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The Central Role of Cardiac MRI in the Management of Heart Failure and Cardiomyopathy Patients Guest: Gosia Wamil, M.D., Ph.D. Host: Malcolm R. Bell, M.D. Cardiac MRI is now central to heart failure care, moving beyond imaging to guide diagnosis and treatment. It distinguishes disease causes, identifies fibrosis and scar, and uncovers specific conditions in both HFrEF and HFpEF. By providing prognostic markers, it helps tailor therapies and improve outcomes—delivering the right treatment at the right time. In this episode of "Interviews With the Experts," Dr. Malcolm Bell interviews Dr. Gosia Wamil from Mayo Clinic London practice on the role of cardiac MRI in practice. Topics Discussed: When does CMR change the management decision? CMR findings Which CMR biomarkers truly predict outcomes—and how should clinicians act on them? From echo-first to CMR-led pathways: what should every HF service implement now? Connect with Mayo Clinic's Cardiovascular Continuing Medical Education online at https://cveducation.mayo.edu or on Twitter @MayoClinicCV and @MayoCVservices. LinkedIn: Mayo Clinic Cardiovascular Services Cardiovascular Education App: The Mayo Clinic Cardiovascular CME App is an innovative educational platform that features cardiology-focused continuing medical education wherever and whenever you need it. Use this app to access other free content and browse upcoming courses. Download it for free in Apple or Google stores today! No CME credit offered for this episode. Podcast episode transcript found here. Recorded on: 14-January-2026
Você otimizou o LDL. Chegou na meta de ApoB. E o paciente volta meses depois com um novo evento. Neste episódio especial, com apoio da Novo Nordisk, Diandro Mota e William Batah recebem o Dr. Eduardo Lima, doutor em Cardiologia pela USP, professor colaborador e supervisor da Residência em Cardiologia da FMUSP/InCor e Head Nacional de Cardiologia da Rede Américas, para uma conversa que pode redefinir como você enxerga o risco residual. A tese é direta: a aterosclerose nunca foi só uma doença de colesterol. Ela é imunometabólica, e a inflamação subclínica pode ser o elo que faltava.O que você vai aprender:
Drs. Dasgupta and Sarswat review how ATTR cardiomyopathy remains under-recognized despite its prevalence in older patients with heart failure, emphasizing clinical red flags across cardiac and systemic manifestations. They outline a practical diagnostic pathway that prioritizes early identification using light-chain evaluation, bone scintigraphy, and genetic testing to distinguish transthyretin subtypes and initiate timely, disease-modifying therapy.
JAMA Medical News Director Jennifer Abbasi and Associate Managing Editor Kate Schweitzer discuss "HFpEF May Be a Different Disease in Patients With Severe Obesity." Related Content: HFpEF May Be a Different Disease in Patients With Severe Obesity
ReferencesFront. Endocrinol., 2019. 02 July Sec. Molecular and Structural Endocrinology Volume 10 -J Cell Physiol. 2026 May;241(5):e70190Thromb Haemost.2009 Sep;102(3):544–554.Guerra, DJ. 2026.Unpublished LecturesCahn and Heusen. 1957. All The Way Frank Sinatrahttps://open.spotify.com/track/7fanCwOck16J9MPJ3SR39P?si=df1d1051137648f4Dvorak, A. 1983. American String Quintet 3. E Flat Major OP.97https://music.youtube.com/watch?v=cip5TJ7H4jg&si=kOTQNlmy93LDJNvL
Witam Państwa, nazywam się Jarosław Drożdż, pracuję w Centralnym Szpitalu Klinicznym Uniwersytetu Medycznego w Łodzi, skąd nagrywam podcast Kardio Know-How. W tym odcinku omawiam drugą część badań opublikowanych podczas kongresu ACC 2026. Nadciśnienie płucne rozpoznajemy przy średnim ciśnieniu powyżej 20 mmHg, a kluczowa jest grupa I WHO związana z przebudową tętnic płucnych. Choroba wynika m.in. z zaburzenia równowagi między aktywiną a BMP, prowadząc do wzrostu oporu, przeciążenia prawej komory i zgonu w ciągu kilku lat.Objawem dominującym jest duszność wysiłkowa, często niewidoczna w spoczynku, ale nasilona nawet przy krótkim marszu. Przełomem okazał się sotatercept, który w badaniu STELLAR poprawił dystans marszu, parametry biochemiczne i znacząco zmniejszył śmiertelność (https://www.nejm.org/doi/full/10.1056/NEJMoa2213558). W badaniu ZENITH u pacjentów wysokiego ryzyka wykazano szybkie i wyraźne zmniejszenie ryzyka zgonu, przeszczepu płuc i hospitalizacji (https://www.nejm.org/doi/abs/10.1056/NEJMoa2415160).Nowe dane dotyczą także grupy II nadciśnienia płucnego w HFpEF, szczególnie postaci mieszanej CpcPH o wysokiej śmiertelności. Sotatercept działa jako inhibitor sygnalizacji aktywiny i jako pierwszy lek nie opiera się na rozszerzaniu naczyń, lecz wpływa na przebudowę naczyń. W badaniu CADENCE poprawiał opór płucny, ciśnienie, NT-proBNP i wydolność wysiłkową przy dobrej tolerancji (https://www.ahajournals.org/doi/10.1161/CIRCULATIONAHA.126.079918). To podejście wpisuje się w nową koncepcję HFpEF Miltona Packera, opisaną m.in. tutaj: https://open.spotify.com/episode/23WzUWHSoF1lZoiE130nEW?si=f12fe0e345e54111 oraz https://www.sciencedirect.com/science/article/pii/S1071916426002289. Szczegółowy TRANSKRYPT do odcinka.Podcast jest przeznaczony wyłącznie dla osób z profesjonalnym wykształceniem medycznym.
Heart failure with preserved ejection fraction, so-called HFpEF, is happening more frequently, especially in those with severe obesity. David Kass, a cardiologist and researcher at Johns Hopkins, and colleagues, have looked closely at heart muscle cells from this group of … How is obesity related to a common form of heart failure? Elizabeth Tracey reports Read More »
Are you up to date on the latest clinical developments for steroidal and nonsteroidal mineralocorticoid receptor antagonists (MRAs) in heart failure with preserved ejection fraction (HFpEF)? Credit available for this activity expires: 04/08/2027 Earn Credit / Learning Objectives & Disclosures: https://www.medscape.org/viewarticle/beyond-headlines-critical-look-mra-evidence-hfpef-2026a1000al7?ecd=bdc_podcast_libsyn_mscpedu
In this episode of Parallax, Dr Ankur Kalra is joined by Dr Michelle Kittleson, Professor of Medicine and Advanced Heart Failure Cardiologist at Cedars-Sinai Medical Center, for a clinically rich breakdown of her standout trial picks from the 2026 ACC Annual Scientific Sessions. Dr Kittleson brings her characteristic precision to four landmark studies spanning heart failure and atrial fibrillation. She unpacks the SPIRIT HF trial — a negative study of spironolactone in HFpEF that, she argues, does not consign the drug to the shelf — and explains why its high discontinuation rate and pandemic-era disruptions complicate the headline result. For clinicians managing cost-conscious patients, her take on spironolactone as a practical alternative to finerenone is a perspective worth hearing. The conversation turns to the CADENCE trial, a Phase 2 study of sotatercept in Group 2 pulmonary hypertension secondary to HFpEF — a phenotype Dr Kittleson treats with particular caution given the risks of misdirected pulmonary vasodilator therapy. She offers measured optimism about what these early results might mean for future treatment of HFpEF-related lung remodelling. Dr Kalra and Dr Kittleson also enter the ongoing debate around left atrial appendage closure, weighing the contrasting conclusions of the CLOSURE AF and CHAMPION AF trials against each other — and against a shared conviction that anticoagulation remains the standard of care for the vast majority of patients with atrial fibrillation. Finally, they examine the STEMI Door to Unload trial, a cautionary study in indication creep: the microaxial flow pump that proves life-saving in cardiogenic shock offered no infarct-size benefit in haemodynamically stable STEMI patients — and came with a meaningful increase in bleeding and vascular complications. Dr Kittleson also shares her stepwise outpatient algorithm for a new HFpEF diagnosis, from ruling out mimics such as cardiac amyloidosis to sequencing SGLT2 inhibitors, MRAs, GLP-1 agonists, and ARNIs based on individual patient profile. The episode closes with a discussion of her new column for NEJM Voices, where she writes on the art of medicine. Questions and comments can be sent to podcast@radcliffe-group.com and may be answered by Ankur in the next episode. Host: @AnkurKalraMD and produced by: @RadcliffeCardio Parallax is Ranked in the Top 100 Health Science Podcasts (#48) by Million Podcasts.
SPIRIT-HF, another spironolactone trial in HFpEF; the ESSENCE imaging study of the drug olezarsen; the SirPAD trial in peripheral artery disease; and ultrasound-guided femoral venous access are the topics John Mandrola, MD, discusses in this week's podcast. This podcast is intended for healthcare professionals only. To read a partial transcript or to comment, visit: https://www.medscape.com/twic I ACC: SPIRIT-HF Trial FINEARTS-HF Trial https://www.nejm.org/doi/full/10.1056/NEJMoa2407107 TOPCAT Trial https://www.nejm.org/doi/full/10.1056/NEJMoa1313731 TOPCAT Americas Trial https://www.ahajournals.org/doi/10.1161/circulationaha.114.013255 II A New Class of Lipid Lowering Drug Has a Dubious Debut At ACC ESSENCE-TIMI 73b Imaging Study https://www.ahajournals.org/doi/10.1161/CIRCULATIONAHA.126.080012 ESSENCE-TIMI 73b Trial https://www.nejm.org/doi/full/10.1056/NEJMoa2507227 IMPROVE IT Trial https://www.nejm.org/doi/full/10.1056/NEJMoa1410489 III Drug-Coated Balloons Looked Quite Good in PAD interventions Sirolimus-Coated Balloon Reduces Amputation Risk in Peripheral Artery Disease https://www.medscape.com/viewarticle/sirolimus-coated-balloon-reduces-amputation-risk-peripheral-2026a1000a83 SirPAD trial https://www.nejm.org/doi/full/10.1056/NEJMoa2600360 IV Another Vascular Story from the European Heart Rhythm Association ULYSSES Trial https://doi.org/10.1093/eurheartj/ehag291 ULTRA-FAST Trial https://doi.org/10.1093/europace/eux175 You may also like: The Bob Harrington Show with the Stephen and Suzanne Weiss Dean of Weill Cornell Medicine, Robert A. Harrington, MD. https://www.medscape.com/author/bob-harrington Questions or feedback, please contact news@medscape.net
Please visit answersincme.com/860/101064703-replay to participate, download slides and supporting materials, complete the post test, and get a certificate. Presented by Muthiah Vaduganathan, MD, MPH and Nosheen Reza, MD, MS. In this activity, experts in cardio-kidney-metabolic syndrome (CKM) discuss emerging evidence on nonsteroidal mineralocorticoid receptor antagonists (nsMRAs) and practical strategies for incorporating these therapies into care for patients with heart failure, with or without chronic kidney disease (CKD) or type 2 diabetes (T2D). Upon completion of this activity, participants should be better able to: Specify the rationale for nonsteroidal mineralocorticoid receptor antagonists (nsMRAs) as treatment for adult patients with HF, with or without CKD or T2D; Differentiate the risk-benefit profiles between nsMRAs and the current standard of care for the treatment of HFmrEF or HFpEF, based on the available evidence; and Recommend patient-centered, long-term care strategies to integrate nsMRAs into clinical practice for patients with HF, with or without overlapping CKD or T2D.
