Cardionerds: A Cardiology Podcast

By CardioNerds

Welcome to CardioNerds, where we bring you in-depth discussions with leading experts, case reports, and updates on the latest advancements in the world of cardiology. Tune in to expand your knowledge... more

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The podcast currently has 451 episodes available.

Cardionerds: A Cardiology Podcast episodes:

March 22, 2026444. 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.
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27min
March 05, 2026443. 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.
CardioNerds Pulmonary Embolism Page
CardioNerds Episode Page
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Cardionerds Healy Honor Roll
CardioNerds Journal Club
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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/
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26min
February 27, 2026442. 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.
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
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
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42min
February 13, 2026441. 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.
CardioNerds Atrial Fibrillation Page
CardioNerds Episode Page
CardioNerds Academy
Cardionerds Healy Honor Roll
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Subscribe to The Heartbeat Newsletter!
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Become a CardioNerds Patron!
PEARLS
Pulmonary veins (PVs) are the dominant triggers in early AF due to their unique myocardial sleeve electrophysiology.
Pulmonary vein isolation (PVI) remains the cornerstone of AF ablation by blocking PV triggers from reaching the left atrium. Posterior wall isolation is sometimes performed in persistent AFib, but large RCTs found no significant benefit over PVI alone.
Paroxysmal AF has the highest ablation success rates. Left atrial health remains the major determinant of outcome.
Ablation modalities include pulsed field ablation, radiofrequency ablation, and cryo-balloon ablation. PFA offers advantage of relative myocardial selectivity with near zero risk of atrio-esophageal fistula.
Long-term anticoagulation decisions after ablation currently depend on CHA₂DS₂-VASc score. Recent evidence suggests the safety of stopping anticoagulation in low-risk patients after ablation.
Early atrial arrhythmia recurrence during a blanking period after ablation (≤3 months) often reflects inflammation — not procedural failure. Late recurrence suggests PV reconnection or residual substrate and often requires repeat ablation.
Hybrid surgical and catheter Afib ablation represent an aggressive strategy for rhythm control in patients with persistent or long-standing persistent AF with extensive substrate and/or patients who have had multiple failed catheter ablations.
Notes
1. What is the mechanism behind AF initiation?
Atrial fibrillation (AF) is a progressive condition.
Early AF is primarily trigger-driven, most commonly from the pulmonary veins.
Pulmonary vein myocardial sleeves have unique electrophysiologic properties that promote premature beats and afterdepolarizations.
As AF progresses, atrial remodeling (fibrosis and scar) leads to a more substrate-driven arrhythmia.
2. How does early catheter ablation for atrial fibrillation work?
Electrical Isolation of pulmonary veins, blocking PV triggers from reaching the left atrium.
By reducing burden of atrial fibrillation, this may slow adverse atrial remodeling.
3. Which patients are good candidates for Afib ablation?
Functional Status: ambulatory, active patients derive the greatest benefit. Advanced frailty or severe end-stage cardiovascular disease reduces expected benefit.
Comorbidity Burden: CHA₂DS₂-VASc score helps risk-stratify not only stroke risk but also rhythm-control outcomes.
Type and Duration of AF
Paroxysmal AF → highest likelihood of success (burden reduction often 95–99%).
Long-standing persistent AF → lower suppression rates (often 50–80%).
Left Atrial Health: a major determinant of outcomes.
LA diameter >5.5 cm associated with significantly worse outcomes.
LA volume index (normal ≤34 mL/m²) is preferred over diameter for assessment.
4. What are the predictors of complications from AFib ablation procedures?
Low and high body mass index (BMI)
Chronic corticosteroid use
Severe enlargement of other cardiac chambers
Female gender is associated with a numerically higher risk of complications.
5. Role of preprocedural imaging with cardiac CT or MRI
Cardiac CT
Faster and convenient
Help define LA geometry and Pulmonary vein anatomy
Anatomic Variants as Right middle pulmonary vein, accessory pulmonary veins common pulmonary vein ostium, Atrial diverticula or Accessory left atrial appendage
Consider Cardiac MRI when:
Strong family history of atrial fibrillation or cardiomyopathy
Suspicion of occult structural heart disease
6. Key Procedural Steps in AF Ablation
There is significant variation across centers in anesthesia, mapping, and ablation strategies.
The following outline reflects a common contemporary approach.
Anesthesia & Monitoring
Most commonly performed under general anesthesia.
Benefits include improved catheter stability, enhanced patient comfort, and controlled ventilation (e.g., low-volume, high-frequency).
Invasive arterial line (A-line) is preferred for rapid detection of hypotension.
Vascular Access
Ultrasound-guided femoral venous access with multiple sheaths.
Micropuncture technique is ideal to minimize complications.
