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Cardionerds: A Cardiology Podcast
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Welcome to CardioNerds, where we bring you in-depth discussions with leading experts, case reports, and updates on the latest advancements in the world of cardiology. Tune in to expand your knowledge, sharpen your skills, and become a true CardioNerd!
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456. ACS Guidelines Question #2 with Dr. Michelle O’Donoghue
1w ago00:10:03Tap to summarizeThis 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? A Proceed with primary PCI to LAD B Medical management with aspirin and enoxaparin C Medical management with aspirin and clopidogrel D Medical management with aspirin and ticagrelor Answer #2 Explanation The Correct answer is D In 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 Takeaway In 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
Transcribe →455. The Long-Term Management Of Patients With Pulmonary Embolism with Dr. Soophia Naydenov
2w ago00:19:12Tap to summarizeCardioNerds (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. CardioNerds Pulmonary Embolism PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! 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...
Transcribe →454. ACHD Surgery 101: Thinking Like a Surgeon with Elizabeth Stephens
4w ago00:42:42Tap to summarizeCardioNerds (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...
Transcribe →453. ACS Guidelines Question #1 with Dr. Sunil Rao
Jun 400:10:29Tap to summarizeThe 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? A Right radial artery only B Radial + bilateral femoral C Bilateral femoral only Answer #1 Explanation The correct answer is B. Radial and bilateral femoral Radial 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 Takeaway For patients with ACS undergoing PCI, radial access is strongly preferred to reduce mortality, bleeding, and vascular complications. Guideline Loc. Section 7.1
Transcribe →452. Risk stratification in Acute Pulmonary Embolism with Dr. Stavros Konstantinides
Jun 100:25:35Tap to summarizeCardioNerds (Dr. Billy-Joe Mullinax, Dr. Dinu Balanescu, and Dr. Jane Ehret) discuss risk stratification in acute pulmonary embolism with Dr. Stavros Konstantinides, Chair of the 2019 ESC Pulmonary Embolism Guidelines. Using a real-world case, this episode explores how modern PE care has moved beyond “massive” and “submassive” labels toward a dynamic, physiology-based approach. The discussion highlights the limitations of static risk scores, the importance of right ventricular dysfunction and biomarkers, and why normotension does not imply stability. Special emphasis is placed on intermediate-high risk PE, early identification of impending hemodynamic collapse, and the role of lactate, serial reassessment, and PERT teams in guiding escalation of care. Audio editing by CardioNerds intern, Joshua Khorsandi.The 2026 American multi-society PE guidelines were published after this episode was recorded. Dr. Dinu Balanescu and Dr. Billy-Joe Mullinax are Co-chairs for the CardioNerds PE Series, developed in collaboration with the PERT Consortium.   Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. CardioNerds Pulmonary Embolism PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls Stable blood pressure does not mean low risk in PEHypotension is a late finding. Patients may have severe RV failure, hypoxia, and tissue hypoperfusion while remaining normotensive — a key concept behind “normotensive shock.” Risk stratification in PE must be dynamic, not staticLegacy scores like PESI and Bova provide a snapshot and predict 30-day mortality, but they do not capture short-term trajectory or impending hemodynamic collapse. Intermediate-high risk PE is a dangerous and heterogeneous groupPatients with RV dysfunction, positive biomarkers, tachycardia, hypoxemia, and elevated lactate may have in-hospital mortality approaching 15%, rivaling STEMI. Lactate is a critical but underutilized marker in PEElevated lactate reflects tissue hypoxia and early circulatory failure and may identify patients at risk for collapse before blood pressure declines. PERT enables physiology-driven, patient-centered PE carePERT teams operationalize continuous reassessment, integrate imaging, labs, and clinical trajectory, and allow timely escalation — shifting PE management from rigid categories to real-time decision-making. Notes Drafted by Dr. Jane Ehret. 