Cardionerds: A Cardiology Podcast

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  463. Multimodality Imaging in Chronic Coronary Artery Disease with Dr. Panithaya Chareonthaitawee 17.08.2026 39мин

  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. Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. CardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! 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/
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  462. Tricuspid Regurgitation with Dr. Sunil Mankad 13.08.2026 18мин

  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. Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. CardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! 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. The Tricuspid Valve: A Review of Pathology, Imaging, and Current Treatment Options: A Scientific Statement From the American Heart Association. Circulation. 2024;149(22):e1223-e1238.
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  461. Pre-Pregnancy Risk Stratification and Counseling with Dr. Katie Young 11.08.2026 52мин

  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. Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. CardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! 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
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  460. Approach to HFpEF and the Metabolic Syndrome with Dr. John Ostrominski 29.07.2026 22мин

  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. CardioNerds Heart Success Series PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls 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
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  459. The Continuum of Prevention and Heart Failure with Dr. Anu Lala and Dr. Martha Gulati 23.07.2026 26мин

  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. 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 Prevention PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! 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, risk-based prevention strategies are needed. Psychological health: Depression is common in HF and independently associated with worse outcomes. Screening with brief questionnaires (e.g., PHQ-2) is recommended. Meditation, spirituality, and holistic wellness approaches remain underutilized. 5. What systems-level and policy changes are needed to move the needle on heart failure prevention? Multidisciplinary HF prevention clinics that bring together preventive cardiologists, HF specialists, endocrinologists, nephrologists, dietitians, pharmacists, exercise physiologists, and genetic counselors are advocated by the statement. EHR-embedded risk stratification could proactively flag patients on a trajectory toward HF—analogous to sepsis alerts or fall risk flags—enabling earlier intervention, particularly for patients who may not reach a cardiologist. Cardiac rehabilitation remains underutilized, particularly in HFrEF (Class 2b recommendation) and HFpEF (not yet covered by Medicare). The HF-ACTION trial showed quality-of-life benefits, and the REHAB-HF trial showed particular benefit in older patients with HFpEF. Policy priorities include expanding insurance coverage for preventive screening and novel therapies (SGLT2i, GLP-1 RAs, nsMRAs), reducing clinical inertia through team-based care models with closer follow-up intervals, and ensuring equitable access to evidence-based therapies across diverse populations. Digital health and AI hold promise for personalized risk prediction, remote monitoring (e.g., wearable devices, implantable PA pressure monitors), and virtual cardiac rehabilitation to overcome access barriers. Figure  Lala A, Beavers C, Blumer V, et al. The continuum of prevention and heart failure in cardiovascular medicine: a joint scientific statement from the Heart Failure Society of America and the American Society for Preventive Cardiology. J Card Fail. 2026;32(1):75-105. doi:10.1016/j.cardfail.2025.06.013) References Key references are bolded. Lala A, Beavers C, Blumer V, et al. The continuum of prevention and heart failure in cardiovascular medicine: a joint scientific statement from the Heart Failure Society of America and the American Society for Preventive Cardiology. J Card Fail. 2026;32(1):75-105. doi:10.1016/j.cardfail.2025.06.013 Heidenreich PA, Bozkurt B, Aguilar D, et al. 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 Lloyd-Jones DM, Allen NB, Anderson CAM, et al. Life’s Essential 8: updating and enhancing the American Heart Association’s construct of cardiovascular health: a presidential advisory from the American Heart Association. Circulation. 