Intracardiac Echocardiography (ICE)
ICE catheter insertion.
Reduces complications, guides transseptal puncture, assesses catheter contact, and monitors for pericardial effusion.
Anticoagulation
Systemic heparin initiated before or immediately after transseptal access.
Activated clotting time (ACT) maintained in therapeutic range (typically >300 seconds).
Transseptal Puncture
Access to the left atrium via transseptal sheath.
Often uses electrocautery-assisted wire, with ICE guidance to improve safety.
Left Atrial Mapping
Creation of electroanatomic map (common in many centers).
Ideally performed in sinus rhythm.
Assesses left atrial geometry, voltage (for scar/substrate), and activation timing.
Ablation Strategy
Core component is pulmonary vein isolation (PVI).
Technology options include pulse field ablation (PFA), radiofrequency ablation, and cryoballoon ablation.
Additional ablation (case-dependent):
Posterior wall isolation
Targeting non-pulmonary vein triggers
Linear lesions
Ablation of organized atrial tachycardias/flutters
Emerging approaches include AI-guided strategies.
Post-Ablation Assessment
Confirm pulmonary vein entrance and exit block.
Remap left atrium (in many practices) to evaluate lesion completeness.
Check for complications (e.g., ICE assessment for pericardial effusion).
7. What is Electroanatomic Mapping?
Combines 3D geometry (anatomic reconstruction of cardiac chamber) with electrophysiology (electrical signals from tissue).
How it works:
Mapping catheter is moved along the atrial wall
Records electrograms
System generates:
3D chamber model
Voltage map (tissue health/scar)
Activation map (depolarization timing)
Key information provided
Voltage map (substrate assessment):
High voltage = healthy tissue
Low voltage = scar/fibrosis
Identifies areas needing additional ablation (e.g., posterior wall scar)
Activation map:
Visualizes wavefront propagation
Essential for diagnosing and ablating macroreentrant atrial flutters and organized atrial tachycardias
8. What is the current role of Afib ablaton outside pulmonary vein isolation?
While Pulmonary Vein Isolation (PVI) remains the cornerstone of atrial fibrillation (AF) ablation, adjunctive strategies are increasingly used for persistent AF, with varying levels of supporting data.
Non-PVI Triggers:
Arrhythmogenic foci found outside the pulmonary veins in 10% to 20% of patients.
Common sites include SVC, LAA, CS, and Crista Terminalis.
Identifying and ablating these inducible triggers—often provoked by isoproterenol—can reduce recurrence in persistent AF.
Posterior Wall Isolation (PWI):
The posterior wall is a driver for persistent AF.
Randomized evidence for routine PWI is conflicting.
Large RCTs found no significant benefit over PVI alone for first-time ablations.
Remains a primary adjunctive target for redo procedures.
AI-Guided Ablation:
Uses AI to identify “spatio-temporal dispersion” areas.
Recent TAILORED-AF trial demonstrate increased freedom from AF at 12 months compared to conventional PVI.
9. Comparison of ablation techniques
Pulsed Field Ablation (PFA) – Non-Thermal
Mechanism: irreversible electroporation
Key advantages:
Shorter procedural time
Comparable efficacy to thermal ablation
Higher myocardial tissue selectivity
No known risk of esophageal fistula or pulmonary vein stenosis
Low risk of phrenic nerve (usually transient)
Disadvantages:
Less flexibility for complex substrate
Hemolysis with possible AKI
Early and delayed coronary spasms
Skeletal muscle stimulation during energy delivery
Loss of all electrograms even with reversible injury can be misleading
Limited long term data
Radiofrequency Ablation (RFA) – Thermal (Heat)
Mechanism: resistive heating
Key advantages:
Highly versatile
Can tailor lesions
Long term experience
Disadvantages:
More procedural time (less with ultrahigh power RFA)
Very small risk of esophageal fistula (1/2000 but 50% mortality!)
Pulmonary vein stenosis
Rare Phrenic nerve palsy
Stem pops
Cryoballoon Ablation (CBA) – Thermal (Cold)
Mechanism: Uses extreme cold
Key Advantages:
Short learning curve
Single shot balloon
Highly reproducible
Good catheter stability (adhesion during freeze)
Low risk of thrombus
Disadvantages:
Similar to RFA
More phrenic nerve palsy
Less esophageal fistula and pulmonary vein stenosis
10. Other Complications of AF Catheter Ablation common to all modalities
Pericardial effusion/tamponade: 0.4–2.2%
Stroke/TIA: ~0.2–1.8%
In-hospital mortality: Very low (0.05–0.46%)
Often overstated in studies based on National Inpatient Sample (NIS) due to selection bias
Vascular access complications: Hematoma
11. Expert approach to Antiarrhythmic Drug (AAD) Therapy After AF Ablation
Continue AAD for the 3-month blanking period after catheter ablation.
