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Explore every episode of the podcast Cardionerds: A Cardiology Podcast
Dive into the complete episode list for Cardionerds: A Cardiology Podcast. Each episode is cataloged with detailed descriptions, making it easy to find and explore specific topics. Keep track of all episodes from your favorite podcast and never miss a moment of insightful content.
| Title | Pub. Date | Duration | |
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| 475. Case Report: The Walls Have a Story: Rapidly Progressive AL Cardiac Amyloidosis – Georgetown/Washington Hospital Center | 29 Oct 2026 | 00:55:13 | |
CardioNerds guest hosts Dr. Apoorva Gangavelli and Dr. Georgia Vasilakis, alongside Dr. Flavia Tejada, Dr. Ahmad Ahmad, and Dr. Blanca Simon Frances from MedStar Washington Hospital Center/Georgetown University for a case discussion on rapidly progressive heart failure and the urgency of recognizing infiltrative cardiomyopathy. They discuss a 65-year-old man with newly diagnosed HFrEF and CKD who presented with acute decompensated heart failure, low-voltage ECG, concentric LV thickening, renal dysfunction, and abnormal lambda free light chains. His course was complicated by PEA arrest when laid supine, cardiogenic shock physiology, bilateral pleural effusions, and biopsy-confirmed AL cardiac amyloidosis. The episode focuses on clinical red flags, diagnostic algorithms, hemodynamic fragility, and why suspected AL amyloidosis is a hematologic and cardiac emergency. Expert commentary is provided by Dr. Ajay Kadakkal. Audio editing for this episode was performed by CardioNerds Intern, Dr. Julia Marques Fernandes. “To study the phenomena of disease without books is to sail an uncharted sea, while to study books without patients is not to go to sea at all.” – Sir William Osler. CardioNerds thank the patients and their loved ones whose stories teach us the Art of Medicine and support our Mission to Democratize Cardiovascular Medicine. US Cardiology Review is now the official journal of CardioNerds! Submit your manuscript here. CardioNerds Case Reports Page CardioNerds Journal Club
Notes were drafted by Dr. Flavia Tejada Frisancho, Dr. Ahmad Ahmad and Dr. Blanca Simon Frances. 1. What clinical features should raise suspicion for cardiac amyloidosis in a patient presenting with heart failure?
This case highlights how patients with cardiac amyloidosis can be extremely hemodynamically fragile. 5. What management principles are important once AL cardiac amyloidosis is suspected or confirmed?
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| 474. Cardiothoracic Surgery in Pulmonary Embolism with Dr. Joshua Goldberg | 26 Oct 2026 | 00:15:11 | |
In this episode, the CardioNerds (Dr. Dinu Balanescu, Dr. Billy Joe Mullinax, and Dr. Akiva Rosenzveig) take a deep dive into the world of the surgical management of pulmonary embolism (PE) with faculty expert, Dr. Joshua Goldberg. We start from the pathophysiology of PE and its impact on right ventricular, and thereby left ventricular, hemodynamics. We then discuss the management of high-risk PE and where catheter-based therapies, surgical management and mechanical circulatory support via ECMO find their roles. Dr. Goldberg also provides a historical overview of the evolution of the surgical management of PE. We conclude by briefly discussing the management of chronic thromboembolic pulmonary hypertension (CTEPH) as a long-term complication of PE. Audio editing for this episode was performed by CardioNerds Intern, Dr. Julia Marques Fernandes. NOTE: this episode was recorded before the publication of the 2026 AHA/ACC Acute PE Guidelines. Dr. Dinu Balanescu and Dr. Billy-Joe Mullinax are Co-chairs for the CardioNerds PE Series, developed in collaboration with the PERT Consortium. CardioNerds Pulmonary Embolism Page CardioNerds Journal Club
Notes: Notes drafted by Dr. Akiva Rosenzveig.
Sudden increase in RV afterload which leads to RV volume and pressure overload which leads to neurohormonal activation, increased oxygen demand and RV ischemia, reduced RV contractility leading to reduced left ventricular (LV) preload and reduced cardiac output
We need to focus on not only treating the clot but supporting the RV concurrently. This is analogous to supporting the LV with mechanical circulatory support while also opening the culprit coronary lesion in acute myocardial infarction related cardiogenic shock (AMI-CS). The reason why High-risk/Massive PE has historically had poor outcomes may be because treatment modalities focused on treating the clot and not supporting the RV as well.
With the increased role of catheter-based therapies, the role of surgery is narrowing to a more nuanced patient population. Surgery should be considered when we don’t have other treatment options. It remains especially useful in more subacute clots where it is more difficult to extract with catheter-based interventions. In those cases, surgical pulmonary embolectomy can be useful as you have direct visualization of the pulmonary arteries and its branches.
In the early 1900’s, the Trendelenburg procedure was performed but had a very high mortality rate. This was because they waited for the patients to decompensate and then once the patient was peri-arrest, they would take them urgently to the operating room, snare the aorta and pulmonary artery and open the artery and remove the clot. By manipulating the PA in this way they detrimentally increased the RV afterload on an already failing RV. In the 1930’s, John Gibbon started working on developing cardiopulmonary bypass. Now, surgeons can put the patient on cardiopulmonary bypass and create incisions on both the left and right pulmonary arteries to extract the clot.
Contrary to what we are used to hearing, the lack of a saddle PE shouldn’t be comforting. The more distal clot is more concerning as that’s where there is more significant flow resistance. The saddle embolus takes up a small proportion of the PA cross-sectional area and, therefore, the flow obstruction does not come from there. References:
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| 473. ACS Guidelines Question #11 with Dr. Venu Menon | 23 Oct 2026 | 00:10:31 | |
This episode is part of our comprehensive Decipher the Guidelines Series covering the 2025 ACC/AHA/ACEP/NAEMSP/SCAI Guideline for the Management of Patients With Acute Coronary Syndromes. The following question refers to Section 8.2 of the 2025 ACS Guidelines. The question is asked by Johns Hopkins pre-medical undergraduate and CardioNerds Academy Intern Joshua Khorsandi, answered first by University of Wisconsin cardiology fellow and member of the CardioNerds Interventional Cardiology Council Dr. Shikha Jha, and then by expert faculty Dr. Venu Menon. Dr. Menon is the Section Head of Clinical Cardiology, Director of the Cardiac Intensive Care Unit, and Program Director of Cardiology Fellowship at the Cleveland Clinic. He is the Mehdi Razavi Endowed Chair and Professor of Medicine at the Cleveland Clinic Lerner College of Medicine. He was also a member of the 2025 ACS Guidelines writing committee. A 58-year-old man with a past medical history of hypertension, hyperlipidemia, schizophrenia, atrial fibrillation (on apixaban), and prior tobacco use presents to the emergency department with chest tightness. ECG shows ST elevations in leads II, III, and aVF with reciprocal depressions in leads I and aVL. Emergency coronary angiography demonstrates 100% occlusion of the proximal RCA, and he undergoes PCI. Transthoracic echocardiogram afterward reveals normal LV function with inferior hypokinesis. On day 2, the patient experienced lightheadedness and has frequent melanic stools. His hemoglobin returns at 6 gm/dL (initial hemoglobin 11 g/dL). He undergoes EGD and colonoscopy with successful endoscopic treatment of a small gastric ulcer. True or False: it is reasonable to administer 3-4 units of packed red blood cells for a goal Hb ≥ 10 g/dL. True False Explanation The correct answer is True – it would be reasonable to administer 3-4 units of packed red blood cells for a goal Hb ≥ 10 g/dL. Anemia is common in patients with ACS and is associated with worse short- and long-term outcomes. Anemia is associated with adverse outcomes irrespective of whether the anemia is chronic and due to comorbid conditions, or acute and the result of bleeding related to antithrombotic therapy and/or invasive procedures. The adverse effects of anemia may be due to decreased myocardial oxygen delivery, increased myocardial oxygen demand due to increased cardiac output, or the avoidance of potentially beneficial antithrombotic drugs and/or procedures. Randomized trials in medically ill patients and those undergoing cardiac surgery have demonstrated similar or better outcomes with a restrictive transfusion strategy (targeting a blood hemoglobin level around 8 g/dL) than with a liberal transfusion strategy (targeting a blood hemoglobin level around 10 g/dL). However, randomized trial evidence for populations with ACS suggests possible clinical benefit for a more liberal transfusion strategy targeting a hemoglobin level above 10 g/dL compared with targeting a hemoglobin level above 7 g/dL to 8 g/dL The MINT (Myocardial Ischemia and Transfusion) trial randomly assigned 3,504 patients with acute STEMI or NSTEMI and anemia with a blood hemoglobin level of <10 g/dL (13% with recent bleeding) to a restrictive transfusion strategy (transfusing if the hemoglobin level was <7-8 g/dL) or a liberal transfusion strategy (transfusing if the hemoglobin level was <10 g/dL). Patients were ineligible for enrollment if they had uncontrolled bleeding, were receiving palliative treatment, or were scheduled to have cardiac surgery. Transfusion could be delayed for patients with volume overload or until the day of dialysis in patients with end-stage renal disease. The primary outcome of 30-day death or recurrent MI occurred in 16.9% of patients in the restrictive strategy and 14.5% of patients in the liberal strategy (relative risk, 1.15 [95% CI, 0.99-1.34]; P = 0.07). Death occurred in 9.9% of patients in the restrictive strategy and 8.3% of patients in the liberal strategy (relative risk, 1.19 [95% CI, 0.94-1.49]), and cardiac death occurred in 5.5% of patients in the restrictive strategy and 3.2% of patients in the liberal strategy (relative risk, 1.74 [95% CI, 1.26-2.40]). Although the MINT trial did not demonstrate a statistically significant reduction in its primary endpoint, the results suggest that a liberal blood transfusion strategy targeting a hemoglobin level around 10 g/dL may provide short-term clinical benefit over a restrictive transfusion strategy targeting a hemoglobin level above 7 g/dL or 8 g/dL in patients with AMI and anemia. The 2025 ACS guidelines give a Class 2b, LOE B-R recommendation for a liberal transfusion strategy targeting a hemoglobin of >10 g/dL in patients with ACS and acute or chronic anemia to reduce cardiovascular events. Main Takeaway In patients with ACS and acute or chronic anemia, blood transfusion to achieve a hemoglobin level of more than 10 g/dL may be reasonable to reduce cardiovascular events. Guideline Loc. Section 10.2 | |||
| 471. ACS Guidelines Question #9 with Dr. Venu Menon | 21 Oct 2026 | 00:15:03 | |
This episode is part of our comprehensive Decipher the Guidelines Series covering the 2025 ACC/AHA/ACEP/NAEMSP/SCAI Guideline for the Management of Patients With Acute Coronary Syndromes. The following question refers to Section 9.2 of the 2025 ACS Guidelines. The question is asked by Johns Hopkins pre-medical undergraduate and CardioNerds Academy Intern Joshua Khorsandi, answered first by University of Wisconsin cardiology fellow and member of the CardioNerds Interventional Cardiology Council Dr. Shikha Jha, and then by expert faculty Dr. Venu Menon. Dr. Menon is the Section Head of Clinical Cardiology, Director of the Cardiac Intensive Care Unit, and Program Director of Cardiology Fellowship at the Cleveland Clinic. He is the Mehdi Razavi Endowed Chair and Professor of Medicine at the Cleveland Clinic Lerner College of Medicine. He was also a member of the 2025 ACS Guidelines writing committee. A 74-year-old man with past medical history significant for hyperlipidemia, obstructive sleep apnea, hypertension, tobacco use, type 2 diabetes mellitus, and chronic obstructive pulmonary disease presents to the emergency department with two days of chest tightness and worsening shortness of breath at rest. He is found to have ST elevations in the anterolateral leads. Emergent coronary angiography demonstrates 90% stenosis of proximal to mid LAD and he is treated with two drug-eluting stents. Transthoracic echocardiograms during hospitalization showed an LVEF of 25% with anterior and apical wall motion abnormalities. He is discharged on dual antiplatelet therapy along with metoprolol, valsartan, spironolactone, SGLT2 inhibitor, and rosuvastatin. At follow-up 3 months later, he reports home BP readings in 90s/50s mm Hg with intermittent shortness of breath and lightheadedness. Blood pressure in the office is 92/54 mmHg. ECG shows normal sinus rhythm with anterior Q waves, a narrow QRS, and no acute ST-segment or T-wave changes. Repeat transthoracic echocardiogram shows an LVEF of 30%. What is the most appropriate next step? A Switch valsartan to sacubitril-valsartan B Consider implantable cardioverter defibrillator (ICD) placement C Consider cardiac resynchronization therapy D Consider additional cardiac rehabilitation sessions Explanation The correct answer is B – consider implantable cardioverter defibrillator (ICD) placement. Generally, arrhythmic complications increase both morbidity and mortality rates in patients after ACS. Patients who present with AMI with reduced LVEF (≤40%) have increased risk of new-onset atrial fibrillation, bradyarrhythmias, and ventricular arrhythmias. Ventricular arrhythmias are common after ACS and more common in patients with reduced LVEF. The MADIT II trial (Multicenter Automatic Defibrillator Implantation Trial) demonstrated a 31% reduction in all-cause mortality (HR, 0.69 [95% CI, 0.51-0.93]) for prophylactic implantation of a cardiac defibrillator in patients with an LVEF ≤30% who were at least 30 days after MI or 3 months after revascularization for MI and had an anticipated life expectancy longer than 1 year. A mortality benefit for prophylactic ICD implantation has also been shown in patients with an LVEF ≤35% and New York Heart Association class II or III HF symptoms, as well as in patients with inducible ventricular tachycardia or ventricular fibrillation and an LVEF ≤40%. This patient has an LVEF of <30% with at least NYHA class II symptoms, now 90 days post-revascularization for MI, which means he is a candidate for ICD placement for primary prevention of sudden cardiac death. Answer choice A is incorrect because hypotension in this patient is a limitation to adding any more guideline-directed medical treatment, such as sacubitril/valsartan. This patient does not meet criteria for CRT implantation given his narrow QRS complex, so answer choice C is incorrect. Additional cardiac rehabilitation sessions (answer choice D) would not treat patients’ ongoing cardiomyopathy and SCD risk. The 2025 ACS guidelines give a Class 1, LOE A recommendation for ICD implantation in patients post-MI with LVEF ≤40% at least 40 days post-MI and at least 90 days post-revascularization to reduce mortality. In addition, in patients post-ACS, ICD implantation is reasonable in patients with clinically relevant ventricular arrhythmias >48 hours and within 40 days post-MI to improve survival (LOE 2a, LOE C-EO). Some may wonder about the use of a temporary wearable cardioverter-defibrillator after the initial presentation. In the VEST trial, this strategy did not significantly reduce the primary endpoint, a composite of sudden death or death from ventricular tachyarrhythmias at 90 days) in patients with AMI and LVEF ≤ 35%. Notably, there was a lower incidence of death from any cause in the wearable vest group compared to the no-device group and overall, greater benefit was seen in those who were compliant with the device. As such, use of a wearable cardioverter-defibrillator could be considered in high-risk patients with reduced LVEF as a bridge to consideration for the need for an ICD. Per the guidelines, in patients early after MI, usefulness of a temporary wearable cardioverter-defibrillator is uncertain in patients with an LVEF ≤35% to improve survival (COR 2b, LOE B-R). Main Takeaway In patients post MI, implantable cardioverter defibrillator (ICD) implantation is recommended in selected patients with an LVEF of less than or equal to 40% at least 40 days post MI and at least 90 days post revascularization to reduced death. Guideline Loc. Section 9.2 | |||
| 470. ACS Guidelines Question #8 with Dr. Venu Menon | 20 Oct 2026 | 00:06:48 | |
This episode is part of our comprehensive Decipher the Guidelines Series covering the 2025 ACC/AHA/ACEP/NAEMSP/SCAI Guideline for the Management of Patients With Acute Coronary Syndromes. The following question refers to Section 9.1 of the 2025 ACS Guidelines. The question is asked by Johns Hopkins pre-medical undergraduate and CardioNerds Academy Intern Joshua Khorsandi, answered first by Washington University cardiology fellow and member of the CardioNerds Interventional Cardiology Council Dr. Colin Martz, and then by expert faculty Dr. Venu Menon. Dr. Menon is the Section Head of Clinical Cardiology, Director of the Cardiac Intensive Care Unit, and Program Director of Cardiology Fellowship at the Cleveland Clinic. He is the Mehdi Razavi Endowed Chair and Professor of Medicine at the Cleveland Clinic Lerner College of Medicine. He was also a member of the 2025 ACS Guidelines writing committee. A 65-year-old female with no significant prior cardiac history presents to the emergency department with 3 days of chest tightness associated with shortness of breath. ECG demonstrates anterior ST-segment elevation with reciprocal depressions. Coronary angiography reveals 100% occlusion of the mid left anterior descending artery. She undergoes PCI of the LAD. Two days later, she develops worsening shortness of breath. Her HR is 115 and BP 95/50. Lungs are clear on auscultation. Cardiac examination is significant for a harsh systolic murmur at the left sternal border with a palpable thrill. Transthoracic echocardiogram showed ventricular septal rupture with left-to-right shunt and Qp:Qs estimated at 2.5:1. What is the best next step? A Continue medical management B Proceed with repeat coronary angiogram and right heart catheterization with shunt run C Percutaneous ventricular septal defect closure D Intra-aortic balloon pump placement and cardiac surgical consultation Explanation The correct answer is D – placement of an intra-aortic balloon pump and CT surgical consultation. Timely reperfusion therapy has reduced the incidence of mechanical complications (ventricular septal rupture, mitral valve insufficiency due to papillary muscle infarction or rupture, or free wall rupture) after AMI. Although occasionally found incidentally, mechanical complications commonly present with recurrent or refractory chest pain or a new murmur accompanied by disproportionate heart failure, cardiogenic shock, or sudden cardiac death on clinical presentation within the first week after an AMI. Medical therapy alone is associated with high risk of early death; definitive surgical correction is frequently the treatment of choice. Mortality rates with surgery are highest in subjects with cardiogenic shock and in those requiring early emergency/urgent intervention after AMI. Observed mortality rates following delayed surgery (>7 days) are lower but patient selection and survivor bias contribute to this observation. The 2025 ACS guidelines give a Class 2a, LOE B-NR recommendation for the use of short-term MCS devices in patients with mechanical complications of ACS for hemodynamic stabilization and bridge to surgery. The availability of temporary MCS devices has led to increasing trends for delayed surgery due to concerns for the initial degree of extensive tissue destruction. Delayed surgical intervention may enable hemodynamic stabilization, lead to recovery of end-organ injury, and promote infarct tissue healing and maturation that could facilitate definitive repair. Percutaneous approaches toward repair have been used in patients with prohibitive surgical risk or contraindications to surgery as a primary or temporizing option in the setting of acute mitral regurgitation and ventricular septal rupture and remain an evolving area of investigation. This patient is not at prohibitive risk for surgery. Select patients with mechanical complications of ACS may be considered for cardiac transplantation or durable LVAD as a primary or bailout treatment strategy to improve survival. No RCTs evaluate the role of transfer of patients with mechanical complications after MI to dedicated centers with cardiac surgical expertise. Although overall surgical mortality is approximately 40%, it remains the treatment strategy of choice. Hemodynamic deterioration is unpredictable and can be precipitous in previously stable subjects. Consequently, transfer to a Level 1 cardiac intensive care unit (CICU) with access to various temporary MCS devices and multidisciplinary experienced teams of surgical, interventional, HF, and palliative care specialists is recommended. The guidelines give a Class 1, LOE C recommendation for management of patients with mechanical complications of ACS at centers with cardiac surgical expertise. Main Takeaway Patients with mechanical complications of ACS should be managed in a center with cardiac surgical expertise. In such patients, short-term MCS devices are reasonable for hemodynamical stabilization as a bridge to surgery. Guideline Loc. Section 9.1, Figure 9
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| 469. ACS Guidelines Question #7 with Dr. Venu Menon | 19 Oct 2026 | 00:05:02 | |
This episode is part of our comprehensive Decipher the Guidelines Series covering the 2025 ACC/AHA/ACEP/NAEMSP/SCAI Guideline for the Management of Patients With Acute Coronary Syndromes. The following question refers to Section 8.2 of the 2025 ACS Guidelines. The question is asked by Johns Hopkins pre-medical undergraduate and CardioNerds Academy Intern Joshua Khorsandi, answered first by University of Wisconsin cardiology fellow and member of the CardioNerds Interventional Cardiology Council Dr. Shikha Jha, and then by expert faculty Dr. Venu Menon. Dr. Menon is the Section Head of Clinical Cardiology, Director of the Cardiac Intensive Care Unit, and Program Director of Cardiology Fellowship at the Cleveland Clinic. He is the Mehdi Razavi Endowed Chair and Professor of Medicine at the Cleveland Clinic Lerner College of Medicine. He was also a member of the 2025 ACS Guidelines writing committee. A 72-year-old gentleman with past medical history significant for hypertension, hyperlipidemia, type 2 diabetes, and tobacco use is brought to the ED with chief complaint of chest tightness. He is found to have ST elevations in leads V1 to V4 and is taken for emergency coronary angiography, which demonstrates 99% proximal LAD occlusion. During the procedure, he becomes hypotensive (BP 74/55 mm Hg) and tachycardic (HR 122 bpm). Norepinephrine is initiated. Right heart catheterization demonstrates elevated left and right-sided filling pressures with low cardiac index. Besides immediate revascularization, which of the following would be the best next step? A Cannulate for VA-ECMO B Placement of microaxial intravascular flow pump C Administration of intravenous fluid D Placement of an intraaortic balloon pump Explanation The correct answer is B – Placement of microaxial intravascular flow pump. Cardiogenic shock is estimated to occur in approximately 10% of patients with STEMI and is associated with an early mortality rate of 40% to 50%. Several types of devices for temporary mechanical circulatory support (MCS) are available and have been studied in patients with cardiogenic shock, with variable efficacy and increased risk of vascular complications. IABP counterpulsation improves coronary perfusion and reduces cardiac afterload. It is relatively easy to use and has a smaller insertion profile (8 French), which is associated with lower rates of vascular access site complications when compared with other MCS devices. Left ventricular percutaneous microaxial flow pumps unload the LV by draining blood from the LV and pumping it to the ascending aorta. They are dependent on adequate right ventricular function to fill the LV and require adequate oxygenation of blood. VA-ECMO provides both blood flow and gas exchange, providing full cardiopulmonary bypass, but increases afterload. Randomized trials of MCS devices remain challenging to conduct due to relative lack of equipoise on the part of treating physicians, leading to selective patient enrollment and limiting the generalizability of study results. The DanGer-Shock randomized 360 patients presenting with STEMI and cardiogenic shock of <24 hours duration to either microaxial flow pump or standard of care. The trial demonstrated a 26% reduction of all-cause mortality at 180 days (HR, 0.74 [95% CI, 0.55-0.99]; P = 0.04; absolute risk reduction, 12.7%; number needed to treat = 8) compared with standard of care. However, this came at the cost of increased risk of complications like bleeding, limb ischemia and renal replacement therapy in the microaxial flow pump group. In light of this and other trial data, the guidelines give a Class 2a, LOE B recommendation for the use of a microaxial intravascular flow pump in patients with STEMI complicated by severe or refractory cardiogenic shock to reduce mortality. These patients should be noncomatose and have adequate peripheral vasculature to accommodate large-bore access. Answer choice A is not correct as the use of VA-ECMO cannulation in this setting has been given a class 3 recommendation for lack of benefit. VA-ECMO has not been shown to reduce death compared with medical therapy alone in patients with cardiogenic shock in the setting of MI but increases major bleeding and vascular complications. In the absence of severe concomitant respiratory failure requiring oxygenation support, this strategy is not indicated in the patient described here. Further fluid resuscitation (answer choice C) is not likely to be helpful as right heart catheterization demonstrated elevated filling pressures. Placement of an intraaortic balloon pump (IABP) is not the next best step. The IABP-SHOCK II trial, which randomized patients with acute MI and severe cardiogenic shock to IABP or medical therapy showed no differences at 30 days or at long-term follow-up in the primary outcome of all-cause death. The use of IABP has a class 3 recommendation for lack of benefit in patients with cardiogenic shock secondary to acute myocardial infarction. Main Takeaway In selected patients with STEMI and severe or refractory cardiogenic shock, insertion of microaxial intravascular flow pump is reasonable to reduce death in a noncomatose patient with adequate vascular access. Guideline Loc. Section 8.2
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| 468. 2026 Acute Pulmonary Embolism Guidelines with Dr. Mark Creager | 12 Oct 2026 | 00:44:25 | |
CardioNerds (Drs. Billy Joe Mullinax, Dinu Balanescu, and Saahil Jumkhawala) discuss the 2026 American Heart Association (AHA)/American College of Cardiology (ACC) multisocietal guidelines for the evaluation and management of acute pulmonary embolism (PE) with Dr. Mark Creager, Director Emeritus of the Heart and Vascular Center at Dartmouth Health, past president of the AHA, and Chair of the Writing Committee for the 2026 AHA/ACC PE Guidelines. Audio editing by CardioNerds intern, Dr. Patrick Pekyi-Boateng. Pulmonary embolism is one of the most rapidly evolving conditions in cardiovascular medicine. The 2026 AHA/ACC multisocietal guideline, endorsed by ten professional societies, is the first de novo comprehensive guideline dedicated exclusively to acute PE in adults. It introduces a new five-category A-E risk classification system, a Class I recommendation for the Pulmonary Embolism Response Team (PERT), updated guidance on anticoagulation and advanced reperfusion therapies, and a structured framework for post-PE follow-up and chronic thromboembolic pulmonary hypertension (CTEPH) screening. This episode walks through all of it, using a high-risk clinical case as the backbone. Dr. Dinu Balanescu and Dr. Billy-Joe Mullinax are Co-chairs for the CardioNerds PE Series, developed in collaboration with the PERT Consortium. CardioNerds Pulmonary Embolism Page CardioNerds Journal Club
Notes drafted by Dr. Saahil Jumkhawala.