2022;146(5):e18-e43. doi:10.1161/CIR.0000000000001078 SPRINT Research Group, Wright JT Jr, Williamson JD, et al. A randomized trial of intensive versus standard blood-pressure control. N Engl J Med. 2015;373(22):2103-2116. doi:10.1056/NEJMoa1511939 Levy D, Larson MG, Vasan RS, Kannel WB, Ho KK. The progression from hypertension to congestive heart failure. JAMA. 1996;275(20):1557-1562. doi:10.1001/jama.1996.03530440037034 Major outcomes in high-risk hypertensive patients randomized to angiotensin-converting enzyme inhibitor or calcium channel blocker vs diuretic: the Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT). JAMA. 2002;288(23):2981-2997. doi:10.1001/jama.288.23.2981 Yusuf S, Sleight P, Pogue J, et al. Effects of an angiotensin-converting-enzyme inhibitor, ramipril, on cardiovascular events in high-risk patients. N Engl J Med. 2000;342(3):145-153. doi:10.1056/NEJM200001203420301 Zinman B, Wanner C, Lachin JM, et al. Empagliflozin, cardiovascular outcomes, and mortality in type 2 diabetes. N Engl J Med. 2015;373(22):2117-2128. doi:10.1056/NEJMoa1504720 Anker SD, Butler J, Filippatos G, et al. Empagliflozin in heart failure with a preserved ejection fraction. N Engl J Med. 2021;385(16):1451-1461. doi:10.1056/NEJMoa2107038 Solomon SD, McMurray JJV, Claggett B, et al. Dapagliflozin in heart failure with mildly reduced or preserved ejection fraction. N Engl J Med. 2022;387(12):1089-1098. doi:10.1056/NEJMoa2206286 Filippatos G, Anker SD, Agarwal R, et al. Finerenone reduces risk of incident heart failure in patients with chronic kidney disease and type 2 diabetes: analyses from the FIGARO-DKD trial. Circulation. 2022;145(6):437-447. doi:10.1161/CIRCULATIONAHA.121.057983 Solomon SD, McMurray JJV, Vaduganathan M, et al. Finerenone in heart failure with mildly reduced or preserved ejection fraction. N Engl J Med. 2024;391(16):1475-1485. doi:10.1056/NEJMoa2407107 Lincoff AM, Brown-Frandsen K, Colhoun HM, et al. Semaglutide and cardiovascular outcomes in obesity without diabetes. N Engl J Med. 2023;389(24):2221-2232. doi:10.1056/NEJMoa2307563 Deanfield J, Verma S, Scirica BM, et al. Semaglutide and cardiovascular outcomes in patients with obesity and prevalent heart failure: a prespecified analysis of the SELECT trial. Lancet. 2024;404(10454):773-786. doi:10.1016/S0140-6736(24)01498-3  Kosiborod MN, Abildstrøm SZ, Borlaug BA, et al. Semaglutide in patients with heart failure with preserved ejection fraction and obesity. N Engl J Med. 2023;389(12):1069-1084. doi:10.1056/NEJMoa2306963 Ndumele CE, Neeland IJ, Tuttle KR, et al. A synopsis of the evidence for the science and clinical management of cardiovascular-kidney-metabolic (CKM) syndrome: a scientific statement from the American Heart Association. Circulation. 2023;148(20):1636-1664. doi:10.1161/CIR.0000000000001175 Khan SS, Matsushita K, Sang Y, et al. Development and validation of the American Heart Association’s PREVENT equations. Circulation. 2024;149(6):430-449. doi:10.1161/CIRCULATIONAHA.123.067626 Khan SS, Ning H, Shah SJ, et al. 10-year risk equations for incident heart failure in the general population. J Am Coll Cardiol. 2019;73(19):2388-2397. doi:10.1016/j.jacc.2019.02.057 Bozkurt B, Fonarow GC, Goldberg LR, et al. Cardiac rehabilitation for patients with heart failure: JACC expert panel. J Am Coll Cardiol. 2021;77(11):1454-1469. doi:10.1016/j.jacc.2021.01.030 Packer M. Leptin-aldosterone-neprilysin axis: identification of its distinctive role in the pathogenesis of the three phenotypes of heart failure in people with obesity. Circulation. 2018;137(15):1614-1631. doi:10.1161/CIRCULATIONAHA.117.032474 Lala A, Tayal U, Hamo CE, et al. Sex differences in heart failure. J Card Fail. 2022;28(3):477-498. doi:10.1016/j.cardfail.2021.10.006 Bozkurt B, Coats AJS, Tsutsui H, et al. Universal definition and classification of heart failure. Eur J Heart Fail. 2021;23(3):352-380. doi:10.1002/ejhf.2115 Hershberger RE, Givertz MM, Ho CY, et al. Genetic evaluation of cardiomyopathy—a Heart Failure Society of America practice guideline. J Card Fail. 2018;24(5):281-302. doi:10.1016/j.cardfail.2018.03.004 Levine GN, Cohen BE, Commodore-Mensah Y, et al. Psychological health, well-being, and the mind-heart-body connection: a scientific statement from the American Heart Association. Circulation. 2021;143(10):e763-e783. doi:10.1161/CIR.0000000000000947 Ezekowitz JA, Colin-Ramirez E, Ross H, et al. Reduction of dietary sodium to less than 100 mmol in heart failure (SODIUM-HF): an international, open-label, randomised, controlled trial. Lancet. 2022;399(10333):1391-1400. doi:10.1016/S0140-6736(22)00369-5
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  458. The Golden Age of Pulmonary Embolism Randomized Controlled Trials with Dr. Jay Giri 10.07.2026 29мин