Supported by multiple trials to reduce early AF recurrences.
Decreases hospitalizations during the healing phase by suppressing inflammation-related arrhythmias.
AADs do not clearly improve long-term freedom from AF.
At the 3-month follow-up:
If the patient is asymptomatic with no documented recurrence → discontinue AAD.
If recurrent AF occurs or high substrate burden persists → consider continuing AAD.
12. Expert approach to Anticoagulation After AF Ablation
All patients require anticoagulation for at least 3 months post–ablation.
Current guidelines recommend long-term anticoagulation decisions guided solely by CHA₂DS₂-VASc score.
Decisions should not be based on ablation success or arrhythmia burden.
New data support discontinuation in low-risk patients after careful shared decision-making.
In high-risk patients:
Observational data indicate ~2.5-fold increased stroke risk when anticoagulation is stopped.
OCEAN trial:
Generally low risk patients (mean CHA2DS2-VASc score 2.2).
Rivaroxaban did not significantly reduce composite stroke outcomes compared with aspirin.
13. Approach to recurrent Atrial Arrhythmias After AF Ablation
Early (≤3 months – blanking period):
True blanking probably less (6 weeks to 2 months)
Likely less with PFA
Often due to inflammation or lesion maturation
Should not be considered procedural failure
Management:
Continue or restart AAD
Electrical cardioversion for persistent symptomatic episodes
Avoid early repeat ablation
Late (>3 months) recurrences:
More likely due to pulmonary vein reconnection or residual atrial substrate
Arrhythmias include:
Recurrent atrial fibrillation
Atypical (macroreentrant) atrial flutter
Typical atrial flutter (cavotricuspid isthmus–dependent)
Focal atrial tachycardia
Management is often challenging and may include AAD, cardioversion, or repeat ablation.
14. When to Consider Hybrid Surgical and Catheter Ablation for Atrial Fibrillation?
Aggressive rhythm control strategy when standard endocardial approaches are insufficient.
Typically for persistent or long-standing persistent AF (>12 months).
Often used in patients with extensive substrate or multiple failed catheter ablations.
Can be performed during concomitant cardiac surgery or as a stand-alone hybrid procedure.
Benefits of surgical approach:
Epicardial posterior wall/dome ablation
PVI
Ligation of the ligament of Marshall
Left atrial appendage closure (e.g., AtriClip)
Approach:
Subxiphoid/minimally invasive surgical access
Endocardial EP confirmation
Additional PVI ablation and gap closure
Evidence suggests increased freedom from atrial arrhythmias at the expense of higher major adverse event risk.
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54min
February 04, 2026440. 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
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27min
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
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48min
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
Velleca A, Shullo MA, Dhital K, et al. The International Society for Heart and Lung Transplantation (ISHLT) guidelines for the care of heart transplant recipients. J Heart Lung Transplant. 2023;42(5):e1-e141. doi:10.1016/j.healun.2022.10.015
Sicim H, Tam WSV, Tang PC. Primary graft dysfunction in heart transplantation: the challenge to survival. J Cardiothorac Surg. 2024;19(1):313. doi:10.1186/s13019-024-02816-6
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34min
December 05, 2025437. Atrial Fibrillation: The Diagnosis and Management of Atrial Flutter with Dr. Joshua Cooper
In this episode, the CardioNerds (Dr. Naima Maqsood, Dr. Akiva Rosenzveig, and Dr. Colin Blumenthal) are joined by renowned educator in electrophysiology, Dr. Joshua Cooper, to discuss everything atrial flutter; from anatomy and pathophysiology to diagnosis and management. Dr. Cooper’s expert teaching comes through as Dr. Cooper vividly describes atrial anatomy to provide the foundational understanding to be able to understand why management of atrial flutter is unique from atrial fibrillation despite their every intertwined relationship. A foundational episode for learners to understand atrial flutter as well as numerous concepts in electrophysiology. Audio editing for this episode was performed by CardioNerds intern Dr. Bhavya Shah.
Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values.
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Pearls
“The biggest mistake is failure to diagnose”. Atrial flutter, especially with 2:1 conduction, is commonly missed in both inpatient and outpatient settings so look carefully at that 12-lead EKG so you can mitigate the stroke and tachycardia induced cardiomyopathy risk
Decremental conduction of the AV node makes it more challenging to rate control atrial flutter than atrial fibrillation
Catheter Ablation is the first line treatment for atrial flutter and is highly successful, but cardioversion can be utilized as well prior to pursuing ablation in some cases.
Class I AADs like propafenone and flecainide may stability the atrial flutter circuit by slowing conduction and thus may worsen the arrhythmia. Therefore, the preferred anti-arrhythmic medication in atrial flutter are class III agents.