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| 467. ACS Guidelines Question #6 with Dr. Binita Shah | 23 Sep 2026 | 00:04:31 | |
This episode is part of our comprehensive Decipher the Guidelines Series covering the 2025 ACC/AHA/ACEP/NAEMSP/SCAI Guideline for the Management of Patients With Acute Coronary Syndromes. The following question refers to Section 4.4 of the 2025 ACS Guidelines. The question is asked by Thomas Jefferson medical student and CardioNerds Academy Intern Dr. Grace Qiu, answered first by University of Miami cardiology fellow and member of the CardioNerds Interventional Cardiology Council Dr. Saahil Jumkhawala, and then by expert faculty Dr. Binita Shah. Dr. Binita Shah is an associate professor of medicine, interventional cardiologist, Director for research in Interventional Cardiology, and Director of the Department of Medicine Clinical Investigator Track at NYU. She is also an associate director of interventional cardiology and director of the transcatheter valve program at the VA New York Harbor Healthcare System. She was a member of the 2025 ACS Guidelines writing committee. A 64-year-old male with a history of hypertension and dyslipidemia presents to the emergency department with crescendo angina. His ECG shows ST-segment depression in leads V4–V6, and high-sensitivity troponin levels are significantly elevated. A diagnosis of NSTE-ACS is made, and the patient is scheduled for an early invasive strategy with percutaneous coronary intervention (PCI). Which of the following parenteral anticoagulants is NOT recommended for use as a standalone agent during the PCI procedure itself? A Fondaparinux B Bivalirudin C Unfractionated Heparin D Enoxaparin Explanation The correct answer is A. The choice of parenteral anticoagulation for a patient with Non-ST-Elevation Acute Coronary Syndrome (NSTE-ACS) undergoing Percutaneous Coronary Intervention (PCI) is governed by both efficacy in preventing ischemic events and the safety profile regarding bleeding. The following are the recommended Agents for PCI: Unfractionated Heparin (UFH): In patients with NSTE-ACS, intravenous unfractionated heparin (UFH) is useful to reduce ischemic events (Class 1, LOE C-EO). Bivalirudin: This direct thrombin inhibitor is recommended as an alternative to UFH. In patients with NSTE-ACS undergoing PCI, bivalirudin may be reasonable as an alternative to UFH to reduce bleeding and mortality (Class 2b, LOE B-R) Enoxaparin: In patients with ACS, intravenous enoxaparin may be considered as an alternative to UFH at the time of PCI to reduce ischemic events (Class 2B, LOE B) In patients with ACS, fondaparinux should not be used to support PCI because of the risk of catheter thrombosis (Class 3: Harm; LOE B-R). The primary reason is due to the risk of catheter thrombosis. Large-scale trials (notably the OASIS-5 trial) demonstrated that using fondaparinux alone during PCI led to a significantly higher rate of thrombus formation on the diagnostic and therapeutic catheters. In the OASIS-5 trial, an increase was observed in the rate of catheter-related thrombus with fondaparinux compared with enoxaparin (0.9% versus 0.4%). Similar results were observed in the OASIS-6 trial, in which a higher rate of guiding-catheter thrombosis and more coronary complications with fondaparinux were observed when used during PCI. Main Takeaway – Parenteral anticoagulation for a patient with Non-ST-Elevation Acute Coronary Syndrome (NSTE-ACS) undergoing Percutaneous Coronary Intervention (PCI) is governed by both efficacy in preventing ischemic events and the safety profile regarding bleeding. Expert Suggestions
Guideline Loc. Section 4.4 | |||
| 466. ACS Guidelines Question #5 with Dr. Binita Shah | 18 Sep 2026 | 00:06:57 | |
This episode is part of our comprehensive Decipher the Guidelines Series covering the 2025 ACC/AHA/ACEP/NAEMSP/SCAI Guideline for the Management of Patients With Acute Coronary Syndromes. The following question refers to Section 4.3 of the 2025 ACS Guidelines. The question is asked by Thomas Jefferson medical student and CardioNerds Academy Intern Dr. Grace Qiu, answered first by Cleveland Clinic interventional and structural cardiology fellow and member of the CardioNerds Interventional Cardiology Council Dr. Eunice Dugan, and then by expert faculty Dr. Binita Shah. Dr. Binita Shah is an associate professor of medicine, interventional cardiologist, Director for research in Interventional Cardiology, and Director of the Department of Medicine Clinical Investigator Track at NYU. She is also an associate director of interventional cardiology and director of the transcatheter valve program at the VA New York Harbor Healthcare System. She was a member of the 2025 ACS Guidelines writing committee. A 64-year-old woman with NSTE-ACS is taken to the cardiac catheterization laboratory. She is P2Y12 inhibitor-naive as she was unable to tolerate oral intake due to severe nausea and vomiting. Coronary angiography reveals a high-grade, thrombotic lesion in the mid-Right Coronary Artery. The interventionalist decides to initiate an intravenous P2Y12 inhibitor before proceeding with PCI. Which of the following is the most appropriate management strategy? A Administer Cangrelor as a 30 mcg/kg IV bolus followed by a 4 mcg/kg/min infusion for at least 2 hours or the duration of PCI, whichever is longer. B Administer Eptifibatide (GP IIb/IIIa inhibitor) as a routine double-bolus followed by an infusion to replace the need for P2Y12 inhibition. C Delay the procedure for 2 hours to allow for the administration and absorption of 600 mg of oral Clopidogrel. D Administer Cangrelor as a 180 mcg/kg bolus followed by a 2 mcg/kg/min infusion for exactly 1 hour. Explanation The correct answer is A. Cangrelor is the only intravenous P2Y12 inhibitor currently available. It is a direct-acting, intravenous antagonist of the P2Y12 receptor characterized by rapid and potent platelet inhibitory effects, with restoration of platelet function occurring within 1 hour of drug discontinuation. It also has a very short half-life (3–6 minutes). Among patients with ACS undergoing PCI who have not received a P2Y12 inhibitor, intravenous cangrelor may be reasonable to reduce periprocedural ischemic events (Class 2B; LOE B-R). Dosing Strategy: Bolus: 30mcg/kg IV bolus administered rapidly (under 1 minute) before PCI begins. Infusion: 4 mcg/kg/min IV infusion. Duration: The infusion must run for at least 2 hours or for the duration of the PCI, whichever is longer. Transition to Oral Therapy: Ticagrelor: 180mg can be given at any time (during or after the infusion). Prasugrel/Clopidogrel: loading dose must be given immediately after the infusion is stopped. Giving these earlier can lead to a drug-drug interaction where the Cangrelor prevents the active metabolite from binding to the receptor. In the CHAMPION PHOENIX trial, cangrelor was studied versus clopidogrel in patients undergoing PCI for acute or stable coronary syndromes. Cangrelor was administered as an intravenous bolus prior to PCI followed by an infusion for at least 2 hours or for the duration of the procedure, whichever was longer. In the control arm, clopidogrel was administered as a 600- or 300-mg loading dose immediately before or after PCI. At 48 hours, the primary endpoint of all- cause death, MI, ischemia-driven revascularization, or stent thrombosis was significantly reduced with cangrelor, with similar effects observed among those presenting with NSTE-ACS or STEMI. Glycoprotein IIb/IIIa receptor inhibitors are parenterally administered drugs that block platelet aggregation by preventing platelet cross-linking via fibrinogen or von Willebrand factor binding to the glycoprotein IIb/IIIa receptor. Routine administration of GP IIb/IIIa inhibitors before PCI is not recommended and is associated with increased bleeding without improving ischemic outcomes. (Class 3 – No Benefit). In current practice, the role of glycoprotein IIb/IIIa receptor inhibitors is largely limited to adjunctive use at the time of PCI in patients with large thrombus burden or as “rescue” or “bailout” therapy in patients with PCI complications such as no-reflow or persistent or recurring thrombus at the lesion. B is incorrect. Routine “upstream” or periprocedural use of GP IIb/IIIa inhibitors (GPI) is Class 3 (No Benefit) for most patients. Large trials (like EARLY-ACS) showed that routine GPI use significantly increases major bleeding without a proportional decrease in ischemic events compared to modern P2Y12 inhibitors. C is incorrect. In patients with NSTE-ACS or STEMI who are already in the lab, delaying the procedure to wait for oral drug absorption is not recommended. D is incorrect. The correct bolus is 30mcg/kg. Cangrelor must be infused for at least 2 hours or the duration of the PCI, whichever is longer. Stopping at 1 hour would leave a “gap” in platelet inhibition before an oral agent can take effect. Because Cangrelor’s half-life is only 3–6 minutes, a premature stop increases the risk of acute stent thrombosis. Main Takeaway Cangrelor may be reasonable among patients with ACS undergoing PCI who have not received a P2Y12 inhibitor to reduce periprocedural ischemic events (Class 2b, LOE B-R). Guideline Loc. Section 4.3.3-4.3.4 | |||
| 465. ACS Guidelines Question #4 with Dr. Binita Shah | 17 Sep 2026 | 00:05:10 | |
This episode is part of our comprehensive Decipher the Guidelines Series covering the 2025 ACC/AHA/ACEP/NAEMSP/SCAI Guideline for the Management of Patients With Acute Coronary Syndromes. The following question refers to Sections 4.3.2 and 4.4 of the 2025 ACS Guidelines. The question is asked by Thomas Jefferson medical student and CardioNerds Academy Intern Dr. Grace Qiu, answered first by University of Miami cardiology fellow and member of the CardioNerds Interventional Cardiology Council Dr. Saahil Jumkhawala, and then by expert faculty Dr. Binita Shah. Dr. Binita Shah is an associate professor of medicine, interventional cardiologist, Director for research in Interventional Cardiology, and Director of the Department of Medicine Clinical Investigator Track at NYU. She is also an associate director of interventional cardiology and director of the transcatheter valve program at the VA New York Harbor Healthcare System. She was a member of the 2025 ACS Guidelines writing committee. A 78-year-old man with a history of hypertension and controlled type 2 diabetes presents to a rural emergency department with 90 minutes of persistent, crushing, substernal chest pain. His ECG reveals 3-mm STE in leads V1 through V4. The nearest PCI-capable center is approximately 140 minutes away by ground transport, and air transport is unavailable due to weather. The patient refuses transfer to another facility for the duration of this admission. The clinical team decides to proceed with fibrinolytic therapy using weight-based Tenecteplase (TNK). Which of the following is the most appropriate initial antithrombotic regimen to accompany the fibrinolytic agent? A Clopidogrel 300 mg loading dose; Enoxaparin 30 mg IV bolus followed by 1.0 mg/kg SC every 12 hours. B Clopidogrel 75 mg (no loading dose); Enoxaparin 0.75 mg/kg SC every 12 hours (no IV bolus). C Ticagrelor 180 mg loading dose; Unfractionated heparin (UFH) weight-based IV bolus and infusion. D Prasugrel 10mg (no loading dose); Fondaparinux 2.5 mg IV bolus followed by 2.5 mg SC daily. Explanation (3-8 min to read) The correct answer is B. Clopidogrel is the only P2Y12 inhibitor with a Class 1 recommendation for use alongside fibrinolytic therapy to reduce death and MACE (Class 1, LOE A). Of note, pharmacodynamic variability in response to clopidogrel has been well described, and hyporesponders may be at increased risk of MACE and stent thrombosis when treated with clopidogrel after PCI. Other P2Y12 inhibitors such as ticagrelor and prasugrel are more potent than clopidogrel and achieve more rapid onset of inhibition of platelet activation but with increased risk of bleeding compared with clopidogrel. When administered concurrently with fibrinolytic as the reperfusion strategy, clopidogrel is recommended to be administered with a loading dose (300 mg, then 75 mg daily) for patients <75 years of age and starting without a loading dose (75 mg daily) for patients ≥75 years of age. In patients treated with a fibrinolytic agent who are undergoing subsequent PCI, either clopidogrel or ticagrelor (age <75 years, within 24 hours after a fibrinolytic agent) or prasugrel (>24 hours after a fibrinolytic agent) are alternatives to support PCI. Parenteral anticoagulation is recommended for all patients with ACS, irrespective of the initial treatment strategy, to treat the underlying pathophysiologic process (coronary atherothrombosis) and reduce the risk of recurrent MACE. The choice of a parenteral anticoagulant can be complex because it is influenced by various factors, including vascular access site, renal function, and concomitant use of other antiplatelet or anticoagulant agents. In patients with STEMI treated with fibrinolytic therapy, parenteral anticoagulation is recommended before and after fibrinolytic therapy to reduce ischemic events. In patients with STEMI who received fibrinolytic therapy and who are not planned for an invasive approach (as with the patient in the question stem), enoxaparin is the preferred anticoagulant over UFH. In the ExTRACT-TIMI 25 study, enoxaparin until hospital discharge or for a maximum of 8 days (whichever came first) was compared with UFH administered for at least 48 hours. The primary endpoint of death or nonfatal recurrent MI through 30 days occurred in 12% in the UFH group compared with 9.9% in the enoxaparin group. In a meta-analysis of 14 randomized trials, UFH did not reduce reinfarction or death in patients treated with fibrinolytic therapy. In contrast, low-molecular- weight heparin reduced the risk of reinfarction and death compared with placebo and the risk of reinfarction. In patients >75 years of age, the dosing must be modified: Omit the initial 30 mg IV bolus. Reduce the subcutaneous dose to 0.75 mg/kg (instead of the standard 1.0 mg/kg). The first two SC doses should also be capped at a maximum of 75 mg each. After receiving the fibrinolytic and adjusted antithrombotics, the patient should be transferred to a PCI center to facilitate immediate or early catheterization depending on the clinical circumstances, if this is in-line with the patient’s wishes. Hospitals should have transfer protocols in place to allow for a seamless transfer to the PCI-capable facility as soon as it is safe to do so. A detailed assessment of clinical status is critical to determine the timing of angiography. A is incorrect: This is the standard dose for patients under 75 years of age. In a 78-year-old, the IV bolus of Enoxaparin and the Clopidogrel load significantly increase the risk of a fatal brain bleed. B is incorrect: Ticagrelor is not recommended as an adjunct to fibrinolysis in the 2025 ACS guidelines. D is incorrect: While fondaparinux may be used alongside lytic therapy when not planning an invasive strategy, prasugrel does not have a Class 1 recommendation for use with fibrinolytic therapy. Main Takeaway – Clopidogrel is the only P2Y12 inhibitor with a Class 1 recommendation for use alongside fibrinolytic therapy Guideline Loc. Sections 4.3.2 and 4.4 Table 10
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| 464. ACS Guidelines Question #3 with Dr. Binita Shah | 16 Sep 2026 | 00:10:30 | |
This episode is part of our comprehensive Decipher the Guidelines Series covering the 2025 ACC/AHA/ACEP/NAEMSP/SCAI Guideline for the Management of Patients With Acute Coronary Syndromes. The following question refers to Section 3.2 of the 2025 ACS Guidelines.The question is asked by Thomas Jefferson medical student and CardioNerds Academy Intern Dr. Grace Qiu, answered first by Cleveland Clinic interventional and structural cardiology fellow and member of the CardioNerds Interventional Cardiology Council Dr. Eunice Dugan, and then by expert faculty Dr. Binita Shah.Dr. Binita Shah is an associate professor of medicine, interventional cardiologist, Director for research in Interventional Cardiology, and Director of the Department of Medicine Clinical Investigator Track at NYU. She is also an associate director of interventional cardiology and director of the transcatheter valve program at the VA New York Harbor Healthcare System. She was a member of the 2025 ACS Guidelines writing committee.
Question #3
A 55-year-old woman is brought to the Emergency Department after an out-of-hospital cardiac arrest. She had a witnessed collapse with an initial shockable rhythm. Return of Spontaneous Circulation (ROSC) was achieved after 15 minutes of Advanced Cardiac Life Support (ACLS). Her post-resuscitation ECG shows diffuse ST-segment depression but no ST-segment elevation. She remains comatose.Which of the following is the most appropriate next step in her management regarding coronary angiography?AImmediate emergency coronary angiography (within 2 hours) should be performed.BRoutine emergency coronary angiography is not recommended in the absence of ST-segment elevation or hemodynamic instability.CCoronary angiography should be delayed for at least 72 hours to allow for neurological recovery.DFibrinolytic therapy should be administered immediately if the patient cannot reach a cath lab within 90 minutes.
Answer #3
ExplanationThe correct answer is B.In resuscitated patients who are comatose after cardiac arrest, electrically and hemodynamically stable, and without evidence of STEMI, immediate angiography is not recommended due to lack of benefit (Class 3: No Benefit; LOE A)Patients who have been resuscitated after cardiac arrest and are noncomatose or who are comatose with favorable prognostic features and with evidence of STEMI, should undergo PPCI to improve survival. (Class 1; LOE B-NR).For patients such as this one, a delayed or selective approach should be taken once the patient is stabilized. Early angiography should not be denied solely based on a comatose state, but it should be deferred if there are clear non-cardiac causes for the arrest or if the patient’s overall prognosis is futile.A is incorrect because recent evidence shows no benefit to “emergency” PPCI for stable patients without ST-elevation.C is incorrect because while we wait for stability, we don’t necessarily have a fixed 72-hour “mandatory” delay for the heart if ischemia is suspected.D is incorrect, as fibrinolysis is generally not indicated for post-arrest patients without clear STEMI and carries risks in a post-CPR setting due to potential trauma.The MIRACLE2 Score is a tool for neuroprognostication. It helps clinicians estimate the likelihood of a poor neurological outcome at 6 months. A high score suggests that the benefit of an invasive procedure may be outweighed by the severity of the brain injury.Components of MIRACLE2:M – Missed (unwitnessed) arrest I – Initial non-shockable rhythm R – Reactive pupils at ROSC A – Age (points increase significantly at >60 and >80) C – Rhythm change (e.g., VF to PEA) L – Low pH (pH < 7.20) E – Epinephrine (any dose given)Clinical Threshold: A score of >5 indicates a high risk of poor neurological recovery, which may lead a Heart Team to favor stabilization over immediate emergency angiography in patients without ST-elevation.Early recognition of STEMI in resuscitated patients and direct transfer to a PCI-capable center is associated with improved survival. Survival-to-hospital discharge in the patient who is comatose with out-of-hospital cardiac arrest is <10% regardless of etiology. Those with a witnessed arrest and a shockable rhythm have improved survival. Outcomes for patients with STEMI who are awake after resuscitated cardiac arrest are comparable to patients with STEMI who were not in cardiac arrest. For this reason, patients with cardiac arrest who have achieved return of spontaneous circulation (ROSC) and are awake with STEMI on ECG are candidates for PPCI. However, care should be individualized in the comatose patient with rapid assessment of the patient’s clinical features and cardiac arrest characteristics before proceeding with invasive angiography. In contrast, patients who are stable without ST-segment elevation after out-of-hospital cardiac arrest do not require immediate coronary angiography. Coronary angiography in this setting can be deferred pending further risk stratification.Main TakeawayPatients with cardiac arrest and STEMI who have been resuscitated should preferentially be transferred by EMS to a PPCI-capable center. Certain prognostic scores can help risk stratify patients prior to catheterization.Guideline Loc.Section 3.2. Management of Patients Presenting With Cardiac Arrest | |||
| 463. Multimodality Imaging in Chronic Coronary Artery Disease with Dr. Panithaya Chareonthaitawee | 17 Aug 2026 | 00:39:49 | |
CardioNerds (Drs. Dr. Natalie Marrero, Dr. Ritika Tuli, and Dr. Rafael Toro Manotas) discuss multimodality imaging for risk stratification, evaluation, and management of chronic coronary artery disease with Dr. Panithaya Chareonthaitawee. Audio editing by CardioNerds intern Iman Razeghian.
This episode was produced as part of the CardioNerds Academy curriculum by House Taussig under the guidance of House Chief, Dr. Natalie Marrero and Academy Program Director, Dr. Gurleen Kaur. A matching review article will be published in US Cardiology Review, the official journal of CardioNerds. This discussion was planned in collaboration with the Mayo Clinic Cardiovascular Board Review Course.
In this episode, we discuss the pathophysiology and risk stratification of chronic coronary artery disease (CAD), as well as the current landscape of non-invasive evaluation of this condition. CAD remains a leading cause of morbidity and mortality despite advances in pharmacological and non-pharmacological strategies for the prevention and treatment of atherosclerotic disease. The concept of chronic CAD has shifted from the traditional model of stable, obstructive, flow-limiting disease, toward the current understanding of a dynamic process that extends beyond obstructive epicardial lesions to include non-obstructive plaque, diffuse atherosclerosis, and microvascular disease. Similarly, the imaging modalities used to evaluate CAD have evolved, and clinicians now have an extensive menu of options, each with distinct advantages and limitations, that must be selected carefully to maximize diagnostic accuracy and optimize treatment guidance, while also considering resource availability, local expertise, and high-value care. By the end of the episode, listeners will understand the pathophysiology of chronic CAD, risk-stratify patients with suspected CAD, recognize the advantages and pitfalls of each non-invasive diagnostic modality, and select the most appropriate diagnostic tool for a given clinical scenario.
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Pearls:
Chronic CAD is a complex process that extends beyond obstructive epicardial stenosis to include non-obstructive disease, dynamic plaque burden and ischemia, diffuse atherosclerosis, microvascular dysfunction, vasospasm, among others.
When evaluating patients with suspected CAD, the diagnostic process should be guided by a specific and appropriate clinical question before ordering any tests.
The current diagnostic tool arsenal is broadly divided into anatomic and functional imaging modalities. These are complementary, each with distinct properties and limitations, addressing different clinical questions and assessing different aspects of disease.
Local availability and expertise, along with patient-specific considerations and contraindications, determine the choice of diagnostic modality. No single test is best for every patient.
INOCA and coronary microvascular dysfunction represent a common and increasingly recognized entity that is diagnosable and treatable; initial evaluation includes non-invasive testing such as stress PET and stress CMR.
References
Gulati M, Levy PD, Mukherjee D, et al. 2021 AHA/ACC/ASE/CHEST/SAEM/SCCT/SCMR Guideline for the Evaluation and Diagnosis of Chest Pain: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. Circulation. 2021;144(22):e368-e454. doi:10.1161/CIR.0000000000001029 https://pubmed.ncbi.nlm.nih.gov/34709879/
Vrints C, Andreotti F, Koskinas KC, et al. 2024 ESC Guidelines for the management of chronic coronary syndromes. Eur Heart J. 2024;45(36):3415-3537. doi:10.1093/eurheartj/ehae177 https://pubmed.ncbi.nlm.nih.gov/39210710/
Virani SS, Newby LK, Arnold SV, et al. 2023 AHA/ACC/ACCP/ASPC/NLA/PCNA Guideline for the Management of Patients With Chronic Coronary Disease: A Report of the American Heart Association/American College of Cardiology Joint Committee on Clinical Practice Guidelines. Circulation. 2023;148(9):e9-e119. doi:10.1161/CIR.0000000000001168 https://pubmed.ncbi.nlm.nih.gov/37471501/
Edvardsen T, Asch FM, Davidson B, et al. Non-Invasive Imaging in Coronary Syndromes: Recommendations of The European Association of Cardiovascular Imaging and the American Society of Echocardiography, in Collaboration with The American Society of Nuclear Cardiology, Society of Cardiovascular Computed Tomography, and Society for Cardiovascular Magnetic Resonance. J Am Soc Echocardiogr. 2022;35(4):329-354. doi:10.1016/j.echo.2021.12.012 https://pubmed.ncbi.nlm.nih.gov/35379446/
Douglas PS, Hoffmann U, Patel MR, et al. Outcomes of anatomical versus functional testing for coronary artery disease. N Engl J Med. 2015;372(14):1291-1300. doi:10.1056/NEJMoa1415516 https://pubmed.ncbi.nlm.nih.gov/39210710/
Sharma A, Coles A, Sekaran NK, et al. Stress Testing Versus CT Angiography in Patients With Diabetes and Suspected Coronary Artery Disease. J Am Coll Cardiol. 2019;73(8):893-902. doi:10.1016/j.jacc.2018.11.056 https://pubmed.ncbi.nlm.nih.gov/30819356/
SCOT-HEART Investigators, Newby DE, Adamson PD, et al. Coronary CT Angiography and 5-Year Risk of Myocardial Infarction. N Engl J Med. 2018;379(10):924-933. doi:10.1056/NEJMoa1805971 https://pubmed.ncbi.nlm.nih.gov/30145934/
Li Z, Xu T, Wang Z, et al. Prognostic Significance of Computed Tomography-Derived Fractional Flow Reserve for Long-Term Outcomes in Individuals With Coronary Artery Disease. J Am Heart Assoc. 2025;14(2):e037988. doi:10.1161/JAHA.124.037988 https://pubmed.ncbi.nlm.nih.gov/39791423/
Bateman TM, Al-Mallah MH, et al. Clinical indications for positron emission tomography myocardial perfusion imaging and myocardial blood flow quantification: An American Society of Nuclear Cardiology position statement. J Nucl Cardiol. 2026;57:102619. doi:10.1016/j.nuclcard.2025.102619 https://pubmed.ncbi.nlm.nih.gov/41482140/
Taqueti VR, Di Carli MF. Coronary Microvascular Disease Pathogenic Mechanisms and Therapeutic Options: JACC State-of-the-Art Review. J Am Coll Cardiol. 2018;72(21):2625-2641. doi:10.1016/j.jacc.2018.09.042 https://pubmed.ncbi.nlm.nih.gov/30466521/
Taqueti VR, Hachamovitch R, Murthy VL, et al. Global coronary flow reserve is associated with adverse cardiovascular events independently of luminal angiographic severity and modifies the effect of early revascularization. Circulation. 2015;131(1):19-27. doi:10.1161/CIRCULATIONAHA.114.011939 https://pubmed.ncbi.nlm.nih.gov/25400060/
Mehta PK, Huang J, Levit RD, Malas W, Waheed N, Bairey Merz CN. Ischemia and no obstructive coronary arteries (INOCA): A narrative review. Atherosclerosis. 2022;363:8-21. doi:10.1016/j.atherosclerosis.2022.11.009 https://pubmed.ncbi.nlm.nih.gov/36423427/
Kunadian V, Chieffo A, Camici PG, et al. An EAPCI Expert Consensus Document on Ischaemia with Non-Obstructive Coronary Arteries in Collaboration with European Society of Cardiology Working Group on Coronary Pathophysiology & Microcirculation Endorsed by Coronary Vasomotor Disorders International Study Group. EuroIntervention. 2021;16(13):1049-1069. doi:10.4244/EIJY20M07_01 https://pubmed.ncbi.nlm.nih.gov/32624456/ | |||
| 462. Tricuspid Regurgitation with Dr. Sunil Mankad | 13 Aug 2026 | 00:18:44 | |
CardioNerds (Dr. Apoorva Gangavelli, Dr. Cory Sejo, and Dr. Joseph Kassab), discuss tricuspid regurgitation evaluation and management with Dr. Sunil Mankad.
This episode was produced as part of the CardioNerds Academy curriculum by House Einthoven under the guidance of House Chief, Dr. Apoorva Gangavelli and Academy Program Director, Dr. Gurleen Kaur. A matching review article will be published in US Cardiology Review, the official journal of CardioNerds. This discussion was planned in collaboration with the Mayo Clinic Cardiovascular Board Review Course.
Audio editing by CardioNerds intern Emma Winakur.
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Key Points:
Tricuspid regurgitation is common and associated with increased mortality at every stage, regardless of etiology. Outcomes are worse with worsening severity, so accurate grading is critical.
Etiology is critical to guide treatment decisions. Etiology includes primary vs secondary (atrial or ventricular) vs CIED-related TR. 3D echocardiography can be very helpful in determining TR etiology, especially in CIED-related TR.
Diuresis with the goal of euvolemia is step one. Additionally, underlying contributory conditions (eg. pulmonary HTN, HFrEF, atrial fibrillation) should be addressed, if appropriate, and then TR severity reassessed.
The choice between T-TEER and TTVR hinges on anatomy, RV function, pulmonary hypertension, and the ability to tolerate anticoagulation. T-TEER is generally first line in atrial functional TR with appropriate anatomy, in patients with poor RV function who cannot tolerate a sudden increase in RV afterload, or in patients who cannot tolerate the necessary anticoagulation with TTVR. TTVR is preferred with wide coaptation gaps and CIED-related TR.
This is a team sport. Multidisciplinary discussions utilizing imaging (TTE/TEE, CT), risk scores (TRI-SCORE or TRIO), patient preference, and prior institutional experience are essential for the effective treatment of severe TR.
Notes:
What is the clinical importance of tricuspid regurgitation?
TR is very common with approximately 4% of people over 75 having moderate or greater severity.
TR (even mild) is associated with increased mortality. Those outcomes worsen as the TR severity worsens, and this phenomenon is independent of the mechanism of regurgitation.
What is unique about the tricuspid valve compared to the other cardiac valves?
It is at an anterior location which allows it to be imaged well with transthoracic echocardiography
It is the largest valve and composed generally of 3 leaflets (but very often can have 4+ leaflets).
Importantly, the RV is compliant and changes size and shape readily based on loading conditions. The TV annulus similarly changes size and shape based on hemodynamic conditions such as preload.
What is a good framework for approaching the causes of tricuspid regurgitation?
Determine the presence and define the severity of TR.
Using TTE, we want to measure the right atrial size, the RV size, and any other concomitant valvular lesions.
Use TTE (2D and 3D) to characterize leaflet anatomy and characteristics.
Subtypes of TR mechanisms (many times etiology is mixed).
Primary: primary leaflet abnormality, occurs in ~10% of cases. Look for prolapse, flail, endocarditis, etc.
Secondary/functional: leaflets normal but surrounding structures are abnormal.
Atrial: RA and tricuspid annular dilation but normal RV size/shape, and can be related to arrhythmias like atrial fibrillation.
Ventricular: RV dilated and/or dysfunctional with leaflet tethering. Can be related to pulmonary hypertension or primary RV disease.
Cardiac implantable electronic device (CIED): Related to device (usually pacemakers or ICD) interaction with TV leaflets.
Includes perforation, entanglement in subvalvular apparatus, impingement, etc.
3D TTE particularly helpful to evaluate
How do we grade TR severity?
It is very important to grade the severity of TR, and this is generally done with echocardiography.
There are both quantitative and qualitative methods which use Doppler and various equations to estimate TR severity.
Current recommendations have expanded TR severity beyond mild/moderate/severe to include “massive” and “torrential” categories.
The most important parameters measured/calculated are vena contracta width, regurgitant volume, regurgitant fraction, and effective regurgitant orifice area. Helpful qualitative metrics include hepatic venous flow reversal.
When should additional studies beyond transthoracic echocardiography, such as transesophageal echocardiography (TEE), cardiac computed tomography (CT), and cardiac magnetic resonance imaging (MRI) be pursued?
TEE is particularly helpful if TTE views are poor. Since TEE is used during transcatheter intervention, a pre-procedure TEE to define anatomy, determine procedure candidacy, and plan for the procedure is critical.
CT is also helpful for procedure planning and has particular strengths in defining annulus size and geometry. A CT is required prior to transcatheter tricuspid valve replacement (TTVR).
MRI is helpful for measuring RV volumes and function, but is not generally used to assess TR severity.
What is the approach to the treatment for severe tricuspid regurgitation?
The first step is to try to determine the etiology. For secondary TR, treating the underlying condition is indicated. For example, pulmonary vasodilators for pulmonary HTN or guideline therapy for heart failure with reduced ejection fraction.
Diuretics are the mainstay for treatment, with the goal to obtain euvolemia. This may require inpatient admission to optimize volume status and medication regimen.
Once reversible etiologies are addressed, if the patient is still symptomatic from TR, additional therapies can be considered.
What is the role of right heart catheterizations (RHC) in patients with severe TR?
RHC is very helpful for many reasons. We use it in TR to help determine volume status, cardiac output, and RV function. Additionally, identifying and characterizing pulmonary hypertension (with pulmonary artery pressures and calculating pulmonary vascular resistance) is an important factor when choosing future therapies.
With severe tricuspid regurgitation, when should we refer for intervention (either with surgery or transcatheter repair or replacement)?
Once reversible etiologies are addressed and euvolemia has been achieved, if the patient is still symptomatic from TR despite aggressive medical optimization, additional therapies can be considered.
Once euvolemic, a repeat TTE should be ordered to reassess the severity of the TR.
Use calculators (for example, either the TRI-SCORE or TRIO score) to predict operative mortality for isolated TR surgery.
What are our transcatheter treatment options in severe tricuspid regurgitation, and how do we choose between them?
The primary approved transcatheter treatment options for severe TR include transcatheter tricuspid edge-to-edge repair (T-TEER) and transcatheter tricuspid valve replacement (TTVR), of which the Edwards EVOQUE valve is the only one currently approved by the FDA. There are other TTVR device under investigation.
These decisions should be made with a multi-disciplinary team including representation from cardiac imaging, interventional cardiology, and cardiothoracic surgery.
Factors that go into the decision between T-TEER and TTVR include anatomy (annulus width, coaptation gap, leaflet length), RV reserve, pulmonary hypertension presence, ability to tolerate anticoagulation, patient preference, and institutional experience.
T-TEER is generally the first line with atrial functional and suitable anatomy. It is successful at reducing TR but does not generally eliminate it.
TTVR with EVOQUE is preferred in certain anatomic considerations like a large coaptation gap or when there is CIED-related TR (as this was excluded in T-TEER trials).
Patients must be suitable for anticoagulation to receive TTVR as there is risk of leaflet thrombosis without it.
If moderate/severe pulmonary hypertension is present, or there is poor RV function, TTVR may be avoided as the sudden elimination of TR causes a sudden increase in RV afterload which may not be tolerated.
What is the role in advanced metrics for evaluating RV function?
Advanced metrics like RV/PA coupling are under investigation but have not made it into the guidelines. The clinical utility is not yet known.
Assessing the RV function is important as stated above. Dr. Mankad prefers using 3D TTE to calculate an RVEF, or tracking RV longitudinal free wall strain.
If you do encounter CIED-related TR, how do you treat it?
Evaluate with TTE or TEE. 3D is very helpful to identify relative anatomy and leaflet-device interactions.
There is no clear consensus about treatment if CIED-related TR is the primary mechanism of severe TR. If recently implanted, repositioning may be a valid option, but requires discussions with multiple teams including electrophysiology, advanced cardiac imaging, CT surgery, and interventional cardiology.
References
O'Gara PT, Lindenfeld J, Hahn RT, et al. 10 Issues for the Clinician in Tricuspid Regurgitation Evaluation and Management: 2025 ACC Expert Consensus Decision Pathway. J Am Coll Cardiol. 2025;S0735-1097(25)07047-0.