  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. 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: 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, SBP <90 for sustained period, mechanical circulatory support, or significant respiratory decompensation/intubation – a less sensitive measure than NEWS), (3) recurrent PE admission, (4) non-deterioration-based bailout crossover at day 3, and (5) 48-hour dyspnea score. The larger sample size compensates for the less sensitive clinical deterioration definition. PE-TRACT: NIH-sponsored, open-label, assessor-blinded RCT of CDT (any FDA-cleared device – CDT or mechanical thrombectomy, strategy trial) plus anticoagulation vs. anticoagulation alone in 500 patients with intermediate-risk PE (most permissive enrollment – includes intermediate-low risk patients). Co-primary endpoints at 3 months (peak VO₂ on cardiopulmonary exercise testing) and 12 months (NYHA functional class), analyzed sequentially. Designed to answer the longer-term functional question rather than early clinical deterioration. Question #4: What does the future of PE research look like? Unprecedented evidence generation: Across STORM-PE, PEERLESS, HI-PEITHO, PEERLESS II, PE-TRACT, PRAGUE-26, PEITHO-3, and high-risk PE trials (PERSEVERE, TORPEDO-NL), approximately 8–9 RCTs are enrolling or recently completed – an unparalleled volume of comparative evidence in any cardiovascular subspecialty over such a short period. Guideline impact: The 2026 AHA/ACC PE Guideline already reflects the evolving evidence landscape, with Class 2a–2b recommendations for CDT and MT in select PE categories. Results from HI-PEITHO, PEERLESS II, PRAGUE-26, and PE-TRACT have the potential to substantially strengthen these recommendations, particularly if clinical deterioration endpoints are positive. PERT evolution: As evidence clarifies which patients benefit from intervention, PERT programs may transition from primarily clinical decision-making bodies to systems-of-care delivery engines – analogous to STEMI systems – focused on efficient, protocol-driven care and real-world evidence generation for quality improvement. Innovation ecosystem: The relatively permissive FDA clearance pathway has fostered a competitive device landscape with multiple manufacturers and device types, contrasting with the prolonged duopoly in the TAVR space. This competition may drive technological improvement and more favorable economics. Caution with real-world evidence: While real-world evidence is valuable for quality improvement and systems-of-care assessment, it should be used cautiously for comparative effectiveness analyses due to irreconcilable confounding and limitations in causal inference. RCTs remain the gold standard for comparative questions. References: ★ Rosenfield K, Klok FA, Piazza G, et al. Ultrasound-facilitated, catheter-directed fibrinolysis for acute pulmonary embolism. N Engl J Med. 2026;394(22):2131-2141. doi:10.1056/NEJMoa2503539 ★ Lookstein RA, Konstantinides SV, Weinberg I, et al. Randomized controlled trial of mechanical thrombectomy with anticoagulation versus anticoagulation alone for acute intermediate-high risk pulmonary embolism: primary outcomes from the STORM-PE trial. Circulation. 2026;153(1):21-34. doi:10.1161/CIRCULATIONAHA.125.077232 ★ Jaber WA, Gonsalves CF, Stortecky S, et al. Large-bore mechanical thrombectomy versus catheter-directed thrombolysis in the management of intermediate-risk pulmonary embolism: primary results of the PEERLESS randomized controlled trial. Circulation. 2025;151(5):260-273. doi:10.1161/CIRCULATIONAHA.124.072364 ★ Gonsalves CF, Gibson CM, Stortecky S, et al. Randomized controlled trial of mechanical thrombectomy vs catheter-directed thrombolysis for acute hemodynamically stable pulmonary embolism: rationale and design of the PEERLESS study. Am Heart J. 2023;266:128-137. doi:10.1016/j.ahj.2023.09.002 ★ Sista AK, Troxel AB, Tarpey T, et al. Rationale and design of the PE-TRACT trial: a multicenter randomized trial to evaluate catheter-directed therapy for the treatment of intermediate-risk pulmonary embolism. Am Heart J. 2025;281:112-122. doi:10.1016/j.ahj.2024.11.016 ★ Giri J, Sista AK, Weinberg I, et al. Interventional therapies for acute pulmonary embolism: current status and principles for the development of novel evidence: a scientific statement from the American Heart Association. Circulation. 