Atrial flutter can be triggered by firing from the left side of the heart, so in patients with both atrial fibrillation and flutter, ablating atrial fibrillation makes atrial flutter less likely to recur.
BONUS PEARL: Dr. Cooper’s youtube video on atrial flutter is a MUST SEE!
Notes
Notes: Notes drafted by Dr. Akiva Rosenzveig
What are the distinguishing features of atrial fibrillation and flutter?
Atrial flutter is an organized rhythm characterized by a wavefront that continuously travels around the same circuit leading to reproducible P-waves on surface EKG as well as a very mathematical and predictable relationship between atrial and ventricular activity
Atrial fibrillation is an ever changing, chaotic rhythm that consists of small local circuits that interplay off each other. Consequently, no two beats are the same and the relationship between the atrial activity and ventricular activity is unpredictable leading to an irregularly irregular rhythm
What are common atrial flutter circuits?
Cavo-tricuspid isthmus (CTI)-dependent atrial flutter is the most common type of flutter. It is characterized by a circuit that circumnavigates the tricuspid valve.
Typical atrial flutter is characterized by the circuit running in a counterclockwise pattern up the septum, from medial to lateral across the right atrial roof, down the lateral wall, and back towards the septum across the floor of the right atrium between the IVC and the inferior margin of the tricuspid valve i.e. the cavo-tricuspid isthmus. Surface EKG will show a gradual downslope in leads II, III, and AvF and a rapid rise at end of each flutter wave.
Atypical CTI-dependent flutter follows the same route but in the opposite direction (clockwise). Therefore, we will see positive flutter waves in the inferior leads
Mitral annular flutter is more commonly seen in atrial fibrillation patients who’ve been treated with ablation leading to scarring in the left atrium.
Roof-dependent flutter is characterized by a circuit that travels around left atrium circumnavigating a lesion (often from prior ablation), traveling through the left atrial roof, down the posterior wall, and around the pulmonary veins
Surgical/scar/incisional flutter is seen in people with a history of prior cardiac surgery and have iatrogenic scars in right atrium due to cannulation sites or incisions
How does atrial flutter pharmacologic management differ from other atrial arrhythmias?
The atrioventricular (AV) node is unique in that the faster it is stimulated, the longer the refractory period and the slower it conducts. This characteristic is called decremental conduction. In atrial fibrillation, the atrial rate is so fast that the AV node becomes overwhelmed and only lets some of those signals through to the ventricles creating an irregular tachycardia but at lower rates. In atrial flutter, the atrial rate is slower, therefore the AV node has more capability to conduct allowing for higher ventricular rates. Therefore, to achieve rate control one will need a higher dose of AV blocking medications. Atrial tachycardia may require even higher doses due to the increased ability of the AV node to conduct, as the atrial rates are slower than in atrial flutter.
Sodium channel blockers (Class I) such as flecainide and propafenone slow wavefront propagation, making it easier for the AV node to handle the atrial rates. This will end up leading to increased ventricular rates which can be dangerously fast. That is why AV nodal blockers should be used in conjunction with flecainide and propafenone.
What is the role of cardioversion in atrial flutter management?
Due to high success rate with atrial flutter ablation, ablation is the first line treatment. However, sometimes cardioversion may be utilized in patients depending on how symptomatic they are and how long it will take to get an ablation. Cardioversion may also be utilized preferentially when the atrial flutter was triggered by infection or cardiac surgery to see if it will come back.
If cardioversion is pursued, the patient will need to be anticoagulated due to the stroke risk after the procedure due to post-conversion stunning.
How effective is atrial flutter ablation?
The landmark Natale et al study in 2000 demonstrated 80% success rate after radiofrequency ablation as compared to 36% in patients on anti-arrhythmic therapy. The LADIP study in 2006 further corroborated these findings. Contemporary data shows above 90% success rate of atrial flutter ablation.
In patients who have had both atrial fibrillation and atrial flutter, most electrophysiologists would ablate both. However, in patients with atrial fibrillation, the atrial flutter usually is initiated by trigger spots firing in the left atrium. Once the atrial fibrillation is ablated, the flutter will become less likely. Therefore, there are those who say there’s no need to ablate the flutter circuit as well. Alternatively, if a patient has severe comorbidities and/or is high risk for ablation, one may consider performing the atrial flutter ablation only since atrial flutter is harder to manage medically compared with atrial fibrillation.
How do you manage atrial flutter in the acute inpatient setting?
In the inpatient setting, electrical cardioversion is often limited by blood pressure and the hypotensive effects of the sedatives required. If one is awake and too hypotensive, chemical cardioversion can be pursued. The most effective anti-arrhythmic for this is ibutilide. Amiodarone is not effective for acute cardioversion. Since ibutilide prolongs refractoriness in atrial and ventricular tissue, there’s a risk of long QT induced torsades de pointes. Pretreating with magneisum reduces the risk to 1-2%.
