Podcasts about hfref

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  

This episode covers: Cardiology This Week: A concise summary of recent studies Biomarkers in heart failure Digoxin in HFrEF Scientific Highlights from Heart Failure 2026 Host: Wilfried Mullens Guests: Lynne Stevenson, Dirk van Veldhuisen, Theresa McDonagh Want to watch that episode? Go to: https://esc365.escardio.org/event/2565 Disclaimer: ESC TV Today is supported by Novartis through an independent funding. The programme has not been influenced in any way by its funding partner. 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. A ny views or opinions expressed are the presenters' own and do not reflect the views of the ESC. All declarations of interest are listed at the end of the episode. The ESC is not liable for any translated content of this video. The English language always prevails. ESC TV Today uses a range of tools and resources (including AI) to support content production. All content is reviewed and approved by the editorial team. Statements and opinions expressed by guest speakers are their own. Declarations of interests: Stephan Achenbach, Yasmina Bououdina, Nicolle Kraenkel, Dirk van Veldhuisen and Lynne Warner Stevenson 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, Novo Nordisk, Pfizer, Sanofi, Servier, Takeda, Tecnimede, Viatris. 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:Abbott Vascular, Bristol Myers Squibb, Daiichi Sankyo, Edwards Lifesciences, Novo Nordisk, Sanofi Aventis, Terumo. David Duncker has declared to have potential conflicts of interest to report: lecture honoraria from Abbott, Astra Zeneca, Biotronik, Boehringer Ingelheim, Boston Scientifics, Bristol Meyers Squibb, CVRx, Daiichi Sankyo, Medtronic, Microport, Pfizer, Sanofi, Zoll. Konstantinos Koskinas has declared to have potential conflicts of interest to report: honoraria from MSD, Daiichi Sankyo, Sanofi.  Theresa McDonagh has declared to have potential conflicts of interest to report: honoraria from Boeringer Ingelheim. Felix Mahfoud has declared to have potential conflicts of interest to report: research grants from Deutsche Forschungsgemeinschaft (SFB TRR219), Deutsche Gesellschaft für Kardiologie (DGK), Deutsche Herzstiftung, Ablative Solutions, ReCor Medical. Consulting fees, payment honoraria lectures, presentations, speaker, support travel costs: Ablative Solutions, Astra-Zeneca, Novartis, Inari, Recor Medical, Medtronic, Philips, Merck. 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.

Time to quadruple therapy, the disappointing AVANT GUARD trial, PFA risks, the TREAT-PVC trial, and NSTEMI care in the frail elderly 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 Time to Quadruple Therapy in HFrEF Time to Quadruple Therapy After Diagnosis of HFrEF https://jamanetwork.com/journals/jamacardiology/fullarticle/2846899 II AVANT GUARD PFA Bests Meds as First-Line Treatment for Persistent AF in Randomized Trial https://www.medscape.com/viewarticle/pulsed-field-ablation-bests-meds-first-line-treatment-2026a1000dsm Pulsed Field Ablation of AF Disappoints in Setup for Success: AVANT GUARD https://www.medscape.com/viewarticle/pulsed-field-ablation-af-disappoints-setup-success-avant-2026a1000ddt AVANT GUARD Trial https://www.nejm.org/doi/full/10.1056/NEJMoa2600929 Persistent AF: Meta-analysis of Invasive Strategies 10.1016/j.ijcard.2018.11.127 External Link III Speaking of Scary News on PFA – The TIFFANY Study Abstract - The TIFFANY Study https://www.heartrhythmjournal.com/article/S1547-5271(26)01747-9/fulltext Delayed Myocardial Ischemia and Malignant Arrhythmias After PFA https://www.ahajournals.org/doi/10.1161/CIRCULATIONAHA.125.077983 Alberto Alfie Comment https://x.com/ALFIEEP1/status/2050029151315189774?s=20 IV TREAT PVC Trial TREAT-PVC Trial https://doi.org/10.1016/j.jacep.2026.01.011 TREAT-AF Study 2020 https://doi.org/10.1016/j.jacep.2019.11.008 V NSTEMI In Frail Older Patients SENIOR-RITA Trial https://www.nejm.org/doi/10.1056/NEJMoa2407791 Subanalysis of Senior RITA Trial https://jamanetwork.com/journals/jamanetworkopen/fullarticle/2847995 Timing of Invasive Strategy in Patients With Non-ST-Elevation Acute Coronary Syndrome -- Meta-analysis https://doi.org/10.1016/S0140-6736(17)31490-3 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

Focus Issue on trials - atrial fibrillation , HFrEF, ACS , ischaemic stroke & renovascular hypertension

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.

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.