Witam Państwa, nazywam się Jarosław Drożdż, pracuję w Centralnym Szpitalu Klinicznym Uniwersytetu Medycznego w Łodzi, skąd nagrywam podcast Kardio Know-How. W tym odcinku omawiam drugą część badań opublikowanych podczas kongresu ACC 2026. Migotanie przedsionków będzie narastać wraz z epidemią otyłości, ponieważ dzieli z nią wspólny szlak patofizjologiczny prowadzący także do HFpEF, dlatego kluczowe znaczenie ma leczenie przyczynowe (upstream therapy), a nie rutynowa kardiowersja. W badaniu CLOSURE-AF porównującym DOAC z zamknięciem uszka lewego przedsionka (LAA) u pacjentów wysokiego ryzyka uzyskano podobną liczbę udarów i krwawień, ale więcej zgonów w grupie LAA, mimo czego publikacja sugeruje „nie gorszość” tej strategii (https://www.nejm.org/doi/full/10.1056/NEJMoa2513310). Z kolei w badaniu CHAMPION-AF u pacjentów niższego ryzyka LAA wiązało się z większą liczbą udarów, ale mniejszą liczbą (głównie nieciężkich) krwawień, przy braku różnic w ciężkich krwawieniach i istotnym ryzyku powikłań okołozabiegowych. Autorzy sugerują możliwość traktowania LAA jako alternatywy dla DOAC w ramach wspólnego podejmowania decyzji, choć dane nie pokazują jednoznacznej przewagi klinicznej (https://www.nejm.org/doi/abs/10.1056/NEJMoa2517213). Całość prowadzi do pytania, czy u typowego pacjenta z FA bez przeciwwskazań do DOAC należy pozostać przy leczeniu zachowawczym, czy rozważać interwencję zabiegową, mimo ograniczonych korzyści twardych punktów końcowych (https://journals.viamedica.pl/polish_heart_journal/article/view/108435). Szczegółowy TRANSKRYPT do odcinka.Podcast jest przeznaczony wyłącznie dla osób z profesjonalnym wykształceniem medycznym.
HelixTalk - Rosalind Franklin University's College of Pharmacy Podcast
In this episode, we discuss the most important annual updates in the American Diabetes Association Guidelines, Standards of Care 2026, particularly focusing on changes in pharmacotherapy recommendations and the supporting evidence. Key Concepts A few existing agents now have ASCVD risk reduction data in patients with existing ASCVD or high indicators for ASCVD. They are: oral semaglutide and tirzepatide. SGLT2is are still first-line in patients with diabetes and HF including HFpEF, but SC semaglutide and tirzepatide are now recommended for those with symptomatic HFpEF and obesity due to positive outcomes in this population. The GLP-1RA and dual GLP-1/GIP RA are the preferred agents for weight management in patients with T2DM, but use of GLP-1RA can be considered for weight loss in patients with T1DM. The guideline also better defines recommendations for medication-induced hyperglycemia from immune checkpoint inhibitors, PI3Kɑ (phosphoinositidylinositol 3-kinase α) inhibitors, mTOR inhibitors, and steroids. References American Diabetes Association. Standards of care in diabetes—2026. Diabetes Care. 2026;49(suppl 1):S1-S377. SOUL study. Darren K. McGuire, Marx N, Mulvagh SL, et al. Oral semaglutide and cardiovascular outcomes in high-risk type 2 diabetes. N Engl J Med. 2025;392(20):2001-2012. doi:10.1056/NEJMoa2501006. SURPASS-CVOT. Nicholls SJ, Pavo I, Bhatt DL, et al. Cardiovascular outcomes with tirzepatide versus dulaglutide in type 2 diabetes. N Engl J Med. 2025;393(24):2409-2420. doi:10.1056/NEJMoa2505928. SUMMIT. Packer M, Zile MR, Kramer CM, et al. Tirzepatide for heart failure with preserved ejection fraction and obesity. N Engl J Med. 2025;392(5):427-437. doi:10.1056/NEJMoa2410027. STEP-HFpEF. Kosiborod MN, Abildstrom 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. STEP-HFpEF DM. Kosiborod MN, Petrie MC, Borlaug BA, et al. Semaglutide in patients with obesity‑related heart failure and type 2 diabetes. N Engl J Med. 2024;390(15):1394‑1407. doi:10.1056/NEJMoa2313917.
Witam Państwa, nazywam się Jarosław Drożdż, pracuję w Centralnym Szpitalu Klinicznym Uniwersytetu Medycznego w Łodzi, skąd nagrywam podcast Kardio Know-How. W tym odcinku omawiam najnowsze doniesienia w kwestii etiologii przewlekłej niewydolności serca z zachowaną frakcją wyrzutową. Niewydolność serca przez lata utożsamiano głównie z obniżoną frakcją wyrzutową (HFrEF), jednak obecnie wiemy, że stanowi ona tylko około połowy przypadków, a coraz częściej dominuje HFpEF. Pierwsze obserwacje HFpEF sięgają 1985 roku, gdy opisano pacjentów z objawami niewydolności serca mimo prawidłowej funkcji skurczowej. Przez dekady choroba ta była trudna do leczenia, a skuteczna farmakoterapia pojawiła się dopiero niedawno dzięki flozynom i agonistom GLP-1. Kluczowym pytaniem pozostawało jednak jej pochodzenie. Tradycyjnie uważano, że wynika z wielochorobowości (np. nadciśnienia, choroby wieńcowej), ale dane epidemiologiczne temu przeczą. Równolegle do wzrostu liczby przypadków HFpEF obserwujemy natomiast gwałtowny wzrost otyłości, szczególnie trzewnej. Tkanka tłuszczowa wisceralna działa jako narząd endokrynny, wydzielając adipokiny wpływające na stan zapalny, przerost i włóknienie mięśnia sercowego oraz retencję wody. Kluczowym wskaźnikiem ryzyka jest stosunek talii do wzrostu (WHtR), a jego wartość powyżej 0,5 silnie koreluje z chorobami, w tym HFpEF. Proponowana sekwencja patogenezy wskazuje, że to otyłość prowadzi do HFpEF, a dopiero później pojawiają się inne choroby współistniejące. Dane pokazują, że aż 96% pacjentów z HFpEF ma WHtR > 0,5, co silnie wspiera tę hipotezę (https://www.nejm.org/doi/abs/10.1056/NEJM198501313120504 , https://www.jacc.org/doi/10.1016/j.jacc.2025.06.055 ). Szczegółowy TRANSKRYPT do odcinka.Podcast jest przeznaczony wyłącznie dla osób z profesjonalnym wykształceniem medycznym.
CME credits: 0.25 Valid until: 26-03-2027 Claim your CME credit at https://reachmd.com/programs/cme/beyond-steroidal-mras-the-nonsteroidal-mra-lens-in-hf/49198/ In this brief podcast, Drs. Maria Pabon and Robert Mentz explore the evolving role of mineralocorticoid receptor antagonism in heart failure, with emphasis on patients who appear clinically stable yet remain at elevated biologic risk. They contrast steroidal and nonsteroidal MRAs, highlighting differences in receptor selectivity, cardiac-renal distribution, and downstream anti-fibrotic and anti-inflammatory signaling. Faculty address the principle that symptom stability does not equate to disease stability, offering strategies to identify patients with HFpEF or HFmrEF who may benefit from a risk-based treatment approach.=
Send a textHerzinsuffizienz zählt zu den wichtigsten Risikofaktoren für perioperative Morbidität und Mortalität. Gleichzeitig gewinnen SGLT2-Inhibitoren als leitliniengerechte Therapie bei Herzinsuffizienz zunehmend an Bedeutung – mit neuen Herausforderungen für die perioperative Medizin. In dieser Episode besprechen wir, worauf es bei präoperativer Risikostratifizierung, intraoperativem Management und dem Umgang mit der potenziell euglykämen SGLT2i-assoziierten Ketoazidose ankommt.Roth S, Wagner NM. Perioperatives Management der Herzinsuffizienz im Kontext der SGLT2-Inhibitor-Therapie. Anästh Intensivmed. 2026;67:4–15. DOI: 10.19224/ai2026.004Die chronische Herzinsuffizienz ist eine häufige und prognostisch hochrelevante Komorbidität bei Patient:innen, die sich nichtkardiochirurgischen Eingriffen unterziehen. Sie ist mit einer deutlich erhöhten perioperativen Morbidität und Mortalität assoziiert. Der Übersichtsartikel von Roth und Wagner stellt die aktuelle Evidenz zur präoperativen Evaluation, zur perioperativen Fortführung leitliniengerechter Herzinsuffizienztherapie und zu den Besonderheiten des perioperativen Managements unter SGLT2-Inhibitoren systematisch dar. Ein zentraler Fokus liegt auf der modernen leitliniengerechten Pharmakotherapie der Herzinsuffizienz. Diese soll perioperativ grundsätzlich fortgeführt werden, sofern keine Kontraindikationen bestehen. Im Kontext von HFrEF, HFmrEF und HFpEF nehmen SGLT2-Inhibitoren inzwischen eine wichtige Rolle ein. Gleichzeitig stellen sie im perioperativen Umfeld eine besondere Herausforderung dar, da sie mit einer SGLT2i-assoziierten, potenziell normoglykämen Ketoazidose assoziiert sein können. Der Artikel erläutert, dass diese Komplikation durch perioperative Nüchternheit, chirurgischen Stress, Inflammation und Volumenmangel begünstigt werden kann und diagnostisch besonders relevant ist, weil Ketone in der üblichen Blutgasanalyse nicht automatisch erfasst werden. Für die Diagnostik empfehlen die Autor:innen bei unklarer metabolischer Azidose unter SGLT2i-Therapie ausdrücklich die Bestimmung von Ketonen, idealerweise von Beta-Hydroxybutyrat im Blut. Die Urindiagnostik kann falsch-niedrige oder negative Ergebnisse liefern, da dort vor allem Acetoacetat nachgewiesen wird. Therapeutisch steht bei Verdacht auf SGLT2i-assoziierte Ketoazidose die kombinierte Gabe von Glukose und Insulin mit engmaschiger Überwachung des Säure-Basen-Haushalts und der Elektrolyte im Vordergrund.Hinsichtlich des präoperativen Umgangs mit SGLT2-Inhibitoren beschreibt der Artikel eine weiterhin unklare Evidenzlage. Mehrere Fachgesellschaften empfehlen ein präoperatives Pausieren, meist etwa 72 Stunden vor elektiven Eingriffen, zugleich weisen neuere Daten darauf hin, dass ein pauschales Absetzen insbesondere bei Hochrisikopatient:innen mit Herzinsuffizienz auch Nachteile haben könnte. Daraus leiten die Autor:innen ein differenziertes, individualisiertes Vorgehen ab, das Nutzen und Risiko sorgfältig gegeneinander abwägt. Im intraoperativen Management wird ein organprotektives, engmaschig hämodynamisch gesteuertes Vorgehen betont, einschließlich früh etablierter invasiver Blutdruckmessung bei Herzinsuffizienzpatient:innen.nsgesamt unterstreicht der Beitrag, dass Patient:innen mit Herzinsuffizienz ein individualisiertes perioperatives Management benötigen und dass der optimale perioperative Umgang mit SGLT2-Inhibitoren derzeit noch nicht abschließend geklärt ist. Die SGLT2i-assoziierte Ketoazidose stellt dabei eine diagnostische und therapeutische Schlüsselherausforderung für die perioperative Medizin dar.