References
Jolly WA, Ritchie WT. Auricular flutter and fibrillation. 1911. Ann Noninvasive Electrocardiol. 2003;8(1):92-96. doi:10.1046/j.1542-474x.2003.08114.x
McMichael J. History of atrial fibrillation 1628-1819 Harvey – de Senac – Laënnec. Br Heart J. 1982;48(3):193-197. doi:10.1136/hrt.48.3.193
Lee KW, Yang Y, Scheinman MM; University of Califoirnia-San Francisco, San Francisco, CA, USA. Atrial flutter: a review of its history, mechanisms, clinical features, and current therapy. Curr Probl Cardiol. 2005;30(3):121-167. doi:10.1016/j.cpcardiol.200
2023 ACC/AHA/ACCP/HRS Guideline for the Diagnosis and Management of Atrial Fibrillation: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. Circulation. 2024;149(1):e167. doi:10.1161/
Cosío F. G. (2017). Atrial Flutter, Typical and Atypical: A Review. Arrhythmia & electrophysiology review, 6(2), 55–62. https://doi.org/10.15420/aer.2017.5.2
https://www.escardio.org/Journals/E-Journal-of-Cardiology-Practice/Volume-11/Atrial-flutter-common-and-main-atypical-forms
Natale A, Newby KH, Pisanó E, et al. Prospective randomized comparison of antiarrhythmic therapy versus first-line radiofrequency ablation in patients with atrial flutter. J Am Coll Cardiol. 2000;35(7):1898-1904. doi:10.1016/s0735-1097(00)00635-5
Da Costa A, Thévenin J, Roche F, et al. Results from the Loire-Ardèche-Drôme-Isère-Puy-de-Dôme (LADIP) trial on atrial flutter, a multicentric prospective randomized study comparing amiodarone and radiofrequency ablation after the first episode of symptomatic atrial flutter. Circulation. 2006;114(16):1676-1681. doi:10.1161/CIRCULATIONAHA.106.638395
https://www.acc.org/Membership/Sections-and-Councils/Fellows-in-Training-Section/Section-Updates/2015/12/15/16/58/Atrial-Fibrillation#:~:text=The%20first%20’modern%20day’%20account,in%20open%20chest%20animal%20models.&text=In%201775%2C%20William%20Withering%20first,(purple%20foxglove)%20in%20AFib.
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31min
November 24, 2025436. Heart Failure: Pre-Heart Transplant Evaluation and Management with Dr. Kelly Schlendorf
In this episode, the CardioNerds (Dr. Rachel Goodman, Dr. Shazli Khan, and Dr. Jenna Skowronski) discuss a case of AMI-shock with a focus on listing for heart transplant with faculty expert Dr. Kelly Schlendorf. We dive into the world of pre-transplant management, discuss the current allocation system, and additional factors that impact transplant timing, such as sensitization. We conclude by discussing efforts to increase the donor pool. Audio editing for this episode was performed by CardioNerds Intern, Julia Marques Fernandes.
Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values.
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Pearls
The current iteration of heart allocation listing is based on priority, with status 1 being the highest priority.
The are multiple donor and recipient characteristics to consider when listing a patient for heart transplantation and accepting a heart offer.
Desensitization is an option for patients who need heart transplantation but are highly sensitized. Protocols vary by center.
Acceptance of DCD hearts is one of many efforts to expand the donor pool
Notes
Notes: Notes drafted by Dr. Rachel Goodman
Once a patient is determined to be a candidate for heart transplantation, how is priority determined?
The current iteration of heart listing statuses was implemented in 2018.  Priority is determined by acuity, with higher statuses indicating higher acuity and given higher priority.  Status 1 is the highest priority status, and Status 7 is inactive patients. (1,2)
What criteria should be considered in organ selection when listing a patient for heart transplant?
Once it is determined that a patient will be listed for heart transplantation, there are certain criteria that should be assessed.  These factors may impact pre-transplant care and/or donor matching (3).
(1) PVR
(2) Height/weight
(3) Milage listing criteria
(4) Blood typing/cPRA/HLA typing
What is desensitization and why would it be considered?
Desensitization is an attempt to reduce or remove anti-HLA antibodies in the recipient.  It is done to increase the donor pool.  In general, desensitization is reserved for patients who are highly sensitized.  Desensitization protocols vary by transplant center, and some may opt against it.  When considering desensitization, it is important to note two key things: first, there is no promise that it will work, and second desensitization involves the use of immunosuppressive agents, thereby putting patients at increased risk of infection and cytopenia. (4)
Can you explain DCD and DBD transplant?