Episode 215: Meth-associated HFrEF.   Abishak and Zat (medical students) explain the cardiotoxic effect of methamphetamine and the diagnosis and treatment of heart failure with reduced ejection fraction (HFrEF). Dr. Arreaza adds insight into the reversibility of meth-associated HFrEF.   Written by Abishak Govindarajan, MSIV and Zat Akbar Shaw. American University of the Caribbean. Edits and comments by Hector Arreaza, MD. Welcome Dr. Arreaza: Welcome to Rio Bravo qWeek. My name is Hector Arreaza, family physician, faculty and associate program director of the Clinica Sierra Vista/Rio Bravo Family Medicine Residency Program. Today we will explore heart failure with reduced ejection fraction, a high-yield and clinically relevant topic in medicine. We will discuss the role of methamphetamine use in the development of HFrEF. This is a pressing issue because about 0.8% of the population 12 and older in the US reported using methamphetamine within the past 12 months in 2024 (National Survey on Drug Use and Health, NSDUH), that's about ≈2.4 million people!We are joined by two aspiring physicians who will help explore this topic. By the way, we will refer to methamphetamine in this episode as “meth”. [Abishak and Akbar introduce themselves] Abishak: [Introduce yourself] The role of meth in HFrEF Dr. Arreaza: Meth is a growing problem in many places, including Bakersfield, where we live. Meth is also known as Meth Crystal, Poor man's cocaine, Ice, Glass, Crank, Speed, Chalk, and Tina. How does meth contribute to the development of HFrEF? Abishak: So, first, let's understand how methamphetamine works. It has a chemical structure similar to dopamine and norepinephrine, and it gets taken up through the neuron transporter proteins. Once it enters the synaptic vesicles (storage sacs for neurotransmitters), it displaces and forces the release of large amounts of dopamine, norepinephrine, and serotonin into the synapse (the space between neurons). Additionally, meth blocks the reuptake of those neurotransmitters into the neuron, ensuring they remain in the synapse for a prolonged period. All this causes a downstream effect of increased sympathetic pathways in the body. Diagnosis Dr. Arreaza: The diagnosis starts with collecting a good history and performing a complete physical exam, and then we confirm with an echocardiogram.  Abishak: Yes, diagnosis requires both symptoms consistent with heart failure and objective evidence of reduced ejection fraction. Echocardiography is the primary diagnostic tool. We also measure BNP. In certain cases, cardiac MRI is used to evaluate myocardial fibrosis and exclude infiltrative or inflammatory etiologies. Coronary angiography may be performed if ischemic disease is suspected.Guideline-Directed Medical Therapy Dr. Arreaza: GDMT Guideline-Directed Medical Therapy started around 1987 when ACE inhibitors were proven to improve mortality in patients with heart failure. Then, during the following decades, many medications have been added to GDMT. Until around 2019–2022 we came out with the main 4 groups of medications that we know as GDMT. Let's talk about GDMT. Akbar: There are four core pillars in GDMT. First, an angiotensin receptor-neprilysin inhibitor, such as sacubitril with valsartan (Entresto), is preferred over ACE inhibitors when tolerated. This medication reduces mortality and heart failure hospitalizations. Second, evidence-based beta blockers including carvedilol, metoprolol succinate, or bisoprolol are used to reduce sympathetic overactivity and improve ventricular remodeling. Third, mineralocorticoid receptor antagonists such as spironolactone or eplerenone reduce fibrosis and improve survival. The Fourth pillar is SGLT2 inhibitors such as dapagliflozin or empagliflozin, which provide significant reductions in heart failure hospitalizations and cardiovascular mortality, regardless of diabetes status. Abishak: Other main parts of the treatment are diuretics, which are used for symptom control but do not reduce long-term mortality. Dr. Arreaza: As a recap: The current 4 pillars of GDMT are: ARNI/ACEi + β-blocker + MRA + SGLT2i)  Beta Blocker Considerations Dr. Arreaza: Sometimes we may be concerned about using beta blockers in active meth users. What did you read about it? Abishak: Historically, there was concern about unopposed alpha stimulation. However, in chronic heart failure, beta blockers remain essential. Carvedilol is often favored because it provides both alpha and beta blockade. Careful titration and close monitoring are critical.Reversibility and Remodeling Dr. Arreaza: Regarding meth-associated HFrEF, we have good news for meth users. Tell us about how reversible this condition is.  Akbar: It can be reversible. One of the most important aspects of this condition is that significant reverse remodeling may occur if the patient stops methamphetamine use and adheres to medical therapy. The Left ventricular ejection fraction can improve substantially and, in some cases, normalize. On the other end of the spectrum, continued meth use may lead to progressive fibrosis, ventricular dilation, and potentially irreversible damage, leading to death.Complications of meth-associated HFrEF Abishak: These patients are at increased risk for ventricular arrhythmias, sudden cardiac death, left ventricular thrombus formation, and progressive pulmonary hypertension. If the ejection fraction remains below 35 percent after at least three months of optimized therapy, implantable cardioverter-defibrillator (known as ICD) placement should be considered for primary prevention.Addiction Treatment as Core Therapy Dr. Arreaza: It sounds like GDMT cannot be done without talking about meth use disorder treatment. Akbar: Absolutely. Treating the myocardium without addressing the substance use disorder is ineffective. Primary care providers can be trained to manage addictions, but if resources are available, you can place a referral to addiction medicine, psychiatric support, behavioral therapy, and social support services. This is an essential part of the treatment. Sustained abstinence is the single most powerful predictor of recovery.Prognosis Abishak: Prognosis is highly dependent on abstinence. Patients who stop using methamphetamine often experience meaningful improvement in EF and even return to normal.  Dr. Arreaza: Yes, the key factor is complete abstinence, plus standard heart failure treatment. If the damage is mostly functional and inflammatory, recovery is possible. If there is extensive fibrosis (scar) recovery is less likely. Observational studies have shown that patients with meth-associated cardiomyopathy who stop using meth have significant improvement in EF over 3–12 months, fewer hospitalizations, and lower mortality. Akbar: Absolutely. Not all meth-associated cardiomyopathy behaves the same way. The extent of fibrosis determines recovery potential. Cardiac MRI with late gadolinium enhancement can help us estimate scar burden. Patients with minimal fibrosis often have better improvement with abstinence and medical therapy. Dr. Arreaza: So, MRI can actually help us determine the prognosis. Abishak: Yes, very much so. If MRI shows extensive fibrosis, the likelihood of full EF recovery is lower. That information helps us counsel patients more accurately. Akbar: Another key issue is right ventricular involvement. Methamphetamine can affect both ventricles. When the right ventricle fails, patients may develop severe peripheral edema, ascites, and hepatic congestion. Right ventricular dysfunction also worsens prognosis significantly. Dr. Arreaza: And pulmonary hypertension can also worsen the whole picture.  Akbar: That's correct. Meth is associated with pulmonary arterial hypertension independently of left-sided heart failure. In some patients, you may see a combined picture of both pulmonary vascular disease and right ventricular dysfunction. That can make management more complicated because pulmonary pressures may remain elevated even after EF improves. Dr. Arreaza: Tells us about the role of BNP in monitoring these patients.  Abishak: Serial BNP levels can help track response to therapy. Additionally, troponin may be elevated at times in meth users due to myocardial injury. Monitoring renal function is critical because many heart failure medications affect kidney function and potassium levels. Akbar:Other lifestyle modifications include sodium restriction, regular follow-ups, vaccination, and avoidance of other cardiotoxic substances such as alcohol or cocaine. Sleep disorders, especially OSA, should be evaluated because untreated OSA worsens heart failure outcomes. Dr. Arreaza: WhatIs there any role for wearable devices or remote monitoring? Abishak: Yes, increasingly so. Remote weight monitoring, blood pressure tracking, and symptom reporting can reduce hospitalization. In select patients, implantable hemodynamic monitors may help detect rising filling pressures before symptoms occur. Dr. Arreaza: It was a great discussion. Thank you, Abishak and Akbar for bringing all that valuable information to us. Let's wrap it up.     