2019;140(20):e774-e801. doi:10.1161/CIR.0000000000000707 ★ Zhang RS, Maqsood MH, Sharp ASP, et al. Efficacy and safety of anticoagulation, catheter-directed thrombolysis, or systemic thrombolysis in acute pulmonary embolism. JACC Cardiovasc Interv. 2023;16(22):2781-2793. doi:10.1016/j.jcin.2023.09.014 Additional References Rosovsky RP, Konstantinides SV, Moriarty JM, et al. A prospective, multicenter, randomized controlled trial evaluating anticoagulation alone vs anticoagulation plus computer assisted vacuum thrombectomy for the treatment of intermediate-high-risk acute pulmonary embolism: rationale and design of the STORM-PE study. Am Heart J. 2025;288:1-14. doi:10.1016/j.ahj.2025.03.018 Klok FA, Piazza G, Sharp ASP, et al. Ultrasound-facilitated, catheter-directed thrombolysis vs anticoagulation alone for acute intermediate-high-risk pulmonary embolism: rationale and design of the HI-PEITHO study. Am Heart J. 2022;251:43-53. doi:10.1016/j.ahj.2022.05.011 Creager MA, Barnes GD, Giri J, et al. 2026 AHA/ACC/ACCP/ACEP/CHEST/SCAI/SHM/SIR/SVM/SVN guideline for the evaluation and management of acute pulmonary embolism in adults. J Am Coll Cardiol. 2026;87(7):e77-e206. doi:10.1016/j.jacc.2025.11.027 Piazza G. Advanced management of intermediate- and high-risk pulmonary embolism: JACC focus seminar. J Am Coll Cardiol. 2020;76(18):2117-2127. doi:10.1016/j.jacc.2020.05.028 Zuo Z, Yue J, Dong BR, et al. Thrombolytic therapy for pulmonary embolism. Cochrane Database Syst Rev. 2021;4(4):CD004437. doi:10.1002/14651858.CD004437.pub6 Kroupa J, Buk M, Weichet J, et al. A pilot randomised trial of catheter-directed thrombolysis or standard anticoagulation for patients with intermediate-high risk acute pulmonary embolism (CANARY). EuroIntervention. 2022;18(8):e657-e665. doi:10.4244/EIJ-D-22-00194 Zuin M, Lang I, Chopard R, et al. Innovation in catheter-directed therapy for intermediate-high-risk and high-risk pulmonary embolism. JACC Cardiovasc Interv. 2024;17(20):2390-2408. doi:10.1016/j.jcin.2024.07.037 Harvey JJ, Huang S, Uberoi R. Catheter-directed therapies for the treatment of high risk (massive) and intermediate risk (submassive) acute pulmonary embolism. Cochrane Database Syst Rev. 2022;8(8):CD013083. doi:10.1002/14651858.CD013083.pub2 Kim JM, Horbal SR, Mewaldt C, et al. Mechanical thrombectomy and catheter-directed thrombolysis in acute pulmonary embolism: trends and practice patterns in the PERT Consortium Registry (2016-2024). J Am Coll Cardiol. 2026;87(13):1271-1283. doi:10.1016/j.jacc.2025.12.044 Planer D, Yanko S, Matok I, et al. Catheter-directed thrombolysis compared with systemic thrombolysis and anticoagulation in patients with intermediate- or high-risk pulmonary embolism: systematic review and network meta-analysis. CMAJ. 2023;195(24):E833-E843. doi:10.1503/cmaj.221655 Farmakis IT, Binder H, Chopard R, et al. Reperfusion strategies for acute pulmonary embolism: design and rationale of RECONNECT-PE – a living systematic review and meta-analysis. Am Heart J. 2026;295:107365. doi:10.1016/j.ahj.2026.107365 Rashedi S, Leyva H, Hamade N, et al. Fibrinolytic therapy for thromboembolic diseases: approved indications and future directions. J Am Coll Cardiol. 2025;86(14):1395-1416. doi:10.1016/j.jacc.2025.07.048 Creager MA, Barnes GD, Giri J. A field in transition: catheter-based therapy in the 2026 AHA/ACC acute pulmonary embolism guideline. J Am Coll Cardiol. 2026;87(13):1284-1288. doi:10.1016/j.jacc.2026.01.024
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  457. Insights into INOCA and ANOCA with Dr. Claire Raphael 03.07.2026 9мин