1. What is the contemporary framework for risk stratification in acute pulmonary embolism? Modern PE risk stratification prioritizes hemodynamics and right ventricular (RV) function rather than clot burden. The 2019 ESC Guidelines classify PE into high risk, intermediate risk (low vs high), and low risk, based on: Hemodynamic status, RV dysfunction on imaging, and Cardiac biomarkers. This framework emphasizes early mortality risk but requires clinical context to guide escalation decisions. 2. Why is normotension insufficient to define “stability” in PE? Blood pressure is a late marker of circulatory failure in PE. Patients can maintain normal BP through Tachycardia, Increased sympathetic tone, and RV compensation. Many patients with preserved BP may already have shock physiology, including hypoxemia, elevated lactate, and RV failure — sometimes referred to as “normotensive shock.” 3. How should intermediate-risk PE be conceptualized clinically? Intermediate-risk PE is heterogeneous, ranging from patients who do well on anticoagulation to those who deteriorate rapidly. Intermediate-high risk PE is defined by RV dysfunction on imaging and positive cardiac biomarkers. Clinical features such as tachycardia, increasing oxygen requirement, and elevated lactate identify patients at highest risk within this group. 4. What are the strengths and limitations of commonly used PE risk scores? Legacy scores are useful for initial risk categorization but are static and limited in predicting short-term deterioration. Most scores were developed to predict mortality or complications at fixed time points rather than dynamic clinical trajectory. 5. What are the commonly used risk scores and clinical tools in PE, and what is each designed to predict? ESC Risk Stratification Algorithm: Identifies high-risk PE by hemodynamics. Uses PESI or sPESI in normotensive patients to distinguish low-risk from non–low-risk PE. Uses RV dysfunction and biomarkers to differentiate intermediate-low from intermediate-high risk. Forms the basis of many institutional PE pathways. PESI and sPESI: Validated to predict 30-day mortality. Widely used to identify low-risk patients appropriate for outpatient management. Heavily influenced by age and comorbidities. Bova Score: Predicts 30-day PE-related complications in normotensive patients. Composite PE Shock Score (CPES): Predicts normotensive shock in hemodynamically stable PE patients. Pulmonary Embolism Progression (PEP) Score: Predicts progression from intermediate-risk to high-risk PE within 72 hours of diagnosis. PE Short-term Clinical Outcomes Risk Estimation (PE-SCORE): Predicts clinical deterioration or death within 5 days of PE diagnosis. Hestia Criteria: Identifies low-risk PE patients safe for outpatient treatment. Wells’ Criteria and Revised Geneva Score: Determine pretest probability for diagnostic triage. PERC Score: Rules out PE in very low-risk patie...
Transcribe →451: CCTA, CT-FFR, and AI Plaque Analysis to Personalize CAD Detection, Prevention, and Management with Dr. Michael Gallagher
May 2700:46:23Tap to summarizeCardioNerds Dr. Joseph Kassab, Dr. Mariana Garcia-Arango, and Dr. Christopher Mason explore the technological revolution of Coronary CT Angiography (CCTA) with expert faculty Dr. Michael Gallagher. The discussion details how CCTA has evolved into a frontline diagnostic and preventive tool, moving beyond simple anatomy to incorporate physiology via CT-FFR and biology through AI-driven plaque quantification. The episode reviews landmark evidence like the SCOT-HEART and PROMISE trials, the nuances of CAD-RADS 2.0 reporting, and the emerging role of AI in monitoring treatment response and personalizing cardiovascular care. Critically, they also discuss some of the assumptions and limitations of these techniques. Stay tuned for a matching review article to be submitted to US Cardiology Review, the official Journal of CardioNerds. This episode was supported by an independent medical education grant from HeartFlow. All CardioNerds education is planned, produced, and reviewed solely by CardioNerds.  