CME credits: 0.75 Valid until: 13-02-2027 Claim your CME credit at https://reachmd.com/programs/cme/safety-clinical-integration-and-the-emerging-fifth-pillar-in-hf-practice/54635/ Patients with heart failure with reduced ejection fraction (HFrEF) who have not experienced a recent worsening event pose a major clinical challenge: persistent and under-recognized cardiovascular (CV) risk. Recent findings show that these patients carry significant annual rates of CV death and heart failure (HF) hospitalization, despite adherence to quadruple guideline-directed medical therapy (GDMT) and device support. For cardiologists, the challenge is twofold: accurately identifying high-risk individuals without overt clinical deterioration and knowing when and how to intensify therapy in patients who appear stable but remain vulnerable. Recent data show that soluble guanylate cyclase (sGC) may provide significant reductions in CV death and all-cause mortality, particularly in individuals with moderately elevated NT-proBNP (≤6,000 pg/mL). These findings are especially important because this population is far more common in routine cardiology practice and has historically been overlooked in discussions of additional therapy. However, cardiologists often underestimate risk in these ambulatory patients and may hesitate to add therapies when GDMT appears to be working well. Tune in to learn best practices for patient selection and the implementation of added sGC therapy.

CME credits: 0.75 Valid until: 13-02-2027 Claim your CME credit at https://reachmd.com/programs/cme/evidence-at-a-glance-the-totality-of-evidence-impacting-clinical-decision-making-in-patients-with-hfref-without-a-recent-worsening-event/54634/ Patients with heart failure with reduced ejection fraction (HFrEF) who have not experienced a recent worsening event pose a major clinical challenge: persistent and under-recognized cardiovascular (CV) risk. Recent findings show that these patients carry significant annual rates of CV death and heart failure (HF) hospitalization, despite adherence to quadruple guideline-directed medical therapy (GDMT) and device support. For cardiologists, the challenge is twofold: accurately identifying high-risk individuals without overt clinical deterioration and knowing when and how to intensify therapy in patients who appear stable but remain vulnerable. Recent data show that soluble guanylate cyclase (sGC) may provide significant reductions in CV death and all-cause mortality, particularly in individuals with moderately elevated NT-proBNP (≤6,000 pg/mL). These findings are especially important because this population is far more common in routine cardiology practice and has historically been overlooked in discussions of additional therapy. However, cardiologists often underestimate risk in these ambulatory patients and may hesitate to add therapies when GDMT appears to be working well. Tune in to learn best practices for patient selection and the implementation of added sGC therapy.

CME credits: 0.75 Valid until: 13-02-2027 Claim your CME credit at https://reachmd.com/programs/cme/do-not-delay-timing-triggers-and-identifying-the-right-patient-for-additional-therapies-in-hfref/54633/ Patients with heart failure with reduced ejection fraction (HFrEF) who have not experienced a recent worsening event pose a major clinical challenge: persistent and under-recognized cardiovascular (CV) risk. Recent findings show that these patients carry significant annual rates of CV death and heart failure (HF) hospitalization, despite adherence to quadruple guideline-directed medical therapy (GDMT) and device support. For cardiologists, the challenge is twofold: accurately identifying high-risk individuals without overt clinical deterioration and knowing when and how to intensify therapy in patients who appear stable but remain vulnerable. Recent data show that soluble guanylate cyclase (sGC) may provide significant reductions in CV death and all-cause mortality, particularly in individuals with moderately elevated NT-proBNP (≤6,000 pg/mL). These findings are especially important because this population is far more common in routine cardiology practice and has historically been overlooked in discussions of additional therapy. However, cardiologists often underestimate risk in these ambulatory patients and may hesitate to add therapies when GDMT appears to be working well. Tune in to learn best practices for patient selection and the implementation of added sGC therapy.