   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. 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: 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
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  456. ACS Guidelines Question #2 with Dr. Michelle O’Donoghue 25.06.2026 10мин

  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? 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 
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  455. The Long-Term Management Of Patients With Pulmonary Embolism with Dr. Soophia Naydenov 21.06.2026 19мин

  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. 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 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.
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  454. ACHD Surgery 101: Thinking Like a Surgeon with Elizabeth Stephens 10.06.2026 42мин

  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
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  453. ACS Guidelines Question #1 with Dr. Sunil Rao 04.06.2026 10мин

  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 
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  452. Risk stratification in Acute Pulmonary Embolism with Dr. Stavros Konstantinides 01.06.2026 25мин

  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. 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 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
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  451: CCTA, CT-FFR, and AI Plaque Analysis to Personalize CAD Detection, Prevention, and Management with Dr. Michael Gallagher 27.05.2026 46мин

  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. 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 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....
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  450. Journal Club: The I-CLASS Registry with Dr. Theofanie Mela and Dr. Pugazhendhi Vijayraman 25.05.2026 19мин

  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.  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!
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  449. Atrial Fibrillation: Challenging Scenarios in Atrial Fibrillation Management with Dr. Bradley Knight 21.05.2026 37мин

  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. 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 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 ‌
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  448. The Braunwald Chronicles: The Complete Series — A CardioNerds Tribute to Dr. Eugene Braunwald 30.04.2026 41мин

  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. 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!
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  447. Pulmonary Embolism: Approach to Systemic Thrombolysis in Acute Pulmonary Embolism with Dr. Allison Burnett 24.04.2026 42мин

  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. 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
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  446. The SGLT2i Effect – Protection Against Cancer Therapy-Related Cardiac Dysfunction with Dr. Manu Mysore 16.04.2026 32мин