DBD: donor that have met the requirements for legal definition of brain death.
DCD: donors that have not met the legal definition of brain death but have been determined to have circulatory death.  Because the brain death criteria have not been met, organ recovery can only take place once death is confirmed based on cessation of circulatory and respiratory function. Life support is only withdrawn following declaration of circulatory death—once the heart has stopped beating and spontaneous respirations have stopped. (5,6)
References
1: Maitra NS, Dugger SJ, Balachandran IC, Civitello AB, Khazanie P, Rogers JG. Impact of the 2018 UNOS Heart Transplant Policy Changes on Patient Outcomes. JACC Heart Fail. 2023;11(5):491-503. doi:10.1016/j.jchf.2023.01.009
2:  Shore S, Golbus JR, Aaronson KD, Nallamothu BK. Changes in the United States Adult Heart Allocation Policy: Challenges and Opportunities. Circ Cardiovasc Qual Outcomes. 2020;13(10):e005795. doi:10.1161/CIRCOUTCOMES.119.005795
3:  Copeland H, Knezevic I, Baran DA, et al. Donor heart selection: Evidence-based guidelines for providers. J Heart Lung Transplant. 2023;42(1):7-29. doi:10.1016/j.healun.2022.08.030
4: Kittleson MM. Management of the sensitized heart transplant candidate. Curr Opin Organ Transplant. 2023;28(5):362-369. doi:10.1097/MOT.0000000000001096
5:  Kharawala A, Nagraj S, Seo J, et al. Donation After Circulatory Death Heart Transplant: Current State and Future Directions. Circ Heart Fail. 2024;17(7):e011678. doi:10.1161/CIRCHEARTFAILURE.124.011678
6: Siddiqi HK, Trahanas J, Xu M, et al. Outcomes of Heart Transplant Donation After Circulatory Death. J Am Coll Cardiol. 2023;82(15):1512-1520. doi:10.1016/j.jacc.2023.08.006
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33min
November 20, 2025435. Atrial Fibrillation: Chronic Management of Atrial Fibrillation with Dr. Edmond Cronin
CardioNerds (Dr. Kelly Arps, Dr. Naima Maqsood, and Dr. Elizabeth Davis) discuss chronic AF management with Dr. Edmond Cronin. This episode seeks to explore the chronic management of atrial fibrillation (AF) as described by the 2023 ACC/AHA/ACCP/HRS Guideline for the Diagnosis and Management of Atrial Fibrillation: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. The discussion covers the different AF classifications, symptomatology, and management including medications and invasive therapies. Importantly, the episode explores current gaps in knowledge and where there is indecision regarding proper treatment course, as in those with heart failure and AF. Our expert, Dr. Cronin, helps elucidate these gaps and apply guideline knowledge to patient scenarios. Audio editing for this episode was performed by CardioNerds intern Dr. Bhavya Shah.
Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values.
CardioNerds Atrial Fibrillation Page
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Pearls
Review the guidelines- Catheter ablation is a Class I recommendation for select patient groups
Appropriately recognize AF stages- preAF conditions, symptomatology, classification system (paroxysmal, persistent, long-standing persistent, permanent)
Be familiar with the EAST-AFNET4 trial, as it changed the approach of rate vs rhythm control
Understand treatment approaches- lifestyle modifications, management of comorbidities, rate vs rhythm control medications, cardioversion, ablation, pulmonary vein isolation, surgical MAZE
Sympathize with patients- understand their treatment goals
Notes
Notes: Notes drafted by Dr. Davis.  
What are the stages of atrial fibrillation?
The stages of AF were redefined in the 2023 guidelines to better recognize AF as a progressive disease that requires different strategies at the different therapies
Stage 1 At Risk for AF: presence of modifiable (obesity, lack of fitness, HTN, sleep apnea, alcohol, diabetes) and nonmodifiable (genetics, male sex, age) risk factors associated with AF
Stage 2 Pre-AF: presence of structural (atrial enlargement) or electrical (frequent atrial ectopy, short bursts of atrial tachycardia, atrial flutter) findings further pre-disposing a patient to AF
Stage 3 AF: patient may transition between these stages
Paroxysmal AF (3A): intermittent and terminates within ≤ 7 days of onset
Persistent AF (3B): continuous and sustained for > 7 days and requires intervention
Long-standing persistent AF (3C): continuous for > 12 months
Successful AF ablation (3D): freedom from AF after percutaneous or surgical intervention
Stage 4 Permanent AF: no further attempts at rhythm control after discussion between patient and clinician
The term chronic AF is considered obsolete and such terminology should be abandoned
What are common symptoms of AF?