CME credits: 0.75 Valid until: 13-02-2027 Claim your CME credit at https://reachmd.com/programs/cme/gdmt-is-working-fine-why-add-more-therapies-the-clinical-rationale-for-layering-therapies-in-patients-with-hfref/54632/ Patients with heart failure with reduced ejection fraction (HFrEF) who have not experienced a recent worsening event pose a major clinical challenge: persistent and under-recognized cardiovascular (CV) risk. Recent findings show that these patients carry significant annual rates of CV death and heart failure (HF) hospitalization, despite adherence to quadruple guideline-directed medical therapy (GDMT) and device support. For cardiologists, the challenge is twofold: accurately identifying high-risk individuals without overt clinical deterioration and knowing when and how to intensify therapy in patients who appear stable but remain vulnerable. Recent data show that soluble guanylate cyclase (sGC) may provide significant reductions in CV death and all-cause mortality, particularly in individuals with moderately elevated NT-proBNP (≤6,000 pg/mL). These findings are especially important because this population is far more common in routine cardiology practice and has historically been overlooked in discussions of additional therapy. However, cardiologists often underestimate risk in these ambulatory patients and may hesitate to add therapies when GDMT appears to be working well. Tune in to learn best practices for patient selection and the implementation of added sGC therapy.

CME credits: 0.75 Valid until: 13-02-2027 Claim your CME credit at https://reachmd.com/programs/cme/when-gdmt-isnt-enough-understanding-residual-risk-in-patients-with-hfref/51036/ Patients with heart failure with reduced ejection fraction (HFrEF) who have not experienced a recent worsening event pose a major clinical challenge: persistent and under-recognized cardiovascular (CV) risk. Recent findings show that these patients carry significant annual rates of CV death and heart failure (HF) hospitalization, despite adherence to quadruple guideline-directed medical therapy (GDMT) and device support. For cardiologists, the challenge is twofold: accurately identifying high-risk individuals without overt clinical deterioration and knowing when and how to intensify therapy in patients who appear stable but remain vulnerable. Recent data show that soluble guanylate cyclase (sGC) may provide significant reductions in CV death and all-cause mortality, particularly in individuals with moderately elevated NT-proBNP (≤6,000 pg/mL). These findings are especially important because this population is far more common in routine cardiology practice and has historically been overlooked in discussions of additional therapy. However, cardiologists often underestimate risk in these ambulatory patients and may hesitate to add therapies when GDMT appears to be working well. Tune in to learn best practices for patient selection and the implementation of added sGC therapy.

CME credits: 0.25 Valid until: 10-02-2027 Claim your CME credit at https://reachmd.com/programs/cme/gdmt-is-working-fine-so-why-add-more-therapies-for-patients-with-hfref/48811/ Contemporary trial data and global registries consistently show that ambulatory patients with heart failure with reduced ejection fraction (HFrEF) who have not experienced a recent worsening event still carry residual risk of cardiovascular death and heart failure hospitalizations. These annual rates have been estimated to exceed 10%–20%, despite adherence to quadruple guideline-directed medical therapy (GDMT) and device support. This paradox of clinical stability on the surface, yet significant residual risk underneath, creates a critical blind spot in the management of chronic HFrEF. Recent data show that the addition of soluble guanylate cyclase (sGC) stimulators provides significant reductions in CV death and all-cause mortality, particularly in individuals with moderately elevated NT-proBNP (≤6,000 pg/mL). These findings are especially important because this population is far more common in routine cardiology practice and has historically been overlooked in discussions of additional therapy. Tune in to explore a case to better understand which patients can derive the most benefit from added therapy.=

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/. 

CME credits: 0.25 Valid until: 30-01-2027 Claim your CME credit at https://reachmd.com/programs/cme/missing-the-window-in-ambulatory-patients-with-hfref-on-gdmt-strategies-for-cv-risk-reduction/48813/ For ambulatory patients with heart failure with reduced ejection fraction (HFrEF) who have not experienced a recent worsening event, cardiologists continue to face a major clinical challenge: persistent and under-recognized cardiovascular (CV) risk. Despite adherence to quadruple guideline-directed medical therapy (GDMT) and device support, these “stable,” guideline-treated patients carry residual risk for CV death. Recent evidence shows that the addition of soluble guanylate cyclase (sGC) stimulators provides significant reductions in CV death and all-cause mortality, particularly in individuals with moderately elevated NT-proBNP (≤6,000 pg/mL). However, cardiologists often underestimate risk in these ambulatory patients and may hesitate to add therapies when GDMT appears to be working well. Our experts break down a case to illustrate how and when to employ recent data regarding the use of additional sGC in appropriate patients with HFrEF.=

Darshan H. Brahmbhatt, Podcast Editor of JACC: Advances, discusses a recently published original research paper on The Association Between Office, Video, and Telemanagement Encounters and GDMT Optimization in Advanced HFrEF.

CRT—now framed as cardiac physiologic pacing—remains a cornerstone for HFrEF patients with LVEF ≤50% and either high ventricular pacing burden or a wide QRS, with the biggest gains in LBBB and QRS ≥150 ms. ⚡

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.

Updates on coffee and AFib, a polypill approach for HFrEF, the first oral PCSK9 inhibitor, vitamin D supplementation for secondary prevention, and more: Joanna Chikwe, MD, chair of the American Heart Association's Scientific Sessions conference and of the Department of Cardiac Surgery in the Smidt Heart Institute at Cedars-Sinai Medical Center, shares clinical research highlights from the recent meeting. Related Content: Coffee and AFib, Oral PCSK9 Drugs, an HFrEF Polypill, and Vitamin D Post-MI—Highlights From AHA 2025

New Lancet Seminar on heart failure with reduced ejection fraction.  