EVOLUT Low Risk data, a provocative meta-analysis, DNR orders, targeted hypothermia, good news in HFpEF evidence, and GLP-1s as AF drugs are the topics John Mandrola, MD, discusses in this week's podcast. This podcast is intended for healthcare professionals only. To read a partial transcript or to comment, visit: https://www.medscape.com/twic I EVOLUT Low Risk 6-year Results and a 5-year Meta-Analysis of TAVR vs SAVR 6-Year Outcomes of TAVR vs SAVR https://www.jacc.org/doi/10.1016/j.jacc.2026.02.5063 EVOLUT Low Risk Trial at 2 years https://www.nejm.org/doi/full/10.1056/NEJMoa1816885 EVOLUT Low Risk Trial at 3 years https://www.jacc.org/doi/10.1016/j.jacc.2023.02.017 EVOLUT Low Risk Trial at 4 years https://www.jacc.org/doi/10.1016/j.jacc.2023.09.813 Nonproportional Hazards for Time-to-Event Outcomes in Clinical Trials https://www.jacc.org/doi/10.1016/j.jacc.2019.08.1034 TAVR vs SAVR 5-Year Outcomes - Systematic Review https://heart.bmj.com/content/early/2026/02/11/heartjnl-2025-327092 TAVR vs SAVR Updated Meta-Analysis of RCTs https://www.jacc.org/doi/10.1016/j.jacc.2024.12.031 UK TAVI Trial https://jamanetwork.com/journals/jama/fullarticle/2792251 Dr David Cohen on X https://x.com/djc795/status/2023556582030852172?s=46&t=zXMCUoVjSsdyemzWlzeBjA II DNR in the Hospital Inadequate Documentation of Unilateral DNR Orders https://jamanetwork.com/journals/jama/fullarticle/2829203 GeriPal Blog Unilateral DNR Orders https://geripal.org/unilateral-dnr-gina-piscitello-erin-demartino-will-parker/ III Yet another failure of Targeted Hypothermia 2-Year Follow-Up of TTM2 Trial https://jamanetwork.com/journals/jamaneurology/fullarticle/2845193 TTM2 Trial https://www.nejm.org/doi/full/10.1056/NEJMoa2100591 IV Good news in HFpEF Evidence ALT-FLOW II Trial https://doi.org/10.1093/ejhf/xuaf016 V GLP-1 as AF drugs Semaglutide as Adjunctive Therapy in Obesity-Related PAF https://doi.org/10.1093/europace/euag018 You may also like: The Bob Harrington Show with the Stephen and Suzanne Weiss Dean of Weill Cornell Medicine, Robert A. Harrington, MD. https://www.medscape.com/author/bob-harrington Questions or feedback, please contact news@medscape.net
Episode 212: Managing HFpEFHyo Mun and Jordan Redden (medical students) explain how to manage HFpEF with medications and touch some basics about nonpharmacologic treatments. Dr. Arreaza asks insightful questions to guide the discussion. Written by Hyo Mun, MSIV, American University of the Caribbean; and Jordan Redden, MSIV, Ross University School of Medicine. Comments by Hector Arreaza, MD.You are listening to Rio Bravo qWeek Podcast, your weekly dose of knowledge brought to you by the Rio Bravo Family Medicine Residency Program from Bakersfield, California, a UCLA-affiliated program sponsored by Clinica Sierra Vista, Let Us Be Your Healthcare Home. This podcast was created for educational purposes only. Visit your primary care provider for additional medical advice.Treatment of HFpEFArreaza: Mike, if you had to name the one therapy everyone with HFpEF should be on, what is it?Mike: That's easy! SGLT-2 inhibitors. This is the one slam-dunk we have in HFpEF. Empagliflozin (Jardiance) or dapagliflozin (Farxiga) should be started in essentially every patient with HFpEF, and it doesn't matter if they have diabetes or not.Jordan: And that's worth repeating, because people still think of these as “diabetes drugs.” They're not anymore. In HFpEF, SGLT-2 inhibitors reduce heart-failure hospitalizations, improve symptoms, improve quality of life, and even reduce cardiovascular death.Dr. Arreaza: They're also simple. Empagliflozin 10 mg daily or dapagliflozin 10 mg daily. No titration, no drama. The effectiveness of these meds was established around 2019 with DAPA-HF and later with DELIVER. These were trials thatdemonstrated that dapagliflozin reduces worsening heart failure and cardiovascular events across the full spectrum of heart failure, from reduced to preserved ejection fraction, independent of diabetes status.Mike: And the number needed to treat is about 28 to prevent one heart-failure hospitalization. That's excellent for a disease where we historically had almost nothing that worked.Jordan: They're also safe in chronic kidney disease down to an eGFR of about 25, which makes them even more useful in this population.Dr. Arreaza: Alright. We got SGLT-2 inhibitor, what's next?Mike: Volume management. Loop diuretics are still the backbone of symptom control in HFpEF. If the patient is volume overloaded, you diurese, and you diurese aggressively.Jordan: The goal is euvolemia. Dry weight, no edema, no orthopnea, no waking up gasping for air. A lot of these patients end up needing chronic oral loop diuretics to stay there.Dr. Arreaza: Something to remember: HFpEF patients don't tolerate congestion well, and being “a little wet” is not benign. Let's move into RAAS inhibition. Where do ARBs and ACE inhibitors fit in?Mike: Between ARBs and ACE inhibitors, ARBs are the winners in HFpEF. They actually reduce heart failure hospitalizations—drugs like candesartan, losartan, valsartan. ACE inhibitors? Not so much. They showed minimal benefit in older HFpEF patients, which is why we go with ARBs instead.Jordan: But a lot of clinicians get nervous about ACE inhibitors and ARBs because of kidney function, so it's worth talking through how these drugs actually work in the kidney.Dr. Arreaza: Yes, misunderstanding may lead to unnecessary drug discontinuation.Jordan: Under normal conditions, the afferent arteriole brings blood into the glomerulus, and the efferent arteriole is constricted by angiotensin II. That constriction keeps pressure high in the glomerulus and maintains filtration.Mike: Here's what happens with an ACE inhibitor: you block angiotensin II, the efferent arteriole relaxes, glomerular pressure drops, and GFR dips slightly. Creatinine bumps up a little, and that scares people, but that's actually the whole point—that's how you get kidney protection long-term.Jordan: High intraglomerular pressure causes hyperfiltration injury and scarring over time. Lowering that pressure protects the kidney long-term. The short-term GFR drop is the price you pay for long-term benefits.Dr. Arreaza: So let's talk about CKD, because this is where people panic.Mike: Right. ACE inhibitors and ARBs are not contraindicated in chronic kidney disease. In fact, they're recommended even in advanced stages. They reduce progression to kidney failure by about a third.Jordan: The key is how you use them. Start low. Check creatinine and potassium one to two weeks after starting, then periodically. A creatinine rise up to 30% from baseline is acceptable. That's not kidney injury, that's physiology.Dr. Arreaza: And what about potassium creeping up?Mike: You adjust the dose or add a potassium binder. You don't just automatically stop the drug.Dr. Arreaza: Now there is one absolute contraindication everyone needs to know about! (board exam test)Jordan: Bilateral renal artery stenosis. This is the big one. In these patients, the kidneys are completely dependent on angiotensin II–mediated efferent constriction to maintain GFR. Take that away, and GFR collapses.Mike: Creatinine can jump dramatically within days. If you see a creatinine rise of 20% or more shortly after starting an ACE inhibitor, you should be thinking about bilateral renal artery stenosis and stopping the drug immediately.Dr. Arreaza: After revascularization, though, many patients can tolerate ACE inhibitors again, so this isn't always permanent. What about cardiorenal syndrome? That's where things get uncomfortable.Mike: It is uncomfortable, but cardiorenal syndrome isn't a contraindication. These patients have severe heart failure and kidney disease, and their mortality is actually higher than patients with heart failure alone.Jordan: ACE inhibitors still reduce mortality and slow kidney disease progression in this group. Studies show that stopping ACE inhibitors during acute heart-failure admissions increases in-hospital mortality three- to four-fold.Dr. Arreaza: So we are cautious, but we don't avoid it.Mike: Exactly. Start low, titrate slowly, monitor labs closely, accept up to a 30% creatinine rise. You only stop if kidney function keeps worsening, or potassium gets dangerously high.Dr. Arreaza: Alright. Let's move on. What about mineralocorticoid receptor antagonists… MRA?Jordan: Spironolactone or eplerenone might reduce hospitalizations in HFpEF, but the data is mixed. This is more of a “select patients” situation.Mike: And you have to watch potassium and kidney function carefully, especially if they're already on an ACE inhibitor or ARB.Dr. Arreaza: What about sacubitril-valsartan, also known as Entresto®?Mike: Entresto may help patients with mildly reduced EF roughly in the 45 to 57% range. It's not first-line for HFpEF, but in select patients, it's reasonable.Dr. Arreaza: Now let's clarify one of the biggest sources of confusion: beta blockers.Jordan: Beta blockers are not a treatment for HFpEF itself. They're only indicated if the patient has another reason to be on them, like coronary disease or atrial fibrillation.Mike: And timing really matters here. You absolutely do not start beta blockers during acute decompensated heart failure. Their negative inotropic effects can make things worse when patients are volume overloaded.Jordan: But, and this is critical, you also don't stop them if the patient is already taking one. Abrupt withdrawal causes a sympathetic surge and dramatically increases mortality.Dr. Arreaza: If a patient is admitted on a beta blocker, what do we do?Mike: Continue it at the same dose or reduce it slightly if they're really unstable. Once they're euvolemic and stable, you can carefully titrate up.Jordan: And watch for chronotropic incompetence. HFpEF patients often rely on heart-rate response to exercise, and beta blockers can worsen exercise intolerance.Dr. Arreaza: Beyond medications, HFpEF is really about treating comorbidities. Aerobic activity can be an initial strategy to improve exercise intolerance and has evidence of improving aerobic function and quality of life. Sodium restriction: improves symptoms, does not decrease risk of death or hospitalizations.Mike: Hypertension control is huge. For diabetes, the SGLT-2 inhibitors will perform double duty. For obesity, weight loss improves symptoms, and GLP-1 agonists like semaglutide are absolute gamechangers.Jordan: Don't forget sleep apnea, atrial fibrillation, and lifestyle. Exercise improves the quality of life, even if it doesn't change hard outcomes. Lifestyle is the main treatment. Dr. Arreaza: And when should you refer to cardiology?Mike: You should refer when the diagnosis isn't clear; symptoms are not responding to treatment, difficult volume management, end-organ dysfunction, or if you are concerned about advanced heart failure.Dr. Arreaza: So, it has been a great discussion. What is the takeaway?Mike: HFpEF treatment isn't about one magic drug -- it's about volume control, SGLT2 inhibitors, smart use of RAAS blockade, and aggressive management of comorbidities.Jordan: And it's understanding the physiology, so you don't withhold life-saving therapies out of fear.Dr. Arreaza: Well said. If you found this helpful, share it with a friend or colleague and rate us wherever you listen. This is Dr. Arreaza, signing off.Jordan/Mike: Thanks! Even without trying, every night you go to bed a little wiser. Thanks for listening to Rio Bravo qWeek Podcast. We want to hear from you, send us an email at RioBravoqWeek@clinicasierravista.org, or visit our website riobravofmrp.org/qweek. See you next week! _____________________References:Barzin A, Barnhouse KK, Kane SF. Heart Failure With Preserved Ejection Fraction. Am Fam Physician. 2025;112(4):435-440.Heidenreich PA, Bozkurt B, Aguilar D, et al. 2022 AHA/ACC/HFSA guideline for the management of heart failure. Circulation. 2022;145(18):e895-e1032.Kittleson MM, Panjrath GS, Amancherla K, et al. 2023 ACC expert consensus decision pathway on management of heart failure with preserved ejection fraction. J Am Coll Cardiol. 2023;81(18):1835-1878.