  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. CardioNerds Cardio-Oncology PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls CTRCD is a spectrum — catch it early. CTRCD ranges from subclinical injury detected by imaging and biomarkers to overt heart failure. Early identification in high-risk patients (preexisting CVD, diabetes, HTN, obesity, anthracycline/HER2/radiation exposure) is essential, and early initiation of guideline-directed medical therapy — including ACE inhibitors/ARBs/ARNIs, mineralocorticoid receptor antagonists, and beta-blockers — remains the backbone of prevention and treatment to preserve LVEF and allow safe continuation of cancer therapy. SGLT2 inhibitors are a promising new pillar of cardioprotection in cardio-oncology. They act through a unique combination of mechanisms: renal effects, metabolic reprogramming of the myocardium, anti-inflammatory and antioxidant pathways, and vascular fibrosis modulation — making them a compelling complement to standard therapies rather than a replacement. Early clinical data is encouraging but not yet definitive. The 2024 EMPACARD-PILOT trial demonstrated preserved LVEF and reduced CTRCD in higher-risk patients with diabetes or kidney disease. Ongoing trials — EMPACT and PROTECT — are actively exploring SGLT2 inhibitors for primary prevention during anthracycline and HER2-targeted therapy. SGLT2 inhibitors are NOT yet indicated for ICI-related myocarditis. Immune checkpoint inhibitor (ICI)-related myocarditis is mechanistically immune-driven. While SGLT2 inhibitors have theoretically anti-inflammatory benefits, there is currently no clinical evidence to support their use in this specific setting. The use of SGLT2 inhibitors should be guided by patient risk, existing indications, and ongoing research. Large prospective trials, clarity on timing and patient selection, long-term safety data, and deeper mechanistic understanding in humans remain the most urgent gaps in the field before broader adoption can be recommended. References Theofilis P, Vlachakis PK, Oikonomou E, et al. Cancer therapy-related cardiac dysfunction: A review of current trends in epidemiology, diagnosis, and treatment. Biomedicines. 2024;12(12):2914. doi:10.3390/biomedicines12122914. https://pubmed.ncbi.nlm.nih.gov/39767820/ Lyon AR, Dent S, Stanway S, et al. Baseline cardiovascular risk assessment in cancer patients scheduled to receive cardiotoxic cancer therapies: a position statement and new risk assessment tools from the Cardio-Oncology Study Group of the Heart Failure Association of the European Society of Cardiology in collaboration with the International Cardio-Oncology Society. Eur J Heart Fail. 2020;22(11):1945-1960. doi:10.1002/ejhf.1920. https://pmc.ncbi.nlm.nih.gov/articles/PMC8019326/ Li X, Li Y, Zhang T, et al. Role of cardioprotective agents on chemotherapy-induced heart failure: A systematic review and network meta-analysis of randomized controlled trials. Pharmacol Res. 2020;151(104577):104577. doi:10.1016/j.phrs.2019.104577. https://pubmed.ncbi.nlm.nih.gov/31790821/ Lee YH, Lim S, Davies MJ. Cardiometabolic and renal benefits of sodium-glucose cotransporter 2 inhibitors. Nat Rev Endocrinol. 2025;21(12):783-798. doi:10.1038/s41574-025-01170-4. https://pubmed.ncbi.nlm.nih.gov/40935880/ Dabour MS, George MY, Daniel MR, Blaes AH, Zordoky BN. The cardioprotective and anticancer effects of SGLT2 inhibitors: JACC: CardioOncology state-of-the-art review. JACC CardioOncol. 2024;6(2):159-182. doi:10.1016/j.jaccao.2024.01.007. https://pubmed.ncbi.nlm.nih.gov/38774006/ Armillotta M, Angeli F, Paolisso P, et al. Cardiovascular therapeutic targets of sodium-glucose co-transporter 2 (SGLT2) inhibitors beyond heart failure. Pharmacol Ther. 2025;270(108861):108861. doi:10.1016/j.pharmthera.2025.10886. https://pubmed.ncbi.nlm.nih.gov/40245989/ Góes-Santos BR, Castro PC, Girardi ACC, Antunes-Correa LM, Davel AP. Vascular effects of SGLT2 inhibitors: evidence and mechanisms. Am J Physiol Cell Physiol. 2025;329(4):C1150-C1160. doi:10.1152/ajpcell.00569.2025. 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.
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  445. Heart Failure: The Essential Role of Palliative Care in Advanced Therapies with Dr. Sarah Chuzi 10.04.2026 54мин