CardioNerds (Dr. Kelly Arps, Dr. Naima Maqsood, and Dr. Elizabeth Davis) discuss chronic AF management with Dr. Edmond Cronin. This episode seeks to explore the chronic management of atrial fibrillation (AF) as described by the 2023 ACC/AHA/ACCP/HRS Guideline for the Diagnosis and Management of Atrial Fibrillation: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. The discussion covers the different AF classifications, symptomatology, and management including medications and invasive therapies. Importantly, the episode explores current gaps in knowledge and where there is indecision regarding proper treatment course, as in those with heart failure and AF. Our expert, Dr. Cronin, helps elucidate these gaps and apply guideline knowledge to patient scenarios. Audio editing for this episode was performed by CardioNerds intern Dr. Bhavya Shah. CardioNerds Atrial Fibrillation PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls Review the guidelines- Catheter ablation is a Class I recommendation for select patient groups  Appropriately recognize AF stages- preAF conditions, symptomatology, classification system (paroxysmal, persistent, long-standing persistent, permanent)  Be familiar with the EAST-AFNET4 trial, as it changed the approach of rate vs rhythm control  Understand treatment approaches- lifestyle modifications, management of comorbidities, rate vs rhythm control medications, cardioversion, ablation, pulmonary vein isolation, surgical MAZE  Sympathize with patients- understand their treatment goals  Notes Notes: Notes drafted by Dr. Davis.    What are the stages of atrial fibrillation?   The stages of AF were redefined in the 2023 guidelines to better recognize AF as a progressive disease that requires different strategies at the different therapies  Stage 1 At Risk for AF: presence of modifiable (obesity, lack of fitness, HTN, sleep apnea, alcohol, diabetes) and nonmodifiable (genetics, male sex, age) risk factors associated with AF  Stage 2 Pre-AF: presence of structural (atrial enlargement) or electrical (frequent atrial ectopy, short bursts of atrial tachycardia, atrial flutter) findings further pre-disposing a patient to AF  Stage 3 AF: patient may transition between these stages  Paroxysmal AF (3A): intermittent and terminates within ≤ 7 days of onset  Persistent AF (3B): continuous and sustained for > 7 days and requires intervention  Long-standing persistent AF (3C): continuous for > 12 months   Successful AF ablation (3D): freedom from AF after percutaneous or surgical intervention  Stage 4 Permanent AF: no further attempts at rhythm control after discussion between patient and clinician   The term chronic AF is considered obsolete and such terminology should be abandoned   What are common symptoms of AF?   Symptoms vary with ventricular rate, functional status, duration, and patient perception  May present as an embolic complication or heart failure exacerbation  Most commonly patients report palpitations, chest pain, dyspnea, fatigue, or lightheadedness. Vague exertional intolerance is common  Some patients also have polyuria due to increased production of atrial natriuretic peptide  Less commonly can present as tachycardia-associated cardiomyopathy or syncope  Cardioversion into sinus rhythm may be diagnostic to help determine if a given set of symptoms are from atrial fibrillation to help guide the expected utility of more aggressive rhythm control strategies.   What are the current guidelines regarding rhythm control and available options?  COR-LOE 1B: In patients with reduced LV function and persistent (or high burden) AF, a trial of rhythm control should be recommended to evaluate whether AF is contributing to the reduced LV function   COR-LOE 2a-B: In patients with reduced LV function and persistent (or high burden) AF, a trial of rhythm control should be recommended to evaluate whether AF is contributing to the reduced LV function. In patients with a recent diagnosis of AF (

What is the main driver of sex differences in heart failure with reduced ejection fraction (HFrEF)? In our latest episode, Associate Editor Dr. Petra Kleinbongard (University of Duisburg-Essen) interviews lead author Dr. Matthieu Ruiz (Montreal Heart Institute) and expert Dr. Catherine Mounier (Université du Québec à Montréal) about the new study by David et al. that explores sex-specific effects of B-vitamin supplementation on heart failure with reduced ejection fraction in mice subjected to pressure overload. The research by Ruiz and co-authors found that B-vitamins improved survival rates, cardiac function, and reduced fibrosis in female mice. However, male mice exhibited persistent inflammation, fibrosis, and unfavorable lipidome remodeling despite the B-vitamin supplementation. The findings underscore the sex-specific benefits of B-vitamins in heart failure, and confirm the importance of animal models of human disease for clinical translation. Listen now and learn more.   Chloé David, Sonia Deschênes, Gabriel Ichkhan, Caroline Daneault, Isabelle Robillard Frayne, Bertrand Bouchard, Anik Forest, Yan Fen Shi, Marie-Ève Higgins, Martin G. Sirois, Jean-Claude Tardif, Mathias Mericskay, Jérôme Piquereau, and Matthieu Ruiz Sex-Specific Modulation of Cardiac Fibrosis and Lipid Metabolism by B-Vitamins in Heart Failure with Reduced Ejection Fraction in Mice Am J Physiol Heart Circ Physiol, published June 12, 2025. DOI: 10.1152/ajpheart.00841.2024

CME credits: 0.50 Valid until: 14-11-2026 Claim your CME credit at https://reachmd.com/programs/cme/the-fifth-pillar-closing-the-gap-in-hfref/37615/ For patients with heart failure with reduced ejection fraction (HFrEF), optimizing therapy is an important part of treatment and care. But not all patients may be reaching their treatment goals and can continue to face substantial residual risk despite the use of quadruple pharmacologic guideline-directed medical therapy (GDMT) and medical devices. A soluble guanylate cyclase (sGC) stimulator that targets a previously unaddressed pathway in HFrEF and complements other GDMT may provide an incremental benefit to patients to positively impact outcomes. =