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.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.Pitt B, Pfeffer MA, Assmann SF, et al. Spironolactone for heart failure with preserved ejection fraction. N Engl J Med. 2014;370(15):1383-1392.Yusuf S, Pfeffer MA, Swedberg K, et al. Effects of candesartan in patients with chronic heart failure and preserved left-ventricular ejection fraction. Lancet. 2003;362(9386):777-781.Solomon SD, McMurray JJV, Anand IS, et al. Angiotensin-neprilysin inhibition in heart failure with preserved ejection fraction. N Engl J Med. 2019;381(17):1609-1620.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.Xie Y, Xu E, Bowe B, Al-Aly Z. Long-term cardiovascular outcomes of COVID-19. Nat Med. 2022;28(3):583-590.Puntmann VO, Carerj ML, Wieters I, et al. Outcomes of cardiovascular magnetic resonance imaging in patients recently recovered from COVID-19. JAMA Cardiol. 2020;5(11):1265-1273.Basso C, Leone O, Rizzo S, et al. Pathological features of COVID-19-associated myocardial injury. Eur Heart J. 2020;41(39):3827-3835.Nalbandian A, Sehgal K, Gupta A, et al. Post-acute COVID-19 syndrome. Nat Med. 2021;27(4):601-615.Badve SV, Roberts MA, Hawley CM, et al. Effects of angiotensin-converting enzyme inhibitors and angiotensin receptor blockers in adults with estimated GFR less than 60 mL/min per 1.73 m². Ann Intern Med. 2024;177(8):953-963.Navis G, Faber HJ, de Zeeuw D, de Jong PE. ACE inhibitors and the kidney: a risk-benefit assessment. Drug Saf. 1996;15(3):200-211.Textor SC, Novick AC, Tarazi RC, et al. Critical perfusion pressure for renal function in patients with bilateral atherosclerotic renal vascular disease. Ann Intern Med. 1985;102(3):308-314.Hackam DG, Spence JD, Garg AX, Textor SC. Role of renin-angiotensin system blockade in atherosclerotic renal artery stenosis and renovascular hypertension. Hypertension. 2007;50(6):998-1003.Ronco C, Haapio M, House AA, et al. Cardiorenal syndrome. J Am Coll Cardiol. 2008;52(19):1527-1539.Prins KW, Neill JM, Tyler JO, et al. Effects of beta-blocker withdrawal in acute decompensated heart failure. JACC Heart Fail. 2015;3(8):647-653.Jondeau G, Neuder Y, Eicher JC, et al. B-CONVINCED: Beta-blocker CONtinuation Vs. INterruption in patients with Congestive heart failure hospitalizED for a decompensation episode. Eur Heart J. 2009;30(18):2186-2192.Theme song, Works All The Time by Dominik Schwarzer, YouTube ID: CUBDNERZU8HXUHBS, purchased from https://www.premiumbeat.com/.
Dr. Alanna Morris-Simon, Senior Medical Director for US Medical Affairs at Bayer, describes the symptoms and diagnostics used to classify heart failure and the key at-risk populations for this condition. The rapidly evolving landscape of heart failure treatments now includes the Bayer drug KERENDIA, a non-steroidal MRA approved to reduce cardiovascular death and heart failure in adults with an ejection fraction of 40% or more. This drug is part of an emerging trend to treat multiple related conditions simultaneously and could prevent the onset of heart failure and treat established heart failure. Alanna explains, "At a basic level, heart failure is a clinical syndrome, and that's important. I'm actually a heart failure cardiologist as well. And so this is important because patients have to have signs and symptoms. And those signs and symptoms really result from the heart being unable to either fill with blood properly or squeeze that blood out in a way that meets the body's demands. Either way, patients experience the same symptoms, and those include symptoms like swelling and weight gain, shortness of breath, either at rest or with activity, fatigue, abdominal swelling and bloating, loss of appetite, as well as other symptoms." "If a doctor or a clinician suspects a diagnosis of heart failure, 99.99% of the time, they'll start by ordering an echocardiogram or a heart ultrasound. Of course, the guidelines tell us to get a chest X-ray, get labs, those sorts of things. But really, we make the diagnosis for the most part based on the results of an echocardiogram because that echocardiogram allows us to visualize how the heart is pumping. It allows us to classify the type of heart failure so that if we see that the squeeze of the heart is impaired, we call that heart failure with reduced ejection fraction. And that's when the ejection fraction or EF is 40% or less. If the EF is in the 41 to 49% range, we classify that as heart failure with mildly reduced ejection fraction. And if patients have an ejection fraction of 50% or greater, we call that heart failure with preserved ejection fraction or HFpEF." "And we were excited that the FDA actually granted a priority review for KERENDIA because this really only occurs when the FDA recognizes that a treatment can fill a significant unmet need for a disease or a population of patients. And lo and behold, in July of 2025, finerenone was approved by the FDA under the trade name KERENDIA to reduce the risk of cardiovascular death, hospitalization for heart failure, and urgent heart failure visits in adults with an ejection fraction of 40% or more." #Bayer #Finerenone #Pharma #HeartFailure #HFpEF #HFmrEF #MRA #UnmetNeed #Cardiology #KERENDIA #FDA #CardiovascularHealth #MedicalBreakthrough #PatientCare #Innovation Bayer.com Download the transcript here
Dr. Alanna Morris-Simon, Senior Medical Director for US Medical Affairs at Bayer, describes the symptoms and diagnostics used to classify heart failure and the key at-risk populations for this condition. The rapidly evolving landscape of heart failure treatments now includes the Bayer drug KERENDIA, a non-steroidal MRA approved to reduce cardiovascular death and heart failure in adults with an ejection fraction of 40% or more. This drug is part of an emerging trend to treat multiple related conditions simultaneously and could prevent the onset of heart failure and treat established heart failure. Alanna explains, "At a basic level, heart failure is a clinical syndrome, and that's important. I'm actually a heart failure cardiologist as well. And so this is important because patients have to have signs and symptoms. And those signs and symptoms really result from the heart being unable to either fill with blood properly or squeeze that blood out in a way that meets the body's demands. Either way, patients experience the same symptoms, and those include symptoms like swelling and weight gain, shortness of breath, either at rest or with activity, fatigue, abdominal swelling and bloating, loss of appetite, as well as other symptoms." "If a doctor or a clinician suspects a diagnosis of heart failure, 99.99% of the time, they'll start by ordering an echocardiogram or a heart ultrasound. Of course, the guidelines tell us to get a chest X-ray, get labs, those sorts of things. But really, we make the diagnosis for the most part based on the results of an echocardiogram because that echocardiogram allows us to visualize how the heart is pumping. It allows us to classify the type of heart failure so that if we see that the squeeze of the heart is impaired, we call that heart failure with reduced ejection fraction. And that's when the ejection fraction or EF is 40% or less. If the EF is in the 41 to 49% range, we classify that as heart failure with mildly reduced ejection fraction. And if patients have an ejection fraction of 50% or greater, we call that heart failure with preserved ejection fraction or HFpEF." "And we were excited that the FDA actually granted a priority review for KERENDIA because this really only occurs when the FDA recognizes that a treatment can fill a significant unmet need for a disease or a population of patients. And lo and behold, in July of 2025, finerenone was approved by the FDA under the trade name KERENDIA to reduce the risk of cardiovascular death, hospitalization for heart failure, and urgent heart failure visits in adults with an ejection fraction of 40% or more." #Bayer #Finerenone #Pharma #HeartFailure #HFpEF #HFmrEF #MRA #UnmetNeed #Cardiology #KERENDIA #FDA #CardiovascularHealth #MedicalBreakthrough #PatientCare #Innovation Bayer.com Listen to the podcast here
Episode 211: Understanding HFpEF. Hyo Mun and Jordan Redden (medical students) explain the pathophysiology of heart failure with preserved ejection fraction (HFpEF) and how it differentiates from HFrEF. Dr. Arreaza asks insightful questions and summarizes some key elements of HFpEF. Written by Hyo Mun, MS4, American University of the Caribbean; and Jordan Redden, MS4, Ross University School of Medicine. Comments and edits by Hector Arreaza, MD.You are listening to Rio Bravo qWeek Podcast, your weekly dose of knowledge brought to you by the Rio Bravo Family Medicine Residency Program from Bakersfield, California, a UCLA-affiliated program sponsored by Clinica Sierra Vista, Let Us Be Your Healthcare Home. This podcast was created for educational purposes only. Visit your primary care provider for additional medical advice.What is EF? Just imagine, the heart is a pump, blood gets into the heart through the veins, the ventricles fill up and then squeeze the blood out. So, the percent of blood that is pumped out is the EF. Let's start at the beginning. What is HFpEF?Mike: HFpEF stands for heart failure with preserved ejection fraction. Basically, these patients squeeze normally—their ejection fraction is 50% or higher—but here's the thing: the heart can't relax and fill the way it should. The muscle gets stiff, almost like a thick leather boot that just won't stretch. And because the ventricle can't fill properly, pressure starts backing up into the lungs and the rest of the body. That's when patients start experiencing shortness of breath, leg swelling, fatigue—all those classic symptoms.Dr. Arreaza: And this is where people get fooled by the ejection fraction.Mike: Exactly. The ejectionfraction tells you total left ventricular emptying, not just forward flow.Jordan: The classic example is severe mitral regurgitation. You can eject 60% of your blood volume and still be in cardiogenic shock because most of that blood is leaking backward into the left atrium instead of going into the aorta. So, you get pulmonary edema, hypotension, fatigue, all with a “normal” EF. Which is honestly terrifying if you're over-relying on echo reports without thinking clinically.Dr. Arreaza: And in HFpEF, functional mitral regurgitation often shows up later in the disease. It's not usually the primary cause; it's more of a marker of advanced disease. Moderate to severe MR in HFpEF independently predicts worse outcomes, including a higher risk of mortality or heart failure hospitalization. So, let's contrast this with HFrEF. How are these two different?Mike: HFrEF—heart failure with reduced ejection fraction—is a pumping problem. The heart muscle is weak and can't contracteffectively. Ejection fraction drops below 40%, and this is your classic systolic dysfunction.Jordan: HFpEF, on the other hand, is diastolic dysfunction. The heart muscle is thick, fibrotic, and noncompliant. It squeezes fine, but it just doesn't relax, even though the EF looks reassuring on paper.Mike: I like to explain it this way: HFrEF is a weak heart that can't squeeze. HFpEF is a stiff heart that can't relax. Totally different problems.Dr. Arreaza: And then there's the gray zone: heart failure with mildly reduced EF, or HFmrEF. That's an EF between 41 and 49% with evidence of elevated filling pressures. It really shares the features of both worlds. So, what actually causes HFpEF versus HFrEF?Jordan: HFpEF is basically what happens when all the problems of modern living catch up with you. You've got chronic hypertension, obesity, diabetes, metabolic syndrome, aging, systemic inflammation—all of these things slowly remodel the heart over years. The muscle gets thick and stiff, and eventually the ventricle just loses its ability to relax. So, HFpEF is really a disease of metabolic dysfunction and chronic stress in the heart. Mike: HFrEF is more about direct injury. Think about myocardial infarctions, ischemic cardiomyopathy, viral myocarditis, alcohol