Enjoy this Circulation Paths to Discovery article to learn more about the CardioNerds mission and journey. US Cardiology Review is now the official journal of CardioNerds! Submit your manuscripts here. CardioNerds Multimodality Cardiovascular Imaging PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll Pearls Shift in Paradigm: CCTA is no longer just an anatomic test; with some key limitations, it can provide anatomy, physiology (CT-FFR), and plaque biology (AI-CPA) in a single non-invasive scan. The “Power of Zero” vs. Plaque: While a normal CCTA has a >95% negative predictive value, future MIs often arise from non-obstructive plaque that traditional stress tests might miss. CAD-RADS 2.0 Utility: The addition of plaque burden modifiers (P1–P4) is a “game changer,” allowing clinicians to identify high-risk patients who need aggressive lipid-lowering despite having only mild stenosis. CT-FFR as a Virtual Stress Test: CT-FFR uses computational fluid dynamics to simulate blood flow, potentially reducing unnecessary invasive catheterizations by approximately 61% without sacrificing safety. Seeing the Invisible: AI-based quantitative plaque analysis (QCPA) can identify “subvisual” plaque and low-attenuation (lipid-rich) components that are the primary drivers of acute coronary syndromes. Show Notes How has the role of CCTA changed compared to traditional functional testing? Historically, stress testing answered “is there ischemia today?”, which often reflects late-stage disease. CCTA identifies disease across the entire spectrum, asking “is there atherosclerosis and how much plaque is present?”. Landmark evidence: SCOT-HEART showed a 41% relative risk reduction in MI at 5 years attributed to intensified preventive therapies, and PROMISE showed CCTA was better at selecting patients who truly needed invasive angiography. Diagnostic CCTA imaging depends on the protocol, contrast timing, heart rate, heart rhythm, breathholding, scanner quality, and several patient factors (obesity, prior stents, heavy calcification, complex bypass anatomy, and motion artifact all may limit imaging). “CCTA is exceptional for the right patient, with the right scanner, and the right team.” What are the key modifiers introduced in CAD-RADS 2.0, and why do they matter? CAD-RADS 2.0 moved beyond stenosis severity to include plaque burden (P0 to P4), high-risk plaque (HRP) features, and the presence of ischemia based on CT-FFR. It serves as a clinical decision support tool: a patient with mild (25-49%) stenosis but “extensive” (P4) plaque burden is considered high risk and warrants aggressive risk factor modification. How is CT-FFR calculated, and when is it most useful in clinical practice? CT-FFR uses resting CCTA data and computational fluid dynamics to create a 3D model of coronary flow during simulated maximal hyperemia. It is often used for intermediate lesions (40–90% stenosis) to predict if they are ischemia-producing, guiding the decision whether to proceed with invasive angiography. The assumptions necessary for this computational modeling may not apply well to patients with microvascular dysfunction, significant myocardial scar or prior infarction, or ventricular hypertrophy. Still, data indicate that CT-FFR performs similarly to PET in predicting hemodynamically significant lesions. CT-FFR performs well at the extremes (either clearly normal or clearly abnormal). Accuracy dips, however, in the intermediate range (~0.75-0.80), where decision-making is most critical. In this grey zone, additional factors can help guide the approach, including the amount of myocardium supplied, translesional gradient, and plaque features. CT-FFR has not been validated in distal segments, stented segments, heavily calcified coronary arteries, or in patients with severe aortic stenosis. Caution with CT-FFR should be utilized in very calcified coronary segments. What is AI-based quantitative plaque analysis (QCPA), and what metrics are ready for clinical use? This is potentially a paradigm shift, moving away from stenosis-centric thinking to a more disease burden and plaque biology focus. QCPA uses deep learning algorithms to automatically segment the vessel wall and quantify plaque volume in mm³. Ready for “prime time” metrics include: Total Plaque Volume (TPV), non-calcified plaque volume, and Low-Attenuation Plaque (LAP) burden. Can serial CCTA be used to monitor the effectiveness of medical therapies like statins? While not yet a routine guideline-driven practice, trials like PARADIGM and EVAPORATE show that therapies can stabilize plaque; notably, CCTA is better for monitoring than CAC scores, which can be misleading as statins often increase plaque calcification as part of the stabilization process. There are no randomized trials that serial CCTAs improve outcomes. Cost and radiation exposure will be notable lim...