O'Gara PT, Little SH, Badhwar V, et al. Operator and Institutional Recommendations and Requirements for Tricuspid Interventions: 2026 ACC/AHA/ASE/HRS/STS Expert Consensus Systems of Care Document. J Am Coll Cardiol. 2026;S0735-1097(26)05481-1.
Hahn RT. Tricuspid Regurgitation. N Engl J Med. 2023;388(20):1876-1891.
Davidson LJ, Tang GHL, Ho EC, et al.... | |||
| 461. Pre-Pregnancy Risk Stratification and Counseling with Dr. Katie Young | 11 Aug 2026 | 00:52:19 | |
CardioNerds (Dr. Apoorva Gangavelli, Dr. Rebecca Garber, and Dr. Tina Reddy), discuss pre-pregnancy risk stratification and counseling with Dr. Katie Young across a range of risks.
This episode was produced as part of the CardioNerds Academy curriculum by House Einthoven under the guidance of House Chief, Dr. Apoorva Gangavelli and Academy Program Director, Dr. Gurleen Kaur. A matching review article will be published in US Cardiology Review, the official journal of CardioNerds. This discussion was planned in collaboration with the Mayo Clinic Cardiovascular Board Review Course.
Audio editing by CardioNerds intern, Dr. Patrick Pekyi-Boateng.
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Notes:
Why is pregnancy considered a “physiologic stress test,” and why does risk extend beyond delivery?
Blood volume, heart rate, and cardiac output rise while systemic vascular resistance falls, peaking in the late second/early third trimester; underlying (even undiagnosed) heart disease can be unmasked or worsened.
Postpartum (“fourth trimester”) is a high-risk period, not a safe zone - fluid shifts, rising SVR, and bleeding risk can precipitate decompensation in patients with heart failure, pulmonary hypertension, valvular disease, or aortopathy.
Adverse pregnancy outcomes (hypertensive disorders, gestational diabetes, preterm birth, fetal growth restriction, peripartum cardiomyopathy) are markers of future cardiovascular risk and warrant long-term preventive follow-up.
What is the practical framework for approaching pre-pregnancy cardiovascular risk?
Four broad categories: (1) patients who may need cardiac screening before pregnancy, (2) patients needing risk-factor/medication optimization, (3) known cardiovascular disease where pregnancy is reasonable with structured risk stratification, and (4) high-risk disease where pregnancy may need to be delayed, modified by intervention, or discouraged.
Testing should be targeted, not blanket - reserved for symptoms, abnormal exam, concerning family history, or reduced functional capacity.
How is risk stratified in patients with known cardiovascular disease?
Use a combination of tools per 2025 ESC guidelines: mWHO 2.0 (broad maternal risk category), CARPREG II (additional predictors of maternal cardiac events), and ZAHARA (useful in congenital heart disease).
Key lesion-specific factors: aortic size/growth, valve severity, ventricular function, symptoms, blood pressure, and family history of dissection.
Translate risk into practical terms for patients rather than leading with a numerical score.
Which cardiovascular medications require review before conception?
ACE inhibitors, ARBs, and ARNIs should be transitioned off before pregnancy; statins, MRAs, and SGLT2 inhibitors also need review.
DOACs are contraindicated in pregnancy and lactation; mechanical valve anticoagulation requires individualized shared decision-making, as no strategy is risk-free for mother and fetus.
Medication changes are best made proactively, before conception, rather than reactively.
This is not an exhaustive list! The medication list needs to be reviewed carefully.
Which conditions carry high or prohibitive risk in pregnancy?
Pulmonary arterial hypertension, Eisenmenger syndrome, severe ventricular dysfunction, prior peripartum cardiomyopathy with residual LV dysfunction, severe left-sided obstructive valve disease (e.g., severe mitral stenosis), mechanical valves, significant aortopathy, cyanotic congenital heart disease, and Fontan physiology.
Common theme: limited cardiovascular reserve and high risk of decompensation, thrombosis, arrhythmia, heart failure, aortic dissection, or death. These patients need expert multidisciplinary evaluation before pregnancy.
Severe mitral stenosis is poorly tolerated because tachycardia shortens diastolic filling time and raises left atrial pressure, risking pulmonary edema and decompensation.
When should genetic testing or counseling be offered?
Consider when a diagnosis may be inherited or affect the patient, pregnancy, or family members: inherited cardiomyopathies, aortopathies, channelopathies, select congenital heart disease, and some pulmonary hypertension syndromes.
Recurrence risk of congenital heart disease in offspring is roughly 6-10% when the mother has CHD; fetal echocardiography should be offered.
How should contraception be approached in high-risk cardiac patients?
Frame contraception as part of the cardiac care and reproductive safety plan to prevent unplanned high-risk pregnancy.
Long-acting reversible contraception is often preferred; progestin-only methods are generally safer than estrogen-containing options with thrombosis risk, pulmonary hypertension, or mechanical valves.
What are key delivery-planning considerations for cardiac patients?
Vaginal delivery is preferred unless there is an obstetric indication for cesarean or a specific cardiac reason (e.g., unstable maternal status, therapeutic INR) to avoid labor.
Planning should address delivery location, anesthesia involvement, telemetry needs, fluid management, and postpartum monitoring, clearly communicated across the multidisciplinary team in advance.
How should clinicians counsel patients when pregnancy is discouraged but strongly desired?
Acknowledge the patient's goals and the emotional weight of the conversation; separate the goal (family building) from the timeline (safety now vs. after optimization).
If pregnancy remains prohibitively risky, discuss alternatives for family building and ensure adequate patient support.
What are the key gaps and future directions in cardio-obstetric risk stratification?
Current risk tools (mWHO, CARPREG II, ZAHARA) provide common language but do not fully capture functional status, prior pregnancy history, or how risk evolves over time.
Future direction: individualized, dynamic risk prediction incorporating imaging, biomarkers, exercise capacity, and social drivers of health, with better long-term links between pregnancy complications and cardiovascular prevention.
References
1. European Society of Cardiology. 2025 ESC Guidelines for the management of cardiovascular disease and pregnancy.
2. Mehta LS, et al. Cardiovascular Considerations in Caring for Pregnant Patients: A Scientific Statement From the American Heart Association. Circulation. 2020;141:e884-e903. PMID: 32362133. doi:https://doi.org/10.1161/CIR.0000000000000772
3. ACOG Practice Bulletin No. 212. Pregnancy and Heart Disease. Obstet Gynecol. 2019;133(5):e320-e356. PMID: 31022123. doi:https://doi.org/10.1097/AOG.0000000000003243 | |||
| 460. Approach to HFpEF and the Metabolic Syndrome with Dr. John Ostrominski | 29 Jul 2026 | 00:22:45 | |
CardioNerds Dr. Rohit Nathani, Dr. Atefeh Ghorbanzadeh, and Dr. Mariam Riad, discuss Obesity-related Heart Failure with Preserved Ejection Fraction (HFpEF) with Dr. John Ostrominski.
This episode was produced as part of the CardioNerds Academy curriculum by House Jones under the guidance of House Chief, Dr. Mariam Riad and Academy Program Director, Dr. Gurleen Kaur. A matching review article will be published in US Cardiology Review, the official journal of CardioNerds.
This episode highlights the diverse clinical phenotypes and complex, multifaceted pathophysiology of HFpEF. We take a deep dive into the therapeutic advances that represent paradigm shift in metabolic modulation aimed at improving outcomes in patients with HFpEF and metabolic syndrome.
Audio editing by CardioNerds intern Pacey Wetstein.
Enjoy this Circulation Paths to Discovery article to learn more about the CardioNerds mission and journey.
US Cardiology Review is now the official journal of CardioNerds! Submit your manuscripts here.
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Pearls
HFpEF is a constellation of symptoms often with different underlying pathophenotypes; cardiometabolic type is rising in incidence.
Diagnosis is predominantly based on the clinical scenario along with supporting evidence from imaging modalities such as echocardiogram, cardiac MRI, and right heart catheterization.
Cardiometabolic HFpEF is a complex syndrome characterized by dysregulated lipid metabolism, systemic inflammation, and hemodynamic abnormalities, all of which contribute to exercise intolerance and frailty.
Lifestyle interventions, comorbidities management, and HFpEF therapeutics go hand in hand for comprehensive HFpEF care and offer opportunities for multispecialty collaboration to achieve optimal patient outcomes.
References
Ostrominski, J, Højbjerg Lassen, M, Butt, J. et al. Adiposity-Related Anthropometrics and Clinical Outcomes in Heart Failure With Mildly Reduced or Preserved Ejection Fraction: A Participant-Level Pooled Analysis of Randomized Clinical Trials. JACC. 2025 Nov, 86 (20) 1760–1777.https://doi.org/10.1016/j.jacc.2025.08.012
Packer, M. The Adipokine Hypothesis of Heart Failure With a Preserved Ejection Fraction: A Novel Framework to Explain Pathogenesis and Guide Treatment. JACC. 2025 Oct, 86 (16) 1269–1373.https://doi.org/10.1016/j.jacc.2025.06.055
Ahmed, N., Dalmasso, C., Turner, M.B. et al. From fat to filter: the effect of adipose tissue-derived signals on kidney function. Nat Rev Nephrol 21, 417–434 (2025). https://doi.org/10.1038/s41581-025-00950-5
Alicic, R.Z., Neumiller, J.J. & Tuttle, K.R. GLP-1 receptor agonists and next-generation metabolic hormone therapies in chronic kidney disease. Nat Rev Nephrol 22, 265–282 (2026). https://doi.org/10.1038/s41581-025-01036-y
Ostrominski, J, Harrington, J, Claggett, B. et al. Anthropometric Measures, Cardiovascular Outcomes, and Treatment Effects of Finerenone in Cardiovascular-Kidney-Metabolic Disease: Pooled Participant-Level Analysis of 3 Global Trials. JACC. 2025 Nov, 86 (20) 1781–1801.https://doi.org/10.1016/j.jacc.2025.08.039 | |||
| 459. The Continuum of Prevention and Heart Failure with Dr. Anu Lala and Dr. Martha Gulati | 23 Jul 2026 | 00:26:30 | |
CardioNerds (Drs. Apoorva Gangavelli, Jenna Skowronski, and Hannah Every) discuss the continuum of prevention and heart failure with Drs. Anu Lala and Martha Gulati. Grounded in a clinical case of a 55-year-old woman with uncontrolled hypertension, type 2 diabetes, and obesity who is on the trajectory toward heart failure, this episode unpacks a paradigm-shifting framework from a joint HFSA/ASPC Scientific Statement. The discussion explores how prevention should not be siloed from heart failure management but rather integrated across a patient's lifespan—from primary prevention in at-risk individuals, to secondary prevention in those with established heart failure, to tertiary prevention in patients with advanced therapies such as LVADs and heart transplantation. The experts highlight the importance of aggressive risk factor management, biomarker-guided screening, the AHA's Life's Essential 8, and the need for multidisciplinary collaboration and systems-level change to shift heart failure care from reactive to proactive. Audio editing for this episode was performed by CardioNerds Intern, Dr. Julia Marques Fernandes.
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Pearls
Systemic inflammatory diseases are associated with an elevated CVD risk that has significant implications for early detection, risk Heart failure prevention is a continuum, not a checkpoint. Prevention applies at every stage—from at-risk (Stage A) through advanced/post-transplant care—and every clinical encounter is an opportunity to intervene. The AHA's Life's Essential 8 (diet, physical activity, nicotine exposure, sleep, BMI, blood lipids, blood glucose, blood pressure) forms the foundation at every stage.
Hypertension carries the highest population-attributable risk for heart failure of any modifiable risk factor. In the Framingham Heart Study, 91% of patients with newly diagnosed HF had pre-existing hypertension. The SPRINT trial demonstrated a 38% reduction in HF incidence with intensive blood pressure targets (<120 mm Hg systolic). Agent selection matters: ACE inhibitors, ARBs, and thiazide diuretics should be prioritized for HF prevention.
Overlapping risk factors should prompt parallel, not sequential, intervention. Pharmacotherapies such as SGLT2 inhibitors and GLP-1 receptor agonists target multiple pathways simultaneously (diabetes, obesity, CKD, HF risk), making them ideal for patients with cardiometabolic multimorbidity. The cardio-kidney-metabolic (CKM) syndrome framework reinforces this integrated approach.
Biomarker screening with BNP/NT-proBNP should be used proactively in high-risk populations, not just reactively in the emergency department. Even modestly elevated natriuretic peptide levels (e.g., BNP >30 ng/L or NT-proBNP >125 ng/L) identify individuals at heightened risk for progression to symptomatic HF. The ACC/AHA/HFSA guidelines give a Class IIa recommendation for natriuretic peptide screening in at-risk patients. Urine albumin-to-creatinine ratio (UACR) is an underutilized screening tool that provides additional insight into CKM risk.
The heart failure label does not close the prevention window—it accentuates it. Secondary prevention through GDMT optimization (quadruple therapy in HFrEF) and continued risk factor management remains critical. Tertiary prevention extends to post-LVAD and post-transplant patients, where hypertension, diabetes, obesity, and CKD management remain essential to long-term outcomes.
Show notes
For a comprehensive review, please review the full HFSA/ASPC Joint Scientific Statement: Lala A, Beavers C, Blumer V, et al. The Continuum of Prevention and Heart Failure in Cardiovascular Medicine. J Card Fail. 2026;32:75-105. doi:10.1016/j.cardfail.2025.06.013
1. What is the "continuum of prevention" framework, and how does it differ from traditional approaches to heart failure prevention?
Historically, prevention and heart failure management have been treated as separate disciplines—primary prevention handled by preventive cardiologists and treatment managed by heart failure specialists. This joint HFSA/ASPC Scientific Statement reframes prevention as a dynamic, continuous process that spans a patient's entire lifespan, regardless of HF stage or ejection fraction.
The framework maps onto the ACC/AHA HF staging system:
Primary prevention targets Stage A ("at risk") and Stage B ("pre-HF") patients to reduce the burden of incident HF.
Secondary prevention targets Stage C (symptomatic) and Stage D (advanced) patients to reduce the impact of established HF through GDMT optimization and ongoing risk factor management.
Tertiary prevention encompasses risk factor management in patients with LVADs or heart transplants—populations where hypertension, diabetes, and obesity still drive outcomes.
The Central Figure of the statement illustrates that Life's Essential 8 (blood pressure and lipid control, diabetes management, exercise, sleep, smoking cessation, weight management, and diet/nutrition counseling) forms the foundation at every stage, with pharmacologic and device-based therapies layered on top as disease progresses (Figure)
2. How do traditional risk factors drive heart failure, and what should clinicians prioritize?
Hypertension carries the greatest population-attributable risk for HF. In the Framingham Heart Study (N=5,143), HTN was associated with a 2- to 3-fold increased risk of HF, with a population-attributable risk of 39% in men and 59% in women. The SPRINT trial showed a 38% reduction in HF incidence and 25% reduction in the primary composite outcome with intensive BP targets (<120 mm Hg). Not all antihypertensives are equal for HF prevention: the ALLHAT trial showed that amlodipine carried a 38% higher risk and lisinopril a 19% higher risk of incident HF compared with chlorthalidone. The statement recommends prioritizing ACE inhibitors, ARBs, or thiazide diuretics as first-line agents when HF prevention is a goal.
Type 2 diabetes confers a 5-fold risk of HF in women and 2-fold in men. Each 5-year increment in diabetes duration is associated with a 17% increased risk of incident HF. SGLT2 inhibitors have a Class 1 recommendation for HF prevention in patients with T2DM and established CVD or high cardiovascular risk. Finerenone (nonsteroidal MRA) reduced new-onset HF by 32% in the FIGARO-DKD trial among patients with T2DM and CKD. GLP-1 receptor agonists reduce CV events in patients with T2DM and ASCVD and are recommended in current guidelines.
Obesity independently leads to myocardial dysfunction through the leptin-aldosterone-neprilysin framework, ectopic fat deposition, and neurohormonal dysregulation. The SELECT trial demonstrated that semaglutide reduced HF composite endpoint events (HR 0.84; 95% CI 0.74–0.97) in patients with obesity and established CVD without T2DM. Women with obesity are at highest risk for HFpEF, while men with obesity are at highest risk for HFrEF.
Chronic kidney disease with albuminuria is deliberately included as a traditional risk factor in this statement. Albuminuria confers a 2- to 3-fold increased risk of incident HF. UACR screening is recommended for patients with T2DM and those at risk for CKD.
3. How can risk stratification tools and biomarkers be used to identify patients on the trajectory toward heart failure?
Natriuretic peptides (BNP/NT-proBNP): The ACC/AHA/HFSA guidelines give a Class IIa recommendation for BNP or NT-proBNP screening in patients at risk for HF. Even modestly elevated levels (BNP >30 ng/L or NT-proBNP >125 ng/L) are associated with heightened risk for progression to symptomatic HF. In the ARIC study, incorporating NT-proBNP reclassified 20% of older adults without HF into Stage B. Factors that affect interpretation include age, sex, obesity (lower values), and CKD (higher values).
High-sensitivity cardiac troponin (hs-cTn): Concentrations above the 99th percentile are now included in the definition of Stage B HF. Troponin testing may complement natriuretic peptides, particularly when BNP/NT-proBNP values are ambiguous.
Risk scores: The PCP-HF equation predicts 10-year HF risk using traditional risk factors plus QRS duration. The AHA PREVENT score incorporates HF risk calculation and includes markers of kidney function (albuminuria, eGFR), though it may underestimate risk in men and Black adults. The CKM syndrome staging framework (Stages 0–4) provides a holistic approach to assessing systemic cardiovascular-kidney-metabolic risk.
4. What are the key nontraditional risk factors and cross-cutting themes in heart failure prevention?
Genetics: Pathogenic cardiomyopathy variants exist in ~1 in 200 individuals in the general population. The HFSA and ACMG recommend cascade testing to identify at-risk family members. Polygenic risk scores for dilated cardiomyopathy show a 3.8-fold risk for DCM in the top 10th percentile compared with the median.
Sex-specific considerations: Women have 2.8 times the odds of developing HFpEF, while men have similarly increased odds of HFrEF. A complete obstetric/gynecologic history is essential—preeclampsia is associated with a 4-fold increased risk of HF. Peripartum cardiomyopathy requires intentional screening in high-risk populations.
Cardiotoxic exposures: Clinicians should be aware of medications that cause direct myocardial toxicity (e.g., anthracyclines, trastuzumab, tyrosine kinase inhibitors). A team-based approach with pharmacists can help optimize medication selection and risk factor modification.
Social determinants of health: Environmental exposures (air pollution, arsenic, lead, cadmium), food insecurity, financial instability, and limited healthcare access contribute to HF risk and progression. Equity-focused,... | |||
| 458. The Golden Age of Pulmonary Embolism Randomized Controlled Trials with Dr. Jay Giri | 10 Jul 2026 | 00:29:09 | |
CardioNerds co-chairs Dr. Dinu Balanescu and Dr. Billy Joe Mullinax, along with FIT lead Dr. Shiavax Rao, discuss the evolving landscape of randomized controlled trials in pulmonary embolism with Dr. Jay Giri, interventional cardiologist, Associate Professor of Medicine, and Director of the Cardiovascular Catheterization Laboratories at the Hospital of the University of Pennsylvania. This episode examines the historical evidence behind systemic thrombolysis, the emergence of catheter-directed therapies and mechanical thrombectomy, and the landmark RCTs - STORM-PE, PEERLESS, HI-PEITHO, and PEERLESS II - that are reshaping intermediate-risk PE management. The discussion highlights challenges in PE trial design, the critical importance of clinical deterioration as an endpoint, and why this era represents an unprecedented wave of evidence generation in PE. Audio editing for this episode was performed by CardioNerds Intern, Dr. Julia Marques Fernandes.
Dr. Dinu Balanescu and Dr. Billy-Joe Mullinax are Co-chairs for the CardioNerds PE Series, developed in collaboration with the PERT Consortium.
Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values.
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Pearls:
Systemic thrombolysis in intermediate-risk PE reduces hemodynamic decompensation but at the cost of ~1.5–2% intracranial hemorrhage risk - a near-zero net benefit that has driven the search for safer catheter-based alternatives.
"Focus on clinical deterioration, not mortality" - Due to crossover design in contemporary PE RCTs, control-arm patients who decompensate are rescued with advanced therapies, biasing mortality toward the null. Clinical deterioration is the most informative endpoint to watch in HI-PEITHO, PRAGUE-26, and PEERLESS II.
HI-PEITHO is the first large RCT to demonstrate that catheter-directed fibrinolysis plus anticoagulation significantly reduces the composite of PE-related death, cardiorespiratory decompensation, or PE recurrence versus anticoagulation alone (RR 0.39; 95% CI 0.20–0.77; P=0.005), with no intracranial hemorrhage in either arm.
The four major upcoming/recently reported PE RCTs (HI-PEITHO, PRAGUE-26, PEERLESS II, PE-TRACT) enroll progressively different risk populations - from the most enriched (HI-PEITHO) to the most permissive (PE-TRACT, which includes intermediate-low risk patients) - enabling a nuanced understanding of which patients benefit most from intervention.
PE device clearance follows a fundamentally different FDA pathway than structural heart devices (single-arm safety/efficacy studies vs. mandated RCTs), yet market forces and clinical need have ultimately driven industry and government to sponsor large-scale RCTs - a lesson in how evidence development can evolve organically alongside regulatory frameworks.
Notes:
Notes drafted by Dr. Shiavax Rao.
Question #1: What is the current evidence behind advanced PE therapies?
Systemic thrombolysis: Sixteen RCTs over 40 years (1972–2014) enrolling nearly 2,000 patients have studied systemic thrombolysis in intermediate-risk PE. The landmark PEITHO trial (n=1,006) showed that tenecteplase reduced the composite of death or hemodynamic collapse (2.6% vs. 5.6%; P=0.015), driven primarily by reduced hemodynamic decompensation (1.6% vs. 5.0%; P=0.002). However, this came at the cost of increased major bleeding (6.3% vs. 1.5%; P<0.001) and a ~2% rate of intracranial hemorrhage. Meta-analyses of systemic thrombolysis trials show a small absolute mortality benefit (~1–2%) that is closely offset by bleeding risk, explaining why guidelines have not broadly recommended systemic thrombolysis for intermediate-risk PE.
Catheter-directed thrombolysis (CDT): The ULTIMA trial (n=59) was the first RCT of ultrasound-assisted CDT (EkoSonic/EKOS system) vs. anticoagulation alone in intermediate-risk PE. CDT showed superior RV/LV ratio improvement at 24 hours (decrease of 0.30 ± 0.20 vs. 0.03 ± 0.16; P<0.001), but this difference was no longer significant at 90 days. The CANARY trial, initiated in Iran in 2019, was halted prematurely due to the COVID-19 pandemic but largely verified ULTIMA's findings, with a signal that RV benefits may persist at 90 days.
Mechanical thrombectomy - single-arm data: The FLARE trial demonstrated a 25% reduction in RV/LV ratio at 48 hours with large-bore aspiration thrombectomy (FlowTriever). The EXTRACT-PE trial showed significant RV/LV ratio reduction with the Indigo aspiration system with a low major adverse event rate. The FLASH registry (FlowTriever) reported a mean 7.6 mmHg drop in mean PA pressure and RV/LV ratio decrease from 1.23 to 0.98 at 48 hours.
STORM-PE (2025): The first RCT of mechanical thrombectomy (computer-assisted vacuum thrombectomy [CAVT] with the Indigo/Penumbra system) vs. anticoagulation alone. One hundred patients were randomized across 22 sites. CAVT was superior for the primary endpoint of 48-hour RV/LV ratio reduction (0.52 vs. 0.24; difference 0.27; P<0.001), with earlier normalization of vital signs and comparable major adverse event rates (4.3% vs. 7.5%; P=0.681). Two PE-related deaths occurred in the CAVT arm. The trial was not powered for mortality or longer-term outcomes.
PEERLESS (2025): The first RCT comparing two interventional strategies head-to-head - large-bore mechanical thrombectomy (FlowTriever) vs. CDT - in 550 patients with intermediate-risk PE. The primary hierarchical win ratio composite favored LBMT (win ratio 5.01; 95% CI 3.68–6.97; P<0.001), driven primarily by fewer clinical deterioration/bailout events (1.8% vs. 5.4%; P=0.04) and substantially less post-procedural ICU use (41.6% vs. 98.6% admission rates). No significant differences in mortality, intracranial hemorrhage, or major bleeding were observed. RV/LV ratio reduction was similar between arms. LBMT was associated with shorter hospital stays and fewer 30-day readmissions.
Question #2: What are the challenges with conducting RCTs in PE?
Crossover and rescue therapy: Unlike early TAVR trials where control-arm patients could not cross over to the device arm, contemporary PE trials allow crossover upon clinical deterioration. This is ethically necessary given available therapies but biases mortality toward the null, making it unlikely that any individual trial - or even a meta-analysis of the four major trials (~2,400–3,000 patients combined) - will demonstrate a mortality difference.
Heterogeneity of intermediate-risk PE: Two patients meeting ESC intermediate-high risk criteria (RV dysfunction + elevated troponin) can look clinically very different - one may be tachypneic on 5 liters of oxygen, while another is comfortable on room air. This heterogeneity complicates enrollment, endpoint detection, and generalizability.
Endpoint selection: Early PE trials relied on surrogate imaging endpoints (RV/LV ratio, PA pressure reduction, Miller score). While these demonstrate proof-of-concept, they have not moved guidelines. Clinically relevant endpoints - mortality, clinical deterioration, functional status, quality of life - are needed but require larger sample sizes and longer follow-up.
Funding and maturation of the field: Trials require buy-in from government or industry funders. It took time for the field to mature enough to estimate effect sizes for trial powering, accumulate sufficient operator experience to ensure internal validity, and for industry to recognize that market adoption required randomized evidence despite existing FDA clearance.
FDA regulatory pathway: PE devices are cleared via a 510(k) pathway requiring single-arm studies (~100–150 patients) demonstrating safety and RV/LV ratio improvement - a much lower bar than the pre-market approval pathway requiring RCTs mandated for structural heart devices (e.g., TAVR, MitraClip). While this has enabled rapid innovation and market competition, it initially reduced the incentive for industry-sponsored RCTs.
Question #3: What are the upcoming/recently reported RCT trials in PE?
HI-PEITHO (published 2026, NEJM): Multinational adaptive-design RCT of ultrasound-facilitated CDT (EkoSonic system, alteplase 2 mg bolus + 1 mg/hr/catheter × 7 hours) plus anticoagulation vs. anticoagulation alone in 544 patients with enriched intermediate-high risk PE (RV/LV ≥1.0, elevated troponin, plus ≥2 of: SBP ≤110, HR ≥100, RR >20). Primary composite of PE-related death, cardiorespiratory decompensation/collapse, or symptomatic PE recurrence within 7 days: 4.0% intervention vs. 10.3% control (RR 0.39; 95% CI 0.20–0.77; P=0.005). Effect driven by reduced cardiorespiratory decompensation. Major bleeding at 7 days: 4.1% vs. 2.2% (P=0.32). No intracranial hemorrhage in either arm. Clinical deterioration measured using the National Early Warning Score (NEWS), a validated ordinal scoring system incorporating vital signs - more sensitive at detecting decompensation than binary clinical criteria.
PRAGUE-26: Czech Republic government-sponsored RCT with a design essentially identical to HI-PEITHO in terms of sample size and primary endpoint, but using standard (non-ultrasound-assisted) CDT catheters in the interventional arm. Enrolling well; results anticipated in the near term.
PEERLESS II: Industry-sponsored (Inari/Boston Scientific) RCT of large-bore mechanical thrombectomy (FlowTriever) plus anticoagulation vs. anticoagulation alone in up to 1,200 patients with enriched intermediate-high risk PE (enrichment criteria slightly less stringent than HI-PEITHO). Five-component hierarchical primary endpoint assessed via win ratio: (1) mortality, (2) clinical deterioration (defined by binary clinical criteria - pressor initiation,... | |||
| 457. Insights into INOCA and ANOCA with Dr. Claire Raphael | 03 Jul 2026 | 00:09:25 | |
CardioNerds (Drs. Apoorva Gangavelli, Rebecca Garber, and Tina Reddy discuss INOCA with Dr. Claire Raphael. Audio editing by CardioNerds Academy intern, student doctor Pacey Wetstein.
This episode was produced as part of the CardioNerds Academy curriculum by House Einthoven under the guidance of House Chief, Dr. Apoorva Gangavelli, and Academy Program Director, Dr. Gurleen Kaur. A matching review article will be published in US Cardiology Review, the official journal of CardioNerds.
Non-obstructive coronary artery disease (CAD) is more common than often recognized, particularly in women and individuals with risk factors like diabetes or hypertension. Conditions such as INOCA, ANOCA, and MINOCA can cause ischemia and chest pain despite “clean” angiograms, often due to microvascular dysfunction, coronary spasms, or subtle plaque. Diagnosing these conditions requires advanced imaging or invasive studies to assess blood flow and vessel function. Treatment focuses on reducing cardiovascular risk with aspirin, statins, ACE inhibitors, or ARBs, and managing symptoms with beta-blockers or calcium channel blockers. The key takeaway: A normal angiogram doesn’t rule out disease, and these patients need a comprehensive, evidence-based approach to care.
Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values.
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Pearls:
When patients present with chest pain but do not have obstructive coronary artery disease, the story does not end there! Other pathologies that must be ruled out include spontaneous coronary artery disease (SCAD), coronary vasospasm, microvascular disease, Takotsubo, and cardiomyopathy. A TTE can help rule out other pathologies. Cardiac MRI can help identify myocardial fibrosis, scarring, or edema that may suggest prior events or alternative diagnoses.
About 60-70% of INOCA cases are in women. However, it is estimated that about half of the patients with so-called “normal” angiograms actually have positive stress tests. Patients with elevated troponins are more likely to have recurrent events. Patients with INOCA are more likely to come back to the ER multiple times before getting diagnosed. These patients have a 1.4x increased risk of adverse cardiovascular events (such as HFpEF, MI, and recurrent hospitalizations for cardiac chest pain).
INOCA is a complex condition with a variety of causes, primarily linked to microvascular disease. Within microvascular disease, there are different "endotypes" (types or subcategories) classified by specific characteristics. In centers that conduct microvascular testing, patients are categorized as endothelium-independent or endothelium-dependent, based on their responses to adenosine or acetylcholine during testing. Additionally, microvascular disease can be classified as either structural or functional, depending on the results of tests measuring microvascular resistance.