toxicity, chemotherapy like doxorubicin, genetic cardiomyopathies, or chronic uncontrolled tachycardia. These insults actually damage or kill heart muscle cells, leading to a dilated, weak ventricle that can't pump effectively.Dr. Arreaza: So the short version: HFpEF is caused by chronic metabolic and hypertensive stress, while HFrEF is caused mainly by myocardial damage. A question we get a lot: does HFpEF eventually turn into HFrEF? What do you guys think?Mike: In most cases, no. HFpEF patients usually stay HFpEF throughout their disease course. They don't just “burn out” and turn into HFrEF.Jordan: They're generally separate disease entities with different pathophysiology. A patient with HFpEF can develop HFrEF if they have a big myocardial infarction or ongoing ischemia that damages the muscle, but that's not the natural progression.Mike: Interestingly though, the opposite can happen. Some HFrEF patients actually improve their ejection fraction with good medical therapy—that's called HF with improved EF—and it's a great sign that treatment is working.Dr. Arreaza: Another question. How do HFpEF and HFrEF compare to restrictive cardiomyopathy and constrictive pericarditis?Jordan: Clinically, they can all look very similar: dyspnea, edema, fatigue, but the underlying mechanisms are completely different.Mike: In HFpEF, the myocardium itself is stiff from hypertrophy and fibrosis. The problem is intrinsic to the heart muscle, and EF stays preserved. Echoshows diastolic dysfunction with elevated filling pressures.Jordan: In HFrEF, the myocardium is weak. The ventricle is often dilated and contracts poorly, with a reduced EF.Mike: Restrictive cardiomyopathy is different. Here, the myocardium gets infiltrated by abnormal stuff—amyloid, iron, sarcoid—and that makes it extremely stiff. It can look like HFpEF on the surface, but it's usually more severe. On Echo You'll see biatrial enlargement, small ventricles, and preserved EF. And importantly, it's a pathologic diagnosis, so you need advanced imaging or biopsy to confirm it.Jordan: Constrictive pericarditis is another mimic, but here the myocardium is usually normal. The problem is that the pericardium is thickened, calcified, and rigid. This will physically prevent the heart from being filled. Imaging shows pericardial thickening, septal bounce, and respiratory variation in flow, and cath shows equalization of diastolic pressures, which is the hallmark of constrictive pericarditis.Dr. Arreaza: So the takeaway is: HFpEF is a clinical syndrome driven by common metabolic and hypertensive causes, while restrictive and constrictive diseases are specific pathologic entities. If “HFpEF” is unusually severe or not responding to treatment, you need to think beyond HFpEF. Which type of heart failure is more common right now?Mike: Good question, the answer is: HFpEF. It now accounts for up to 60% of all heart failure cases, and it's still rising.Dr. Arreaza: Why is that?Jordan: Because people are living longer, gaining weight, and developing more metabolic syndrome. HFpEF thrives in older, or people with obesity, hypertension, or diabetes: basically, the modern American population. At the same time, better treatment of acute MIs means fewer people are developing HFrEF from massive heart attacks.Mike: HFpEF is the heart failure epidemic of the 21st century. It's honestly the cardiology equivalent of type 2 diabetes.Dr. Arreaza: Let's talk aboutCOVID-19. (2025 and still talking about it) Does it actually increase heart failure risk?Mike: Yes, absolutely. COVID increases both acute and long-term heart failure risk.Jordan: During acute infection, COVID can cause myocarditis, trigger massive inflammation, and precipitate acute decompensated heart failure, especially in patients with pre-existing disease. It also causes microthrombi, which can injure the myocardium.Mike: And after infection, even mild cases are linked to a significantly higher risk of developing new heart failure within the following year. Both HFpEF and HFrEF rates go up.Dr. Arreaza: I remember seeing this in 2021, we had a patient with acute COVID and HFrEF, her EF was about 10%, I lost contact with the patient and at the end I don't know what happened to her. What's the pathophysiology of COVID and heart failure?Mike: COVID causes direct viral injury through ACE2 receptors, triggers massive inflammation that damages the endothelium and heart muscle, leads to microvascular clotting and fibrosis—all mechanisms that promote HFpEF.Jordan: Add autonomic dysfunction, persistent low-grade inflammation, and worsening metabolic syndrome, and you've got a perfect storm for heart failure.Dr. Arreaza: Bottom line: COVID is a cardiovascular disease as much as a respiratory one. If someone had COVID and now has unexplained dyspnea or fatigue, think about heart failure. Get an echo, get a BNP, start treatment. Last big question: why did we have so many therapies for HFrEF but essentially none for HFpEF for years?Mike: HFrEF is mechanistically straightforward. You've got a weak heart with excessive neurohormonal activation going on — so you block RAAS, block the sympathetic system, drop the afterload. The drugs make sense.Jordan: HFpEF is messy. It's not one disease. It's stiffness, fibrosis, inflammation, microvascular dysfunction, metabolic disease, atrial fibrillation, all overlapping. One drug can't fix all of that.Mike: And some drugs that worked beautifully in HFrEF actually made HFpEF worse. Take Beta blockers, for example. They slow heart rate, which is a problem because HFpEF patients rely on heart rate to maintain their cardiac output.Jordan: The breakthrough came with SGLT-2 inhibitors: diabetes drugs that unexpectedly addressed multiple HFpEF mechanisms at once: volume, metabolism, inflammation, and myocardial energetics.Dr. Arreaza: The miracle drug for HFpEF! Alright, let's wrap up.Mike: Bottom line: HFpEF is common, complex, and dangerous: even if the EF looks “normal.”Jordan: And if you're relying on ejection fraction alone, HFpEF will humble you every time.Dr. Arreaza: If you liked this episode, share it with a friend or a colleague and rate us wherever you listen. This is Dr. Arreaza, signing off.Even without trying, every night you go to bed a little wiser. Thanks for listening to Rio Bravo qWeek Podcast. We want to hear from you, send us an email at RioBravoqWeek@clinicasierravista.org, or visit our website riobravofmrp.org/qweek. See you next week! _____________________References:Barzin A, Barnhouse KK, Kane SF. Heart Failure With Preserved Ejection Fraction. Am Fam Physician. 2025;112(4):435-440.Heidenreich PA, Bozkurt B, Aguilar D, et al. 2022 AHA/ACC/HFSA guideline for the management of heart failure. Circulation. 2022;145(18):e895-e1032.Kittleson MM, Panjrath GS, Amancherla K, et al. 2023 ACC expert consensus decision pathway on management of heart failure with preserved ejection fraction. J Am Coll Cardiol. 2023;81(18):1835-1878.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.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.Pitt B, Pfeffer MA, Assmann SF, et al. Spironolactone for heart failure with preserved ejection fraction. N Engl J Med. 2014;370(15):1383-1392.Yusuf S, Pfeffer MA, Swedberg K, et al. Effects of candesartan in patients with chronic heart failure and preserved left-ventricular ejection fraction. Lancet. 2003;362(9386):777-781.Solomon SD, McMurray JJV, Anand IS, et al. Angiotensin-neprilysin inhibition in heart failure with preserved ejection fraction. N Engl J Med. 2019;381(17):1609-1620.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.Xie Y, Xu E, Bowe B, Al-Aly Z. Long-term cardiovascular outcomes of COVID-19. Nat Med. 2022;28(3):583-590.Puntmann VO, Carerj ML, Wieters I, et al. Outcomes of cardiovascular magnetic resonance imaging in patients recently recovered from COVID-19. JAMA Cardiol. 2020;5(11):1265-1273.Basso C, Leone O, Rizzo S, et al. Pathological features of COVID-19-associated myocardial injury. Eur Heart J. 2020;41(39):3827-3835.Nalbandian A, Sehgal K, Gupta A, et al. Post-acute COVID-19 syndrome. Nat Med. 2021;27(4):601-615.Badve SV, Roberts MA, Hawley CM, et al. Effects of angiotensin-converting enzyme inhibitors and angiotensin receptor blockers in adults with estimated GFR less than 60 mL/min per 1.73 m². Ann Intern Med. 2024;177(8):953-963.Navis G, Faber HJ, de Zeeuw D, de Jong PE. ACE inhibitors and the kidney: a risk-benefit assessment. Drug Saf. 1996;15(3):200-211.Textor SC, Novick AC, Tarazi RC, et al. Critical perfusion pressure for renal function in patients with bilateral atherosclerotic renal vascular disease. Ann Intern Med. 1985;102(3):308-314.Hackam DG, Spence JD, Garg AX, Textor SC. Role of renin-angiotensin system blockade in atherosclerotic renal artery stenosis and renovascular hypertension. Hypertension. 2007;50(6):998-1003.Ronco C, Haapio M, House AA, et al. Cardiorenal syndrome. J Am Coll Cardiol. 2008;52(19):1527-1539.Prins KW, Neill JM, Tyler JO, et al. Effects of beta-blocker withdrawal in acute decompensated heart failure. JACC Heart Fail. 2015;3(8):647-653.Jondeau G, Neuder Y, Eicher JC, et al. B-CONVINCED: Beta-blocker CONtinuation Vs. INterruption in patients with Congestive heart failure hospitalizED for a decompensation episode. Eur Heart J. 2009;30(18):2186-2192.Theme song, Works All The Time by Dominik Schwarzer, YouTube ID: CUBDNERZU8HXUHBS, purchased from https://www.premiumbeat.com/.
In this episode of the MyHeart.net podcast, Dr. Alain Bouchard discusses the interplay between Heart Failure with Preserved Ejection Fraction, or HFpEF, and obesity with Dr. Michelle Kittleson, Director of Heart Failure Research at the Smidt Heart Institute at Cedars-Sinai.Learn more about the diagnosis, challenges, and management of this condition by exploring our article, Managing Obesity in Heart Failure with Preserved Ejection Fraction (HFpEF).About the TeamDr. Alain Bouchard is a clinical cardiologist at Cardiology Specialists of Birmingham, AL. He is a native of Quebec, Canada and trained in Internal Medicine at McGill University in Montreal. He continued as a Research Fellow at the Montreal Heart Institute. He did a clinical cardiology fellowship at the University of California in San Francisco. He joined the faculty at the University of Alabama Birmingham from 1986 to 1990. He worked at CardiologyPC and Baptist Medical Center at Princeton from 1990-2019. He is now part of the Cardiology Specialists of Birmingham at UAB Medicine.Dr. Philip Johnson is originally from Selma, AL. Philip began his studies at Vanderbilt University in Nashville, TN, where he double majored in Biomedical and Electrical Engineering. After a year in the “real world” working for his father as a machine design engineer, he went to graduate school at UAB in Birmingham, AL, where he completed a Masters and PhD in Biomedical Engineering before becoming a research assistant professor in Biomedical Engineering. After a short stint in academics, he continued his education at UAB in Medical School, Internal Medicine Residency, and is currently a cardiology fellow in training with a special interest in cardiac electrophysiology.Medical DisclaimerThe contents of the MyHeart.net podcast, including as textual content, graphical content, images, and any other content contained in the Podcast (“Content”) are purely for informational purposes. The Content is not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a medical condition. Never disregard professional medical advice or delay in seeking it because of something you have read or heard on the Podcast!If you think you may have a medical emergency, call your doctor or 911 immediately. MyHeart.net does not recommend or endorse any specific tests, physicians, products, procedures, opinions, or other information that may be mentioned on the Podcast. Reliance on any information provided by MyHeart.net, MyHeart.net employees, others appearing on the Podcast at the invitation of MyHeart.net, or other visitors to the Podcast is solely at your own risk.The Podcast and the Content are provided on an “as is” basis.