Transcribe →450. Journal Club: The I-CLASS Registry with Dr. Theofanie Mela and Dr. Pugazhendhi Vijayraman
May 2500:19:54Tap to summarizeJoin CardioNerds EP Council Chair Dr. Naima Maqsood and Episode Lead Dr. Sukriti Banthiya as they discuss the results of the International Collaborative LBBAP Study (I-CLAS) with expert faculty Dr. Theofanie Mela and Dr. Pugazhendhi Vijayraman. Audio editing by CardioNerds academy intern, Grace Qiu. The International Collaborative LBBAP Study (I-CLAS) evaluated clinical outcomes between biventricular pacing (BVP) and left bundle branch area pacing (LBBAP) in patients with left ventricular ejection fraction (LVEF) ≤50% undergoing cardiac resynchronization therapy. Between January 2018 and June 2023, 2,579 patients were enrolled across 18 centers. The primary composite outcome was defined as all-cause mortality or heart failure hospitalization. LBBAP demonstrated a shorter paced QRS duration and was associated with a lower risk of primary composite outcome and heart failure hospitalization. No significant difference was observed in all-cause mortality. Additionally, procedural complications were lower with LBBAP. This episode was planned in collaboration with Heart Rhythm TV with mentorship from Dr. Daniel Alyesh and Dr. Mehak Dhande.  Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. US Cardiology Review is now the official journal of CardioNerds! Submit your manuscript here. CardioNerds Journal Club PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron!
Transcribe →449. Atrial Fibrillation: Challenging Scenarios in Atrial Fibrillation Management with Dr. Bradley Knight
May 2100:37:54Tap to summarizeIn this episode, CardioNerds Dr. Colin Blumenthal, Dr. Kelly Arps, and Dr. Yong Hao Yeo are joined by electrophysiology expert Dr. Bradley Knight to discuss atrial fibrillation (AF) management in challenging clinical scenarios. We explore arrhythmias in patients with pre-excitation syndromes, particularly Wolff-Parkinson-White (WPW) syndrome, and strategies for rhythm control. We also discuss AF management in pregnancy, adult congenital heart disease, and patients with tachycardia-bradycardia (tach-brady) syndrome. This episode provides essential insights into nuanced decision-making for the care of patients with complex arrhythmia profiles. Audio editing by CardioNerds academy intern, Grace Qiu. Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. CardioNerds Atrial Fibrillation PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! PEARLS AF in WPW is a true emergency—AV nodal blocking agents can be deadly. In patients with WPW syndrome, AF can rapidly conduct through the accessory pathway, risking ventricular fibrillation and sudden death. Avoid AV nodal blockers like beta-blockers and calcium channel blockers. Catheter ablation is the first-line rhythm control strategy in WPW. Catheter ablation carries a Class I recommendation and offers >90% success. If antiarrhythmic drugs are needed, sodium channel blockers like flecainide or propafenone are preferred in patients without structural heart disease. In pregnancy, protecting the mother is protecting the fetus. An unstable mother means an unstable fetus. Rate control is the first step in AF with rapid ventricular responses and electrical cardioversion is safe when needed. Multidisciplinary care is essential. AF in congenital heart disease is often outside the pulmonary veins. Surgical scars and chamber remodeling in ACHD patients often lead to AF from non-pulmonary vein foci. Electrogram-based mapping and targeted ablation strategies are essential to increase success rate of durable rhythm control. Tachy-brady syndrome may require pacing to unlock therapy. AF may cause atrial myopathy and sinus node dysfunction. These patients often require permanent pacing to allow safe use of rate-controlling medications like beta-blockers and to prevent syncope or chronotropic incompetence. Notes: Notes drafted by Dr. Yong Hao Yeo Why is atrial tachycardia in patients with WPW syndrome dangerous? Patients with WPW commonly present with supraventricular tachycardia (SVT) due to atrioventricular reentrant circuits, either orthodromic or antidromic. This SVT can degenerate into AF. In the absence of AV nodal as the governor between the atrium and ventricles, the accessory pathway may conduct impulses rapidly and frequently. This can lead to dangerously high ventricular rates, predisposing patients to ventricular fibrillation and sudden cardiac arrest. What are some strategies for rhythm control in patients with WPW and atrial tachycardia? Catheter ablation is the first-line therapy (Class I recommendation), with