The field is moving towards the term ANOCA, or angina with non-obstructive coronary arteries, to include patients with anginal symptoms without objective ischemia.
The field is moving toward using genotyping and hemodynamic testing to guide first-line therapies for microvascular disease, a heterogeneous condition. Current treatments mostly come from obstructive coronary artery disease, but specialized approaches—like the coronary sinus reducer—may offer unique benefits for microvascular disease.
Treatment includes sublingual nitroglycerin, ACE inhibitors/ARBs, and beta-blockers. Remember to also treat any additional comorbidities, such as diabetes, hypertension, and hyperlipidemia. Unfortunately, many of these patients may still have refractory chest pain, so it is important to reassure them. These patients can still exercise, but they may be hesitant to do so for fear of having chest pain. Cardiac rehab may be helpful for these patients as it helps them build up their tolerance.
References
Lawton JS, Tamis-Holland JE, Bangalore S, et al; Writing Committee Members. 2021 ACC/AHA/SCAI guideline for coronary artery revascularization: a report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. Circulation. 2022;145(3):e18-e114. doi:10.1161/CIR.0000000000001039
Hwang D, Park S, Koo B-K. Ischemia with nonobstructive coronary artery disease. JACC: Asia. 2023;3(2):169-180. doi:10.1016/j.jacasi.2023.01.004
Yukselen Z, Majmundar V, Dasari M, Kumar PA, Singh Y. Chest pain risk stratification in the emergency department: current perspectives. Open Access Emerg Med. 2024;16:29-43. doi:10.2147/OAEM.S419657 | |||
| 456. ACS Guidelines Question #2 with Dr. Michelle O’Donoghue | 25 Jun 2026 | 00:10:03 | |
This episode is part of our comprehensive Decipher the Guidelines Series covering the 2025 ACC/AHA/ACEP/NAEMSP/SCAI Guideline for the Management of Patients With Acute Coronary Syndromes. The following question refers to Section 5.2.1 of the 2025 ACS Guidelines.The question is asked by Thomas Jefferson medical student and CardioNerds Academy Intern Dr. Grace Qiu, answered first by Henry Ford Interventional cardiology fellow and member of the CardioNerds Interventional Cardiology Council Dr. Li Pang, and then by expert faculty Dr. Michelle O’Donoghue.Dr. O’Donoghue is a cardiologist, senior investigator with the TIMI Study Group, and Associate Professor of Medicine at Harvard Medical School who holds the McGillycuddy-Logue Endowed Chair in Cardiology at Brigham and Women’s Hospital. She was the Vice Chair of the Writing Committee for the 2025 ACS Guidelines.
Question #2
A 63-year-old woman presented to the emergency room for chest pain. She described having exertional chest pain for the past two months and had an episode of severe pain after dinner 3 days ago. She went to bed and slept it off. She told her children today at a family gathering, and was immediately brought to the ED by her daughter. She has a history of hypertension and hyperlipidemia. She was asymptomatic and normotensive in the ED. Labs show a down-trending troponin and an elevated NT-proBNP but are otherwise unremarkable. Her ECG showed Q waves with ST elevation in V2-V4. She was treated with aspirin and heparin drip, and taken to the cath lab. Coronary angiogram showed complete proximal LAD occlusion with right-to-left collaterals, without significant residual disease elsewhere. She remains asymptomatic and is stable, both hemodynamically and electrically.What is the next best step with regard to reperfusion and anti-thrombotic management?AProceed with primary PCI to LAD BMedical management with aspirin and enoxaparin CMedical management with aspirin and clopidogrelDMedical management with aspirin and ticagrelor
Answer #2
Explanation The Correct answer is DIn patients who are stable with STEMI and have a totally occluded infarct-related artery >24 hours after symptom onset and are without evidence of ongoing ischemia, acute severe HF, or life-threatening arrhythmia, PPCI should not be performed due to lack of benefit. (Class 3, LOE B-R)The benefit of PPCI begins to diminish after >12 hours from symptom onset, but there appears to be continued benefit through approximately 24 hours. In stable asymptomatic patients with an occluded artery >48 hours after symptom onset, routine PCI has not been shown to be beneficial in the absence of ongoing ischemia. The relative utility of routine PCI for asymptomatic patients with STEMI between 24 and 48 hours from symptom onset is less rigorously tested.PCI is not recommended for an occluded infarct-related artery if the patient is asymptomatic and has a completed infarct. MACE outcomes were similar in those with an occluded infarct-related artery who underwent medical therapy versus those who underwent PCI 3 to 28 days after an MI (Occluded Artery Trial [OAT]), and results were no different at 7-year follow-up. Similar findings were noted in the DECOPI (Desobstruction Coronaire en Post-Infarctus) trial, which enrolled patients with an occluded artery and Q waves on the ECG presenting 2 to 15 days after symptom onset.However, coronary revascularization should be considered for patients with late presentations with continued signs and symptoms of ischemia, including cardiogenic shock, acute severe HF, persistent angina, and life-threatening arrhythmias. Main TakeawayIn patients who are stable with STEMI who have a totally occluded infarct-related artery >24 hours after symptom onset and are without evidence of ongoing ischemia, acute severe HF, or life-threatening arrhythmia, PPCI should not be performed due to lack of benefit.Guideline Loc.Section 5.2.1 | |||
| 455. The Long-Term Management Of Patients With Pulmonary Embolism with Dr. Soophia Naydenov | 21 Jun 2026 | 00:19:12 | |
CardioNerds (Amit and Dan), Billy Joe Mullinax, and Saahil Jumkhawala discuss the long term management of pulmonary embolism with Dr. Soophia Naydenov. The episode focuses on the approach to patients who struggle with persistent symptoms like dyspnea and fatigue even after completing the acute phase of anticoagulation. This spectrum of disease, ranging from mild post-PE impairment to chronic thromboembolic pulmonary hypertension (CTEPH), requires a structured follow-up. The discussion covers the critical importance of identifying CTEPH early, the necessary timelines for follow-up, and the appropriate objective screening tools and invasive testing to guide patient care toward full functional recovery. Audio editing by CardioNerds academy intern, Grace Qiu.
Dr. Dinu Balanescu and Dr. Billy-Joe Mullinax are Co-chairs for the CardioNerds PE Series, developed in collaboration with the PERT Consortium.
Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values.
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Acronyms
PE: Pulmonary Embolism
PERT: Pulmonary Embolism Response Team
CTEPH: Chronic Thromboembolic Pulmonary Hypertension
QL: Quality of Life
VTE: Venous Thromboembolism
DASH: D-dimer, Age, Sex, History of non-provoked PE (a risk score)
CPET: Cardiopulmonary Exercise Testing
PFTs: Pulmonary Function Tests
VQ Scan: Ventilation-Perfusion Scan
DOACs: Direct Oral Anticoagulants
TPA: Tissue Plasminogen Activator (Thrombolytics)
ECMO: Extracorporeal Membrane Oxygenation
Pearls:
Post-PE "Syndrome" is a Spectrum: It is more accurately a spectrum of disease (sequelae of PE) rather than a single syndrome, ranging from mild fatigue/dyspnea to the most severe form, CTEPH.
Structured Follow-up is Mandatory: All PE survivors need a structured follow-up, typically with checkpoints at 3, 6, 12, and 16–24 months, with the primary goal being to detect CTEPH, the deadliest, yet potentially curable, disease on the spectrum.
Screening Should Be Objective and Practical: When screening for persistent symptoms, use objective assessment tools like the Post-VTE Functional Status (PVFS) scale or the Modified Medical Research Council (MMR-C) scale, as highly comprehensive but cumbersome tools (like the PE Quality of Life questionnaire) may not be practical for routine clinical use. Recurrence Risk Scores Aid in Anticoagulation Duration: Simple scores like the DASH score or the HERDO2 score (for women) can provide guidance when considering the continuation versus discontinuation of anticoagulation after the initial treatment phase.
Invasive Testing for Persistent Symptoms: If a patient remains symptomatic at the 6-month mark despite normal non-invasive testing (chest X-ray, ECG, PFTs, six-minute walk, echo, VQ scan, CPET), consider invasive testing such as Right Heart Catheterization (RHC) at rest or with exercise, or an invasive CPET.
Notes:
Notes drafted by Saahil Jumkhawala.
1. The Spectrum of Post-PE Disease
The term "post-PE syndrome" should be used with caution, as it refers to a spectrum of disease rather than a single entity.
This spectrum includes symptoms (sequelae) that exist in a patient's life following an incidental PE event that they did not have before.
On one extreme is Chronic Thromboembolic Pulmonary Hypertension (CTEPH):
The definition is clear, but it is the most deadly type, though thankfully rare (2% to 4%).
It involves a residual clot and pulmonary hypertension identifiable at rest.
In the middle is Chronic Thromboembolic Disease (CTED):
Patients may have residual defects seen on a VQ or CT scan, but they do not have pulmonary hypertension.
On the other side is a milder disease, which can include fatigue, dyspnea, or a patient's perceived impairment, where the definitions of CTEPH and CTED are not met, but the patient remains symptomatic.
2. Structured Follow-up and Screening for Post-PE Symptoms
Structured follow-up is key for all PE survivors, though the structure may vary based on available resources (PCP, Cardiology, Pulmonary, or multidisciplinary clinic).
Recommended Timeline for Follow-up: Data from studies like ELOPE and FOCUS suggest checkpoints at 3, 6, 12, and up to 16 to 24 months.
This timeline is designed to identify patients who may develop CTEPH.
88% of patients who develop CTEPH will be identified within about a year.
A structured follow-up can reduce the delay in CTEPH diagnosis from 10–12 months to 4–6 months.
Personal Practice Note: A quick 2–3 week/30-day check-in is recommended for severely ill patients (e.g., those who had TPA, profound shock, or ECMO support) to ensure medication compliance, manage symptoms, and identify red flags.
Screening Tools (Objective Assessment):
The first step is an inventory of patient symptoms, leaning toward objective rather than subjective assessment.
Recommended Simple Tools:
Modified Medical Research Council (MMR-C) for dyspnea evaluation.
Post-VTE Functional Status (PVFS) scale.
The Pulmonary Embolism Quality of Life (QL) questionnaire is comprehensive but long, making it tedious and better suited for research.
Future Utility: Technology (AI/electronic tools) may assist in administering these questionnaires before the clinic visit, presenting the information as a "dashboard" for the provider.
3. Management of Persistent Symptoms and Further Testing
Initial Non-Invasive Tests (Often done at 3 months):
Echocardiogram
VQ Scan
Full PFTs
Six-minute walk
CPET
Further Evaluation for Persistent Symptoms (e.g., at 6 months): If non-invasive tests (Chest X-ray, ECG, CPET) are normal but symptoms persist, more invasive testing should be considered as the patient has not returned to baseline.
Repeat VQ scan or echocardiogram if symptoms have changed.
Right Heart Catheterization (RHC) at rest or with exercise.
Invasive CPET.
PA gram (Pulmonary Angiogram) to assess vasculature.
4. Recurrence Risk and Anticoagulation Duration
The decision to continue or discontinue anticoagulation depends on the patient's risk factors, the situation of the PE (provoked or unprovoked), presence of active cancer, and patient preference.
Recurrence Risk Scores:
Simple scores are preferred for practicality.
DASH Score.
HERDO2 Score (particularly for women).
The Vienna Score can be considered if the question is whether to restart anticoagulation after a disruption.
Role of D-dimer in Abbreviation: While D-dimer can be used to guide the decision to restart anticoagulation after a planned pause (if D-dimer is high, resume), patient symptoms are preferable to guide management decisions like early abbreviation.
5. Prevention of Post-PE Syndrome
Currently, there is no clear tool known to prevent the post-PE syndrome/spectrum of disease.
Best Current Advice for Prevention/Recovery:
Anticoagulation compliance.
Pulmonary rehabilitation, which aids in faster recovery.
General precautions, such as smoking cessation and body weight management.
Future Research: Ongoing trials are investigating whether acute management strategies (e.g., using thrombolytics in intermediate-risk PE) can prevent long-term sequelae. (The PYTHO trial did not show a reduced rate of CTEPH in intermediate-risk PE patients who received thrombolytics).
References:
Khan, F., Tritschler, T., Kahn, S. R., & Rodger, M. A. "Venous Thromboembolism." The Lancet, vol. 398, no. 10294, 2021, pp. 64-77. doi:10.1016/S0140-6736(20)32658-1.
Kearon, C., & Kahn, S. R. "Long-Term Treatment of Venous Thromboembolism." Blood, vol. 135, no. 5, 2020, pp. 317-325. doi:10.1182/blood.2019002364.
Kahn, S. R., & de Wit, K. "Pulmonary Embolism." The New England Journal of Medicine, vol. 387, no. 1, 2022, pp. 45-57. doi:10.1056/NEJMcp2116489.
Di Nisio, M., van Es, N., & Büller, H. R. "Deep Vein Thrombosis and Pulmonary Embolism." The Lancet, vol. 388, no. 10063, 2016, pp. 3060-3073. doi:10.1016/S0140-6736(16)30514-1.
Chopard, R., Albertsen, I. E., & Piazza, G. "Diagnosis and Treatment of Lower Extremity Venous Thromboembolism: A Review." JAMA, vol. 324, no. 17, 2020, pp. 1765-1776. doi:10.1001/jama.2020.17272. | |||
| 454. ACHD Surgery 101: Thinking Like a Surgeon with Elizabeth Stephens | 10 Jun 2026 | 00:42:42 | |
CardioNerds (Drs. Rawan Amir, Tripti Gupta, and Alysha Joseph) discuss the fundamentals of adult congenital heart disease (ACHD) surgery with Dr. Elizabeth Stephens. Audio editing by CardioNerds academy intern, Grace Qiu.
Using a case of a young adult undergoing a Ross procedure, the episode walks through what happens in the operating room—from induction and intraoperative transesophageal echocardiography (TEE) to cardiopulmonary bypass (CPB), myocardial protection, and surgical repair. The discussion highlights key concepts including cardioplegia, cross-clamp and bypass times, hypothermic circulatory arrest, and the complexity of redo sternotomy. This episode provides learners with a practical framework to interpret operative reports, anticipate postoperative physiology, and better collaborate with surgical teams.
This episode was produced by the CardioNerds ACHD Council and planned by Dr. Rawan Amir.
CardioNerds Adult Congenital Heart Disease PageCardioNerds Episode Page
Pearls
“LV distension kills patients.”Preventing left ventricular distension with appropriate venting and awareness of aortic insufficiency is critical to intraoperative safety.
TEE can change the surgical plan in real time.Findings such as underestimated aortic regurgitation, mitral pathology, or a PFO may directly alter cannulation and cardioplegia strategy.
Cross-clamp time = myocardial ischemic time; bypass time = systemic stress.Both are key predictors of postoperative complications including renal injury, bleeding, and ventricular dysfunction.
Redo sternotomy risk is driven by anatomy, not just number.Aorta adherent to the sternum, conduit position, and chamber pressurization define risk more than the number of prior surgeries.
Think longitudinally—ACHD surgery is lifetime planning.Surgical materials and strategies must account for future interventions, especially in younger patients.
Notes:
Notes drafted by Dr. Alysha Joseph, aided by generative artificial intelligence.
What are the key steps in congenital cardiac surgery from incision to closure?
Preoperative planning is multidisciplinary, involving surgeon, anesthesia, cardiology, and ICU teams; high-risk inductions (e.g., critical AS, Williams syndrome) are identified early
TEE is performed immediately after induction to reassess anatomy and may reveal new findings (e.g., underestimated AI, mitral disease, PFO)
Median sternotomy is performed, followed by creation of a pericardial well to optimize exposure
Heparin is administered prior to cannulation; arterial and venous cannulas are placed for initiation of CPB
Cross-clamp is applied and cardioplegia delivered to arrest the heart, allowing a still and protected operative field
Surgical repair (e.g., Ross procedure) is performed, followed by de-airing, cross-clamp removal, and reperfusion
Patient is weaned from bypass with TEE reassessment, hemostasis achieved, and chest closed
What is cardioplegia and how is it delivered?
Cardioplegia is a potassium-rich solution that arrests myocardial activity and reduces metabolic demand
Most commonly used solution in the U.S. is Del Nido cardioplegia, originally developed for pediatric myocardium
Delivery strategies include:
Antegrade (via aortic root) – standard approach
Ostial (direct coronary delivery) – used when aortic root cannot be relied upon
Retrograde (via coronary sinus) – useful in severe AI or coronary disease
NOTE: Severe aortic regurgitation can impair antegrade delivery and requires alternative strategies and LV venting
What do cross-clamp time and bypass time represent clinically?
Cross-clamp time = duration of myocardial ischemia while the heart is arrested
Bypass time = total duration on CPB, reflecting systemic exposure to non-physiologic circulation
Prolonged cross-clamp time (>2–3 hours) increases risk of myocardial dysfunction, especially with poor baseline function
Longer bypass time is associated with increased risk of renal injury, coagulopathy, and bleeding
These metrics often reflect both case complexity and intraoperative challenges
What is hypothermic circulatory arrest (HCA) and when is it used?
HCA involves complete cessation of blood flow to allow a bloodless surgical field
Typically used in complex aortic arch repairs
Patients are cooled to ~18°C to reduce metabolic demand and protect organs
Duration is ideally limited to <30 minutes to minimize neurologic injury
Adjuncts include:
Antegrade cerebral perfusion (ACP) – provides targeted brain perfusion
Retrograde cerebral perfusion (RCP) – less effective for oxygen delivery
What makes redo congenital cardiac surgery high risk?
Re-entry risk depends on anatomical relationships:
Aorta adherent to sternum (especially midline) poses high risk of catastrophic bleeding
RVOT conduits or pressurized chambers near sternum increase injury risk
Loss of peripheral vascular access from prior procedures limits bailout options
Accumulated comorbidities (renal, hepatic dysfunction) increase perioperative risk
Diastolic dysfunction and ventricular impairment complicate weaning from bypass
Complexity of planned repair and institutional/surgeon experience significantly influence outcomes
What does “venting the ventricle” mean and why is it important?
Venting refers to decompression of the left ventricle using a cannula (often via right superior pulmonary vein)
Prevents LV distension, which can impair myocardial protection and lead to hemodynamic collapse
Particularly important in the presence of aortic insufficiency or inadequate forward flow
Failure to adequately vent can result in arrhythmias, poor recovery, and adverse outcomes
What materials are used in congenital surgery and how do they impact long-term care?
Common patch materials include bovine pericardium (durable, non-stretch), Dacron, Gore-Tex, and autologous pericardium
Conduits (e.g., homografts, Contegra, Hancock) are used to connect cardiac structures and often contain valves
Most materials do not grow with the patient and are prone to calcification over time
Surgical decisions must consider future transcatheter or surgical interventions
Limited availability of certain graft sizes (e.g., pulmonary homografts) impacts real-world decision-making
References:
1. Salis, S. et al. Cardiopulmonary bypass duration is an independent predictor of morbidity and mortality after cardiac surgery. J Cardiothorac Vasc Anesth. 2008;22(6):814-822. doi:10.1053/j.jvca.2008.08.004
2. Al-Sarraf, N. et al. Cross-clamp time is an independent predictor of mortality and morbidity in low- and high-risk cardiac patients. International journal of surgery (London, England). 2011; 9(1):104–109. https://doi.org/10.1016/j.ijsu.2010.10.007
3. Weiland, A. P. et al. Physiologic principles and clinical sequelae of cardiopulmonary bypass. Heart & lung : the journal of critical care. 1986;15(1):34–39.
4. Park, C. B. et al. Identifying patients at particular risk of injury during repeat sternotomy: analysis of 2555 cardiac reoperations. The Journal of thoracic and cardiovascular surgery. 2010;140(5):1028–1035. https://doi.org/10.1016/j.jtcvs.2010.07.086
5. Morales, D. L. et al. Repeat sternotomy in congenital heart surgery: no longer a risk factor. The Annals of thoracic surgery. 2008; 86(3):897–902. https://doi.org/10.1016/j.athoracsur.2008.04.044
6. Francica, A. et al. Cardioplegia between Evolution and Revolution: From Depolarized to Polarized Cardiac Arrest in Adult Cardiac Surgery. Journal of clinical medicine. 2021;10(19):4485. https://doi.org/10.3390/jcm10194485
7. Ghia, S. et al. Hypothermic Circulatory Arrest in Adult Aortic Arch Surgery: A Review of Hypothermic Circulatory Arrest and its Anesthetic Implications. Journal of cardiothoracic and vascular anesthesia. 2023; 37(12): 2634–2645. https://doi.org/10.1053/j.jvca.2023.08.139
8. Peivandi, A. D. et al. Grafts and Patches: Optimized but Not Optimal Materials for Congenital Heart Surgery. Pediatric cardiology. 2023;44(5):996–1002. https://doi.org/10.1007/s00246-023-03153-6 | |||
| 453. ACS Guidelines Question #1 with Dr. Sunil Rao | 04 Jun 2026 | 00:10:29 | |
The following question refers to Section 7.1 of the 2025 ACS Guidelines.
The question is asked by Thomas Jefferson medical student and CardioNerds Academy Intern Dr. Grace Qiu, answered first by University of Michigan fellow and CardioNerds FIT Ambassador Dr. Kayla Secrest, and then by expert faculty Dr. Sunil Rao.
Dr. Rao is an interventional cardiologist, Professor of Medicine at NYU Grossman School of Medicine, Deputy Director of the Leon H. Charney Division of Cardiology, and the Director of Interventional Cardiology for the NYU Langone Health System. He is the Editor-in-Chief for Circulation Cardiovascular Interventions and was the Chair of the Writing Committee for the 2025 ACS Guidelines.
This episode is part of our comprehensive Decipher the Guidelines Series covering the 2025 ACC/AHA/ACEP/NAEMSP/SCAI Guideline for the Management of Patients With Acute Coronary Syndromes.
Question #1
A 68-year-old man with a history of hypertension, hyperlipidemia, stage III chronic kidney disease, and prior tobacco use presents to a local emergency department with reports of chest pain while raking leaves at home. Upon arrival, he is hemodynamically stable with a heart rate of 86 beats per minute and a blood pressure of 133/85 mmHg. His EKG reveals ST elevations in the septal and anterior leads (V1-V4). He is given 324mg of aspirin and is promptly evaluated by the interventional cardiology team, who elects to take him emergently to the catheterization lab. Upon arrival to the catheterization lab, the nurse asks the interventional fellow which access sites they should prep for this case? How should the interventional fellow respond?ARight radial artery onlyBRadial + bilateral femoralCBilateral femoral only
Answer #1
Explanation The correct answer is B. Radial and bilateral femoralRadial artery access is the preferred vascular access site for coronary angiography and PCI in patients with ACS. Transradial access has been shown to reduce mortality, bleeding, and vascular complications compared with transfemoral access (Class I, LOE A). Radial access also allows earlier ambulation and is associated with greater patient comfort.Although the right radial artery is the most widely studied upper-extremity access site, alternative sites such as the ulnar and distal radial arteries have demonstrated similar outcomes.However, the radial artery may be required as a bypass conduit for CABG. In institutions where the radial artery is routinely used for surgical grafting, this potential future use should be considered when selecting vascular access.In addition, transfemoral access—preferably performed with ultrasound guidance—should be considered in patients in whom temporary mechanical circulatory support (MCS) is anticipated or in those for whom radial access is not feasible due to anatomical or technical constraints. Prepping bilateral groins in addition to the radial artery provides a backup strategy for urgent MCS placement or for transition to femoral access should radial access fail.For these reasons, prepping both the radial artery and bilateral groins is the most appropriate response.Radial-only preparation is incorrect because, although radial access is preferred, patients with STEMI may still require emergent MCS or alternative access if the radial artery is unsuitable. Preparing only the wrist without backup femoral access may delay care should hemodynamic instability occur.Femoral-only preparation is incorrect because transradial access provides superior outcomes in ACS, including significant reductions in all-cause mortality, major bleeding, and vascular complications. RCTs and meta-analyses, including MATRIX (which showed lower MACE and net adverse clinical events with radial access) and SAFARI-STEMI (which showed no difference in mortality but was underpowered)—support radial as first-line access when feasible.Main TakeawayFor patients with ACS undergoing PCI, radial access is strongly preferred to reduce mortality, bleeding, and vascular complications.Guideline Loc.Section 7.1 | |||
| 452. Risk stratification in Acute Pulmonary Embolism with Dr. Stavros Konstantinides | 01 Jun 2026 | 00:25:35 | |
CardioNerds (Dr. Billy-Joe Mullinax, Dr. Dinu Balanescu, and Dr. Jane Ehret) discuss risk stratification in acute pulmonary embolism with Dr. Stavros Konstantinides, Chair of the 2019 ESC Pulmonary Embolism Guidelines. Using a real-world case, this episode explores how modern PE care has moved beyond “massive” and “submassive” labels toward a dynamic, physiology-based approach. The discussion highlights the limitations of static risk scores, the importance of right ventricular dysfunction and biomarkers, and why normotension does not imply stability. Special emphasis is placed on intermediate-high risk PE, early identification of impending hemodynamic collapse, and the role of lactate, serial reassessment, and PERT teams in guiding escalation of care. Audio editing by CardioNerds intern, Joshua Khorsandi.The 2026 American multi-society PE guidelines were published after this episode was recorded.
Dr. Dinu Balanescu and Dr. Billy-Joe Mullinax are Co-chairs for the CardioNerds PE Series, developed in collaboration with the PERT Consortium.
Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values.
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Pearls
Stable blood pressure does not mean low risk in PEHypotension is a late finding. Patients may have severe RV failure, hypoxia, and tissue hypoperfusion while remaining normotensive — a key concept behind “normotensive shock.”
Risk stratification in PE must be dynamic, not staticLegacy scores like PESI and Bova provide a snapshot and predict 30-day mortality, but they do not capture short-term trajectory or impending hemodynamic collapse.
Intermediate-high risk PE is a dangerous and heterogeneous groupPatients with RV dysfunction, positive biomarkers, tachycardia, hypoxemia, and elevated lactate may have in-hospital mortality approaching 15%, rivaling STEMI.
Lactate is a critical but underutilized marker in PEElevated lactate reflects tissue hypoxia and early circulatory failure and may identify patients at risk for collapse before blood pressure declines.
PERT enables physiology-driven, patient-centered PE carePERT teams operationalize continuous reassessment, integrate imaging, labs, and clinical trajectory, and allow timely escalation — shifting PE management from rigid categories to real-time decision-making.
Notes
Drafted by Dr. Jane Ehret.
1. What is the contemporary framework for risk stratification in acute pulmonary embolism?
Modern PE risk stratification prioritizes hemodynamics and right ventricular (RV) function rather than clot burden.
The 2019 ESC Guidelines classify PE into high risk, intermediate risk (low vs high), and low risk, based on: Hemodynamic status, RV dysfunction on imaging, and Cardiac biomarkers.
This framework emphasizes early mortality risk but requires clinical context to guide escalation decisions.
2. Why is normotension insufficient to define “stability” in PE?
Blood pressure is a late marker of circulatory failure in PE.
Patients can maintain normal BP through Tachycardia, Increased sympathetic tone, and RV compensation.
Many patients with preserved BP may already have shock physiology, including hypoxemia, elevated lactate, and RV failure — sometimes referred to as “normotensive shock.”
3. How should intermediate-risk PE be conceptualized clinically?
Intermediate-risk PE is heterogeneous, ranging from patients who do well on anticoagulation to those who deteriorate rapidly.
Intermediate-high risk PE is defined by RV dysfunction on imaging and positive cardiac biomarkers.
Clinical features such as tachycardia, increasing oxygen requirement, and elevated lactate identify patients at highest risk within this group.
4. What are the strengths and limitations of commonly used PE risk scores?
Legacy scores are useful for initial risk categorization but are static and limited in predicting short-term deterioration.
Most scores were developed to predict mortality or complications at fixed time points rather than dynamic clinical trajectory.
5. What are the commonly used risk scores and clinical tools in PE, and what is each designed to predict?
ESC Risk Stratification Algorithm: Identifies high-risk PE by hemodynamics. Uses PESI or sPESI in normotensive patients to distinguish low-risk from non–low-risk PE. Uses RV dysfunction and biomarkers to differentiate intermediate-low from intermediate-high risk. Forms the basis of many institutional PE pathways.
PESI and sPESI: Validated to predict 30-day mortality. Widely used to identify low-risk patients appropriate for outpatient management. Heavily influenced by age and comorbidities.
Bova Score: Predicts 30-day PE-related complications in normotensive patients.
Composite PE Shock Score (CPES): Predicts normotensive shock in hemodynamically stable PE patients.
Pulmonary Embolism Progression (PEP) Score: Predicts progression from intermediate-risk to high-risk PE within 72 hours of diagnosis.
PE Short-term Clinical Outcomes Risk Estimation (PE-SCORE): Predicts clinical deterioration or death within 5 days of PE diagnosis.
Hestia Criteria: Identifies low-risk PE patients safe for outpatient treatment.
Wells’ Criteria and Revised Geneva Score: Determine pretest probability for diagnostic triage.
PERC Score: Rules out PE in very low-risk patients.
6. What is the role of biomarkers in PE risk stratification?
Troponin and natriuretic peptides reflect RV myocardial injury and strain.
Current guidelines treat biomarkers as binary (positive vs negative), despite risk being continuous.
Biomarkers are most helpful for: Initial risk classification.
They are less useful for: Short-interval monitoring and Detecting rapid clinical deterioration.
7. Why is lactate an important physiologic marker in PE?
Lactate reflects global tissue hypoxia and impaired perfusion.
Elevated lactate may identify patients with: Early circulatory failure and Increased risk of imminent hemodynamic collapse.
Lactate is not currently included in ESC risk algorithms but may add important prognostic information in intermediate-risk patients.
8. How does trajectory influence decision-making in PE management?
Risk stratification should be viewed as a dynamic process, not a one-time label.
Worsening clinical trajectory may include: Rising heart rate, Increasing oxygen needs, Rising lactate, and Progressive RV dysfunction.
Serial reassessment is essential for timely escalation of care.
9. What role do Pulmonary Embolism Response Teams (PERT) play in risk stratification?
PERT facilitates: Multidisciplinary decision-making and Integration of imaging, biomarkers, and clinical physiology.