Mode of Death in Patients With Heart Failure With Mildly Reduced or Preserved Ejection Fraction: The FINEARTS-HF RCT
PDFs available here: https://rhesusmedicine.com/pages/cardiologyConsider subscribing (if you found any of the info useful!): https://www.youtube.com/channel/UCRks8wB6vgz0E7buP0L_5RQ?sub_confirmation=1Timestamps:0:00 What is Heart Failure / Heart Failure Definition0:11 Systolic vs Diastolic Heart Failure 0:31 How is Cardiac Output Calculated2:28 Causes of Heart Failure 4:39 Heart Failure Risk Factors5:24 Signs and Symptoms of Heart Failure6:12 Diagnosis of Heart Failure 7:41 Treatment of Heart Failure (HFrEF vs HFpEF) ReferencesNaing, P., Forrester, D., Kangaharan, N., Muthumala, A.S.M., Myint, S.M. & Playford, D., 2019. Heart failure with preserved ejection fraction. July 2019. [online] Available at: https://www1.racgp.org.au/ajgp/2019/july/heart-failure-with-preserved-ejection-fraction. RACGPLi, P., Zhao, H., Zhang, J., Ning, Y. & Tu, Y., 2021. Similarities and differences between HFmrEF and HFpEF. , 8:678614. [online] Available at: https://www.frontiersin.org/articles/10.3389/fcvm.2021.678614/full. Cellular and molecular differences between HFpEF and HFrEF: a step ahead in an improved pathological understanding, National Center for Biotechnology Information (NCBI), 2020. Available at: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7016826/. NCBIAlbakri, A., 2018. Heart failure with reduced ejection fraction: clinical status and meta-analyses of diagnosis by 3D echocardiography and natriuretic peptides-guided therapy. Paolucci, L., 2022. New guideline-directed treatments for heart failure. Journal of the American College of Cardiology: Case Reports. Available at: https://www.jacc.org/doi/10.1016/j.jaccases.2021.11.006. jacc.orgNicolas, D., 2024. Sacubitril-Valsartan. In: StatPearls . Treasure Island (FL): StatPearls Publishing. Available at: https://www.ncbi.nlm.nih.gov/books/NBK507904/. NCBINational Center for Biotechnology Information (NCBI), 2024. Heart failure: diagnosis, management and prognosis. Available at: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4961993/.National Center for Biotechnology Information (NCBI), 2024. Heart failure with preserved ejection fraction (HFpEF). Available at: https://www.ncbi.nlm.nih.gov/books/NBK599960/. NCBIDisclaimer: Please remember this podcast and all content from Rhesus Medicine is for educational and entertainment purposes only and is not a guide to diagnose or to treat any form of condition. The content is not to be used to guide clinical practice and is not medical advice. Please consult a healthcare professional for medical advice.
Obesity, Hypertension, and Risk Factors in Terms of Prevention and Decreasing the Risk of HfpEF Guest: Affan Irfan, M.D., Ph.D. Host: Stephen L. Kopecky, M.D. HFpEF is a type of heart failure where the heart pumps normally but becomes stiff. This leads to fatigue, shortness of breath, and fluid retention. It is closely linked to obesity, hypertension, and metabolic disorders, with cases rising as these conditions become more common. Topics Discussed: What is HFpEF and its risk factors? How common are obesity and hypertension, and how often do they lead to HFpEF? How do you diagnose HFpEF? How effective are weight loss, diet, and exercise in preventing HFpEF? What medical and public health strategies help reduce these risk factors and HFpEF cases? Connect with Mayo Clinic's Cardiovascular Continuing Medical Education online at https://cveducation.mayo.edu or on Twitter @MayoClinicCV and @MayoCVservices. LinkedIn: Mayo Clinic Cardiovascular Services Cardiovascular Education App: The Mayo Clinic Cardiovascular CME App is an innovative educational platform that features cardiology-focused continuing medical education wherever and whenever you need it. Use this app to access other free content and browse upcoming courses. Download it for free in Apple or Google stores today! No CME credit offered for this episode. Podcast episode transcript found here.
The FiltrateJoel Topf @kidneyboy.bsky.socialSwapnil Hiremath@hswapnil.medsky.socialAC @medpeedskidneys.bsky.socialSpecial GuestMike Walsh Associate Professor in the Departments of Medicine and Health Research Methods, Evidence, and Impact, McMaster University as well as a Scientist at the Population Health Research Institute and a nephrologist at St. Joseph's Healthcare Hamilton where he is the Chair of the Clinical Nephrology Research Group. Editing and Show Notes bySophia AmbrusoThe Kidney Connection written and performed by Tim YauShow NotesALCHEMIST (NephJC Shorts, Rossignol et al Lancet 2025)AC is in her 83rd year of med-peds fellowship.Joel's monologue brings us all down.Prophylactic ICD therapy doesn't improve sudden cardiac death or all-cause mortality in HD patients in the ICD2 trial (Jukema JW et al. Circulation 2019)Initiation with statins do not impact MACE endpoints or atherosclerotic events (4D AURORA trial Fellstrom BC et al. NEJM 2009 & SHARP trial Baigent C et al. Lancet 2011)Mike tries to liven up the mood by mentioning positive outcomes with iron therapy in heart failure with the PIVOTAL trial (Macdougall IC et al. NEJM 2018)TOPHAT trial revealed treatment with spironolactone in HFpEF did not affect MACE outcomes. (Pitt B et al. NEJM 2014)NephTrials ‘Run-in periods in clinical trials: What can we ACHIEVE?'SPIN D trial - spironolactone dose finding trial in ESRD (Charytan DM et al. Kidney Int 2018)Mike shares the human experience of the trial after being instructed to end the trial prematurely and being told they have “answered their question”Study in Japan - spironolactone predominantly benefits male over females (cannot find this)Male vs female benefit not observed in ACHIEVE despite Mike's initial hypothesisSwap compares and contrasts ACHIEVE, ALCHEMIST & Meta-analysis (Pyne L et al. Lancet 2025)Mike discusses how nonadherence to spironolactone impacted the intention to treat outcomes in the trial.What is a high risk of bias for dummies?Mike, Swap & Joel ponder future nsMRA or ASI trials hemodialysis?Tubular secretionsSwap is probably stalking Martha Wells by now, has moved on from Witch King, now onto Queen Demon on Good ReadsAC is adding to her brood, 2 dogs (Snickers & Harper), 1 childDungeon Crawler Call - a science fantasy book series by Matt Dinniman (on goodreads), which he lovingly referred to as complete nerd trash.Joel is binging on the series Task on HBO max, featuring Mark Ruffalo as FBI agent.NephJC is having its annual fundraiser (get your tickets here) at ASN. Providing a party shuttle that is leaving every 30 minutes from the conference center. As always, it will feature a live podcast recording covering the ASN late breaking, high impact clinical trials.Swap describes the high impact model at ASN this year - go big or go home.
JACC Editor-in-Chief Harlan M. Krumholz, MD, SM, introduces the October 21, 2025 issue of JACC, which is devoted entirely to Dr. Milton Packer's adipokine hypothesis. Dr. Krumholz explains the rationale behind dedicating the issue to this bold conceptual framework, which proposes that dysfunctional visceral fat and its secreted adipokines drive HFpEF. We're also thrilled to present readers with 10 accompanying expert commentaries that explore, challenge, and contextualize the hypothesis.
This episode covers: Cardiology This Week: A concise summary of recent studies Visceral adiposity: paradigm shift in HFpEF management Artificial Intelligence in echocardiography Milestones: ISIS-2 Host: Susanna Price Guests: Carlos Aguiar, Milton Packer, Rudolf de Boer Want to watch the episode? Go to: https://esc365.escardio.org/event/2175 Want to watch the extended interview on AI in echocardiography? Go to: https://esc365.escardio.org/event/2175?resource=interview Disclaimer: ESC TV Today is supported by Bristol Myers Squibb and Novartis. This scientific content and opinions expressed in the programme have not been influenced in any way by its sponsors. This programme is intended for health care professionals only and is to be used for educational purposes. The European Society of Cardiology (ESC) does not aim to promote medicinal products nor devices. Any views or opinions expressed are the presenters' own and do not reflect the views of the ESC. The ESC is not liable for any translated content of this video. The English language always prevails. Declarations of interests: Stephan Achenbach, Yasmina Bououdina, Nicolle Kraenkel and Susanna Price have declared to have no potential conflicts of interest to report. Carlos Aguiar has declared to have potential conflicts of interest to report: personal fees for consultancy and/or speaker fees from Abbott, AbbVie, Alnylam, Amgen, AstraZeneca, Bayer, BiAL, Boehringer-Ingelheim, Daiichi-Sankyo, Ferrer, Gilead, GSK, Lilly, Novartis, Pfizer, Sanofi, Servier, Takeda, Tecnimede. John-Paul Carpenter has declared to have potential conflicts of interest to report: stockholder Mycardium AI. Davide Capodanno has declared to have potential conflicts of interest to report: Bristol Myers Squibb, Daiichi Sankyo, Sanofi Aventis, Novo Nordisk, Terumo. Rudolf de Boer has declared to have potential conflicts of interest to report: the institution of Rudolf de Boer has received research grants and/or fees from Alnylam, AstraZeneca, Abbott, Bristol-Myers Squibb, NovoNordisk, and Roche; Rudolf de Boer has had speaker engagements with and/or received fees from and/or served on an advisory board for Abbott, AstraZeneca, Bristol Myers Squibb, NovoNordisk, Roche, and Zoll; Rudolf de Boer received travel support from Abbott and NovoNordisk. Konstantinos Koskinas has declared to have potential conflicts of interest to report: honoraria from MSD, Daiichi Sankyo, Sanofi. Milton Packer has declared to have potential conflicts of interest to report: 89bio, Abbvie, Actavis, Altimmune, Alnylam, Amarin, Amgen, Ardelyx, ARMGO, AstraZeneca, Attralus, Biopeutics, Boehringer Ingelheim, Caladrius, Casana, CSL Behring, Cytokinetics, Daiichi Sankyo, Imara, Lilly, Medtronic, Moderna, Novartis, NovoNordisk, Pharmacocosmos, Regeneron, Roche, Salamandra. Steffen Petersen has declared to have potential conflicts of interest to report: consultancy for Circle Cardiovascular Imaging Inc. Calgary, Alberta, Canada. Emma Svennberg has declared to have potential conflicts of interest to report: Abbott, Astra Zeneca, Bayer, Bristol-Myers, Squibb-Pfizer, Johnson & Johnson.