GLP-1 use in HFrEF, left atrial posterior wall isolation during AF ablation, peri-device leaks for LAAO, new findings in post-cardiac surgery AF, and imaging before AF ablation 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. Listener Feedback HYPERION trial https://www.nejm.org/doi/10.1056/NEJMoa2508170 ZENITH trial https://www.nejm.org/doi/full/10.1056/NEJMoa2415160 II GLP1 Use in HFrEF Effects of GLP-1s in Patients With HFrEF https://doi.org/10.1016/j.jchf.2025.102573 FIGHT Study https://jamanetwork.com/journals/jama/fullarticle/2540402 FIGHT Study Post-hoc Analysis https://dom-pubs.pericles-prod.literatumonline.com/doi/10.1111/dom.14862 Substudy of EXSCEL Trial https://www.ahajournals.org/doi/10.1161/CIRCULATIONAHA.119.041659 III LA Posterior Wall Isolation Saga Failure of PW Wall Isolation by PFA with Epicardial Mapping https://doi.org/10.1016/j.jacep.2025.08.017 IV Peridevice Leaks After LAAO IMPRESSION LAAC Study https://doi.org/10.1016/j.jacep.2025.08.014 V Post Cardiac Surgery AF Monitoring of New-Onset AF After CABG https://jamanetwork.com/journals/jama/fullarticle/2839710 PACES trial https://clinicaltrials.gov/study/NCT04045665 VI TEE vs ICE Before AF ablation ICE vs TEE Study https://jamanetwork.com/journals/jamacardiology/fullarticle/2839370 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

CME credits: 1.00 Valid until: 24-09-2026 Claim your CME credit at https://reachmd.com/programs/cme/tbd/37671/ Patients with chronic kidney disease (CKD) and heart failure with reduced ejection fraction (HFrEF) will achieve improved benefits from optimized use of guideline directed medical therapy, however healthcare providers may not be utilizing renin–angiotensin aldosterone system inhibitors (RAASi) and mineralocorticoid receptor antagonists (MRA) use due to hyperkalemia concerns. Using a multidisciplinary approach, experts in cardiology and nephrology address the clinical implications of suboptimal RAASi and MRA use, compare real-world data on the efficacy and safety of oral potassium binders, and developing evidence-based treatment strategies that incorporate potassium binders to improve outcomes in patients with CKD and HF who are at risk for or experiencing hyperkalemia.

CME credits: 1.00 Valid until: 24-09-2026 Claim your CME credit at https://reachmd.com/programs/cme/tbd/37675/ Patients with chronic kidney disease (CKD) and heart failure with reduced ejection fraction (HFrEF) will achieve improved benefits from optimized use of guideline directed medical therapy, however healthcare providers may not be utilizing renin–angiotensin aldosterone system inhibitors (RAASi) and mineralocorticoid receptor antagonists (MRA) use due to hyperkalemia concerns. Using a multidisciplinary approach, experts in cardiology and nephrology address the clinical implications of suboptimal RAASi and MRA use, compare real-world data on the efficacy and safety of oral potassium binders, and developing evidence-based treatment strategies that incorporate potassium binders to improve outcomes in patients with CKD and HF who are at risk for or experiencing hyperkalemia.

CME credits: 1.00 Valid until: 24-09-2026 Claim your CME credit at https://reachmd.com/programs/cme/tbd/37673/ Patients with chronic kidney disease (CKD) and heart failure with reduced ejection fraction (HFrEF) will achieve improved benefits from optimized use of guideline directed medical therapy, however healthcare providers may not be utilizing renin–angiotensin aldosterone system inhibitors (RAASi) and mineralocorticoid receptor antagonists (MRA) use due to hyperkalemia concerns. Using a multidisciplinary approach, experts in cardiology and nephrology address the clinical implications of suboptimal RAASi and MRA use, compare real-world data on the efficacy and safety of oral potassium binders, and developing evidence-based treatment strategies that incorporate potassium binders to improve outcomes in patients with CKD and HF who are at risk for or experiencing hyperkalemia.

CME credits: 1.00 Valid until: 24-09-2026 Claim your CME credit at https://reachmd.com/programs/cme/tbd/37672/ Patients with chronic kidney disease (CKD) and heart failure with reduced ejection fraction (HFrEF) will achieve improved benefits from optimized use of guideline directed medical therapy, however healthcare providers may not be utilizing renin–angiotensin aldosterone system inhibitors (RAASi) and mineralocorticoid receptor antagonists (MRA) use due to hyperkalemia concerns. Using a multidisciplinary approach, experts in cardiology and nephrology address the clinical implications of suboptimal RAASi and MRA use, compare real-world data on the efficacy and safety of oral potassium binders, and developing evidence-based treatment strategies that incorporate potassium binders to improve outcomes in patients with CKD and HF who are at risk for or experiencing hyperkalemia.