PERT is most valuable for: Intermediate-risk and high-risk PE and Patients with complex comorbidities or uncertain trajectory.
PERT enables a shift from category-based to physiology-driven PE care.
References
1. Konstantinides SV, Meyer G, Becattini C, et al. 2019 ESC Guidelines for the diagnosis and management of acute pulmonary embolism developed in collaboration with the European Respiratory Society (ERS): The Task Force for the diagnosis and management of acute pulmonary embolism of the European Society of Cardiology (ESC). Eur Respir J. 2019;54(3):1901647. Published 2019 Oct 9. doi:10.1183/13993003.01647-2019
2. Leidi A, Bex S, Righini M, Berner A, Grosgurin O, Marti C. Risk Stratification in Patients with Acute Pulmonary Embolism: Current Evidence and Perspectives. J Clin Med. 2022;11(9):2533. Published 2022 Apr 30. doi:10.3390/jcm11092533
3. Choi WH, Kwon SU, Jwa YJ, et al. The pulmonary embolism severity index in predicting the prognosis of patients with pulmonary embolism. Korean J Intern Med. 2009;24(2):123-127. doi:10.3904/kjim.2009.24.2.123
4. Jiménez D, Aujesky D, Moores L, et al. Simplification of the pulmonary embolism severity index for prognostication in patients with acute symptomatic pulmonary embolism. Arch Intern Med. 2010;170(15):1383-1389. doi:10.1001/archinternmed.2010.199
5. Chen X, Shao X, Zhang Y, et al. Assessment of the Bova score for risk stratification of acute normotensive pulmonary embolism: A systematic review and meta-analysis. Thromb Res. 2020;193:99-106. doi:10.1016/j.thromres.2020.05.047
6. Zhang RS, Yuriditsky E, Zhang P, et al. Composite Pulmonary Embolism Shock Score and Risk of Adverse Outcomes in Patients With Pulmonary Embolism. Circ Cardiovasc Interv. 2024;17(8):e014088. doi:10.1161/CIRCINTERVENTIONS.124.014088
7. Zhang RS, Alam U, Sharp ASP, et al. Validating the Composite Pulmonary Embolism Shock Score for Predicting Normotensive Shock in Intermediate-Risk Pulmonary Embolism. Circ Cardiovasc Interv. 2024;17(2):e013399. doi:10.1161/CIRCINTERVENTIONS.123.013399
8. Ehret J, Wakefield D, Badlam J, Antkowiak M, Erdreich B. Development of the Pulmonary Embolism Progression (PEP) score for predicting short-term clinical deterioration in intermediate-risk pulmonary embolism: a single-center retrospective study. J Thromb Thrombolysis. 2025;58(2):243-253. doi:10.1007/s11239-024-03051-5
9. Weekes AJ, Raper JD, Lupez K, et al. Development and validation of a prognostic tool: Pulmonary embolism short-term clinical outcomes risk estimation (PE-SCORE). PLoS One. 2021;16(11):e0260036. Published 2021 Nov 18. doi:10.1371/journal.pone.0260036
10. Zondag W, Hiddinga BI, Crobach MJ, et al. Hestia criteria can discriminate high- from low-risk patients with pulmonary embolism. Eur Respir J. 2013;41(3):588-592. doi:10.1183/09031936.00030412
11. Wells PS, Anderson DR, Rodger M, et al. Excluding pulmonary embolism at the bedside without diagnostic imaging: management | |||
| 451: CCTA, CT-FFR, and AI Plaque Analysis to Personalize CAD Detection, Prevention, and Management with Dr. Michael Gallagher | 27 May 2026 | 00:46:23 | |
CardioNerds Dr. Joseph Kassab, Dr. Mariana Garcia-Arango, and Dr. Christopher Mason explore the technological revolution of Coronary CT Angiography (CCTA) with expert faculty Dr. Michael Gallagher. The discussion details how CCTA has evolved into a frontline diagnostic and preventive tool, moving beyond simple anatomy to incorporate physiology via CT-FFR and biology through AI-driven plaque quantification. The episode reviews landmark evidence like the SCOT-HEART and PROMISE trials, the nuances of CAD-RADS 2.0 reporting, and the emerging role of AI in monitoring treatment response and personalizing cardiovascular care. Critically, they also discuss some of the assumptions and limitations of these techniques.
Stay tuned for a matching review article to be submitted to US Cardiology Review, the official Journal of CardioNerds.
This episode was supported by an independent medical education grant from HeartFlow. All CardioNerds education is planned, produced, and reviewed solely by CardioNerds.
Enjoy this Circulation Paths to Discovery article to learn more about the CardioNerds mission and journey.
US Cardiology Review is now the official journal of CardioNerds! Submit your manuscripts here.
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Pearls
Shift in Paradigm: CCTA is no longer just an anatomic test; with some key limitations, it can provide anatomy, physiology (CT-FFR), and plaque biology (AI-CPA) in a single non-invasive scan.
The "Power of Zero" vs. Plaque: While a normal CCTA has a >95% negative predictive value, future MIs often arise from non-obstructive plaque that traditional stress tests might miss.
CAD-RADS 2.0 Utility: The addition of plaque burden modifiers (P1–P4) is a "game changer," allowing clinicians to identify high-risk patients who need aggressive lipid-lowering despite having only mild stenosis.
CT-FFR as a Virtual Stress Test: CT-FFR uses computational fluid dynamics to simulate blood flow, potentially reducing unnecessary invasive catheterizations by approximately 61% without sacrificing safety.
Seeing the Invisible: AI-based quantitative plaque analysis (QCPA) can identify "subvisual" plaque and low-attenuation (lipid-rich) components that are the primary drivers of acute coronary syndromes.
Show Notes
How has the role of CCTA changed compared to traditional functional testing?
Historically, stress testing answered "is there ischemia today?", which often reflects late-stage disease.
CCTA identifies disease across the entire spectrum, asking "is there atherosclerosis and how much plaque is present?".
Landmark evidence: SCOT-HEART showed a 41% relative risk reduction in MI at 5 years attributed to intensified preventive therapies, and PROMISE showed CCTA was better at selecting patients who truly needed invasive angiography.
Diagnostic CCTA imaging depends on the protocol, contrast timing, heart rate, heart rhythm, breathholding, scanner quality, and several patient factors (obesity, prior stents, heavy calcification, complex bypass anatomy, and motion artifact all may limit imaging). “CCTA is exceptional for the right patient, with the right scanner, and the right team.”
What are the key modifiers introduced in CAD-RADS 2.0, and why do they matter?
CAD-RADS 2.0 moved beyond stenosis severity to include plaque burden (P0 to P4), high-risk plaque (HRP) features, and the presence of ischemia based on CT-FFR.
It serves as a clinical decision support tool: a patient with mild (25-49%) stenosis but "extensive" (P4) plaque burden is considered high risk and warrants aggressive risk factor modification.
How is CT-FFR calculated, and when is it most useful in clinical practice?
CT-FFR uses resting CCTA data and computational fluid dynamics to create a 3D model of coronary flow during simulated maximal hyperemia.
It is often used for intermediate lesions (40–90% stenosis) to predict if they are ischemia-producing, guiding the decision whether to proceed with invasive angiography.
The assumptions necessary for this computational modeling may not apply well to patients with microvascular dysfunction, significant myocardial scar or prior infarction, or ventricular hypertrophy. Still, data indicate that CT-FFR performs similarly to PET in predicting hemodynamically significant lesions.
CT-FFR performs well at the extremes (either clearly normal or clearly abnormal). Accuracy dips, however, in the intermediate range (~0.75-0.80), where decision-making is most critical. In this grey zone, additional factors can help guide the approach, including the amount of myocardium supplied, translesional gradient, and plaque features.
CT-FFR has not been validated in distal segments, stented segments, heavily calcified coronary arteries, or in patients with severe aortic stenosis. Caution with CT-FFR should be utilized in very calcified coronary segments.
What is AI-based quantitative plaque analysis (QCPA), and what metrics are ready for clinical use?
This is potentially a paradigm shift, moving away from stenosis-centric thinking to a more disease burden and plaque biology focus.
QCPA uses deep learning algorithms to automatically segment the vessel wall and quantify plaque volume in mm³.
Ready for "prime time" metrics include: Total Plaque Volume (TPV), non-calcified plaque volume, and Low-Attenuation Plaque (LAP) burden.
Can serial CCTA be used to monitor the effectiveness of medical therapies like statins?
While not yet a routine guideline-driven practice, trials like PARADIGM and EVAPORATE show that therapies can stabilize plaque; notably, CCTA is better for monitoring than CAC scores, which can be misleading as statins often increase plaque calcification as part of the stabilization process.
There are no randomized trials that serial CCTAs improve outcomes. Cost and radiation exposure will be notable limitations. Serial scan timing, scan acquisition and interpretation standardization would be key.
Dr. Gallagher notes that we are moving toward a world in which plaque burden may become a "treatment biomarker," similar to tumor burden in oncology.
References
1. Coronary Computed Tomography Angiography From Clinical Uses to Emerging Technologies: JACC State-of-the-Art Review. Abdelrahman KM, Chen MY, Dey AK, et al. Journal of the American College of Cardiology. 2020;76(10):1226-1243. doi:10.1016/j.jacc.2020.06.076.
2. Non-Invasive Imaging in Coronary Syndromes: Recommendations of the European Association of Cardiovascular Imaging and the American Society of Echocardiography, in Collaboration With the American Society of Nuclear Cardiology, Society of Cardiovascular Computed Tomography, and Society for Cardiovascular Magnetic Resonance. Edvardsen T, Asch FM, Davidson B, et al. Journal of the American Society of Echocardiography : Official Publication of the American Society of Echocardiography. 2022;35(4):329-354. doi:10.1016/j.echo.2021.12.012.
3. 2021 AHA/ACC/ASE/CHEST/SAEM/SCCT/SCMR Guideline for the Evaluation and Diagnosis of Chest Pain: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. Gulati M, Levy PD, Mukherjee D, et al. Journal of the American College of Cardiology. 2021;78(22):e187-e285. doi:10.1016/j.jacc.2021.07.053.
4. Contemporary, Non-Invasive Imaging Diagnosis of Chronic Coronary Artery Disease. van der Bijl P, Gulati M, Saraste A, et al. Lancet (London, England). 2025;406(10519):2577-2587. doi:10.1016/S0140-6736(25)01586-7.
5. State of the Art: Evaluation and Medical Management of Nonobstructive Coronary Artery Disease in Patients With Chest Pain: A Scientific Statement From the American Heart Association. Slipczuk L, Blankstein R, Bucciarelli-Ducci C, et al. Circulation. 2025;152(23):e443-e466. doi:10.1161/CIR.0000000000001394.
6. Diagnostic Performance of Fractional Flow Reserve Derived From Coronary CT Angiography: The ACCURATE-CT Study. Li C, Hu Y, Jiang J, et al. JACC. Cardiovascular Interventions. 2024;17(17):1980-1992. doi:10.1016/j.jcin.2024.06.027.
7. Clinical Outcomes Based on Coronary Computed Tomography-Derived Fractional Flow Reserve and Plaque Characterization. Sato Y, Motoyama S, Miyajima K, et al. JACC. Cardiovascular Imaging. 2024;17(3):284-297. doi:10.1016/j.jcmg.2023.07.013.
8. Clinical Use of Coronary Computed Tomography Angiography-Derived Fractional Flow Reserve: Expert Consensus by an International Working Group. Tang CX, Leipsic JA, Nørgaard BL, et al. European Radiology. 2026;:10.1007/s00330-025-12313-6. doi:10.1007/s00330-025-12313-6.
9. Diagnostic accuracy of computed tomography–derived fractional flow reserve: a systematic review. Cook CM, Petraco R, Shun-Shin MJ, et al. JAMA Cardiol. 2017;2(7):803-810. Doi:10.1001/jamacardio.2017.1314
10. Diagnostic performance of noninvasive fractional flow reserve derived from coronary computed tomography angiography in suspected coronary artery disease: the NXT trial (Analysis of Coronary Blood Flow Using CT Angiography: Next Steps). Nørgaard BL, Leipsic J, Gaur S, et al. J Am Coll Cardiol. 2014;63(12):1145-1155. Doi:10.1016/j.jacc.2013.11.043
11. Comparison of coronary computed tomography angiography, fractional flow reserve, and perfusion imaging for ischemia diagnosis. Driessen RS, Danad I, Stuijfzand WJ, et al. J Am Coll Cardiol. 2019;73(2):161-173. Doi:10.1016/j.jacc.2018.10.056.
12. 1-year outcomes of FFRCT-guided care in patients with suspected coronary disease: the PLATFORM study. Douglas PS, De Bruyne B, Pontone G, et al. J Am Coll Cardiol. 2016;68(5):435-445. Doi:10.1016/j.jacc.2016.05.057.
13. Comparison of an initial risk-based testing strategy vs usual testing in stable symptomatic patients with suspected coronary artery disease: the PRECISE randomized clinical trial.... | |||
| 450. Journal Club: The I-CLASS Registry with Dr. Theofanie Mela and Dr. Pugazhendhi Vijayraman | 25 May 2026 | 00:19:54 | |
Join CardioNerds EP Council Chair Dr. Naima Maqsood and Episode Lead Dr. Sukriti Banthiya as they discuss the results of the International Collaborative LBBAP Study (I-CLAS) with expert faculty Dr. Theofanie Mela and Dr. Pugazhendhi Vijayraman. Audio editing by CardioNerds academy intern, Grace Qiu.
The International Collaborative LBBAP Study (I-CLAS) evaluated clinical outcomes between biventricular pacing (BVP) and left bundle branch area pacing (LBBAP) in patients with left ventricular ejection fraction (LVEF) ≤50% undergoing cardiac resynchronization therapy. Between January 2018 and June 2023, 2,579 patients were enrolled across 18 centers. The primary composite outcome was defined as all-cause mortality or heart failure hospitalization. LBBAP demonstrated a shorter paced QRS duration and was associated with a lower risk of primary composite outcome and heart failure hospitalization. No significant difference was observed in all-cause mortality. Additionally, procedural complications were lower with LBBAP.
This episode was planned in collaboration with Heart Rhythm TV with mentorship from Dr. Daniel Alyesh and Dr. Mehak Dhande.
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| 449. Atrial Fibrillation: Challenging Scenarios in Atrial Fibrillation Management with Dr. Bradley Knight | 21 May 2026 | 00:37:54 | |
In this episode, CardioNerds Dr. Colin Blumenthal, Dr. Kelly Arps, and Dr. Yong Hao Yeo are joined by electrophysiology expert Dr. Bradley Knight to discuss atrial fibrillation (AF) management in challenging clinical scenarios. We explore arrhythmias in patients with pre-excitation syndromes, particularly Wolff-Parkinson-White (WPW) syndrome, and strategies for rhythm control. We also discuss AF management in pregnancy, adult congenital heart disease, and patients with tachycardia-bradycardia (tach-brady) syndrome. This episode provides essential insights into nuanced decision-making for the care of patients with complex arrhythmia profiles. Audio editing by CardioNerds academy intern, Grace Qiu.
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PEARLS
AF in WPW is a true emergency—AV nodal blocking agents can be deadly. In patients with WPW syndrome, AF can rapidly conduct through the accessory pathway, risking ventricular fibrillation and sudden death. Avoid AV nodal blockers like beta-blockers and calcium channel blockers.
Catheter ablation is the first-line rhythm control strategy in WPW. Catheter ablation carries a Class I recommendation and offers >90% success. If antiarrhythmic drugs are needed, sodium channel blockers like flecainide or propafenone are preferred in patients without structural heart disease.
In pregnancy, protecting the mother is protecting the fetus. An unstable mother means an unstable fetus. Rate control is the first step in AF with rapid ventricular responses and electrical cardioversion is safe when needed. Multidisciplinary care is essential.
AF in congenital heart disease is often outside the pulmonary veins. Surgical scars and chamber remodeling in ACHD patients often lead to AF from non-pulmonary vein foci. Electrogram-based mapping and targeted ablation strategies are essential to increase success rate of durable rhythm control.
Tachy-brady syndrome may require pacing to unlock therapy. AF may cause atrial myopathy and sinus node dysfunction. These patients often require permanent pacing to allow safe use of rate-controlling medications like beta-blockers and to prevent syncope or chronotropic incompetence.
Notes: Notes drafted by Dr. Yong Hao Yeo
Why is atrial tachycardia in patients with WPW syndrome dangerous?
Patients with WPW commonly present with supraventricular tachycardia (SVT) due to atrioventricular reentrant circuits, either orthodromic or antidromic. This SVT can degenerate into AF.
In the absence of AV nodal as the governor between the atrium and ventricles, the accessory pathway may conduct impulses rapidly and frequently. This can lead to dangerously high ventricular rates, predisposing patients to ventricular fibrillation and sudden cardiac arrest.
What are some strategies for rhythm control in patients with WPW and atrial tachycardia?
Catheter ablation is the first-line therapy (Class I recommendation), with a success rate of over 90%.
Ablation reduces the risk of sudden cardiac arrest, though some patients may remain prone to AF.
If ablation is not feasible/ contraindicated, sodium channel blockers such as flecainide and propafenone are good options in patients without ischemia or structural heart disease (Class IIa recommendation).
Amiodarone should be avoided because it has a long half-life, can accumulate in the system, and may delay definitive treatment with catheter ablation.
AV nodal blocking agents like beta blockers and calcium channel blockers should be avoided, as they are less effective at controlling ventricular rate in WPW and can increase conduction over the accessory pathway. These agents can also exacerbate the risk of rapid ventricular rates during AF and worsen left ventricular function.
What are some special considerations in managing AF in pregnant patients?
The primary goal in managing cardiovascular disease during pregnancy is to protect the mother, as fetal outcomes depend on maternal well-being. Therefore, while caution is necessary, we should avoid undertreating pregnant patients with AF.
In cases of AF with rapid ventricular response (RVR), rate control is usually the first-line strategy, with beta blockers preferred over digoxin or non-dihydropyridine calcium channel blockers. It is then reasonable to initially observe for spontaneous conversion in stable patients.
Antiarrhythmic drugs (AADs) are generally avoided during the first trimester, but clinical judgment on a case-by-case basis is essential.
Evidence for the safety of AADs in pregnancy is limited, often derived from their use in other conditions such as fetal SVT. Flecainide and sotalol are reasonable options for rhythm control (Class IIa recommendation).
Electrical cardioversion is considered safe in pregnancy and should be utilized when indicated (Do not forget!).
There is no pregnancy-specific thromboembolic risk stratification tool. CHA₂DS₂-VASc scoring and the presence of risk factors like mitral stenosis can help guide anticoagulation decisions, though the magnitude of thromboembolic risk during pregnancy remains unclear.
Rate control agents are typically continued during delivery due to the increased physiologic stress of labor and delivery.
Multidisciplinary care is crucial and should involve obstetrics, maternal-fetal medicine, cardiology, and electrophysiology specialists.
What are some key considerations for AF management in patients with adult congenital heart disease (ACHD)?
Patients with repaired congenital heart disease are at increased risk for arrhythmias due to two main factors: surgical scars that create arrhythmogenic foci and mechanical remodeling of the atria or ventricles resulting from the underlying disease.
In these patients with structural heart disease, sodium channel blockers may not be ideal antiarrhythmic options.
When selecting an antiarrhythmic drug, clinicians must consider the nature of structural or surgical impairments, such as right bundle branch block or prolonged QT interval.
It is also essential to assess renal and hepatic function (often impaired in patients with ACHD) to ensure appropriate metabolism and clearance of antiarrhythmic medications.
Electrogram-based ablation strategies (those leveraging artificial intelligence are developing!) may help identify effective ablation targets, which are often outside the pulmonary veins in patients with ACHD. These individualized approaches can improve ablation success rates in this complex patient population.
What makes tachycardia-bradycardia (tach-brady) syndrome a unique challenge in arrhythmia management?
Patients who present with both AF and bradycardia, especially with syncope, require a thoughtful diagnostic approach to identify the underlying rhythm disturbance.
Extended cardiac monitoring, including event monitors or implantable loop recorders, can help capture intermittent arrhythmias and correlate them with symptoms.
AF may lead to atrial myopathy, and since the sinus node resides within the atrium, this can result in sinus node dysfunction—a hallmark of tachy-brady syndrome.
Following spontaneous conversion from AF to sinus rhythm, sinus node dysfunction may persist, leading to prolonged pauses or chronotropic incompetence.
Management becomes more complex when beta-blockers are needed for AF with RVR, as they can exacerbate bradycardia. Permanent pacemaker implantation is often the next step to consider.
Permanent pacemaker implantation is often considered to facilitate safe rate control in these cases.
In younger patients, aggressive AF burden reduction may prevent atrial remodeling and the development of true atrial myopathy, potentially avoiding pacemaker implantation.
References
Joglar JA, Chung MK, Armbruster AL, et al. 2023 ACC/AHA/ACCP/HRS Guideline for the Diagnosis and Management of Atrial Fibrillation: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. Circulation. 2023;149(1). doi:https://doi.org/10.1161/CIR.0000000000001193
Van IC, Rienstra M, Bunting KV, et al. 2024 ESC Guidelines for the management of atrial fibrillation developed in collaboration with the European Association for Cardio-Thoracic Surgery (EACTS). European Heart Journal. 2024;45(36). doi:https://doi.org/10.1093/eurheartj/ehae176
Joglar JA, Kapa S, Saarel EV, et al. 2023 HRS expert consensus statement on the management of arrhythmias during pregnancy. Heart Rhythm. Published online May 1, 2023. doi:https://doi.org/10.1016/j.hrthm.2023.05.017
Stout KK, Daniels CJ, Aboulhosn JA, et al. 2018 AHA/ACC Guideline for the Management of Adults With Congenital Heart Disease: Executive Summary. Journal of the American College of Cardiology. 2019;73(12):1494-1563. doi:https://doi.org/10.1016/j.jacc.2018.08.1028 | |||
| 448. The Braunwald Chronicles: The Complete Series — A CardioNerds Tribute to Dr. Eugene Braunwald | 30 Apr 2026 | 00:41:43 | |
CardioNerds (Amit Goyal, Daniel Ambinder, Carine Hamo, and Karan Desai) are honored to bring you The Braunwald Chronicles — a special tribute to the life and legacy of Dr. Eugene Braunwald.
Originally released as a 6-part series, we are now bringing these chapters together as one complete experience. These are stories of discovery, innovation, accidents, perseverance, and more… truly, these are the stories of cardiology itself — told firsthand by the father of modern cardiology. Dr. Braunwald’s life and work form the very foundation of contemporary cardiovascular medicine, and his story is, in many ways, the story of our field. Join us as we journey through the history of cardiology across six extraordinary chapters — from the early days of physiologic discovery, to the development of transseptal access, to defining the natural history of valvular disease, to shaping modern therapies for myocardial infarction, and beyond. Through it all, Dr. Braunwald reflects on the principles that guided his career — curiosity, perseverance, mentorship, and the importance of being in the right place, at the right time, with the right people.We hope this collection serves not only as an educational experience, but as a tribute to one of the greatest minds in the history of medicine.
We thank Dr. Karan Desai, Editorial APD with the CardioNerds Academy and fellow at the University of Maryland, for all the work he put into designing The Braunwald Chronicles. Audio editing by Pace Wetstein.
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| 447. Pulmonary Embolism: Approach to Systemic Thrombolysis in Acute Pulmonary Embolism with Dr. Allison Burnett | 24 Apr 2026 | 00:42:43 | |
CardioNerds Drs. Dinu Balanescu, Billy-Joe Mullinax, and Mariana Garcia discuss systemic thrombolysis in pulmonary embolism with expert Dr. Allison Burnett. Audio editing by CardioNerds Academy intern, student doctor, Pace Wetstein.
Pulmonary embolism is the third leading cause of cardiovascular death in the US, and high-risk PE carries a 30-day mortality risk as high as 30-50%. In this episode, we discuss the indications for systemic thrombolysis, including high-risk PE and cardiac arrest. We addressed how to appropriately select candidates for systemic thrombolysis, balancing the high risk of bleeding. Additionally, we discussed anticoagulation management and timing concurrent with lytic therapy, as well as the importance of multidisciplinary PERT teams.
The 2026 American multi-society PE guidelines were published after this episode was recorded.
Dr. Dinu Balanescu and Dr. Billy-Joe Mullinax are Co-chairs for the CardioNerds PE Series, developed in collaboration with the PERT Consortium.
Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values.
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Pearls
Risk stratification is crucial in acute pulmonary embolism care. Based on the ESC 2019 guidelines, low-risk PE patients are those who are normotensive with no evidence of right ventricular dysfunction. Intermediate risk includes two categories: intermediate-low, with normotensive patients who have a high PE score with negative biomarkers, and intermediate-high risk, which has elevated biomarkers or signs of RV strain. High-risk PE includes hemodynamically unstable patients (SBP<90) who have end-organ dysfunction, shock, or cardiac arrest.
The 2026 American multi-society PE guidelines presented a new clinical classification scheme is presented, entitled “Acute Pulmonary Embolism Clinical Categories,” with 5 categories (A-E) and subcategories, ranging from low to high risk for adverse outcomes.
Systemic lysis has been studied in patients at high and intermediate risk. Overall, the reduction in mortality has been seen in patients with high-risk PE.
Systemic thrombolysis is associated with high rates of bleeding, 2% fatal or high-risk intracranial hemorrhage per the PEITHO trial; therefore, selecting the appropriate population is critical to improve outcomes and balance the risks and benefits.
Multidisciplinary PERT teams are crucial for making high-quality decisions, and stewardship is necessary to optimize the care of patients with PE.
Notes
Notes: Notes drafted by Dr. Mariana Garcia-Arango
What is the role of systemic thrombolysis in the current era of available catheter-directed therapies?
Thrombolytic therapy reduces mortality, PE recurrence, and PE-related mortality in patients with acute PE.
The evidence supports use during high-risk PE and cardiac arrest.
The clinical presentation is often severe, with high stakes and limited time to mobilize to the cath lab on time for catheter therapies, especially in rural populations.
How to approach the use of systemic thrombolysis during CPR?
Cardiac arrest from PE carries a very poor outlook, with survival rates under 10%. Rapid, targeted interventions to restore circulation are critical.
Systemic thrombolysis may be considered for patients in cardiac arrest due to confirmed or strongly suspected pulmonary embolism, especially when standard ACLS interventions have not been successful.
What is the best anticoagulation approach while using lytics?
Most of the time, we should opt for low-molecular-weight heparin over unfractionated heparin, which has been shown to lead to less major bleeding and reduction of recurrent PE.
Exceptions to the rule include renal dysfunction or if there is consideration of cannulation for ECMO or other invasive procedures.
There is variation in practice regarding timing and initiation of anticoagulation while using lytics. There are different protocols given the variety of how studies were conducted.
If they are going to get mechanical catheter-based therapy, the trend is to prefer LMWH.
When lytics are included, either systemic or catheter-directed lytics, there is flexibility and room to discuss with the multidisciplinary PERT team which strategy to use.
Future studies and trials are needed to standardize the best therapies.
What are the pharmacologic properties of available thrombolytics?
Thrombolytics catalyze the conversion of plasminogen to plasmin, leading to fibrin degradation and thrombus dissolution.
Alteplase is a recombinant tissue plasminogen activator, administered intravenously at a dose of IV 100 mg infusion over 2 hours. In cardiac arrest, the initial: 50 mg bolus over 2 minutes and continue CPR; after 15 minutes, if return of spontaneous circulation is not achieved and the medical team decides to continue CPR, repeat 50 mg bolus.
Tenecteplase is a modified variant of alteplase with increased fibrin specificity. The usual dose is weight-based and delivered via IV bolus, which facilitates rapid delivery in emergency settings. Dose per weight: ≥60 to <70 kg: 35 mg, ≥70 to <80 kg: 40 mg, ≥80 to <90 kg: 45 mg, ≥90 kg: 50 mg
Are there any ongoing clinical trials and emerging therapies investigating novel thrombolytics and strategies to optimize efficacy while minimizing bleeding risk?
PEITHO-3 is a large, randomized, double-blind, multinational study comparing reduced-dose intravenous alteplase with standard heparin in patients with intermediate-high-risk PE.
References
Sedhom R, Megaly M, Elbadawi A, et al. Contemporary national trends and outcomes of pulmonary embolism in the United States. Am J Cardiol. 2022;176:132-138. doi:10.1016/j.amjcard.2022.03.060
Marti C, John G, Konstantinides S, Combescure C, Sanchez O, Lankeit M, Meyer G, Perrier A. Systemic thrombolytic therapy for acute pulmonary embolism: a systematic review and meta-analysis. Eur Heart J. 2015 Mar 7;36(10):605-14. Epub 2014 Jun 10.
Zuo Z, Yue J, Dong BR, Wu T, Liu GJ, Hao Q. Thrombolytic therapy for pulmonary embolism. Cochrane Database Syst Rev. 2021;CD004437.
Feltes J, Popova M, Hussein Y, Pierce A, Yamane D. Thrombolytics in cardiac arrest from pulmonary embolism: a systematic review and meta-analysis. J Intensive Care Med. 2023;39(5):477-483.
Javaudin F, Lascarrou JB, Le Bastard Q, Bourry Q, Latour C, De Carvalho H, Le Conte P, Escutnaire J, Hubert H, Montassier E, Leclère B; Research Group of the French National Out-of-Hospital Cardiac Arrest Registry (GR-RéAC). Thrombolysis during resuscitation for out-of-hospital cardiac arrest caused by pulmonary embolism increases 30-day survival: findings from the French National Cardiac Arrest Registry. Chest. 2019 Dec;156(6):1167-1175. Epub 2019 Aug 2.
Bonnard T, Tennant Z, Niego B, Kanojia R, Alt K, Jagdale S, Law LS, Rigby S, Medcalf RL, Peter K, Hagemeyer CE. Novel thrombolytic drug based on thrombin cleavable microplasminogen coupled to a single-chain antibody specific for activated GPIIb/IIIa. J Am Heart Assoc. 2017 Feb 3;6(2):e004535.
Kearon C, Akl EA, Comerota AJ, Prandoni P, Bounameaux H, Goldhaber SZ, Nelson ME, Wells PS, Gould MK, Dentali F, Crowther M, Kahn SR. Antithrombotic therapy for VTE disease: Antithrombotic Therapy and Prevention of Thrombosis, 9th ed: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines. Chest. 2012 Feb;141(2 Suppl):e419S-e496S. Erratum in: Chest. 2012 Dec;142(6):1698-1704.