a success rate of over 90%. Ablation reduces the risk of sudden cardiac arrest, though some patients may remain prone to AF. If ablation is not feasible/ contraindicated, sodium channel blockers such as flecainide and propafenone are good options in patients without ischemia or structural heart disease (Class IIa recommendation). Amiodarone should be avoided because it has a long half-life, can accumulate in the system, and may delay definitive treatment with catheter ablation. AV nodal blocking agents like beta blockers and calcium channel blockers should be avoided, as they are less effective at controlling ventricular rate in WPW and can increase conduction over the accessory pathway. These agents can also exacerbate the risk of rapid ventricular rates during AF and worsen left ventricular function. What are some special considerations in managing AF in pregnant patients? The primary goal in managing cardiovascular disease during pregnancy is to protect the mother, as fetal outcomes depend on maternal well-being. Therefore, while caution is necessary, we should avoid undertreating pregnant patients with AF. In cases of AF with rapid ventricular response (RVR), rate control is usually the first-line strategy, with beta blockers preferred over digoxin or non-dihydropyridine calcium channel blockers. It is then reasonable to initially observe for spontaneous conversion in stable patients. Antiarrhythmic drugs (AADs) are generally avoided during the first trimester, but clinical judgment on a case-by-case basis is essential. Evidence for the safety of AADs in pregnancy is limited, often derived from their use in other conditions such as fetal SVT. Flecainide and sotalol are reasonable options for rhythm control (Class IIa recommendation). Electrical cardioversion is considered safe in pregnancy and should be utilized when indicated (Do not forget!). There is no pregnancy-specific thromboembolic risk stratification tool. CHA₂DS₂-VASc scoring and the presence of risk factors like mitral stenosis can help guide anticoagulation decisions, though the magnitude of thromboembolic risk during pregnancy remains unclear. Rate control agents are typically continued during delivery due to the increased physiologic stress of labor and delivery. Multidisciplinary care is crucial and should involve obstetrics, maternal-fetal medicine, cardiology, and electrophysiology specialists. What are some key considerations for AF management in patients with adult congenital heart disease (ACHD)? Patients with repaired congenital heart disease are at increased risk for arrhythmias due to two main factors: surgical scars that create arrhythmogenic foci and mechanical remodeling of the atria or ventricles resulting from the underlying disease. In these patients with structural heart disease, sodium channel blockers may not be ideal antiarrhythmic options. When selecting an antiarrhythmic drug, clinicians must ...
Transcribe →448. The Braunwald Chronicles: The Complete Series — A CardioNerds Tribute to Dr. Eugene Braunwald
Apr 3000:41:43Tap to summarizeCardioNerds (Amit Goyal, Daniel Ambinder, Carine Hamo, and Karan Desai) are honored to bring you The Braunwald Chronicles — a special tribute to the life and legacy of Dr. Eugene Braunwald. Originally released as a 6-part series, we are now bringing these chapters together as one complete experience. These are stories of discovery, innovation, accidents, perseverance, and more… truly, these are the stories of cardiology itself — told firsthand by the father of modern cardiology. Dr. Braunwald’s life and work form the very foundation of contemporary cardiovascular medicine, and his story is, in many ways, the story of our field. Join us as we journey through the history of cardiology across six extraordinary chapters — from the early days of physiologic discovery, to the development of transseptal access, to defining the natural history of valvular disease, to shaping modern therapies for myocardial infarction, and beyond. Through it all, Dr. Braunwald reflects on the principles that guided his career — curiosity, perseverance, mentorship, and the importance of being in the right place, at the right time, with the right people.We hope this collection serves not only as an educational experience, but as a tribute to one of the greatest minds in the history of medicine. We thank Dr. Karan Desai, Editorial APD with the CardioNerds Academy and fellow at the University of Maryland, for all the work he put into designing The Braunwald Chronicles. Audio editing by Pace Wetstein. CardioNerds Braunwald Chronicles Series PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron!