CME credits: 1.00 Valid until: 24-09-2026 Claim your CME credit at https://reachmd.com/programs/cme/tbd/37674/ Patients with chronic kidney disease (CKD) and heart failure with reduced ejection fraction (HFrEF) will achieve improved benefits from optimized use of guideline directed medical therapy, however healthcare providers may not be utilizing renin–angiotensin aldosterone system inhibitors (RAASi) and mineralocorticoid receptor antagonists (MRA) use due to hyperkalemia concerns. Using a multidisciplinary approach, experts in cardiology and nephrology address the clinical implications of suboptimal RAASi and MRA use, compare real-world data on the efficacy and safety of oral potassium binders, and developing evidence-based treatment strategies that incorporate potassium binders to improve outcomes in patients with CKD and HF who are at risk for or experiencing hyperkalemia.

CME credits: 1.00 Valid until: 24-09-2026 Claim your CME credit at https://reachmd.com/programs/cme/tbd/37670/ Patients with chronic kidney disease (CKD) and heart failure with reduced ejection fraction (HFrEF) will achieve improved benefits from optimized use of guideline directed medical therapy, however healthcare providers may not be utilizing renin–angiotensin aldosterone system inhibitors (RAASi) and mineralocorticoid receptor antagonists (MRA) use due to hyperkalemia concerns. Using a multidisciplinary approach, experts in cardiology and nephrology address the clinical implications of suboptimal RAASi and MRA use, compare real-world data on the efficacy and safety of oral potassium binders, and developing evidence-based treatment strategies that incorporate potassium binders to improve outcomes in patients with CKD and HF who are at risk for or experiencing hyperkalemia.

CME credits: 1.00 Valid until: 24-09-2026 Claim your CME credit at https://reachmd.com/programs/cme/tbd/36194/ Patients with chronic kidney disease (CKD) and heart failure with reduced ejection fraction (HFrEF) will achieve improved benefits from optimized use of guideline directed medical therapy, however healthcare providers may not be utilizing renin–angiotensin aldosterone system inhibitors (RAASi) and mineralocorticoid receptor antagonists (MRA) use due to hyperkalemia concerns. Using a multidisciplinary approach, experts in cardiology and nephrology address the clinical implications of suboptimal RAASi and MRA use, compare real-world data on the efficacy and safety of oral potassium binders, and developing evidence-based treatment strategies that incorporate potassium binders to improve outcomes in patients with CKD and HF who are at risk for or experiencing hyperkalemia.

CME credits: 1.00 Valid until: 24-09-2026 Claim your CME credit at https://reachmd.com/programs/cme/the-critical-interplay-ckd-hf-and-hyperkalemia/36193/ Patients with chronic kidney disease (CKD) and heart failure with reduced ejection fraction (HFrEF) will achieve improved benefits from optimized use of guideline directed medical therapy, however healthcare providers may not be utilizing renin–angiotensin aldosterone system inhibitors (RAASi) and mineralocorticoid receptor antagonists (MRA) use due to hyperkalemia concerns. Using a multidisciplinary approach, experts in cardiology and nephrology address the clinical implications of suboptimal RAASi and MRA use, compare real-world data on the efficacy and safety of oral potassium binders, and developing evidence-based treatment strategies that incorporate potassium binders to improve outcomes in patients with CKD and HF who are at risk for or experiencing hyperkalemia.

CME credits: 1.00 Valid until: 24-09-2026 Claim your CME credit at https://reachmd.com/programs/cme/tbd/37676/ Patients with chronic kidney disease (CKD) and heart failure with reduced ejection fraction (HFrEF) will achieve improved benefits from optimized use of guideline directed medical therapy, however healthcare providers may not be utilizing renin–angiotensin aldosterone system inhibitors (RAASi) and mineralocorticoid receptor antagonists (MRA) use due to hyperkalemia concerns. Using a multidisciplinary approach, experts in cardiology and nephrology address the clinical implications of suboptimal RAASi and MRA use, compare real-world data on the efficacy and safety of oral potassium binders, and developing evidence-based treatment strategies that incorporate potassium binders to improve outcomes in patients with CKD and HF who are at risk for or experiencing hyperkalemia.

In this episode, we give a wrap-up of late-breaking clinical science presented at the ESC Congress 2025 in Madrid. First, David Berg presents the DAPA ACT HF-TIMI 68 trial, reporting on dapagliflozin in patients hospitalized for acute heart failure, along with a meta-analysis of SGLT2 inhibitors in this setting. Next, Javed Butler highlights results of the VICTOR trial, a large phase 3 study of vericiguat in chronic heart failure with reduced ejection fraction. Then, Andre Zimerman discusses the PhysioSync-HF trial, comparing conduction system pacing with biventricular resynchronization therapy in patients with HFrEF. Finally, Kieran Docherty shares insights from a community-based study on the benefits of early initiation of disease-modifying therapy in suspected heart failure.   Additional information: Topic 1: With Gregorio Tersalvi, Mayo Clinic, Rochester, MN - USA, David Berg, Brigham and Women's Hospital, Boston - USA and Novi Yanti Sari, Siloam Hospitals Group, Jakarta - Indonesia Results paper: Dapagliflozin in Patients Hospitalized for Heart Failure: Primary Results of the DAPA ACT HF-TIMI 68 Randomized Clinical Trial and Meta-Analysis of Sodium-Glucose Cotransporter-2 Inhibitors in Patients Hospitalized for Heart Failure Replay ESC Congress Hot Line: https://esc365.escardio.org/presentation/312142 Circulation. 2025 Aug 29. doi: 10.1161/CIRCULATIONAHA.125.076575.    Topic 2: With Javed Butler, Baylor Scott & White Health, Dallas - USA and Henrike Arfsten, Medical University of Vienna, Vienna - Austria Results papers: Vericiguat in patients with chronic heart failure and reduced ejection fraction (VICTOR): a double-blind, placebo-controlled, randomised, phase 3 trial Lancet. 2025 Replay ESC Congress hotline: https://esc365.escardio.org/presentation/312148 doi: 10.1016/S0140-6736(25)01665-4.  Vericiguat for patients with heart failure and reduced ejection fraction across the risk spectrum: an individual participant data analysis of the VICTORIA and VICTOR trials Lancet. 2025 Aug 29:S0140-6736(25)01682-4. doi: 10.1016/S0140-6736(25)01682-4.   Topic 3: With Andre Zimerman, Hospital Moinhos De Vento, Porto Alegre - Brazil and Floran Sahiti, University Hospital of Wurzburg, Wurzburg - Germany Methods paper: Conduction system pacing vs biventricular resynchronization in heart failure with reduced ejection fraction and left bundle branch block: Rationale and design of the PhysioSync-HF Trial Am Heart J. 2025 Dec:290:38-45. Replay ESC Congress: https://esc365.escardio.org/session/50327 doi: 10.1016/j.ahj.2025.06.002.   Topic 3: With Kieran Docherty, University of Glasgow, Glasgow - UK and Jolie Bruno, Inserm UMR-S942, Paris - France Results paper: Benefit of early initiation of disease-modifying therapy in community-based patients with suspected heart failure Eur Heart J. 2025 Aug 29:ehaf675. doi: 10.1093/eurheartj/ehaf675.    This 2025 HFA Cardio Talk podcast series is supported by Bayer AG in the form of an unrestricted financial support. The discussion has not been influenced in any way by its sponsor. 