Levine M, Hirsh J, Weitz J, Cruickshank M, Neemeh J, Turpie AG, Gent M. A randomized trial of a single bolus dosage regimen of recombinant tissue plasminogen activator in patients with acute pulmonary embolism. Chest. 1990 Dec;98(6):1473-1479.
Rivera-Lebron B, Weinberg AS. Acute pulmonary embolism in adults: Reperfusion therapy in intermediate- and high-risk patients. In: Connor RF, ed. UpToDate. Waltham, MA: UpToDate Inc. Accessed August 28, 2025. | |||
| 446. The SGLT2i Effect – Protection Against Cancer Therapy-Related Cardiac Dysfunction with Dr. Manu Mysore | 16 Apr 2026 | 00:32:38 | |
CardioNerds (Drs. Natalie Marrero, Shivani Reddy, and Rebecca S. Steinberg), discuss the role of SGLT2i in cancer therapy-related cardiac dysfunction (CTRCD) with Dr. Manu Murali Mysore.
This episode was produced as part of the CardioNerds Academy curriculum by House Taussig under the guidance of House Chief, Dr. Natalie Marrero, and Academy Program Director, Dr. Gurleen Kaur. A matching review article will be published in US Cardiology Review, the official journal of CardioNerds. Audio editing for this episode was performed by CardioNerds Intern, Dr. Julia Marques Fernandes.
Summary: Cancer therapy-related cardiac dysfunction (CTRCD) spans a spectrum from subclinical biomarker elevation to overt heart failure, with risk amplified by preexisting cardiovascular disease, diabetes, hypertension, obesity, and exposure to therapies, such as anthracyclines, HER2-targeted therapies, or radiation. This episode explores the emerging and promising role of SGLT2 inhibitors as a cardioprotective adjunct in cardio-oncology — examining mechanisms, clinical evidence, ongoing trials, and critical knowledge gaps — while affirming that guideline-directed medical therapy remains the cornerstone of prevention and treatment.
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Pearls
CTRCD is a spectrum — catch it early. CTRCD ranges from subclinical injury detected by imaging and biomarkers to overt heart failure. Early identification in high-risk patients (preexisting CVD, diabetes, HTN, obesity, anthracycline/HER2/radiation exposure) is essential, and early initiation of guideline-directed medical therapy — including ACE inhibitors/ARBs/ARNIs, mineralocorticoid receptor antagonists, and beta-blockers — remains the backbone of prevention and treatment to preserve LVEF and allow safe continuation of cancer therapy.
SGLT2 inhibitors are a promising new pillar of cardioprotection in cardio-oncology. They act through a unique combination of mechanisms: renal effects, metabolic reprogramming of the myocardium, anti-inflammatory and antioxidant pathways, and vascular fibrosis modulation — making them a compelling complement to standard therapies rather than a replacement.
Early clinical data is encouraging but not yet definitive. The 2024 EMPACARD-PILOT trial demonstrated preserved LVEF and reduced CTRCD in higher-risk patients with diabetes or kidney disease. Ongoing trials — EMPACT and PROTECT — are actively exploring SGLT2 inhibitors for primary prevention during anthracycline and HER2-targeted therapy.
SGLT2 inhibitors are NOT yet indicated for ICI-related myocarditis. Immune checkpoint inhibitor (ICI)-related myocarditis is mechanistically immune-driven. While SGLT2 inhibitors have theoretically anti-inflammatory benefits, there is currently no clinical evidence to support their use in this specific setting.
The use of SGLT2 inhibitors should be guided by patient risk, existing indications, and ongoing research. Large prospective trials, clarity on timing and patient selection, long-term safety data, and deeper mechanistic understanding in humans remain the most urgent gaps in the field before broader adoption can be recommended.
References
Theofilis P, Vlachakis PK, Oikonomou E, et al. Cancer therapy-related cardiac dysfunction: A review of current trends in epidemiology, diagnosis, and treatment. Biomedicines. 2024;12(12):2914. doi:10.3390/biomedicines12122914. https://pubmed.ncbi.nlm.nih.gov/39767820/
Lyon AR, Dent S, Stanway S, et al. Baseline cardiovascular risk assessment in cancer patients scheduled to receive cardiotoxic cancer therapies: a position statement and new risk assessment tools from the Cardio-Oncology Study Group of the Heart Failure Association of the European Society of Cardiology in collaboration with the International Cardio-Oncology Society. Eur J Heart Fail. 2020;22(11):1945-1960. doi:10.1002/ejhf.1920. https://pmc.ncbi.nlm.nih.gov/articles/PMC8019326/
Li X, Li Y, Zhang T, et al. Role of cardioprotective agents on chemotherapy-induced heart failure: A systematic review and network meta-analysis of randomized controlled trials. Pharmacol Res. 2020;151(104577):104577. doi:10.1016/j.phrs.2019.104577. https://pubmed.ncbi.nlm.nih.gov/31790821/
Lee YH, Lim S, Davies MJ. Cardiometabolic and renal benefits of sodium-glucose cotransporter 2 inhibitors. Nat Rev Endocrinol. 2025;21(12):783-798. doi:10.1038/s41574-025-01170-4. https://pubmed.ncbi.nlm.nih.gov/40935880/
Dabour MS, George MY, Daniel MR, Blaes AH, Zordoky BN. The cardioprotective and anticancer effects of SGLT2 inhibitors: JACC: CardioOncology state-of-the-art review. JACC CardioOncol. 2024;6(2):159-182. doi:10.1016/j.jaccao.2024.01.007. https://pubmed.ncbi.nlm.nih.gov/38774006/
Armillotta M, Angeli F, Paolisso P, et al. Cardiovascular therapeutic targets of sodium-glucose co-transporter 2 (SGLT2) inhibitors beyond heart failure. Pharmacol Ther. 2025;270(108861):108861. doi:10.1016/j.pharmthera.2025.10886. https://pubmed.ncbi.nlm.nih.gov/40245989/
Góes-Santos BR, Castro PC, Girardi ACC, Antunes-Correa LM, Davel AP. Vascular effects of SGLT2 inhibitors: evidence and mechanisms. Am J Physiol Cell Physiol. 2025;329(4):C1150-C1160. doi:10.1152/ajpcell.00569.2025. https://pubmed.ncbi.nlm.nih.gov/40908107/
Daniele AJ, Gregorietti V, Costa D, López-Fernández T. Use of EMPAgliflozin in the prevention of CARDiotoxicity: the EMPACARD - PILOT trial. CardioOncology. 2024;10(1):58. doi:10.1186/s40959-024-00260-y. https://pubmed.ncbi.nlm.nih.gov/39237985/
Clinicaltrials.gov. Clinicaltrials.gov. Accessed April 16, 2026. https://clinicaltrials.gov/study/NCT05271162
Greco A, Quagliariello V, Rizzo G, et al. SGLT2i Dapagliflozin in primary prevention of chemotherapy induced cardiotoxicity in breast cancer patients treated with neo-adjuvant anthracycline-based chemotherapy +/- trastuzumab: rationale and design of the multicenter PROTECT trial. CardioOncology. 2025;11(1):79. doi:10.1186/s40959-025-00368-9. https://pmc.ncbi.nlm.nih.gov/articles/PMC12400668/
Key Guideline Reference: Lyon AR, López-Fernández T, Couch LS, et al. 2022 ESC guidelines on cardio-oncology developed in collaboration with the European hematology association (EHA), the European society for therapeutic radiology and oncology (ESTRO) and the international cardio-oncology society (IC-OS). Eur Heart J Cardiovasc Imaging. 2022;23(10):e333-e465. doi:10.1093/ehjci/jeac106. https://pubmed.ncbi.nlm.nih.gov/36017575/
Be sure to check out the corresponding review article on the cardioprotective role of SGLT2 inhibitors in CTRCD that will be published in US Cardiology Review, the official journal of CardioNerds. Additionally, please reference CardioNerds Cardio-Oncology Episodes 261 and 274 for related content. | |||
| 445. Heart Failure: The Essential Role of Palliative Care in Advanced Therapies with Dr. Sarah Chuzi | 10 Apr 2026 | 00:54:56 | |
Dr. Jenna Skowronski, Dr. Shazli Khan, and Dr. Alix Barnes discuss the involvement of palliative care throughout the heart failure spectrum with Dr. Sarah Chuzi. Audio editing for this episode was performed by CardioNerds Intern, Dr. Julia Marques Fernandes.
In this episode, we discuss utilizing palliative care principles while caring for patients with heart failure, particularly those being considered for advanced therapies. We emphasize utilization of communication frameworks when discussing prognosis and making decisions on pursuing therapies such as palliative inotropes, left ventricular assist devices (LVADs), and heart transplant. Additionally, we discuss when to involve specialty palliative care services. Finally, we highlight the difference between palliative care and hospice and how to help patients navigate the transition from life-prolonging care to hospice.
Dr. Jenna Skowronski is the Chair for the CardioNerds Heart Failure Council. Dr. Jenna Skowronski and Dr. Shazli Khan are the Co-chairs for the CardioNerds Advanced Heart Failure Therapies Series. Dr. Alix Barnes is the CardioNerds FIT Ambassador at UPMC and member of the CardioNerds Critical Care Cardiology Council.
Enjoy this Circulation Paths to Discovery article to learn more about the CardioNerds mission and journey.
US Cardiology Review is now the official journal of CardioNerds! Submit your manuscripts here.
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Pearls
Primary palliative care is care provided by a clinician that is not a palliative care specialist, such as a heart failure clinician having a conversation with a patient about their goals and values in clinic.
Taking time to get to know a patient as an individual and learning their goals and values prior to diving into conversations about prognosis and change in treatment plan facilitates more effective goals of care discussions.
Utilizing and practicing a communication framework can improve our skills at goals of care discussions.
Palliative inotropes should be reserved for patients experiencing symptomatic benefit from the therapy that outweighs the associated risks including arrhythmias and infections. The burden of managing these therapies at home should also be considered.
Partnerships between cardiologists and hospice agencies can improve the experience for patients with heart failure who enroll in hospice. Cardiologists can continue to see their patients even after hospice enrollment and help with symptom management.
Notes
Notes: Notes drafted by Dr. Barnes.
1. What is the difference between primary palliative care and specialty palliative care?
Primary palliative care is the delivery of palliative care services that any clinician can deliver.
This includes aligning treatment with a patient’s goals and basic symptom management. For heart failure patients, symptom management can include cardiac symptoms such as dyspnea and chest pain as well as managing comorbid mood disorders such as adjustment disorder, depression, and anxiety.
Advanced palliative care skills take additional training and time to develop. These include leading a difficult family meeting, managing symptoms that are not controlled with standard therapies and responding to emotional and spiritual distress. When these situations are encountered, referral to a specialty palliative care service should be considered. 1
2. How is palliative care integrated throughout the disease trajectory of a patient with heart failure?
Heart failure clinicians deliver primary palliative care when assessing a patient’s preferences, goals and values or managing symptoms.
As a patient’s disease progresses, the heart failure team also engages in primary palliative care when delivering news about prognosis.
When advanced therapies are being considered, utilization of shared decision-making (SDM) should be employed (see question 3 for further discussion on SDM).
For patients being considered for LVAD, the Centers for Medicare and Medicaid Services (CMS) mandates that patients are seen by a palliative care specialist prior to implantation. 2
Despite this, there remains variability in how institutions involve specialty palliative care in this decision-making process. Thoughtful consideration of what palliative care resources are available at your institution should guide how best to integrate specialty palliative care teams into the LVAD decision tree.
One example of a model for meeting this mandate is having a small team of heart failure clinicians with additional palliative care training meet all patient’s being evaluate for LVAD.
3. What is shared decision-making (SDM) and how is it utilized when evaluating a patient for advanced therapies?
SDM is a collaborative process where patients and clinicians work together to make medical decisions that are aligned with a patient’s goals and values.3
There are a variety of communication frameworks that can be used to engage in effective SDM.
One framework is the Serious Illness Conversation guide. This is an evidenced based framework that can be used to deliver the news about a patient’s current condition and then assess their goals, values and preferences for next steps in their treatment plan.4 This framework can be helpful when discussing prognosis prior to introducing the idea of an evaluation for advanced therapies.
REMAP is a second commonly used framework which stands for Reframe, Expect Emotion, Map What’s Important, Align, and Plan.5 This framework is similarly helpful when starting a discussion about advanced therapies with a patient.
Both frameworks prioritize learning about a patient’s goals, values, and preferences prior to making a recommendation for a treatment plan. Listening more than speaking and accepting that a patient and their family may choose a path that is different than what you personally might choose for yourself or your loved ones are vital pillars to engaging in these conversations effectively.
When discussing LVAD, it is important to avoid framing the decision as “LVAD or no LVAD,” rather LVAD versus best supportive care.
The “Best Case, Worst Case” framework is an effective way to create choice awareness for patients when they are faced with making this decision. This is a way to discuss both the best outcomes after LVAD implantation as well as the potential complications so a patient is better able to understand the full spectrum of possible outcomes. 6
4. How do you select which patients would benefit from home inotrope therapy?
There is no data demonstrating a survival benefit with use of palliative inotropes. There may be subsets of patients who derive a survival benefit, such as patients whose renal function worsens when the agent is withdrawn, however there is no concrete data proving this. 7
Therefore, the benefit of home inotrope therapy should be based on if the patient derives symptomatic benefit from these agents. Additionally, risks of the therapy such as arrhythmias and infection as well as the burden of managing these therapies at home should also be weighed in the decision.8
Life expectancy for patients being initiated on palliative inotropes likely ranges from 6 to 9 months. Given this prognosis, concordant palliative care efforts should be intensified when starting patients on these agents. This can either be through involvement in specialty palliative care or increasing primary palliative care interventions. 9
5. How do you determine if a patient would be a candidate for hospice and how do you discuss hospice with patients and their families?
Hospice is a comprehensive program that provides supportive care to patients at end of life. This includes a team of physicians, nurses, aids, social workers and chaplains that can deliver care in the home, at a nursing facility, or in an inpatient hospice facility. 10
Patients with a prognosis of 6 months or less can qualify for hospice services.
Even if a patient qualifies for hospice based on their prognosis, it is important to assess if a patient’s goals and values align with hospice. Introducing hospice to patients who still desire life prolonging care can cause mistrust between the patient and their health care team.
When introducing hospice, it is helpful to describe the services hospice offers in addition to naming the service as some patients may have a negative connotation with the word “hospice.”
6. How can cardiologists partner with hospice agencies to provide better care for these patients?
Heart failure specialists can continue to see their patients even after they enroll in hospice. Partnering in hospice agencies in this way can help improve symptom management for patients while also allowing them to continue meaningful relationships with providers with whom they’ve developed a longitudinal relationship with.
Guideline directed medical therapy (GDMT) and diuretics can be continued while enrolled in hospice as long as they are offering symptomatic benefit. Heart failure specialists can help with adjusting GDMT to cheaper formulations, such as exchanging angiotensin receptor-neprilysin inhibitors (ANRIs) for angiotensin receptor blockers (ARBs).
Many hospice agencies cannot accept patients receiving palliative inotropes due to the resources and training required to safely care for these patients. Understanding what hospice agencies in your area can and cannot support allows heart failure specialists to have informed discussions with patients and make appropriate referrals.
References
Quill TE, Abernethy AP. Generalist plus Specialist Palliative Care — Creating a More Sustainable Model. N Engl J Med. 2013;368(13):1173-1175. doi:10.... | |||
| 444. Heart Failure: LVAD Part 2 with Dr. Mark Belkin and Dr. Chris Salerno | 22 Mar 2026 | 00:26:44 | |
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.
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Pearls
“The right ventricle sets the stage.” — LVAD success hinges on RV performance; a struggling RV can turn a perfect LVAD surgery into a perfect storm.
“Watch the ratios.” — A PAPi < 2 and RA:PCWP >0.6 signal high risk for RV failure post-implant; trends and response to optimization matter more than static numbers.
“From hemocompatibility to hemodynamics.” — The LVAD field has moved from fighting pump thrombosis to mastering long-term RV failure and aortic insufficiency.
“Not all antibodies are created equal.” — LVAD-related sensitization often resolves post-transplant, reminding clinicians to interpret PRA trends in context.
“Recovery is possible.” — The RESTAGE-HF trial and emerging SGLT2 data hint at a new era: not just sustaining life with LVADs but restoring native heart function.
Notes
Notes drafted by Dr. Hamza Patel.
1. Hemodynamic & Vasoactive Management of the RV
Use norepinephrine and vasopressin for pressor support; consider dobutamine as inotrope of choice.
Consider avoiding early milrinone due to hypotension and reduced coronary perfusion.
Use inhaled NO or epoprostenol selectively; institutional variation depends on cost and supply.
Key hemodynamic markers:
PAPi = (PA systolic – PA diastolic) / RA pressure.
PAPi < 2 → increased RV failure risk.
RA:PCWP ratio ≈ 0.6 normal; ≈ 1 → severe RV dysfunction.
RV reserve—the ability to improve these indices with optimization—is a stronger predictor of outcomes than baseline numbers alone.
NOTE: there is no robust data to guide vasoactive medical decision-making and there is substantial institutional variability in practive.
2. Long-Term LVAD Complications
MOMENTUM 3 trial: HeartMate 3 reduced pump thrombosis (10 → 1 %), stroke (14 → 5%), and GI bleed (77 → 43 %).
Persistent issues: driveline infections, RV failure, and aortic insufficiency.
Driveline care: silver sulfadiazine (Silvadene) cream linked to lower infection rates (Cowher & Kenmore 2025).
Field now focuses on hemodynamic-related adverse events—the next frontier in LVAD outcomes.
Innovation ahead: smaller drivelines and fully implantable LVADs to eliminate infection risk.
3. Sensitization and Transplant Candidacy
LVADs may induce de novo HLA antibodies, complicating transplant matching.
These antibodies tend to be transient and less cytotoxic, often resolving post-transplant.
Sensitization degree varies by device and patient; management strategies are center-dependent.
The field is redefining which antibodies are truly LVAD-induced versus incidental.
4. GDMT & Myocardial Recovery
GDMT data in LVAD patients limited—excluded from major HFrEF trials.
RESTAGE-HF: aggressive GDMT post-LVAD yielded 52% explant rate within 18 months.
SGLT2 inhibitors: emerging evidence of reverse remodeling and reduced LV size (Belkin et al., THT 2025).
GDMT promotes recovery but requires cautious titration to avoid hypotension and RV strain.
5. Future of LVAD Therapy
The fully implantable LVAD remains the goal—wireless energy, no driveline, and fewer infections.
Short-term focus: device miniaturization, improved energy efficiency, and better hemocompatibility.
HeartMate 3 remains gold standard until next-generation systems mature.
References
Mehra MR et al. NEJM 2018 — MOMENTUM 3 Final Report.
Takeda K et al. JHLT 2020 — Predictors of RV Failure After LVAD.
Imamura T et al. Circ Heart Fail 2017 — Hemodynamics and RV Adaptation Post-LVAD.
RESTAGE-HF Trial, JHLT 2019.
Cowher J, Kenmore C et al. 2025 — Driveline Care & Infection Outcomes.
Belkin M et al. THT 2025 — SGLT2 Inhibition and Reverse Remodeling Post-LVAD. | |||
| 443. Pulmonary Embolism: The Modern Approach to Pulmonary Embolism Care with Dr. Kenneth Rosenfield | 05 Mar 2026 | 00:25:56 | |
This inaugural episode of the CardioNerds Pulmonary Embolism (PE) Series explores the evolution of acute PE care. Dr. Ibrahim Zahid, Dr. Dinu Balanescu, and Dr. Billy Joe Mullinax join guest expert Dr. Kenneth Rosenfield to discuss the shifting landscape of PE management.
Pulmonary embolism (PE) remains a leading cause of cardiovascular mortality and a frequent diagnostic challenge, often masquerading as myocardial infarction or a benign illness. Over the past decade, PE care has evolved from anticoagulation-only strategies to nuanced, risk-stratified, multidisciplinary management. Modern approaches integrate hemodynamics, biomarkers, and advanced imaging to guide therapy, including catheter-directed interventions and large-bore thrombectomy. The Pulmonary Embolism Response Team (PERT) model addresses historical gaps by coordinating rapid, multispecialty decision-making and standardizing care pathways. The PERT Consortium further advances PE care through education, research, and the world’s largest PE registry, while fostering leadership and research opportunities for trainees. Despite advances, long-term outcomes and post-PE syndromes remain important areas for future investigation. Audio editing by CardioNerds Academy intern, student doctor, Pace Wetstein.
Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values.
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Pearls
PE is a “master masquerader”—maintain suspicion for atypical presentations like myocardial infarction, heart failure, flu, or anxiety.
Multidisciplinary management mediated through pulmonary embolism response teams improves outcomes and standardizes care.
Risk stratification integrates hemodynamics, biomarkers, and imaging.
Advanced therapies have expanded beyond anticoagulation.
Long‑term follow‑up and post‑PE syndrome need more research.
Notes
Notes: Notes drafted by Dr. Ibrahim Zahid.
1. How has the clinical approach to PE changed over the past decade?
PE is the third leading cause of cardiovascular death and historically under‑recognized.
Symptoms mimic MI, HF, asthma, syncope, and more.PE is a silent killer, and it should be recognized more as a cause of spontaneous cardiac arrest.
Where life threatening disease like stroke which is owned by neurological specialists and MI is primarily managed by cardiac specialists, PE is an entity without a professional home. The PERT Consortium brings the specialties together for PE care.
2. Ten years ago, a 58-year-old patient with a large bilateral PE, RV dilation, and positive biomarkers might have been managed with anticoagulation and close observation alone. Today, with evolving—but still uneven—data on advanced therapies, PE care feels far more nuanced and highly dependent on where you practice. What are the major gaps in traditional PE management that clinicians should recognize, and what care pathways should they be aware of across different hospital systems?
Care has shifted from anticoagulation‑only to multidisciplinary approaches like catheter directed thrombectomy.
Risk‑based pathways and the use of CT angiogram has improved early recognition. Risk stratification tools must be used as tools for early recognition of intermediate risk PE.
Untreated PE leads to chronic complications like chronic thromboembolic disease and chronic thromboembolic pulmonary hypertension, which requires long term clinic follow up.
3. What is the role of risk stratification tools such as PeSI, sPeSI scores, cardiac biomarkers, and imaging findings in PE, and how do they guide treatment decisions in real world practice?
Integrate vitals (blood pressure and heart rate), biomarkers (troponin, pro-BNP), RV/LV ratio assessment, acid‑base status, and scores.
Tools include PESI, sPESI, BOVA, HESTIA, FAST, Geneva, NEWS, shock index.
Vitals, lactate, acid-base status, and tools like NEWS or shock index track clinical evolution.
PESI/sPESI estimate 30-day mortality and help identify low-risk patients who may be candidates for early discharge or outpatient therapy.
Clinical judgment matters—scores don’t fully capture clot burden, trajectory, or bleeding risk.
4. How was the pulmonary embolism response team created, and since its creation, what evidence or outcome data became available to support the PERT model?
Originated after a sentinel case at MGH: A young, pregnant woman in her 30s, who collapsed at home, underwent thrombectomy, and had to be on ECMO for a few days. The case brought cardiology, cardiac surgeons and critical care physicians together for planning and improvement in her health, which was rewarding.
Thereby, it was decided to bring specialties involved in PE care together to create a response team.
The name of the team, Pulmonary Embolism Response Team (PERT), was coined by Richard Channick in the first meeting.
Posters were set up all over the hospital to call a centralized line when an acute PE is recognized
A meeting was held to present the concept of putting together a consortium, with development of action items and a PERT database.
Enabled rapid multidisciplinary input using early teleconferencing tools.
5. Given concerns about having too many ‘cooks in the kitchen’ during the initial PE call—especially with rotating teams—how can institutions reconcile workflow complexity with standardized pathways in a way that meaningfully supports and justifies the added burden on frontline clinicians?
Every hospital’s PERT is different, catering to their needs and workflow
At least two disciplines are needed to make a PERTData is currently being collected to guide further on how the workflow can be standardized
Most importantly, the team brings in resources that were not available prior to PERT formation.
6. What are the main goals of the PERT consortium, and how does it support clinicians and institutions involved?
To improve care and improve outcomes for patients with PE
Expand education, refine algorithms, standardize care with Centers of Excellence.
Maintain the largest PE registry for research and outcomes improvement.
7. Beyond global networking, shared learning from successful systems, and the pathway toward Center of Excellence designation, what additional benefits can clinicians and health systems gain by participating in the PERT Consortium?
The ability to learn from other systems, the ability to share experiences.
Allow people to develop their professional careers like leadership experience, becoming a member of the trainee council
Initiate projects and receive funding for your ideas
8. For trainees interested in pulmonary embolism care, how can a trainee be a champion at their institution? Does PERT provide assistance and how can they really contribute meaningfully even before becoming a fellow/attending?
Medical students and residents interested in PE should reach out to the consortium and the consortium will hook you up with the correct mentors who can nurture you along.
Listen to the podcasts.
Participate with your local PERT team
PERT wants involvement of people who are social media savvy to help spread the word on PE.
Top three take-away points from this episode
Acute PE care has advanced and multiple treatment modalities for acute PE including catheter directed therapy, large bore thrombectomy, are becoming standard of care.
Multidisciplinary models like PERT improve coordination and outcomes.
Trainees play a vital role in advancing PE care through involvement, research, and education
References
Konstantinides SV, Meyer G, Becattini C, Bueno H, Geersing GJ, Harjola VP, Huisman MV, Humbert M, Jennings CS, Jiménez D, Kucher N, Lang IM, Lankeit M, Lorusso R, Mazzolai L, Meneveau N, Ní Áinle F, Prandoni P, Pruszczyk P, Righini M, Torbicki A, Van Belle E, Zamorano JL; ESC Scientific Document Group. 2019 ESC Guidelines for the diagnosis and management of acute pulmonary embolism developed in collaboration with the European Respiratory Society (ERS). Eur Heart J. 2020 Jan 21;41(4):543-603. doi: 10.1093/eurheartj/ehz405. PMID: 31504429. https://pubmed.ncbi.nlm.nih.gov/31504429/
Rosovsky R, Zhao K, Sista A, Rivera-Lebron B, Kabrhel C. Pulmonary embolism response teams: Purpose, evidence for efficacy, and future research directions. Res Pract Thromb Haemost. 2019 Jun 9;3(3):315-330. doi: 10.1002/rth2.12216. PMID: 31294318; PMCID: PMC6611377. https://pmc.ncbi.nlm.nih.gov/articles/PMC6611377/
Rosenfield K, Bowers TR, Barnett CF, Davis GA, Giri J, Horowitz JM, Huisman MV, Hunt BJ, Keeling B, Kline JA, Klok FA, Konstantinides SV, Lanno MT, Lookstein R, Moriarty JM, Ní Áinle F, Reed JL, Rosovsky RP, Royce SM, Secemsky EA, Sharp ASP, Sista AK, Smith RE, Wells P, Yang J, Whatley EM; Pulmonary Embolism Research Collaborative (PERC) Attendees. Standardized Data Elements for Patients With Acute Pulmonary Embolism: A Consensus Report From the Pulmonary Embolism Research Collaborative. Circulation. 2024 Oct;150(14):1140-1150. doi: 10.1161/CIRCULATIONAHA.124.067482. Epub 2024 Sep 12. PMID: 39263752; PMCID: PMC11698503. https://pubmed.ncbi.nlm.nih.gov/39263752/
Sharifi M, Awdisho A, Schroeder B, Jiménez J, Iyer P, Bay C. Retrospective comparison of ultrasound facilitated catheter-directed thrombolysis and systemically administered half-dose thrombolysis in treatment of pulmonary embolism. Vasc Med. 2019 Apr;24(2):103-109. doi: 10.1177/1358863X18824159. Epub 2019 Mar 5. PMID: 30834822. https://pubmed.ncbi.nlm.nih.gov/30834822/
Pandya V, Chandra AA, Scotti A, Assafin M, Schenone AL, Latib A, Slipczuk L, Khaliq A. Evolution of Pulmonary Embolism Response Teams in the Unite | |||
| 442. Heart Failure: LVAD Part 1 with Dr. Jeff Teuteberg and Dr. Mani Daneshmand | 27 Feb 2026 | 00:41:37 | |
CardioNerds (Dr. Jenna Skowronski [Heart Failure Council Chair], Dr. Shazli Khan, and Dr. Josh Longinow) are joined by renowned leaders in the field of AHFTC (Advanced Heart Failure and Transplant Cardiology) and mechanical circulatory support, Dr. Jeff Teuteberg and Dr. Mani Daneshmand to continue the discussion of advanced heart failure therapies by taking a deep dive into the world of durable LVADs (Left Ventricular Assist Devices). In this episode, we will review the history of ventricular assist devices, the basics of LVAD function, selection criteria for LVAD therapy, and surgical nuances of LVAD implantation. Audio Editing by CardioNerds intern, Joshua Khorsandi.
Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values.
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Pearls
There have been significant advances in the field of MCS/LVAD therapy since the first implanted LVAD in the 1960s, to the first FDA approved device in the early 2000’s, to now the HM3 LVAD, with the most important change being a centrifugal flow/magnetically levitated design that led to minimized hemocompatibility-related adverse events (HRAE’s) (MOMENTUM 3 trial comparing HM2 and HM3).
The REMATCH trial in 2001 was a pivotal trial for LVAD therapy, demonstrating that in a population of patients with advanced HF (70% IV inotrope dependent), LVAD therapy significantly improved survival at both 1 and 2 years as compared to medical therapy alone.
MOMENTUM 3 trial was a landmark trial for the HM3 device, showing that in a population of end stage HF patients (86% inotrope dependent, 32% INTERMACS 1-2, and 60% DT strategy), 5-year survival with HM3 was 58% and HM3 had lower HRAE’s compared with HM2.
There are both patient-specific factors and surgical considerations when it comes to candidacy for LVAD therapy.
RV function prior to LVAD is a key determinant for success post-LVAD
Many patients being considered for LVAD may not have robust RV function, however, predicting RV failure after LVAD is exceedingly difficult.
In general, it doesn't matter how bad the RV may look on imaging; we care more about the pre-LVAD hemodynamics (look at the PAPi and RA/wedge ratio).