Transcribe →447. Pulmonary Embolism: Approach to Systemic Thrombolysis in Acute Pulmonary Embolism with Dr. Allison Burnett
Apr 2400:42:43Tap to summarizeCardioNerds Drs. Dinu Balanescu, Billy-Joe Mullinax, and Mariana Garcia discuss systemic thrombolysis in pulmonary embolism with expert Dr. Allison Burnett. Audio editing by CardioNerds Academy intern, student doctor, Pace Wetstein. Pulmonary embolism is the third leading cause of cardiovascular death in the US, and high-risk PE carries a 30-day mortality risk as high as 30-50%. In this episode, we discuss the indications for systemic thrombolysis, including high-risk PE and cardiac arrest. We addressed how to appropriately select candidates for systemic thrombolysis, balancing the high risk of bleeding. Additionally, we discussed anticoagulation management and timing concurrent with lytic therapy, as well as the importance of multidisciplinary PERT teams.  The 2026 American multi-society PE guidelines were published after this episode was recorded. Dr. Dinu Balanescu and Dr. Billy-Joe Mullinax are Co-chairs for the CardioNerds PE Series, developed in collaboration with the PERT Consortium. Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. CardioNerds Pulmonary Embolism PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls Risk stratification is crucial in acute pulmonary embolism care. Based on the ESC 2019 guidelines, low-risk PE patients are those who are normotensive with no evidence of right ventricular dysfunction. Intermediate risk includes two categories: intermediate-low, with normotensive patients who have a high PE score with negative biomarkers, and intermediate-high risk, which has elevated biomarkers or signs of RV strain. High-risk PE includes hemodynamically unstable patients (SBP<90) who have end-organ dysfunction, shock, or cardiac arrest. The 2026 American multi-society PE guidelines presented a new clinical classification scheme is presented, entitled “Acute Pulmonary Embolism Clinical Categories,” with 5 categories (A-E) and subcategories, ranging from low to high risk for adverse outcomes. Systemic lysis has been studied in patients at high and intermediate risk. Overall, the reduction in mortality has been seen in patients with high-risk PE. Systemic thrombolysis is associated with high rates of bleeding, 2% fatal or high-risk intracranial hemorrhage per the PEITHO trial; therefore, selecting the appropriate population is critical to improve outcomes and balance the risks and benefits. Multidisciplinary PERT teams are crucial for making high-quality decisions, and stewardship is necessary to optimize the care of patients with PE. Notes Notes: Notes drafted by Dr. Mariana Garcia-Arango What is the role of systemic thrombolysis in the current era of available catheter-directed therapies? Thrombolytic therapy reduces mortality, PE recurrence, and PE-related mortality in patients with acute PE. The evidence supports use during high-risk PE and cardiac arrest. The clinical presentation is often severe, with high stakes and limited time to mobilize to the cath lab on time for catheter therapies, especially in rural populations. How to approach the use of systemic thrombolysis during CPR? Cardiac arrest from PE carries a very poor outlook, with survival rates under 10%. Rapid, targeted interventions to restore circulation are critical. Systemic thrombolysis may be considered for patients in cardiac arrest due to confirmed or strongly suspected pulmonary embolism, especially when standard ACLS interventions have not been successful. What is the best anticoagulation approach while using lytics? Most of the time, we should opt for low-molecular-weight heparin over unfractionated heparin, which has been shown to lead to less major bleeding and reduction of recurrent PE. Exceptions to the rule include renal dysfunction or if there is consideration of cannulation for ECMO or other invasive procedures.  There is variation in practice regarding timing and initiation of anticoagulation while using lytics. There are different protocols given the variety of how studies were conducted. If they are going to get mechanical catheter-based therapy, the trend is to prefer LMWH. When lytics are included, either systemic or catheter-directed lytics, there is flexibility and room to discuss with the multidisciplinary PERT team which strategy to use. Future studies and trials are needed to standardize the best therapies.  What are the pharmacologic properties of available thrombolytics? Thrombolytics catalyze the conversion of plasminogen to plasmin, leading to fibrin degradation and thrombus dissolution. Alteplase is a recombinant tissue plasminogen activator, administered intravenously at a dose of IV 100 mg infusion over 2 hours. In cardiac arrest, the initial: 50 mg bolus over 2 minutes and continue CPR; after 15 minutes, if return of spontaneous circulation is not achieved and the medical team decides to continue CPR, repeat 50 mg bolus. Tenecteplase is a modified variant of alteplase with increased fibrin specificity. The usual dose is weight-based and delivered via IV bolus, which facilitates rapid delivery in emergency settings. Dose per weight: ≥60 to <70 kg: 35 mg, ≥70 to <80 kg: 40 mg, ≥80 to <90 kg: 45 mg, ≥90 kg: 50 mg Are there any ongoing clinical trials and emerging therapies investigating novel thrombolytics and strategies to optimize efficacy while minimizing bleeding risk? <ul cl...
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