

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Episodes Archives - Cardionerds episodes

April 24447. Pulmonary Embolism: Approach to Systemic Thrombolysis in Acute Pulmonary Embolism with Dr. Allison Burnett
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.
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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.
43 min
April 16446. The SGLT2i Effect – Protection Against Cancer Therapy-Related Cardiac Dysfunction with Dr. Manu Mysore
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 Page
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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.
33 min
April 10445. Heart Failure: The Essential Role of Palliative Care in Advanced Therapies with Dr. Sarah Chuzi
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 Page
CardioNerds Episode Page
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CardioNerds Journal Club
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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/
55 min
March 22444. Heart Failure: LVAD Part 2 with Dr. Mark Belkin and Dr. Chris Salerno
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 Page
CardioNerds Episode Page
CardioNerds Academy
Cardionerds Healy Honor Roll
CardioNerds Journal Club
Subscribe to The Heartbeat Newsletter!
Check out CardioNerds SWAG!
Become a CardioNerds Patron!
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.
27 min
March 05443. Pulmonary Embolism: The Modern Approach to Pulmonary Embolism Care with Dr. Kenneth Rosenfield
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.
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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/
26 min
February 27442. Heart Failure: LVAD Part 1 with Dr. Jeff Teuteberg and Dr. Mani Daneshmand
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.
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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
42 min
February 13441. Atrial Fibrillation: Ablation of Atrial Fibrillation with Dr. Jon Piccini
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.
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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.
54 min
February 04440. Heart Failure: Post-Heart Transplant Management with Dr. Shelly Hall and Dr. MaryJane Farr
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.
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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
27 min
December 25, 2025439. Atrial Fibrillation: Anti-Arrhythmic Drugs in the Management of Atrial Arrhythmias with Dr. Andrew Epstein
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.
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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
48 min
December 16, 2025438. Heart Failure: Perioperative Heart Transplant Management with Dr. Dave Kaczorowski and Dr. Jason Katz
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.
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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
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34 min

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Episodes Archives - Cardionerds

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About Episodes Archives - Cardionerds