  Dr. Jenna Skowronski, Dr. Shazli Khan, and Dr. Alix Barnes discuss the involvement of palliative care throughout the heart failure spectrum with Dr. Sarah Chuzi. Audio editing for this episode was performed by CardioNerds Intern, Dr. Julia Marques Fernandes. In this episode, we discuss utilizing palliative care principles while caring for patients with heart failure, particularly those being considered for advanced therapies. We emphasize utilization of communication frameworks when discussing prognosis and making decisions on pursuing therapies such as palliative inotropes, left ventricular assist devices (LVADs), and heart transplant. Additionally, we discuss when to involve specialty palliative care services. Finally, we highlight the difference between palliative care and hospice and how to help patients navigate the transition from life-prolonging care to hospice. Dr. Jenna Skowronski is the Chair for the CardioNerds Heart Failure Council. Dr. Jenna Skowronski and Dr. Shazli Khan are the Co-chairs for the CardioNerds Advanced Heart Failure Therapies Series. Dr. Alix Barnes is the CardioNerds FIT Ambassador at UPMC and member of the CardioNerds Critical Care Cardiology Council. Enjoy this Circulation Paths to Discovery article to learn more about the CardioNerds mission and journey. US Cardiology Review is now the official journal of CardioNerds! Submit your manuscripts here. CardioNerds Heart Success Series PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls Primary palliative care is care provided by a clinician that is not a palliative care specialist, such as a heart failure clinician having a conversation with a patient about their goals and values in clinic.  Taking time to get to know a patient as an individual and learning their goals and values prior to diving into conversations about prognosis and change in treatment plan facilitates more effective goals of care discussions.   Utilizing and practicing a communication framework can improve our skills at goals of care discussions.   Palliative inotropes should be reserved for patients experiencing symptomatic benefit from the therapy that outweighs the associated risks including arrhythmias and infections. The burden of managing these therapies at home should also be considered. Partnerships between cardiologists and hospice agencies can improve the experience for patients with heart failure who enroll in hospice. Cardiologists can continue to see their patients even after hospice enrollment and help with symptom management.   Notes Notes: Notes drafted by Dr. Barnes. 1. What is the difference between primary palliative care and specialty palliative care? Primary palliative care is the delivery of palliative care services that any clinician can deliver. This includes aligning treatment with a patient’s goals and basic symptom management. For heart failure patients, symptom management can include cardiac symptoms such as dyspnea and chest pain as well as managing comorbid mood disorders such as adjustment disorder, depression, and anxiety. Advanced palliative care skills take additional training and time to develop. These include leading a difficult family meeting, managing symptoms that are not controlled with standard therapies and responding to emotional and spiritual distress. When these situations are encountered, referral to a specialty palliative care service should be considered. 1 2. How is palliative care integrated throughout the disease trajectory of a patient with heart failure? Heart failure clinicians deliver primary palliative care when assessing a patient’s preferences, goals and values or managing symptoms. As a patient’s disease progresses, the heart failure team also engages in primary palliative care when delivering news about prognosis. When advanced therapies are being considered, utilization of shared decision-making (SDM) should be employed (see question 3 for further discussion on SDM). For patients being considered for LVAD, the Centers for Medicare and Medicaid Services (CMS) mandates that patients are seen by a palliative care specialist prior to implantation. 2 Despite this, there remains variability in how institutions involve specialty palliative care in this decision-making process. Thoughtful consideration of what palliative care resources are available at your institution should guide how best to integrate specialty palliative care teams into the LVAD decision tree. One example of a model for meeting this mandate is having a small team of heart failure clinicians with additional palliative care training meet all patient’s being evaluate for LVAD. 3. What is shared decision-making (SDM) and how is it utilized when evaluating a patient for advanced therapies? SDM is a collaborative process where patients and clinicians work together to make medical decisions that are aligned with a patient’s goals and values.3 There are a variety of communication frameworks that can be used to engage in effective SDM. One framework is the Serious Illness Conversation guide. This is an evidenced based framework that can be used to deliver the news about a patient’s current condition and then assess their goals, values and preferences for next steps in their treatment plan.4  This framework can be helpful when discussing prognosis prior to introducing the idea of an evaluation for advanced therapies. REMAP is a second commonly used framework which stands for Reframe, Expect Emotion, Map What’s Important, Align, and Plan.5 This framework is similarly helpful when starting a discussion about advanced therapies with a patient. 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....
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  444. Heart Failure: LVAD Part 2 with Dr. Mark Belkin and Dr. Chris Salerno 22.03.2026 26мин