On this episode of JHLT: The Podcast, the Digital Media Editors invite author Dr. Ayumi Goda, from the Kyorin University Hospital in Tokyo, Japan, to discuss her team's paper, “Prevalence of occult HFpEF and age-specific efficacy of passive leg raise in pulmonary hypertension.” The discussion explores: How clinical observations led to the idea for a study on whether the passive leg raise could unmask occult HFpEF The potential diagnostic value of the passive leg raise in differing patient populations Age-specific cutoffs that may influence what kind of testing to use in clinical practice For the latest studies from JHLT, visit www.jhltonline.org/current, or, if you're an ISHLT member, access your Journal membership at www.ishlt.org/jhlt. Don't already get the Journal and want to read along? Join the International Society of Heart and Lung Transplantation at www.ishlt.org for a free subscription, or subscribe today at www.jhltonline.org.
In this episode, Dr. Harlan Krumholz reviews the September 9, 2025 issue of JACC, covering key studies on artificial intelligence in cardiovascular research, the effects of tirzepatide in heart failure with preserved ejection fraction (HFpEF), and how social, racial, and genetic factors influence heart failure risk. He discusses the growing burden of heart failure in the elderly, the need to disaggregate data in Asian American and Pacific Islander populations, and the role of rare genetic variants in atrial fibrillation outcomes. The episode also features perspectives on clinical trial design, complex case reports, and emphasizes the need for AI submissions to meet high standards of clinical relevance, feasibility, and long-term impact.
Please visit answersincme.com/QWE860 to participate, download slides and supporting materials, complete the post test, and obtain credit. In this activity, an expert in cardiology discusses the evolving role of mineralocorticoid receptor antagonists (MRAs) to treat patients with heart failure. Upon completion of this activity, participants should be better able to: Identify the evolving role of mineralocorticoid receptor antagonists (MRAs) to treat patients with heart failure; Evaluate clinical implications of the latest data on nonsteroidal MRAs for the treatment of heart failure and mildly reduced ejection fraction (HFmrEF) or heart failure and preserved ejection fraction (HFpEF), in the context of current standard-of-care; and Describe strategies to incorporate nonsteroidal MRAs into the treatment plans of patients with HFmrEF or HFpEF.
Interview with Margaret Infeld, MD, MS, author of Clinical Outcomes With Personalized Accelerated Physiologic Pacing in Heart Failure With Preserved Ejection Fraction: Follow-Up of the myPACE Trial. Hosted by Robert Bonow, MD. Related Content: Clinical Outcomes With Personalized Accelerated Physiologic Pacing in Heart Failure With Preserved Ejection Fraction
Interview with Margaret Infeld, MD, MS, author of Clinical Outcomes With Personalized Accelerated Physiologic Pacing in Heart Failure With Preserved Ejection Fraction: Follow-Up of the myPACE Trial. Hosted by Robert Bonow, MD. Related Content: Clinical Outcomes With Personalized Accelerated Physiologic Pacing in Heart Failure With Preserved Ejection Fraction
Join us as we review recent practice-changing articles on cannabidiol (CBD)-induced liver injury, IV iron for HFrEF, bedtime administration of blood pressure meds, carpal tunnel syndrome & rheumatoid arthritis , & FDA approval of finerenone for HFpEF. Fill your brain hole with a delicious stack of hotcakes! Featuring Paul Williams (@PaulNWilliamz), Rahul Ganatra (@rbganatra), Nora Taranto (@norataranto) and Matt Watto (@doctorwatto). Claim CME for this episode at curbsiders.vcuhealth.org! Patreon | Episodes | Subscribe | Spotify | YouTube | Newsletter | Contact | Swag! | CME Credits Written and Hosted by: Rahul Ganatra MD, MPH; Nora Taranto MD, Paul Williams, MD, FACP, Matthew Watto MD, FACP Cover Art: Rahul Ganatra MD, MPH Reviewer: Emi Okamoto, MD Technical Production: Pod Paste Showrunners: Matthew Watto MD, FACP; Paul Williams MD, FACP Show Segments Intro, disclaimer CBD-induced liver injury IV Iron in HFrEF Bedtime administration of BP medications Carpal tunnel syndrome and RA FDA approves Finerenone for HFpEF Outro Sponsor: Permanente Want to join thousands of physicians who've made TPMG their career destination? Discover more at northerncalifornia.permanente.org
CardioNerds (Drs. Rick Ferraro and Georgia Vasilakis Tsatiris) discuss ATTR cardiac amyloidosis with expert Dr. Justin Grodin. This episode is a must-listen for all who want to know how to diagnose and treat ATTR with current available therapies, as well as management of concomitant diseases through a multidisciplinary approach. We take a deep dive into the importance of genetic testing, not only for patients and families, but also for gene-specific therapies on the horizon. Dr. Grodin draws us a roadmap, guiding us through new experimental therapies that may reverse the amyloidosis disease process once and for all. Audio editing by CardioNerds academy intern, Christiana Dangas. This episode was developed in collaboration with the American Society of Preventive Cardiology and supported by an educational grant from BridgeBio. 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 Cardiac Amyloid PageCardioNerds Episode Page Pearls: You must THINK about your patient having amyloid to recognize the pattern and make the diagnosis. Start with a routine ECG and TTE, and look for a disproportionately large heart muscle with relatively low voltages on the ECG. Before you diagnose ATTR amyloidosis, AL amyloidosis must be ruled out (or ruled in) with serum light chains, serum/urine immunofixation, and/or tissue biopsy. Genetic testing is standard of care for all patients and families with ATTR amyloidosis, and the future is promising for gene-specific treatments. Current FDA-approved treatments for TTR amyloidosis are TTR stabilizers and TTR silencers, but TTR fibril-depleting agents are on their way. Early diagnosis of ATTR affords patients maximal benefit from current amyloidosis therapies. TTR amyloidosis patients require a multidisciplinary approach for success, given the high number of concomitant diseases with cardiomyopathy. Notes: Notes: Notes drafted by Dr. Georgia Vasilakis Tsatiris. What makes you most suspicious of a diagnosis of cardiac amyloidosis from the typical heart failure patient? You must have a strong index of suspicion, meaning you THINK that the patient could have cardiac amyloidosis, to consider it diagnostically. Some characteristics or “red flags” to not miss: Disproportionately thick heart muscle with a relatively low voltages on EKG Bilateral carpal tunnel syndrome – estimated that 1 in 10 people >65 years old will have amyloidosis Previously tolerated antihypertensive medications Atraumatic biceps tendon rupture Bilateral carpal tunnel syndrome Spinal stenosis Concomitant with other diseases: HFpEF, low-flow low-gradient aortic stenosis How would you work up a patient for cardiac amyloidosis? Start with a routine ECG (looking for disproportionally low voltage) and routine TTE (looking for thick heart muscle) CBC, serum chemistries, hepatic function panel, NT proBNP, and troponin levels NOTE: It is critical to differentiate between amyloid light chain (AL amyloidosis) and transthyretin ATTR amyloidosis, as both make up 95-99% of amyloidosis cases. Obtain serum free light chains, serum & urine electrophoresis, and serum & urine immunofixation to rule out AL amyloidosis. (See table below) AL Amyloidosis ATTR Amyloidosis → Positive serum free light chains and immunofixation (Abnormal M protein) → Tissue biopsy (endomyocardial, fat pad) to confirm diagnosis → Negative serum free light chains and immunofixation (ruled out AL amyloidosis) → Cardiac scintigraphy (Technetium pyrophosphate with SPECT imaging) What treatment options do we have to offer now for ATTR CM, and how has this compared to prior years? Before 2019, treatment options were limited outside of cardiac tr...
Welcome to my podcast. I am Doctor Warrick Bishop, and I want to help you to live as well as possible for as long as possible. I'm a practising cardiologist, best-selling author, keynote speaker, and the creator of The Healthy Heart Network. I have over 20 years as a specialist cardiologist and a private practice of over 10,000 patients. Dr. Warick Bishop, a cardiologist and CEO of the Healthy Heart Network, invites Dr. Fiona Foo, a cardiologist specializing in heart failure, to discuss heart failure with preserved ejection fraction (HFpEF). HFpEF is defined as the heart's inability to relax well, leading to symptoms like shortness of breath and fluid buildup. Risk factors for HFpEF include age, hypertension, obesity, diabetes, and certain medical conditions like chronic kidney disease and chronic obstructive pulmonary disease. Women, especially after menopause, are at higher risk due to specific factors like pregnancy-related hypertensive disorders. The podcast concludes with a teaser for a part two episode focusing on HFpEF management and prevention strategies. Dr. Bishop emphasizes the importance of feedback and sharing the podcast to help raise awareness about heart health.
Drs. Rick Ferraro and Sneha Nandy discuss ‘Diagnosis of ATTR Cardiac Amyloidosis' with Dr. Venkatesh Murthy. In this episode, we explore the diagnosis of ATTR cardiac amyloidosis, a condition once considered rare but now increasingly recognized due to advances in imaging and the availability of effective therapies. Dr. Venkatesh Murthy, a leader in multimodality imaging, discusses key clinical and laboratory features that should raise suspicion for the disease. We also examine the role of nuclear imaging and genetic testing in confirming the diagnosis, as well as the importance of early detection. Tune in for expert insights on navigating this challenging diagnosis and look out for our next episode on treatment approaches for cardiac amyloidosis! Audio editing for this episode was performed by CardioNerds Intern, Julia Marques Fernandes. 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 Cardiac Amyloid PageCardioNerds Episode Page Pearls: - Diagnosis of Transthyretin amyloid cardiomyopathy 1. Recognizing the Red Flags – ATTR cardiac amyloidosis often presents with subtle but telling signs, such as bilateral carpal tunnel syndrome, low-voltage ECG, and a history of lumbar spinal stenosis or biceps tendon rupture. If you see these features in a patient with heart failure symptoms, think amyloidosis! 2. “Vanilla Ice Cream with a Cherry on Top” – On strain echocardiography, apical sparing is a classic pattern for cardiac amyloidosis. While helpful, it's not foolproof—multimodal imaging and clinical suspicion are key! 3. Nuclear Imaging is a Game-Changer – When suspicion for cardiac amyloidosis is high à a positive PYP scan with SPECT imaging (grade 2 or 3 myocardial uptake) in the absence of monoclonal protein (ruled out by SPEP, UPEP, and free light chains) is diagnostic for ATTR amyloidosis—no biopsy needed! 4. Wild-Type vs. Hereditary? Know the Clues – Older patients (70+) are more likely to have wild-type ATTR, while younger patients (40s-60s), especially those with neuropathy and a family history of heart failure, should raise suspicion for hereditary ATTR. Genetic testing is crucial for distinguishing between the two. Note that some ATTR variants may predispose to a false negative PYP scan! 5. Missing Amyloidosis = Missed Opportunity – With multiple disease-modifying therapies now available, early diagnosis is critical. If you suspect cardiac amyloidosis, don't delay the workup—early treatment improves outcomes! Notes - Diagnosis of Transthyretin amyloid cardiomyopathy What clinical features should raise suspicion for ATTR cardiac amyloidosis? ATTR cardiac amyloidosis is underdiagnosed because symptoms overlap with other forms of heart failure. Red flags include bilateral carpal tunnel syndrome (often years before cardiac symptoms), low-voltage ECG despite increased LV wall thickness, heart failure with preserved ejection fraction (HFpEF) with a restrictive pattern, and history of lumbar spinal stenosis, biceps tendon rupture, and/or peripheral neuropathy, including possible autonomic dysfunction (e.g., orthostatic hypotension). Remember: If an older patient presents with heart failure and unexplained symptoms like neuropathy or musculoskeletal issues, think amyloidosis! What is the differential diagnosis for a thick left ventricle (LVH) and how does ATTR amyloidosis fit into it? Hypertension: Most common cause of LVH, typically with a history of uncontrolled high blood pressure. Aortic stenosis: May present with concentric LVH. Hypertrophic cardiomyopathy (HCM): Genetic disorder typically presenting with asymmetric LVH, especially in younger patients. Infiltrative cardiomyopathy: Often due to amyloidosis, sarcoidosis,
In this episode of JACC This Week, Editor-in-Chief Dr. Harlan Krumholz introduces the journal's new design and highlights key studies from the July 29, 2025 issue. Topics include the under-expansion analysis of the ACURATE NEO2 valve, the impact of tirzepatide in obesity-related HFpEF, the effects of private equity ownership on heart failure care, and evolving strategies for managing multivalve disease.