Symptoms vary with ventricular rate, functional status, duration, and patient perception
May present as an embolic complication or heart failure exacerbation
Most commonly patients report palpitations, chest pain, dyspnea, fatigue, or lightheadedness. Vague exertional intolerance is common
Some patients also have polyuria due to increased production of atrial natriuretic peptide
Less commonly can present as tachycardia-associated cardiomyopathy or syncope
Cardioversion into sinus rhythm may be diagnostic to help determine if a given set of symptoms are from atrial fibrillation to help guide the expected utility of more aggressive rhythm control strategies.
What are the current guidelines regarding rhythm control and available options?
COR-LOE 1B: In patients with reduced LV function and persistent (or high burden) AF, a trial of rhythm control should be recommended to evaluate whether AF is contributing to the reduced LV function
COR-LOE 2a-B: In patients with reduced LV function and persistent (or high burden) AF, a trial of rhythm control should be recommended to evaluate whether AF is contributing to the reduced LV function. In patients with a recent diagnosis of AF (<1 year), rhythm control can be useful to reduce hospitalizations, stroke, and mortality. In patients with AF and HF, rhythm control can be useful for improving symptoms and improving outcomes, such as mortality and hospitalizations for HF and ischemia. In patients with AF, rhythm-control strategies can be useful to reduce the likelihood of AF progression.
COR-LOE 2b-C: In patients with AF where symptoms associated with AF are uncertain, a trial of rhythm control (eg, cardioversion or pharmacological therapy) may be useful to determine what if any symptoms are attributable to AF.
COR-LOE 2b-B: In patients with AF, rhythm-control strategies may be useful to reduce the likelihood of development of dementia or worsening cardiac structural abnormalities.
While both rate and rhythm control can improve AF symptoms, several studies (such as AF-CHF) show improved quality of life with rhythm control
EAST-AFNET 4 was significant in that it showed rhythm control was associated with a 25% reduction in the combined endpoint of mortality rate, stroke, and hospitalizations due to HF or ACS
Acute rhythm control can be achieved with electrical or pharmacological cardioversion. Electrical is more effective and faster than pharmacological and is preferred for patients with hemodynamic instability attributable to AF. However, both approaches involved considerations for anticoagulation and thromboembolic risk. Pharmacologic options for cardioversion include ibutilide, amiodarone, flecainide, propafenone, procainamide, dofetilide, and sotalol.
COR-LOE 1-A: In patients with symptomatic AF in whom antiarrhythmic drugs have been ineffective, contraindicated, not tolerated or not preferred, and continued rhythm control is desired, catheter ablation is useful to improve symptoms.
AF ablation is also a suitable first-line option in some patients with paroxysmal AF to reduce recurrence and burden. Patient selection is important. Younger patients, those with minimal atrial enlargement, less myocardial fibrosis, and less persistent forms are more likely to have successful ablations, meaning less likely to have recurrence of AF after ablation.
HFrEF patients derive greater benefit than others from AF ablation in terms of improved functional status, LV function, and cardiovascular outcomes
Surgical ablation can be considered in those undergoing cardiac surgery for some other etiology such as valve surgery or CABG and is associated with increased survival, but some risk of pacemaker placement and renal dysfunction
How would you monitor for AF recurrence in post-ablation or cardioversion? Is there a role for monitoring in every patient?
Cardiac monitoring may be advised to AF patients for various reasons, such as for detecting recurrences, screening, or response to therapy
Long-term surveillance to detect recurrent AF can be beneficial and can be accomplished by various modalities, including wearable devices, smart watches, random monitoring (Holter, event, mobile telemetry), and implantable loop recorders. This is especially helpful in those who had AF-induced cardiomyopathy, especially if their LVEF recovered after rate/rhythm control. This is a population in whom recurrence of AF would want to be promptly noted and addressed.
Loop recorders can also be helpful in detecting subclinical AF or in patients with stroke or TIA of undetermined cause (COR-LOE 2a-B)
What AF burden warrants intervention?
It is important to recognize that AF is a chronic condition and tends to recur, so treatment often is focused on reducing risk of recurrence
Patient-clinician shared decision making is important when deciding when/how to intervene, as there is no cut-off for “significant” burden (COR-LOE 1-B)
What are some options for antiarrhythmic drugs and their characteristics?
Antiarrhythmic drugs are reasonable for long-term maintenance of sinus rhythm for patients with AF who are not candidates for, or decline, catheter ablation, or who prefer antiarrhythmic therapy
Amiodarone can be used in patients with or without HFrEF, as opposed to many other anti-arrhythmics that are (relatively) contraindicated in HFrEF or should be used with caution in such patients, such as flecainide, propafenone, dronedarone, and sotalol. However, due to its adverse effects and multiple drug interactions, is should be used only in patients in which other antiarrhythmic drugs are contraindications, ineffective, or not preferred. Dofetilide can also be used in patients with HFrEF.