  CardioNerds (Dr. Hamza Patel, Dr. Jenna Skowronski, and Dr. Apoorva Gangavelli) discuss advanced heart failure and LVAD management with Dr. Mark Belkin, Advanced Heart Failure & Transplant Cardiologist, and Dr. Chris Salerno, Cardiothoracic Surgeon. They explore the nuances of right ventricular (RV) physiology, perioperative hemodynamic optimization, long-term complications, sensitization and transplant considerations, and the evolving role of GDMT in LVAD patients.  This episode highlights the delicate interplay between surgical and medical management in achieving optimal outcomes for patients living with durable mechanical circulatory support.Audio editing by CardioNerds Academy intern, student doctor, Pace Wetstein. Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. CardioNerds Heart Success Series PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls “The right ventricle sets the stage.” — LVAD success hinges on RV performance; a struggling RV can turn a perfect LVAD surgery into a perfect storm.  “Watch the ratios.” — A PAPi < 2 and RA:PCWP >0.6 signal high risk for RV failure post-implant; trends and response to optimization matter more than static numbers.  “From hemocompatibility to hemodynamics.” — The LVAD field has moved from fighting pump thrombosis to mastering long-term RV failure and aortic insufficiency.  “Not all antibodies are created equal.” — LVAD-related sensitization often resolves post-transplant, reminding clinicians to interpret PRA trends in context.  “Recovery is possible.” — The RESTAGE-HF trial and emerging SGLT2 data hint at a new era: not just sustaining life with LVADs but restoring native heart function.  Notes Notes drafted by Dr. Hamza Patel. 1. Hemodynamic & Vasoactive Management of the RV  Use norepinephrine and vasopressin for pressor support; consider dobutamine as inotrope of choice.  Consider avoiding early milrinone due to hypotension and reduced coronary perfusion.  Use inhaled NO or epoprostenol selectively; institutional variation depends on cost and supply.  Key hemodynamic markers:  PAPi = (PA systolic – PA diastolic) / RA pressure.  PAPi < 2 → increased RV failure risk.  RA:PCWP ratio ≈ 0.6 normal; ≈ 1 → severe RV dysfunction.  RV reserve—the ability to improve these indices with optimization—is a stronger predictor of outcomes than baseline numbers alone.  NOTE: there is no robust data to guide vasoactive medical decision-making and there is substantial institutional variability in practive.  2. Long-Term LVAD Complications  MOMENTUM 3 trial: HeartMate 3 reduced pump thrombosis (10 → 1 %), stroke (14 → 5%), and GI bleed (77 → 43 %).  Persistent issues: driveline infections, RV failure, and aortic insufficiency.  Driveline care: silver sulfadiazine (Silvadene) cream linked to lower infection rates (Cowher & Kenmore 2025).  Field now focuses on hemodynamic-related adverse events—the next frontier in LVAD outcomes.  Innovation ahead: smaller drivelines and fully implantable LVADs to eliminate infection risk.  3. Sensitization and Transplant Candidacy  LVADs may induce de novo HLA antibodies, complicating transplant matching.  These antibodies tend to be transient and less cytotoxic, often resolving post-transplant.  Sensitization degree varies by device and patient; management strategies are center-dependent.  The field is redefining which antibodies are truly LVAD-induced versus incidental.  4. GDMT & Myocardial Recovery  GDMT data in LVAD patients limited—excluded from major HFrEF trials.  RESTAGE-HF: aggressive GDMT post-LVAD yielded 52% explant rate within 18 months.  SGLT2 inhibitors: emerging evidence of reverse remodeling and reduced LV size (Belkin et al., THT 2025).  GDMT promotes recovery but requires cautious titration to avoid hypotension and RV strain.  5. Future of LVAD Therapy  The fully implantable LVAD remains the goal—wireless energy, no driveline, and fewer infections.  Short-term focus: device miniaturization, improved energy efficiency, and better hemocompatibility.  HeartMate 3 remains gold standard until next-generation systems mature.  References Mehra MR et al. NEJM 2018 — MOMENTUM 3 Final Report.  Takeda K et al. JHLT 2020 — Predictors of RV Failure After LVAD.  Imamura T et al. Circ Heart Fail 2017 — Hemodynamics and RV Adaptation Post-LVAD.  RESTAGE-HF Trial, JHLT 2019.  Cowher J, Kenmore C et al. 2025 — Driveline Care & Infection Outcomes.  Belkin M et al. THT 2025 — SGLT2 Inhibition and Reverse Remodeling Post-LVAD.