What happens in the OR may be the most important determinant of how the RV will do with the LVAD!
Notes
Notes drafted by Dr. Josh Longinow.
1. Historical background of heart pumps and LVADs
LVAD Evolution FDA approval year 2001 2008 2012 2017 Pump HeartMate XVE HeartMate II Heartware HVAD HeartMate III Flow/Design Features Pulsatile Technology Continuous flow Axial design Continuous flow Centrifugal design Continuous flow Full MagLev + Centrifugal design
The 1960’s ushered in the first ‘LVADs’, when the first air-powered ‘LVAD’ was implanted. It kept the patient alive for four days before the patient expired.
The first generation of LVADs were pulsatile pumps
The first nationally recognized, FDA approved LVAD was the HeartMate XVE (late 1990s to early 2000s, REMATCH trial). The XVE pump used compressed air (pneumatically driven) to power the pump.
Prior to the XVE, OHT was the standard of care for patients with advanced, end-stage heart failure.
The second and third generations of LVADs were non-pulsatile, continuous flow devices and included the HVAD, HM2, and HM3 devices.
MOMENTUM 3 was a landmark trial for the HM3 device, showing that in a population of sick patients with end stage HF (86% inotrope dependent, 32% INTERMACS 1-2, and 60% DT strategy), 5-year survival with HM3 was 58% and HM3 had lower HRAE’s compared with HM2.
The only pump that is currently FDA approved for implant is the HM3, although other pumps are in clinical trials (BrioVAD system, INNOVATE Trial).
2. What are LVADs, and how do they work?
In simplest terms, the LVAD is a heart pump comprised of several key mechanistic components:
Inflow cannula
Mechanical pump
Outflow cannula
Driveline
Controller/Power source
The HM3 differs from its predecessors (HM2 and HVAD) in several key ways;
HM3 is placed intrapericardial whereas the HM2 was placed pre-peritoneal.
Perhaps most importantly, the HM3 is a fully magnetically levitated, centrifugal flow pump, whereas the HM2 is an axial flow device.
Axial flow pumps are not magnetically levitated, leading to more friction produced between the ruby bearing’s contact with the pump rotors, and higher rates of hemocompatibility related adverse events (HRAEs, i.e. pump thrombosis) and the HM2 was ultimately discontinued in favor of the HM3 (MOMENTUM 3 trial).
3. What do the terms ‘Destination Therapy’ (DT) or ‘Bridge to Transplant’ (BTT) mean when it comes to LVADs?
When LVADs first came on the stage, EVERYONE was a BTT; these early pumps weren’t designed for long term use (I.e. REMATCH Trial, Heartmate XVE)
Destination therapy means the LVAD was placed in leu of transplant because there are contraindications to transplant
REMATCH trial brought about the concept of “Destination therapy”, comparing outcomes in patients (with contraindications for transplant) who received an LVAD vs optimal medical therapy
Bridge to transplant means we are placing the LVAD in a patient who may not be a transplant candidate at this moment in time (is too sick, or conversely, not sick enough), but may be down the line
Bridge to recovery is another term used when the LVAD is being placed for a patient we think may have a recoverable cardiomyopathy
4. What are some factors we should consider when assessing a patient's candidacy for LVAD, in general, and from a surgical perspective?
Patient factors
Older age might push us towards thinking LVAD rather than transplant
In general, age > 70 is the cutoff for transplant, but this is not a hard cut off and varies institution to institution
In general, think about things that help predict recovery after a major surgery; Frailty and Nutritional status are important, we try to optimize these prior to LVAD implant
Right ventricular function remains the Achilles heel of LV support
We know that needing temporary RV support post LVAD puts you on a different survival curve than patients who don't need RVAD support
Studies have not been able to successfully predict who will develop RV failure after LVAD implantation
What happens in the time between when the patient goes to the OR and when they get back to the ICU is an important determinant who might develop RV failure post LVAD
Surgical techniques such as implanting the HM3 in the intra-thoracic cavity, rather than intra-pericardial may help maintain LV/RV geometry to help optimize the RV post LVAD
Surgical considerations for LVAD candidacy
Small, hypertrophied LV: HM3 inflow cannula is small, but small hypertrophied ventricles tend towards chamber collapse during systole causing suction, needing to run slower with lower flow rates
Chest size/diameter: pumps have gotten so small now, that for adults, these have become less of a consideration
BMI: low BMI used to be more of a concern with the older pumps due to where they were placed, and the relative size of the pump itself, not so much now with the smaller HM 3 pumps
Calcified LV apex: would increase risk of stroke, bleeding
Driveline tunneling becomes a concern in the super obese population, higher risk for driveline infections (might tunnel these driveline’s shorter, and to a less fatty region of the abdomen, could even tunnel out the thoracic cavity in the super obese to limit skin motion)
5. Is there a role for MCS (i.e. temporary LVAD such as Impella) in pre-habilitation of patients prior to LVAD surgery?
The theory of being able to improve systemic perfusion, decongest the organs, and make the patient feel better prior to surgery makes sense, but becomes problematic due to the lack of a hard end point/time for prehabilitation which might risk delays in surgery
More likely that it can lead to delay in the surgery, with less-than-optimal benefit; you don’t want to prolong the wait for surgery and increase the risk for complications prior to surgery
An Impella 5.5 is currently FDA approved for 2 weeks of support, not 2 months so timing is important to keep in mind
It's unlikely that you will take a patient and convert them from a malnourished, cachectic person in 2 weeks' time
6. Is there a role for LVAD therapy in the younger patient population? Should we be thinking of LVAD up front for these patients, with the goal of transplanting down the line?
Recovery may be more likely in certain populations, particularly younger females with smaller LV’s; in those populations, perhaps bridge to recovery should be the focus, optimizing them on GDMT etc.
The replacement of transplant, with MCS (LVAD) in young patients has become a topic of discussion, because these pumps have become better and better, with the thinking that an LVAD could bridge a patient for 10 years or so, and they could get a transplant later
It is still a big unknown, but several concerns exist
Patients who get LVADs might end up with complications that become contraindication to transplant down the line (stroke, sensitization etc)
Patients and providers are more hesitant because of the more recent iteration for the UNOS criteria for OHT listing which no longer gives patients with an uncomplicated LVAD higher priority, and therefore they could end up waiting a longer time for a heart after undergoing LVAD
... | |||
| 441. Atrial Fibrillation: Ablation of Atrial Fibrillation with Dr. Jon Piccini | 13 Feb 2026 | 00:53:39 | |
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.
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PEARLS
Pulmonary veins (PVs) are the dominant triggers in early AF due to their unique myocardial sleeve electrophysiology.
Pulmonary vein isolation (PVI) remains the cornerstone of AF ablation by blocking PV triggers from reaching the left atrium. Posterior wall isolation is sometimes performed in persistent AFib, but large RCTs found no significant benefit over PVI alone.
Paroxysmal AF has the highest ablation success rates. Left atrial health remains the major determinant of outcome.
Ablation modalities include pulsed field ablation, radiofrequency ablation, and cryo-balloon ablation. PFA offers advantage of relative myocardial selectivity with near zero risk of atrio-esophageal fistula.
Long-term anticoagulation decisions after ablation currently depend on CHA₂DS₂-VASc score. Recent evidence suggests the safety of stopping anticoagulation in low-risk patients after ablation.
Early atrial arrhythmia recurrence during a blanking period after ablation (≤3 months) often reflects inflammation — not procedural failure. Late recurrence suggests PV reconnection or residual substrate and often requires repeat ablation.
Hybrid surgical and catheter Afib ablation represent an aggressive strategy for rhythm control in patients with persistent or long-standing persistent AF with extensive substrate and/or patients who have had multiple failed catheter ablations.
Notes
1. What is the mechanism behind AF initiation?
Atrial fibrillation (AF) is a progressive condition.
Early AF is primarily trigger-driven, most commonly from the pulmonary veins.
Pulmonary vein myocardial sleeves have unique electrophysiologic properties that promote premature beats and afterdepolarizations.
As AF progresses, atrial remodeling (fibrosis and scar) leads to a more substrate-driven arrhythmia.
2. How does early catheter ablation for atrial fibrillation work?
Electrical Isolation of pulmonary veins, blocking PV triggers from reaching the left atrium.
By reducing burden of atrial fibrillation, this may slow adverse atrial remodeling.
3. Which patients are good candidates for Afib ablation?
Functional Status: ambulatory, active patients derive the greatest benefit. Advanced frailty or severe end-stage cardiovascular disease reduces expected benefit.
Comorbidity Burden: CHA₂DS₂-VASc score helps risk-stratify not only stroke risk but also rhythm-control outcomes.
Type and Duration of AF
Paroxysmal AF → highest likelihood of success (burden reduction often 95–99%).
Long-standing persistent AF → lower suppression rates (often 50–80%).
Left Atrial Health: a major determinant of outcomes.
LA diameter >5.5 cm associated with significantly worse outcomes.
LA volume index (normal ≤34 mL/m²) is preferred over diameter for assessment.
4. What are the predictors of complications from AFib ablation procedures?
Low and high body mass index (BMI)
Chronic corticosteroid use
Severe enlargement of other cardiac chambers
Female gender is associated with a numerically higher risk of complications.
5. Role of preprocedural imaging with cardiac CT or MRI
Cardiac CT
Faster and convenient
Help define LA geometry and Pulmonary vein anatomy
Anatomic Variants as Right middle pulmonary vein, accessory pulmonary veins common pulmonary vein ostium, Atrial diverticula or Accessory left atrial appendage
Consider Cardiac MRI when:
Strong family history of atrial fibrillation or cardiomyopathy
Suspicion of occult structural heart disease
6. Key Procedural Steps in AF Ablation
There is significant variation across centers in anesthesia, mapping, and ablation strategies.
The following outline reflects a common contemporary approach.
Anesthesia & Monitoring
Most commonly performed under general anesthesia.
Benefits include improved catheter stability, enhanced patient comfort, and controlled ventilation (e.g., low-volume, high-frequency).
Invasive arterial line (A-line) is preferred for rapid detection of hypotension.
Vascular Access
Ultrasound-guided femoral venous access with multiple sheaths.
Micropuncture technique is ideal to minimize complications.
Intracardiac Echocardiography (ICE)
ICE catheter insertion.
Reduces complications, guides transseptal puncture, assesses catheter contact, and monitors for pericardial effusion.
Anticoagulation
Systemic heparin initiated before or immediately after transseptal access.
Activated clotting time (ACT) maintained in therapeutic range (typically >300 seconds).
Transseptal Puncture
Access to the left atrium via transseptal sheath.
Often uses electrocautery-assisted wire, with ICE guidance to improve safety.
Left Atrial Mapping
Creation of electroanatomic map (common in many centers).
Ideally performed in sinus rhythm.
Assesses left atrial geometry, voltage (for scar/substrate), and activation timing.
Ablation Strategy
Core component is pulmonary vein isolation (PVI).
Technology options include pulse field ablation (PFA), radiofrequency ablation, and cryoballoon ablation.
Additional ablation (case-dependent):
Posterior wall isolation
Targeting non-pulmonary vein triggers
Linear lesions
Ablation of organized atrial tachycardias/flutters
Emerging approaches include AI-guided strategies.
Post-Ablation Assessment
Confirm pulmonary vein entrance and exit block.
Remap left atrium (in many practices) to evaluate lesion completeness.
Check for complications (e.g., ICE assessment for pericardial effusion).
7. What is Electroanatomic Mapping?
Combines 3D geometry (anatomic reconstruction of cardiac chamber) with electrophysiology (electrical signals from tissue).
How it works:
Mapping catheter is moved along the atrial wall
Records electrograms
System generates:
3D chamber model
Voltage map (tissue health/scar)
Activation map (depolarization timing)
Key information provided
Voltage map (substrate assessment):
High voltage = healthy tissue
Low voltage = scar/fibrosis
Identifies areas needing additional ablation (e.g., posterior wall scar)
Activation map:
Visualizes wavefront propagation
Essential for diagnosing and ablating macroreentrant atrial flutters and organized atrial tachycardias
8. What is the current role of Afib ablaton outside pulmonary vein isolation?
While Pulmonary Vein Isolation (PVI) remains the cornerstone of atrial fibrillation (AF) ablation, adjunctive strategies are increasingly used for persistent AF, with varying levels of supporting data.
Non-PVI Triggers:
Arrhythmogenic foci found outside the pulmonary veins in 10% to 20% of patients.
Common sites include SVC, LAA, CS, and Crista Terminalis.
Identifying and ablating these inducible triggers—often provoked by isoproterenol—can reduce recurrence in persistent AF.
Posterior Wall Isolation (PWI):
The posterior wall is a driver for persistent AF.
Randomized evidence for routine PWI is conflicting.
Large RCTs found no significant benefit over PVI alone for first-time ablations.
Remains a primary adjunctive target for redo procedures.
AI-Guided Ablation:
Uses AI to identify "spatio-temporal dispersion" areas.
Recent TAILORED-AF trial demonstrate increased freedom from AF at 12 months compared to conventional PVI.
9. Comparison of ablation techniques
Pulsed Field Ablation (PFA) – Non-Thermal
Mechanism: irreversible electroporation
Key advantages:
Shorter procedural time
Comparable efficacy to thermal ablation
Higher myocardial tissue selectivity
No known risk of esophageal fistula or pulmonary vein stenosis
Low risk of phrenic nerve (usually transient)
Disadvantages:
Less flexibility for complex substrate
Hemolysis with possible AKI
Early and delayed coronary spasms
Skeletal muscle stimulation during energy delivery
Loss of all electrograms even with reversible injury can be misleading
Limited long term data
... | |||
| 440. Heart Failure: Post-Heart Transplant Management with Dr. Shelly Hall and Dr. MaryJane Farr | 04 Feb 2026 | 00:26:16 | |
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 | |||
| 439. Atrial Fibrillation: Anti-Arrhythmic Drugs in the Management of Atrial Arrhythmias with Dr. Andrew Epstein | 25 Dec 2025 | 00:47:13 | |
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.
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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.... | |||
| 438. Heart Failure: Perioperative Heart Transplant Management with Dr. Dave Kaczorowski and Dr. Jason Katz | 16 Dec 2025 | 00:33:38 | |
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.... | |||
| 437. Atrial Fibrillation: The Diagnosis and Management of Atrial Flutter with Dr. Joshua Cooper | 05 Dec 2025 | 00:30:07 | |
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.
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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. | |||
| 436. Heart Failure: Pre-Heart Transplant Evaluation and Management with Dr. Kelly Schlendorf | 24 Nov 2025 | 00:32:11 | |
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 | |||
| 435. Atrial Fibrillation: Chronic Management of Atrial Fibrillation with Dr. Edmond Cronin | 20 Nov 2025 | 00:47:54 | |
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.
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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,... | |||
| 434. Heart Failure: Advanced Therapies Evaluation with Dr. Michelle Kittleson | 07 Nov 2025 | 00:14:01 | |
CardioNerds kicks off its advanced therapies series with Chair of the CardioNerds Heart Failure Council, Dr. Jenna Skowronski, co-chair of the series, Dr. Shazli Khan, and Episode FIT lead, Dr. Jason Feinman. In this first episode, they discuss the process of advanced therapies evaluation with Dr. Michelle Kittleson, Professor of Medicine and Director of Education in Heart Failure and Transplantation at Cedars-Sinai. In this case-based discussion, they cover the signs and symptoms of end-stage heart failure, the initial management strategies, and the diagnostic workup required when considering advanced therapies. Importantly, they discuss the special considerations for pursuing left-ventricular assist device (LVAD) versus heart transplantation as well as the multidisciplinary, team-based approach needed when advanced therapies are indicated.
Notes were drafted by Dr. Shazli Khan. Audio editing for this episode was performed by CardioNerds Intern, Julia Marques Fernandes.
Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values.
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Pearls
Guideline-directed medical therapy (GDMT) is indicated in all heart failure patients and improves survival, but progressive symptoms and intolerance to GDMT can be warning signs of disease progression. The I-NEED-HELP mnemonic is an excellent reference when considering referral for advanced therapies (Figure).
Management of acute decompensation includes diuretics and possible inotropic support. The inotropic agent used should be whichever best suits your specific patient. Milrinone may result in more hypotension, whereas dobutamine may result in more tachycardia. Tachycardic and normotensive patients may do better with milrinone, while hypotensive patients with normal heart rates may do better with dobutamine. Notably, DoReMi found no difference between milrinone and dobutamine for patients with cardiogenic shock.
The initial diagnostic evaluation includes an echocardiogram, right heart catheterization (RHC), and often cardiopulmonary exercise testing (CPET) to objectively assess the status of the heart. Comprehensive labs, imaging and cancer screening are also needed to assess all other organs.
When making the decision to pursue advanced therapies, always ask:
Is the heart sick enough?
Is the rest of the body well enough?
These two questions provide a framework to guide if patients are optimal candidates for transplant versus LVAD.
The advanced therapies evaluation is a team sport! Patients will meet not only with advanced heart failure cardiologists, but also cardiac surgeons, psychiatrists, social workers, nutritionists and pharmacists. All team members are of critical value in the process.
Notes
1.) What are the key features of advanced cardiomyopathy, and when should providers consider referral for advanced therapies?
Advanced cardiomyopathy may present as recurrent hospitalizations for decompensated heart failure, intolerance to GDMT with symptomatic orthostasis and hypotension, and progressive symptoms of heart failure despite medical therapy.
The I-NEED-HELP mnemonic is a helpful tool to identify patients at risk of heart failure and is defined as follows: Need for Inotropic support, New York Heart Association (NYHA) Class IV symptoms, End-Organ Dysfunction, Ejection fraction <20%, Defibrillator shocks for ventricular arrhythmias, Recurrent HF hospitalizations, Escalating diuretic dose, Low blood pressure and Progressive intolerance of GDMT. See the Figure designed by Dr. Gurleen Kaur.
When patients demonstrate any of the above warning signs, they should be referred to advanced heart failure specialists for consideration of advanced therapies.
2.) What diagnostic testing is pursued when working up patients for advanced therapies? How does this workup differ whether you are in the inpatient or outpatient setting?
Work-up generally answers two key questions: is the heart sick enough and is the rest of the body well enough?
Workup includes an echocardiogram that may show specific features concerning for end-stage heart failure (EF <20%, dilated and remodeled left ventricle, reduced right ventricular function, etc.).
A RHC provides information on the filling pressures of the heart for management in the acute setting, but also helps give an objective measure of the cardiac output to assess how sick the heart is. Importantly the RHC also provides key information on the presence of pulmonary hypertension.
Obtaining a comprehensive metabolic panel provides valuable information on end-organ dysfunction, as kidney or liver abnormalities are suggestive of worsening disease.
Outpatients presenting for referral may also undergo CPET as an objective confirmation of decreased functional capacity. Typically, a peak VO2 max of <14 mL/kg/min is indicative of advanced disease.
CT imaging, as well as other cancer screening tools, may be employed to ensure there is no systemic disease that would prohibit advanced therapies.
3.) Who makes up the multidisciplinary advanced therapies team?
The ACC/AHA/HFSA 2022 guidelines for heart failure support using a multidisciplinary team approach in managing HF. This collaborative care model has been shown to reduce hospital admissions and healthcare expenses while enhancing patient adherence to self-care practices and recommended medical treatments.
The multidisciplinary team consists of cardiologists, cardiac surgeons, advanced practice providers, psychiatrists, pharmacists, social workers, nutritionists, and other specialists.
4.) What are the medical factors to consider when deciding between transplant versus LVAD, and what social determinants of health play a role?
The medical evaluation and workup done during the advanced therapies evaluation help answer two crucial questions: Is the heart sick enough? Is the rest of the body well enough? All patients should be assessed for extracardiac disease that may impact survival after advanced therapies.
While selection between transplant versus LVAD varies by program and institution, general principles considered include the allocation system and regional wait times, patient’s age, and extracardiac comorbidities.
Generally, patients being considered for heart transplantation should be devoid of conditions that have a five-year survival of <70% or a ten-year survival of <50%. This is also because patients undergoing organ transplantation require immunosuppressive medications, which may further exacerbate their other systemic conditions.
Social support and internal motivation also play a role, as it is important for patients to attend multiple follow-up appointments and maintain strict adherence to their immunosuppressive medications.
Graphic - Stage D (Advanced) Heart Failure
Designed by Dr. Gurleen Kaur
References
Morris AA, Khazanie P, Drazner MH, et al; American Heart Association Heart Failure and Transplantation Committee of the Council on Clinical Cardiology; Council on Arteriosclerosis, Thrombosis and Vascular Biology; Council on Cardiovascular Radiology and Intervention; Council on Hypertension. Guidance for timely and appropriate referral of patients with advanced heart failure: a scientific statement from the American Heart Association. Circulation. 2021;144(15):e238-e250. doi:10.1161/CIR.0000000000001016 https://www.ahajournals.org/doi/10.1161/CIR.0000000000001016
Truby LK, Rogers JG. Advanced heart failure: epidemiology, diagnosis, and therapeutic approaches. JACC Heart Fail. 2020;8(7):523-536. doi:10.1016/j.jchf.2020.01.014 https://www.sciencedirect.com/science/article/pii/S2213177920302080?via%3Dihub
Heidenreich PA, Bozkurt B, Aguilar D, Allen LA, Byun JJ, Colvin MM, Deswal A, et al; ACC/AHA Joint Committee Members. 2022 AHA/ACC/HFSA guideline for the management of heart failure: a report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. Circulation. 2022;145(18):e895-e1032. doi:10.1161/CIR.0000000000001063 https://www.ahajournals.org/doi/10.1161/CIR.0000000000001063
Guglin M, Zucker MJ, Borlaug BA, Breen E, Cleveland J, Johnson MR, Panjrath GS, et al; ACC Heart Failure and Transplant Member Section and Leadership Council. Evaluation for heart transplantation and LVAD implantation: JACC Council perspectives. J Am Coll Cardiol. 2020;75(12):1471-1487. doi:10.1016/j.jacc.2020.01.034 https://www.sciencedirect.com/science/article/pii/S0735109720304150?via%3Dihub | |||
| 433. The Evolution and Future of Cardio-Obstetrics with Dr. Afshan Hameed, Dr. Doreen DeFaria Yeh, Dr. Garima Sharma, and Dr. Rina Mauricio | 05 Nov 2025 | 00:31:35 | |
In this second episode of a collaborative series with the AHA Women in Cardiology (WIC) Committee, CardioNerds (Dr. Gurleen Kaur and Dr. Anna Radhakrishnan) are joined by four leading experts in Cardio-Obstetrics to explore this rapidly evolving field. Dr. Rina Mauricio (Director of Women's Cardiovascular Health and Cardio-Obstetrics at UT Southwestern Medical Center), Dr. Afshan Hameed (Director of Maternal Fetal Medicine and Cardio-Obstetrics at UC Irvine), Dr. Doreen DeFaria Yeh (Co-director of the MGH Cardiovascular Disease and Pregnancy Program), and Dr. Garima Sharma (Director of Women's Cardiovascular Health and Cardio-Obstetrics at Inova) define Cardio-Ob as encompassing not only care of women during pregnancy, but also the complex decision-making that extends through the preconception and postpartum periods. From counseling patients with pre-existing or congenital heart disease before pregnancy to managing cardiovascular health during pregnancy and after delivery, they trace how the field has developed in response to the urgent need to address maternal mortality. Listeners will gain valuable insight into the multidisciplinary teamwork, patient-centered decision-making, and advocacy that drive this field - along with the importance of expanding Cardio-Ob education for clinicians and trainees, and innovations and system-level changes shaping its future. Audio editing by CardioNerds academy intern, Grace Qiu.
This episode was planned in collaboration with the AHA CLCD Women in Cardiology Committee with mentorship from Dr. Monika Sanghavi.
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| 432. Journal Club: The TRANSFORM-AF Trial with Dr. Sanjeev Saksena and Dr. Varun Sundaram | 29 Oct 2025 | 00:43:05 | |
Dr. Jeanne De Lavallaz and Dr. Ramy Doss discuss the results of the TRANSFORM-AF Trial with expert faculty Dr. Sanjeev Saksena and Dr. Varun Sundaram.
The TRANSFORM-AF trial enrolled 2,510 patients with atrial fibrillation (AF), type 2 diabetes, and obesity across 170 Veterans Affairs hospitals to evaluate the impact of diabetes-dose GLP-1 receptor agonists on AF-related outcomes. Participants were assigned to receive either a GLP-1 receptor agonist, a DPP-IV inhibitor, or a sulfonylurea. The primary composite outcome included AF-related hospitalizations, cardioversions, ablation procedures, and all-cause mortality. Over a median follow-up of 3.2 years, GLP-1 use was associated with a 13% reduction in major AF-related events compared to other therapies. The study population was predominantly male, with a high prevalence of severe obesity (BMI >40 kg/m²) in whom the benefit appeared most pronounced. Notably, the observed benefit occurred despite only modest additional weight loss, suggesting potential non-weight-mediated effects of GLP-1 therapy
This episode was planned in collaboration with Heart Rhythm TV with mentorship from Dr. Daniel Alyesh and Dr. Mehak Dhande.
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| 431. Atrial Fibrillation: Acute Management of Atrial Fibrillation with Dr. Jonathan Chrispin | 24 Oct 2025 | 00:37:21 | |
Dr. Naima Maqsood, Dr. Kelly Arps, and Dr. Jake Roberts discuss the acute management of atrial fibrillation with guest expert Dr. Jonathan Chrispin. Episode audio was edited by CardioNerds Intern Dr. Bhavya Shah.
This episode reviews acute management strategies for atrial fibrillation. Atrial fibrillation is the most common chronic arrhythmia worldwide and is associated with increasingly prevalent comorbidities, including advanced age, obesity, and hypertension. Atrial fibrillation is a frequent indication for hospitalization and a complicating factor during hospital stays for other conditions. Here, we discuss considerations for the acute management of atrial fibrillation, including indications for rate versus rhythm control strategies, treatment targets for these approaches, considerations including pharmacologic versus electrical cardioversion, and management in the post-operative setting.
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Pearls
A key component to the management of acute atrial fibrillation involves addressing the underlying cause of the acute presentation. For example, if a patient presents with rapid atrial fibrillation and signs of infection, treatment of the underlying infection will help improve the elevated heart rate.
Selecting a rate control versus rhythm control strategy in the acute setting involves considerations of comorbid conditions such as heart failure and competing risk factors such as critical illness that may favor one strategy over another. Recent data strongly supports the use of rhythm control in heart failure patients. Patients should be initiated on anticoagulation prior to pursuing a rhythm control strategy.
There are several strategies for rate control medications with therapies including beta-blockers, non-dihydropyridine calcium channel blockers, and digoxin. The selection of which agent to use depends on additional comorbidities and the overall clinical assessment. For example, a patient with severely decompensated low-output heart failure may not tolerate a beta-blocker or calcium channel blocker in the acute phase due to hypotension risks but may benefit from the use of digoxin to provide rate control and some inotropic support.
Thromboembolic prevention remains a cornerstone of atrial fibrillation management, and considerations must always be made in terms of the duration of atrial fibrillation, thromboembolic risk, and risks of anticoagulation.
While postoperative atrial fibrillation is more common after cardiac surgeries, there is no major difference in management between patients who undergo cardiac versus non-cardiac procedures. Considerations involve whether the patient has a prior history of atrial fibrillation, surgery-specific bleeding risks related to anticoagulation, and monitoring in the post-operative period to assess for recurrence.
Notes
1. Our first patient is a 65-year-old man with obesity, hypertension, obstructive sleep apnea, and pre-diabetes presenting for evaluation of worsening shortness of breath and palpitations. The patient has no known history of heart disease. Telemetry shows atrial fibrillation with ventricular rates elevated to 130-140 bpm. What would be the initial approach to addressing the acute management of atrial fibrillation in this patient? What are some of the primary considerations in the initial history and chart review?
An important first step involves taking a careful history to understand the timing of symptom onset and potential underlying causes contributing to a patient’s acute presentation with rapid atrial fibrillation.
Understanding the episode trigger determines management by targeting reversible causes of the acute presentation and elucidating whether the episode is triggered by a cardiac or non-cardiac condition. For example, if a patient presents with a few days of infectious symptoms, treating the infection is likely to lead to improvements in heart rate.
Determining the tempo of symptoms has further importance for assessing the risk of thromboembolism and anticoagulation consideration.
2. How would the initial evaluation be different for patients who have a new diagnosis of atrial fibrillation compared to those who have a known prior history of this arrhythmia?
The acuity of symptom onset plays an essential role in these considerations. For example, a patient may describe symptoms that have been ongoing for several months, which indicate a diagnosis beyond the acute phase of their presentation and would involve different considerations than for a patient who first noticed symptoms within the past few hours.
One way to view RVR rates in a patient with longstanding or permanent atrial fibrillation is to consider this vital sign as that patient’s version of sinus tachycardia in response to another physiologic process. In that setting, you would not try an approach to directly lower their heart rate but would instead attempt to determine and address the underlying cause of their presentation.
An additional consideration for patients without known prior atrial fibrillation is that they have likely never been on any rate-controlling agents and may have variable initial responses to these interventions.
3. In cases for which acute rate control of atrial fibrillation is indicated, what is the recommended heart rate target and how quickly should we aim to reach that target?
The initial first step in management should focus on addressing the underlying cause of the patient’s elevated heart rate while in atrial fibrillation. Once those factors are addressed and elevated heart rates persist, a rate-controlling agent can be considered.
Often, a primary reason for rate control is for symptom relief since patients can be very symptomatic from an elevated heart rate alone.
A reasonable goal for the intermediate setting is to achieve a heart rate of less than 100-110 bpm. One study compared lenient (resting heart rate <110 bpm) versus strict (resting heart rate <80 bpm and heart rate during moderate exercise <110 bpm) rate control in patients with atrial fibrillation and found no difference in outcomes related to mortality, hospitalization for heart failure, stroke, embolism, bleeding, or life-threatening arrhythmic events but that lenient control was easier to achieve.1 For this reason, aggressive rate control in the acute setting may not have a significant impact apart from symptom relief. There are not often clear indications to rapidly lower a patient’s heart rate, for example, from 140 to 90 bpm. Conversely, lowering a patient’s heart rate too rapidly can be detrimental by causing bradycardia or hypotension with excessive use of nodal blocking agents.