In this episode of Medicine Grand Rounders, Dr. Sanjeeb Bhattacharya - Director of the HFpEF clinic and Associate Program Director of the HVTI heart failure fellowship - goes over various clinical presentations of heart failure with preserved ejection fraction. Moderated by: Yasmine K. Elghoul, MD
Listener feedback on cardiac sarcoidosis, out-of-hospital cardiac arrest, less is more when it comes to post-stent antiplatelets, lipoprotein(a), and atrial fibrillation in HFpEF are discussed by John Mandrola, MD, in this week's podcast. This podcast is intended for healthcare professionals only. To read a partial transcript or to comment, visit: https://www.medscape.com/twic I Listener Feedback Mathijssen https://doi.org/10.1093/eurheartj/ehaf338 Poyhonen https://doi.org/10.1161/CIRCEP.124.013239 II News in out of hospital cardiac arrest AHA Press Release https://newsroom.heart.org/news/nfl-safety-justin-reid-expands-cpr-education-for-youth-through-summer-program Chan et al https://www.ahajournals.org/doi/abs/10.1161/CIRCOUTCOMES.124.011799 III Post-Stent Antiplatelet 4D ACS trial https://eurointervention.pcronline.com/article/one-month-dual-antiplatelet-therapy-followed-by-prasugrel-monotherapy-at-a-reduced-dose-the-4d-acs-randomised-trial IV Lp(a) and the new PREVENT equation for Predicting cardiac events Aug 02, 2024 This Week in Cardiology Podcast https://www.medscape.com/viewarticle/1001429 Bhatia et al https://jamanetwork.com/journals/jamacardiology/fullarticle/2835022 V AF in HFpEF Saksena et al https://doi.org/10.1093/europace/euad095 You may also like: The Bob Harrington Show with the Stephen and Suzanne Weiss Dean of Weill Cornell Medicine, Robert A. Harrington, MD. https://www.medscape.com/author/bob-harrington Questions or feedback, please contact news@medscape.net
In this episode, CardioNerds Dr. Anna Radakrishnan and Dr. Apoorva Gangavelli are joined by prevention expert Dr. Martha Gulati and heart failure expert Dr. Anu Lala to discuss heart failure with preserved ejection fraction (HFpEF), a multifactorial, evolving challenge, particularly in women. In this episode, we delve into the distinctive clinical presentation and pathophysiology of HFpEF among women, exploring both traditional and gender-specific risk factors, from metabolic and inflammatory processes to the impact of obesity, sleep apnea, and gender-specific conditions. We also discussed the latest evidence on prevention strategies and emerging therapies that not only target HFpEF symptoms but also address underlying risk factors. This conversation highlights the importance of multidisciplinary, holistic care to advance diagnosis, management, and ultimately, patient outcomes for women with HFpEF. Audio editing by CardioNerds academy intern, Christiana Dangas. 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 - HFpEF in Women HFpEF Is a Multisystem Syndrome:HFpEF in women involves more than just diastolic dysfunction—it represents a convergence of metabolic, inflammatory, and hormonal factors that make its diagnosis and management uniquely challenging. Visceral Adiposity Drives Risk:Obesity isn't just excess weight; central or visceral adiposity actively promotes inflammation, insulin resistance, and microvascular dysfunction, which are crucial in triggering HFpEF in women. Early Identification Is Key:Recognizing—and treating—subtle risk factors such as sleep-disordered breathing, hypertension, and subtle metabolic dysfunction early, especially in women who may underreport symptoms, can prevent progression to HFpEF. Holistic, Lifespan Approach Matters:Effective HFpEF care involves managing the whole cardiometabolic profile with tailored lifestyle interventions, advanced medications (e.g., SGLT2 inhibitors, GLP-1 agonists), and even cardiac rehabilitation, which remain critical at every stage, even after diagnosis. Tailoring Prevention to Unique Risks in Women:Gender-specific factors such as postmenopausal hormonal changes, pregnancy-related complications, and autoimmune conditions demand a customized prevention strategy, reminding us that prevention isn't one-size-fits-all. Show notes - HFpEF in Women Notes drafted by Dr. Apoorva Gangavelli 1. What are the gender-based differences in HFpEF presentation? HFpEF in women often presents with more subtle symptoms such as exertional dyspnea and fatigue, which may be mistakenly attributed to aging or obesity. Women tend to have a higher prevalence of preserved ejection fraction despite a similar heart failure symptom burden to men. The diagnostic challenge is compounded by lower natriuretic peptide levels influenced by hormonal factors, particularly postmenopausal estrogen deficiency, leading to false negatives and underdiagnosis. 2. How do traditional and gender-specific risk factors contribute to the development of HFpEF in women? Traditional risk factors include obesity, hypertension, diabetes, and metabolic syndrome. Gender-specific risk factors encompass pregnancy-related complications, menopause, and autoimmune diseases, which may uniquely affect cardiovascular structure and function in women. The interaction between visceral adiposity and systemic inflammation is central in predisposing women to HFpEF. 3. What underlying pathophysiological mechanisms make women more susceptible to HFpEF? Chronic inflammation and endothelial dysfunction contribute to myocardial stiffness and diastolic dysfunction. ...
CardioNerds Cardiac Amyloidosis Series Chair Dr. Rick Ferraro and Episode Lead Dr. Anna Radakrishnan discuss the biology of transthyretin amyloid cardiomyopathy (ATTR-CM ) with Dr. Daniel Judge. Notes were drafted by Dr. Anna Radakrishnan. The audio was engineered by student Dr. Julia Marques. This episode provides a comprehensive overview of transthyretin (ATTR) cardiac amyloidosis, a complex and rapidly evolving disease process. The discussion covers the key red flags for cardiac amyloidosis, the diagnostic pathway, and the implications of hereditary versus wild-type ATTR. Importantly, the episode delves into the current and emerging therapies for ATTR, including stabilizers, gene silencers, and promising treatments like CRISPR-Cas9 and antibody-based approaches. Dr. Judge shares his insights and excitement about the rapidly advancing field, highlighting the need for early diagnosis and the potential to improve long-term outcomes for patients with this condition. 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 Cardiac Amyloid PageCardioNerds Episode Page Pearls: - Biology of Transthyretin amyloid cardiomyopathy Maintain a high index of suspicion! Look for subtle (yet telling) signs like ventricular hypertrophy, discordant EKG findings, bilateral carpal tunnel syndrome, and spontaneous biceps tendon rupture. Utilize the right diagnostic tests. Endomyocardial biopsy remains the gold standard, but non-invasive tools like PYP scan with SPECT imaging and genetic testing are essential for accurate diagnosis. Differentiating hereditary from wild-type ATTR is critical, as genetic forms may have a more aggressive course and familial implications. Early diagnosis and intervention significantly improve prognosis, making vigilance in screening and prompt treatment initiation essential. The future is now! Cutting-edge therapies are transforming the treatment landscape, including TTR stabilizers, gene silencers, and emerging technologies like CRISPR-Cas9 and antibody-based treatments. Notes - Biology of Transthyretin amyloid cardiomyopathy What is transthyretin amyloid (aTTR) and how is it derived? Transthyretin (TTR) is a transport protein primarily synthesized by the liver, responsible for carrying thyroid hormones (thyroxine) and retinol (vitamin A) in the blood. It circulates as a tetramer, composed of four identical monomers, which is essential for its stability and function. In transthyretin amyloid (ATTR) amyloidosis, the TTR protein becomes unstable, leading to its dissociation into monomers. These monomers misfold and aggregate into insoluble amyloid fibrils, which deposit extracellularly in tissues such as the heart, nerves, and gastrointestinal tract. This progressive amyloid deposition leads to organ dysfunction, including restrictive cardiomyopathy and neuropathy. There are two main forms of ATTR amyloidosis: hereditary (variant) and wild-type (senile) ATTR. Hereditary ATTR (ATTRv) is caused by mutations in the TTR gene. These mutations destabilize the TTR tetramer, making it more prone to dissociation. This increases misfolding and amyloid fibril formation, resulting in systemic amyloid deposition. Wild-type ATTR (ATTRwt) occurs without genetic mutations and is primarily age-related. Over time, even normal TTR tetramers can become unstable, leading to gradual misfolding and amyloid deposition, particularly in the heart. ATTRwt is a common but often underdiagnosed cause of heart failure with preserved ejection fraction (HFpEF) in elderly individuals. How does aTTR lead to deleterious effects in the heart and other organ systems? Transthyretin amyloidosis leads to organ dysfunction through the deposition of misfolded TTR protein as amyloid fib...
Renal denervation, the obesity paradox, JACC and the FINEARTS trial of finerenone in HFpEF, a setback for a PFA system, and coffee are the topics Jon Mandrola, MD, covers this week. This podcast is intended for healthcare professionals only. To read a partial transcript or to comment, visit: https://www.medscape.com/twic I. RDN CMS https://www.cms.gov/medicare-coverage-database/view/ncacal-tracking-sheet.aspx?ncaid=318 Messerli https://doi.org/10.1016/j.jacc.2024.09.1244 Filippone https://doi.org/10.1016/j.amjmed.2023.05.010 II. Finerenone FINEHEARTS -HF NEJM https://www.nejm.org/doi/full/10.1056/NEJMoa2407107 FIDELIO-DKD https://www.nejm.org/doi/full/10.1056/NEJMoa2025845 FIGARO-DKD https://www.nejm.org/doi/full/10.1056/NEJMoa2110956 Why Have We Not Been Able to Demonstrate Reduced Mortality in Patients With HFmrEF/HFpEF? https://doi.org/10.1016/j.jacc.2024.08.033 Regional Variation TOPCAT https://www.ahajournals.org/doi/10.1161/circulationaha.114.013255 Time from WHF Subanalysis https://doi.org/10.1016/j.jacc.2024.09.004 REDEFINE - https://clinicaltrials.gov/study/NCT06008197 Health status paper https://doi.org/10.1016/j.jacc.2024.09.023 Obesity subanalysis https://doi.org/10.1016/j.jacc.2024.10.111 Kidney outcomes https://www.sciencedirect.com/science/article/pii/S0735109724102525 Kidney outcomes 2 https://doi.org/10.1016/j.jacc.2024.11.020 Kaul editorial https://doi.org/10.1016/j.jacc.2024.11.024 III. PFA Setback J&J Halts Varipulse Field Ablation for AFib https://www.medscape.com/viewarticle/j-j-halts-varipulse-field-ablation-afib-2025a10000j8 IV. Coffee Stop the Coffee Studies https://www.medscape.com/viewarticle/883709 Coffee drinking timing and mortality in US adults You may also like: The Bob Harrington Show with the Stephen and Suzanne Weiss Dean of Weill Cornell Medicine, Robert A. Harrington, MD. https://www.medscape.com/author/bob-harrington Questions or feedback, please contact news@medscape.net
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