In patients on amiodarone, labs should be checked regularly for thyroid, liver and kidney functions. There is also a role for pulmonary function testing and chest x-rays to monitor for pulmonary fibrosis, but frequency is not clearly established. It should be noted that amiodarone-induced lung toxicity occurs between 6 months and 2 years of use.
Flecainide is well tolerated, but is contraindicated in patients with significant coronary artery disease and possibly structural heart disease in general. It can also lead to the development of atrial flutter.
Dofetilide and sotalol require regular renal function monitoring and QTC monitoring
When should AV node ablation (AVNA) be considered?
In patients with AF and uncontrolled rapid ventricular response refractory to rate-control medications (who are not candidates for or in whom rhythm control has been unsuccessful), AVNA can be useful to improve symptoms and QOL (COR-LOE 2a-B)
AVNA is effective for rate control and does not require continuation of medications; however, patients become dependent on pacing and lifelong pacemaker implantation, and the potential for device complications
AVNA does not prevent progression or recurrence of AF
The type of device is dependent on patient comorbidities but the advent of conduction system pacing may improve outcomes in these patients compared with RV pacing.
What are some recommendations for managing atrial fibrillation in the perioperative period?
In patients with AF (excluding those with recent stroke or TIA, or a mechanical valve) and on oral anticoagulation with either warfarin or DOAC who are scheduled to undergo an invasive procedure or surgery, temporary cessation of oral anticoagulation without bridging anticoagulation is recommended (COR-LOE 1-B)
In patients with AF on DOAC that has been interrupted for an invasive procedure or surgery, in general, resumption of anticoagulation the day after low bleeding risk surgery and between the evening of the second day and the evening of the third day after high bleeding risk surgery is reasonable, as long as hemostasis has been achieved and further bleeding is not anticipated (COR-LOE 2a-B)
Preop prophylaxis to prevent AF after cardiac surgery with either beta blocker or amiodarone shows mixed benefit and carries a 2a-B recommendation; however, beta blocker is a class 1-A recommendation in patients who do develop AF in the postop period
It should be noted that patients who develop AF in the setting of an acute illness or surgery are at risk of recurrence
References
Joglar, J, Chung, M. et al. 2023 ACC/AHA/ACCP/HRS Guideline for the Diagnosis and Management of Atrial Fibrillation: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. JACC. 2024 Jan, 83 (1) 109–279. https://doi.org/10.1016/j.jacc.2023.08.017
Fuster F, Rydén L, et al. ACC/AHA/ESC Guidelines for the Management of Patients With Atrial Fibrillation: Executive Summary A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and the European Society of Cardiology Committee for Practice Guidelines and Policy Conferences (Committee to Develop Guidelines for the Management of Patients With Atrial Fibrillation) Developed in Collaboration With the North American Society of Pacing and Electrophysiology. Circulation. 2001 Oct, 104 (17). https://doi.org/10.1161/circ.104.17.2118
Kirchhof P, Camm A, et al. Early Rhythm-Control Therapy in Patients with Atrial Fibrillation. N Engl J Med. 2020 Aug, 383 (14) 1305-1416. DOI: 10.1056/NEJMoa2019422
Olshansky, B, Rosenfeld, L, Warner, A. et al. The Atrial Fibrillation Follow-up Investigation of Rhythm Management (AFFIRM) study: Approaches to control rate in atrial fibrillation. JACC. 2004 Apr, 43 (7) 1201–1208.https://doi.org/10.1016/j.jacc.2003.11.032
Whitlock R, Belley-Cote E, et al. Left Atrial Appendage Occlusion during Cardiac Surgery to Prevent Stroke. N Engl J Med. 2021 May, 384 (22) 2081-2091. DOI: 10.1056/NEJMoa2101897
Kirchhof P, Toennis T, et al. Anticoagulation with Edoxaban in Patients with Atrial High-Rate Episodes. N Engl J Med. 2023 Aug, 389 (13) 1167-1179. DOI: 10.1056/NEJMoa2303062
Healey J, Lopes R, et al. Apixaban for Stroke Prevention in Subclinical Atrial Fibrillation. N Engl J Med. 2023 Nov, 390 (2) 107-117. DOI: 10.1056/NEJMoa2310234
Roy D, Talajic M, et al. Rhythm Control versus Rate Control for Atrial Fibrillation and Heart Failure. N Engl J Med. 2008 Jun, 358 (25) 2667-2677. DOI: 10.1056/NEJMoa0708789
Gillinov A, Bagiella E, et al. Rate Control versus Rhythm Control for Atrial Fibrillation after Cardiac Surgery. N Engl J Med. 2016 Mar, 374 (20) 1911-1921. DOI: 10.1056/NEJMoa1602002
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