4. What are some of the considerations for the selection of rate-controlling agents?
Beta-blockers and non-dihydropyridine calcium channel blockers remain the mainstay of therapies used for rate control. The choice between these agents often depends on the comorbidities present. For example, if a patient has a known reduced LVEF, you may often avoid calcium channel blockers and opt for careful titration of beta-blockers. Often, the use of beta-blockers also allows for the management of additional comorbidities, including heart failure and coronary disease.
Digoxin is another agent to consider when a patient presents with acutely decompensated heart failure with a low LVEF and may not tolerate a beta-blocker or calcium channel blocker due to the risk of hypotension or worsening cardiogenic shock. Digoxin provides rate control while adding some positive inotropy. In terms of chronic management, digoxin use can be more challenging with close follow-up required to monitor levels. In some cases, amiodarone can be used as an acute rate-control agent, but there is a risk of conversion to sinus rhythm and thromboembolism if not on anticoagulation.
5. In what clinical scenarios might it be more optimal to consider an upfront rhythm control strategy?
Recent data support the benefit of an upfront rhythm control approach in heart failure patients, with complications including cardiovascular death, stroke, or hospitalization for worsening of heart failure or for acute coronary syndrome, reduced in heart failure patients managed with any early rhythm control strategy.2,3
In certain patients with known atrial fibrillation and heart failure, cardioversion can be considered as a strategy to help improve their heart failure symptoms. In these patients, initiating an anti-arrhythmic drug (AAD) prior to cardioversion can improve the likelihood of remaining in sinus rhythm after cardioversion.
6. Our second patient is a 58-year-old woman with a history of heart failure with reduced EF presenting to the ED with progressive lower extremity swelling and shortness of breath. She has a prior diagnosis of paroxysmal atrial fibrillation, and her most recent echo demonstrated an LVEF of 35%. She is found to have bilateral lower extremity pitting edema to her knees and elevated jugular venous pressure while requiring 2L of oxygen by nasal cannula. She is in rapid atrial fibrillation on presentation. Interrogation of her primary prevention ICD shows that she has been in atrial fibrillation for the past 3 weeks. In this scenario involving a patient with an acute heart failure exacerbation, are there considerations for a more upfront rhythm control strategy and perhaps electrical cardioversion?
In this scenario, there is an indication for utilizing an early rhythm control strategy. Even if an initial trial of diuresis and beta-blockers is used initially, the fact that this patient has been in atrial fibrillation for several weeks with only prior paroxysmal episodes indicates that her arrhythmia is likely contribut | |||
| 430. Women Leaders in Advanced Heart Failure and Transplant Cardiology with Dr. Mariell Jessup and Dr. Nosheen Reza | 09 Oct 2025 | 00:46:18 | |
In this powerful kickoff to a collaborative series with the AHA Women in Cardiology (WIC) Committee, CardioNerds (Dr. Apoorva Gangavelli, Dr. Gurleen Kaur, and Dr. Jenna Skowronski) explore the evolving landscape of women in advanced heart failure and transplant cardiology, featuring insights from two inspiring leaders in the field. Dr. Mariell Jessup, Chief Science and Medical Officer of the American Heart Association, reflects on her decades-long journey in heart failure cardiology, from navigating early career barriers to becoming a trailblazer in clinical leadership and research. Dr. Nosheen Reza, an advanced heart failure and transplant cardiologist at the University of Pennsylvania, shares how Dr. Jessup’s pioneering work has inspired her own career and shaped her approach to mentorship, advocacy, and academic development. Together, they discuss the systemic challenges women continue to face, the importance of sponsorship, and the evolving culture within cardiology. Listeners will gain a multigenerational perspective on how far the field has come and what is still needed to ensure equity, excellence, and innovation in advanced heart failure care.
Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values.
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References
DeFilippis EM, Moayedi Y, Reza N. Representation of Women Physicians in Heart Failure Clinical Practice. Card Fail Rev. 2021;7:e05. Published 2021 Mar 31. doi:10.15420/cfr.2020.31 | |||
| 429. Walking Both Paths: A Physician and Patient in Adult Congenital Heart Disease with Dr. Leigh Reardon | 28 Sep 2025 | 00:43:56 | |
CardioNerds (Dr. Abby Frederickson, Dr. Claire Cambron, and Dr. Rawan Amir) are joined by Dr. Leigh Reardon for a powerful conversation on navigating adult congenital heart disease as both a patient and provider. Dr. Reardon shares his personal journey with congenital heart disease and how it shaped his path to becoming an expert in the field himself. The discussion highlights patient-centered perspectives, barriers to care within the healthcare system, and the importance of advocacy and empathy.
This episode was planned by the CardioNerds ACHD Council.
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| 428. Atrial Fibrillation: The Impact of Modifiable Risk Factors and Lifestyle Management on Atrial Fibrillation with Dr. Prash Sanders | 15 Sep 2025 | 00:17:35 | |
Dr. Kelly Arps, Dr. Naima Maqsood, and Dr. Sahi Allam discuss modifiable risk factors and lifestyle management of atrial fibrillation with Dr. Prash Sanders. Atrial fibrillation is becoming more prevalent across the world as people are living longer with cardiovascular disease. While much of our current focus lies on the pharmacological and procedural management of atrial fibrillation, several studies have shown that targeted reduction of risk factors, such as obesity, sleep apnea, hypertension, and alcohol use, can also significantly reduce atrial fibrillation burden and symptoms. Today, we discuss the data behind lifestyle management and why it is considered the “4th pillar” of atrial fibrillation treatment. We also explore ways to incorporate prevention strategies into our general cardiology and electrophysiology clinics to better serve the growing atrial fibrillation population. Audio editing for this episode was performed by CardioNerds Intern, Julia Marques Fernandes.
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Pearls
More people have atrial fibrillation because it is being detected earlier using wearable technology, and patients are living longer with subclinical or clinical cardiovascular disease
There are 3 components of atrial fibrillation: an electrical “trigger” + a susceptible substrate (due to age, sex, genetics) + “perpetuators” that cause the trigger to continue stimulating the substrate (lifestyle risk factors such as obesity, smoking, diabetes, etc.)
Obesity is the highest attributable risk factor for atrial fibrillation. Treating obesity often helps to treat other risk factors, such as hypertension and sleep apnea.
Counseling is patient-dependent. Most patients are unable to make major behavioral changes cold-turkey and will need to make small, incremental changes.
Dr. Sanders’ tip: He tells his own patients that “atrial fibrillation is the body’s response to stress.” The key to treating atrial fibrillation is to control your underlying stressors - procedures and medications are simply band-aids that do not fix the root of the problem.
Notes
Notes drafted by Dr. Allam.
1. How common is atrial fibrillation?
Atrial fibrillation is the most common sustained arrhythmia. Currently, an estimated 50-60 million individuals worldwide are estimated to have atrial fibrillation, or roughly 1 in 4 individuals over the age of 45.1
The rising global prevalence of atrial fibrillation can be attributed to the aging of the population, increased rates of obesity, and greater accumulation of cardiovascular risk factors and survival with clinical cardiovascular disease.2 Atrial fibrillation is also being detected earlier through digital and wearable devices.2
Annually, we spend approximately $5,312 per adult on the management of atrial fibrillation in the United States.3
2. What is the underlying pathophysiology of atrial fibrillation? How do risk factors like sleep apnea or obesity “trigger” atrial fibrillation?
For atrial fibrillation to occur, there is an electrical “trigger”, a susceptible substrate (due to age, sex, genetics), and “perpetuators” that allow the trigger to continue stimulating the substrate.2
90% of electrical “triggers” come from the pulmonary veins
“Perpetuators” influence how the autonomic nervous system interacts with the triggers and substrate to perpetuate atrial fibrillation. Sleep apnea, obesity, and other risk factors are the “perpetuators”
Over time, as atrial fibrillation recurs, the substrate remodels to result in persistent atrial fibrillation.
3. What are some of the risk factors for atrial fibrillation and what are the possible benefits of controlling them?
Reference 4 provides an excellent review of the individual risk factors
Tobacco use
Nicotine patches/gums and counseling are associated with successful nicotine cessation in RCTs.
In the long term, nicotine itself can cause atrial fibrosis. However, it is safe to use patches and gums in the short term to abet cessation.
Obesity
The highest attributable risk factor for atrial fibrillation. Treating obesity often helps to treat other risk factors, such as hypertension and sleep apnea
In addition to regular exercise, reducing caloric intake can help combat obesity. Eating more fiber-laden food such as vegetables instead of carbohydrates, limiting portions, sugary drinks, and alcohol, and increasing fasting periods can all help decrease weight.
GLP-1 agonists can significantly reduce obesity and improve both symptoms and mortality for patients with comorbid conditions, such as HFpEF.
Obstructive sleep apnea
This is an evolving area of research with upcoming randomized trial data
Sleep apnea is probably not a static condition. Our likelihood of having sleep apnea changes with how rested we are, how much we’ve exercised, or whether we’ve consumed alcohol, etc. The testing and treatment of the future will reflect the changeable nature of sleep apnea.
Current data:
In the atrial fibrillation ablation population, treatment of sleep apnea was associated with an improvement in time to arrhythmia recurrence.
Another observational study from Norway, which included various patients who used dental sleep appliances, found no significant difference in atrial fibrillation between those who were treated for sleep apnea and those who were not. It was severely underpowered to detect a difference.
Caffeine
There is no evidence to support cessation of caffeine in patients with atrial fibrillation
For patients with bothersome palpitations, caffeine cessation can be tried if it improves their symptoms
Alcohol use
Per data from the UK Biobank, a single drink of alcohol daily does not increase your risk for developing atrial fibrillation. However, multiple drinks per day will increase your risk.
A proof-of-concept study showed that patients who abstained from alcohol for at least 6 months had complete resolution of atrial fibrillation. However, the dropout rate was very high as most patients could not completely abstain from alcohol
Dr. Sanders recommends alcohol consumption of ≤ 3 drinks/week, which is the cutoff used in lifestyle management studies.
Heart Failure
For patients with heart failure, the 4 pillars of heart failure management are also crucial to treating atrial fibrillation. SGLT2 inhibitors in particular are likely to confer benefits. 40-50% of patients in the SGLT2 inhibitor clinical trials had co-morbid atrial fibrillation.
About half of patients undergoing atrial fibrillation ablation appear to have HFpEF based on their hemodynamics.
4. Can atrial fibrillation be treated with only lifestyle modifications?
Potentially. This is an evolving area of research without much published data. Empirically, Dr. Sanders has noticed that in patients referred for atrial fibrillation ablation, aggressive lifestyle modifications result in 40% of them no longer requiring ablation. After a 10-year follow-up, 20% still do not require ablation.
However, ablation is still an effective modality to achieve rhythm control. It is also becoming a safer procedure owing to novel techniques, such as pulse field ablation.
In the future, we foresee most patients utilizing a combination of lifestyle modification and rhythm control strategies (ablation and/or medications) to control their atrial fibrillation.
5. What are the benefits of exercise in patients with atrial fibrillation? How much exercise do you recommend to your patients? Also, on the other end of the spectrum, does participation in endurance sports paradoxically promote atrial fibrillation?
The ACTIVE-AF study tested whether an intensive aerobic exercise regimen, up to 210 minutes per day, is safe and effective in controlling atrial fibrillation. Intensive exercise was associated with a significant reduction in atrial fibrillation burden and symptoms as well as an increase in quality of life and maintenance of sinus rhythm.5
Endurance athletes do have an approximately 5-fold higher risk of atrial fibrillation compared to sedentary people.6 However, this occurs at very high levels of exercise, exceeding 4 hours per day. Low to moderate levels of exercise have been shown to reduce rates of atrial fibrillation.4,5
6. How should we counsel patients about lifestyle management? Are there any good resources to use?
Dr. Sanders’ tip: Counseling is patient-dependent. For the majority of patients, the key to behavioral change is to make incremental adjustments over time, accompanied by encouragement. Some patients respond well to continuous feedback from digital devices. We can also supplement pharmacological therapies, such as medications to assist with weight loss or tobacco/alcohol cessation, to behavioral counseling.
Risk factor modification should be the central pillar of atrial fibrillation management and reviewed early on with patients in their atrial fibrillation course. It may be beneficial to have clinic sessions specifically dedicated to lifestyle counseling, which can be run by a multidisciplinary team of electrophysiologists, general cardiologists, and nurse educators.
7. How should we explain what atrial fibrillation is to our patients?
Dr. Sanders’ tip: He tells his own patients that “atrial fibrillation is the body’s response to stress. It occurs because the heart is not coping well with increased stress. Procedures and medications for atrial fibrillation are simply band-aids that do not fix the root of the problem, but controlling the risk factors contributing to increased stress will.”
... | |||
| 427. Management of Asymptomatic Severe Aortic Stenosis with Dr. Parth Desai and Dr. Tony Bavry | 11 Sep 2025 | 00:36:07 | |
CardioNerds (Drs. Amit Goyal, Elizabeth Davis, and Keerthi Gondi) discuss the approach to asymptomatic severe aortic stenosis with expert faculty Drs. Parth Desai and Tony Bavry.
They review the natural history of aortic stenosis, current guidelines for treating severe aortic stenosis, multiparametric risk stratification, trial data on aortic valve replacement for patients with asymptomatic severe aortic stenosis, and a practical approach for our patients today.
This episode was supported by an educational grant from Edwards Lifesciences. All CardioNerds education is planned, produced, and reviewed solely by CardioNerds. Managing asymptomatic severe aortic stenosis | AKH CME
Enjoy this Circulation Paths to Discovery article to learn more about the CardioNerds mission and journey.
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| 426. Case Report: A Ruptured Saccular Aortic Aneurysm into the Right Ventricle – University of Tennessee, Nashville | 08 Sep 2025 | 00:36:09 | |
CardioNerds join Dr. Neel Patel, Dr. Victoria Odeleye, and Dr. Jay Ramsay from the University of Tennessee, Nashville, for a deep dive into cardiovascular medicine in the vibrant city of Nashville. They discuss the following case: A 57-year-old male with a history of prior cardiac surgery, hypertension, and polysubstance use presented with syncope and chest pain. Initial workup revealed a large saccular ascending aortic aneurysm. While under conservative management, he experienced acute hemodynamic collapse, leading to the discovery of an unprecedented aorto-right ventricular fistula. This episode examines the clinical presentation, diagnostic journey, and management challenges of this rare and complex aortic pathology, highlighting the role of multimodal imaging and the interplay of multifactorial risk factors. Expert commentary is provided by Dr. Andrew Zurick III. Episode audio was edited by CardioNerds Intern student Dr. Pacey Wetstein.
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Pearls
Saccular Aneurysm Risk: Saccular aortic aneurysms, though less common than fusiform, carry a higher inherent rupture risk due to concentrated wall shear stress, often exacerbated by prior cardiac surgery, chronic hypertension, and polysubstance use.
Unprecedented Rupture: The direct rupture of an aortic aneurysm into a cardiac chamber, specifically the right ventricle, is an exceedingly rare event, with no prior reported cases in the literature, highlighting the unpredictable nature of complex aortic pathology.
Hemodynamic Catastrophe: A large aorto-right ventricular fistula creates a massive left-to-right shunt, leading to acute right ventricular pressure and volume overload, culminating in rapid cardiogenic shock and refractory right ventricular failure.
Multimodal Imaging Imperative: Multimodal imaging (CT angiography for anatomy, TTE/TEE for real-time hemodynamics and fistula detection, CMR for tissue characterization) is indispensable for rapid diagnosis and comprehensive characterization of life-threatening cardiovascular emergencies.
High-Risk Intervention: Emergent surgical repair of a ruptured aortic aneurysm with an aorto-right ventricular fistula is a high-risk procedure associated with significant mortality, underscoring the need for prompt multidisciplinary care and realistic outcome expectations.
Notes -
Notes (drafted by Dr Neel Patel):
What are the unique characteristics and rupture risk of saccular aortic aneurysms?
Saccular aortic aneurysms are less common than fusiform aneurysms.
They are generally considered more prone to rupture due to higher wall shear stress concentrated at the neck of the aneurysm, acting as a focal point of weakness.
Contributing Factors to Aneurysm Formation and Rupture in this Case:
Prior Cardiac Surgery: Aortic cannulation during the VSD/ASD repair decades ago likely created a localized structural weakness or predisposition.
Chronic, Poorly Controlled Hypertension: Imposed relentless systemic stress on the arterial walls, accelerating dilation and weakening.
Polysubstance Use: Particularly stimulants like cocaine and methamphetamines, which directly contribute to vascular damage by inducing severe, uncontrolled hypertension and direct arterial wall injury. This significantly increases the risk of aneurysm formation and rupture, especially with pre-existing conditions.
The direct rupture of an aortic aneurysm into a cardiac chamber, specifically the right ventricle, is an exceedingly rare event, with no prior reported cases in the literature, making this a "first of its kind" report.
What are the hemodynamic consequences and management challenges associated with aorto-right ventricular fistulas?
Hemodynamic Impact: A large aorto-right ventricular fistula results in a significant anatomic left-to-right shunt, where blood from the high-pressure aorta is shunted directly into the lower-pressure right ventricle.
This leads to acute right ventricular pressure and volume overload, causing rapid right ventricular dilation, increased right ventricular wall stress, and ultimately, acute right ventricular failure.
This directly explained the sudden onset of cardiogenic shock, as the right ventricle was unable to maintain forward flow, leading to systemic hypoperfusion and shock.
Management Challenges:
The patient required emergent, extremely high-risk salvage aortic aneurysm repair surgery.
Marked hemodynamic instability occurred immediately after anesthesia induction (systolic blood pressure dropped to 50 mmHg), necessitating immediate initiation of external cardiopulmonary bypass.
Intra-operatively, a large (2 cm diameter) hole in the ascending aorta communicating with the saccular aneurysm was found, along with a massive (4-5 cm) fistula into the right ventricular outflow tract (RVOT) area, just proximal to the pulmonic valve, with several smaller holes.
Surgical repair involved a 5x10 cm bovine pericardial patch for the right ventricular wall and replacement of a 5 cm segment of the ascending aorta with a 34 mm gelweave straight graft.
Post-operative Course: Severely complicated by severe coagulopathy and extensive bleeding (requiring multiple blood products and a Cabral fistula).
Continued severe right ventricular dysfunction necessitated the placement of a Right Ventricular Assist Device (RVAD).
Despite support, hemodynamic function continued to decline, with severely depressed Left Ventricular (LV) function observed.
The patient ultimately passed away due to refractory right heart failure and hemodynamic collapse, highlighting the extremely high mortality risk associated with such complex, emergent cardiac surgical interventions.
What is the role of multimodal imaging in diagnosing this complex and rare cardiovascular emergency?
CT Angiography: Crucial for initial identification and comprehensive characterization of the large saccular ascending aortic aneurysm, providing precise dimensions, revealing layered thrombus, and understanding anatomical relationships. Its high spatial resolution and wide field of view are excellent for aortic assessment.
Transthoracic and Transesophageal Echocardiography (TTE/TEE): Absolutely critical for real-time diagnosis of the fistula during acute deterioration. Bedside echocardiography, particularly TEE, allowed for visualization of the new continuous, turbulent flow from the aorta directly into the right ventricle, quantification of acute right ventricular dilation, and estimation of significantly increased RVSP. Its accessibility and real-time capabilities are unmatched for acute hemodynamic assessment and shunt detection.
Cardiac MRI (CMR): Provided additional tissue characterization of the aneurysm, confirming partial thrombosis and, importantly, showing no significant late gadolinium enhancement (LGE) in the myocardium, which was reassuring regarding the absence of significant myocardial scar related to the aneurysm itself. CMR offers superior soft tissue characterization compared to CT.
Complementary Nature: This case demonstrated the complementary nature of these modalities: CT provided the initial anatomical roadmap, echocardiography offered real-time hemodynamic assessment and immediate diagnosis of the acute rupture and shunt, and CMR contributed valuable tissue characterization. Imaging choices are guided by clinical questions, urgency, and specific information needed for critical management decisions.
What are the multi-factorial risk factors contributing to complex aortic disease, including the often-overlooked impact of polysubstance use?
Prior Cardiac Surgery: The patient's history of open-heart surgery decades prior, involving aortic cannulation for cardiopulmonary bypass, is a recognized risk factor for the subsequent development of iatrogenic aneurysms, creating a localized structural weakness or predisposition.
Chronic, Poorly Controlled Hypertension: Imposes relentless systemic stress on the arterial walls, accelerating dilation and weakening, significantly contributing to aneurysm progression.
Polysubstance Use:
The patient's long-standing history of polysubstance use, particularly stimulants like cocaine and methamphetamines, represents a significant contributing factor to his vascular pathology.
These substances are not merely comorbidities; they directly contribute to vascular damage.
Chronic stimulant use can induce severe, uncontrolled hypertension and direct arterial wall injury.
This significantly increases the risk of aneurysm formation and rupture, especially when combined with pre-existing conditions like essential hypertension and prior cardiac surgery.
Multi-hit Phenomenon: This case illustrates a multi-factorial pathology where various insults on vascular integrity over time converge to create a highly complex and catastrophic cardiovascular event. The presence of these factors emphasizes the critical importance of a thorough social history in cardiovascular risk assessment, moving beyond a superficial listing to understanding the profound pathophysiological impact on vascular health.
References -
Lavall D, Schäfers HJ, Böhm M, Laufs U. Aneurysms of the ascending aorta. Dtsch Arztebl Int. 2012 Mar;109(13):227-33. doi: 10.3238/arztebl.2012.0227. Epub 2012 Mar 30. PMID: 22532815; PMCID: PMC3334714.
Shang EK, Nathan DP, Boonn WW, Lys-Dobradin IA,... | |||
| 425. Case Report: The Hidden Culprit – Unraveling the Cause of Malignant Ventricular Arrhythmias in a Young Adult – Trinity Health Livonia Hospital | 29 Aug 2025 | 00:54:43 | |
CardioNerds guest host Dr. Colin Blumenthal joins Dr. Juma Bin Firos and Dr. Aishwarya Verma from the Trinity Health Livonia Hospital to discuss a fascinating case involving malignant ventricular arrhythmias. Expert commentary is provided by Dr. Mohammad-Ali Jazayeri. Audio editing for this episode was performed by CardioNerds Intern,Julia Marques Fernandes.
This case explores the puzzling presentation of exercise-induced ventricular tachycardia in a young, otherwise healthy male who suffered recurrent out-of-hospital cardiac arrests. With no traditional risk factors and an unremarkable ischemic workup, the challenge lay in uncovering the underlying cause of his malignant arrhythmias. Electrophysiology studies and advanced imaging played a pivotal role in systematically narrowing the differentials, revealing an unexpected arrhythmogenic substrate. This episode delves into the diagnostic dilemma, the role of EP testing, and the critical decision-making surrounding ICD placement in a patient with a concealed but life-threatening condition.
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Pearls- Malignant Ventricular Arrhythmias
This case highlights the challenges and importance of diagnosing and managing ventricular arrhythmias in young, seemingly healthy individuals. Here are five key takeaways from the episode:
Electrophysiology (EP) studies play a crucial role in identifying arrhythmogenic substrates in patients with exercise-induced ventricular tachycardia (VT) without obvious structural heart disease. In this case, substrate mapping revealed late abnormal ventricular afterdepolarizations in the basal inferior left ventricle, providing valuable insights into the underlying mechanism.
Cardiac MRI can be a powerful tool for detecting subtle myocardial abnormalities. The subepicardial late gadolinium enhancement (LGE) in the lateral and inferior LV walls suggested an underlying myocardial process, even when other imaging modalities appeared normal.
The VT morphology can provide clues about the underlying mechanism. In this case, the right bundle branch block pattern with a northwest axis and shifting exit sites pointed towards a scar-mediated mechanism rather than a channelopathy or idiopathic VT.
Implantable cardioverter-defibrillator (ICD) placement is crucial for secondary prevention of sudden cardiac death (SCD) in patients with malignant ventricular arrhythmias, even in young individuals. The patient's initial deferral of ICD implantation highlights the importance of shared decision-making and patient education in these complex cases.
"Scar-mediated VT introduces the risk of new arrhythmogenic substrates over time, reinforcing the need for ICD therapy even when catheter ablation is considered." This pearl emphasizes the dynamic nature of the arrhythmogenic substrate and the importance of long-term risk mitigation strategies.
Notes - Malignant Ventricular Arrhythmias
Notes were drafted by Juma Bin Firos.
1. What underlying pathologies cause ventricular arrhythmias in young patients without overt structural heart disease?
Myocardial fibrosis:
Detected via late gadolinium enhancement (LGE) on cardiac MRI
Present in 38% of nonischemic cardiomyopathy cases
Increases sudden cardiac death (SCD) risk 5-fold
Often localized to subepicardial regions, particularly in the inferolateral left ventricle (LV)
May precede overt systolic dysfunction by years
Subclinical cardiomyopathy:
67% of young VT patients show subtle cardiac dysfunction
Suggests VT may be the first manifestation of cardiomyopathy
Can include early-stage genetic cardiomyopathies (e.g., ARVC, LMNA mutations)
Often associated with preserved ejection fraction (EF >50%)
Arrhythmogenic substrate:
EP studies localize re-entry circuits to specific regions:
Basal inferior LV near the mitral annulus (as in this case)
Right ventricular outflow tract (RVOT) in idiopathic VT
Papillary muscles or fascicular regions
Substrate can exist even with normal EF and no visible structural abnormalities on echocardiography
Channelopathies:
Long QT syndrome (LQTS): QTc >460ms in males, >470ms in females
Brugada syndrome: Coved ST elevation in V1-V3
Catecholaminergic polymorphic VT (CPVT): Normal resting ECG, bidirectional VT with exercise
Short QT syndrome: QTc <330ms
Inflammatory conditions:
Myocarditis: Can cause transient or persistent arrhythmogenic substrate
Cardiac sarcoidosis: Patchy inflammation and fibrosis, often affecting the septum
2. How do electrophysiology studies differentiate scar-mediated VT from channelopathies?
Substrate mapping:
Identifies late abnormal potentials (LAPs) with 92% specificity for re-entry circuits
Utilizes multi-electrode catheters (e.g., Penta Ray) for high-density mapping
LAPs indicate slow conduction through fibrotic tissue, key for re-entry
Absent in purely electrical disorders like channelopathies
Inducibility:
Programmed electrical stimulation (PES) protocols:
Up to triple extra stimuli at multiple sites (RV apex, RVOT, LV)
Burst pacing at cycle lengths down to 200-250ms
Scar-mediated VT is often inducible with aggressive stimulation
Polymorphic VT/VF induction suggests a structural substrate
Channelopathies like Catecholaminergic polymorphic ventricular tachycardia CPVT) typically requires isoproterenol or exercise for induction
VT morphology analysis:
Right bundle branch block (RBBB) + northwest axis localizes to LV basal inferior wall
Left bundle branch block (LBBB) + inferior axis suggests RVOT origin
Fascicular VT: RBBB + left anterior or posterior fascicular block pattern
Papillary muscle VT: RBBB or LBBB with variable axis
Entrainment mapping:
Performed during sustained monomorphic VT
Post-pacing interval minus tachycardia cycle length (PPI-TCL) <30ms indicates critical isthmus
Not applicable to polymorphic VT or channelopathies
Electroanatomic voltage mapping:
Low voltage areas (<1.5mV bipolar) indicate scar tissue
Normal voltage throughout suggests functional (non-scar) VT mechanism
3. What are key management considerations for recurrent VT/VF in young patients?
ICD for secondary prevention:
Class I indication after cardiac arrest or sustained VT without a reversible cause
Reduces mortality from 13% (8-year untreated) to <5%, especially with LGE present
Device selection:
Single-chamber ICD if no pacing indication
Subcutaneous ICD (S-ICD) in young patients to avoid transvenous lead complications
Consider cardiac resynchronization therapy defibrillator (CRT-D) if LBBB or wide QRS
LifeVest limitations:
Bridges ≤3 months; not a long-term solution
Recurrent arrests double mortality vs. prompt ICD implantation
Compliance issues: must be worn consistently to be effective
Oral antiarrhythmic medications:
Amiodarone:
Effective for acute VT suppression
Long-term use limited by side effects (thyroid, liver, pulmonary toxicity)
Beta-blockers: First line for most VT/VF, especially exercise-induced
Sotalol: Alternative for those with preserved LV function
Mexiletine: Adjunct for frequent ICD shocks, especially with LQT3
Catheter ablation:
Consider early in the course for recurrent ICD shocks
Success rates 60-80% for scar-related VT
May reduce ICD shocks and improve quality of life
Limitations: deep intramural or epicardial substrates may require specialized approaches
Lifestyle modifications:
Exercise restrictions: Avoid high-intensity activities that trigger arrhythmias
Stress management: Consider cognitive behavioral therapy or mindfulness training
Avoidance of QT-prolonging medications in LQTS patients
Genetic testing and family screening:
Recommended for suspected inherited arrhythmia syndromes
Can guide management and risk stratification for family members
4. Why does exercise exacerbate arrhythmia risk in these patients?
Sympathetic surge:
Increases myocardial oxygen demand
Enhances automaticity and triggered activity
Can unmask concealed conduction abnormalities
Hemodynamic changes:
Increased preload and afterload stress fibrotic regions
Volume shifts may alter electrolyte concentrations locally
Metabolic factors:
Lactic acid accumulation can promote ectopic beats
Catecholamine release exacerbates ion channel dysfunction in channelopathies
Exercise-induced VT/VF correlates with 8× higher SCD risk vs. rest-onset arrhythmias:
Warrants activity restrictions tailored to individual risk profile
May indicate more malignant substrate or advanced disease process
Treadmill testing:
Should guide therapy in asymptomatic patients with exercise-related VT
Protocols:
Bruce protocol for general assessment
Modified protocols (e.g., longer stages) for specific arrhythmia provocation
Endpoints:
Induction of sustained VT/VF
Achieving target heart rate (85% of age-predicted maximum)
Development of concerning symptoms (pre-syncope, chest pain)
Cardiac rehabilitation:
Supervised exercise programs can improve outcomes
Gradual increase in intensity with continuous monitoring
Helps define safe exercise thresholds for patients
5. How does LGE on cardiac MRI refine risk stratification?
Late gadolinium enhancement (LGE) on cardiac MRI acts like a "scar map" of the heart, revealing areas of damaged or fibrotic tissue. These scars create electrical instability, increasing the risk of dangerous heart rhythms and sudden cardia | |||
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