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

In this episode, we review the pharmacology, indications, adverse effects, monitoring, and unique drug characteristics of angiotensin receptor blockers (ARBs).  Key Concepts ARBs are equally efficacious as ACE inhibitors when used for hypertension, heart failure with reduced ejection fraction (HFrEF), chronic kidney disease (CKD) with proteinuria, and post-MI care. Some limited evidence suggests that they might be better in reducing albuminuria in patients with diabetes. ARBs are generally better tolerated than ACEi due to a lower risk of angioedema and dry cough.  While most ARBs are comparable to each other, small differences exists regarding hepatic metabolism (CYP metabolism for losartan, telmisartan, and azilsartan), degree of blood pressure lowering (generally better with azilsartan, olmesartan, valsartan, and candesartan), and additional pharmacological effects (telmisartan with PPAR-Y agonism, losartan with uricosuric effect). ARBs are contraindicated in pregnancy, those with bilateral renal artery stenosis, and those with previous angioedema to ARBs. The most common adverse effects include hypotension and hyperkalemia, but in rare cases acute renal impairment can also occur. Baseline serum creatinine and potassium should be monitored in patients taking ARBs. After initiation or dose adjustment, blood pressure, serum creatinine, and potassium should be repeated in 1-2 weeks. Signs and symptoms of hypotension as well as angioedema should be monitored throughout the treatment period.

Join us at patreon.com/curbsiders today and save 20% on NEW Annual Memberships with promo code: UNLOCKED. *This offer expires at 3am EST on May 15, 2025. Matt and Paul recap top pearls from a recent episode on heart failure with reduced ejection fraction (HFrEF) and the importance of understanding the underlying causes of heart failure with Dr. Michelle Kittleson (video version). They also answer listener questions and share their picks of the week. Chapters: 00:00 Introduction and Humor 01:41 Understanding Heart Failure 04:50 Guideline-Directed Medical Therapy 09:57 Practical Approaches to Treatment 13:58 The Importance of Medication Adherence 16:22 Dietary Considerations in Heart Failure 18:24 ED Follow-Ups and Patient Management 20:38 SGLT2 Inhibitors and Infections 25:58 Patient Counseling and Preventative Care 26:33 Picks of the Week

We're taking a break this week, but we'll be back next week with a brand-new episode.  Provide superb outpatient care for your patients with HFrEF. Identify underlying causes of heart failure and titrate medications with ease. Dr Michelle Kittleson @MKittlesonMD (Cedars Sinai) breaks down the nuances of treating this common cardiac condition.  Claim CME for this episode at curbsiders.vcuhealth.org! Patreon | Episodes | Subscribe | Spotify | YouTube | Newsletter | Contact | Swag! | CME Show Segments 00:00 Introduction  03:22 Case Presentation: Newly Diagnosed Heart Failure 07:26 Using Physical Exam Findings to Guide Diuresis 11:58 The Four Pillars of Guideline-Directed Medical Therapy for Heart Failure 15:07 Optimizing Therapy and Follow-Up in Heart Failure Patients 22:10 The Benefits of High-Intensity Initiation and Titration of Guideline-Directed Medical Therapy 28:02 Consideration of Other Medications 40:02 Referral to Advanced Heart Failure Specialist 49:11 Optimizing Therapy and Follow-Up 55:33 Conclusion and Book Recommendation Credits Writer and Producer: Deborah Gorth MD, PhD Infographic and Cover Art: Zoya Surani Hosts: Matthew Watto MD, FACP; Paul Williams MD, FACP    Reviewer: Emi Okamoto MD Showrunners: Matthew Watto MD, FACP; Paul Williams MD, FACP Technical Production: PodPaste Guest: Michelle Kittleson MD, PhD Sponsor: Mint Mobile  Get your summer savings and shop premium wireless plans at MINTMOBILE. com/CURB. Sponsor: American College of Physicians Order ACP MKSAP today at acponline.org. Curbsiders Listeners who use promo code  CORECS will receive a MKSAP gift pack with their subscription. Sponsor: Panacea Legal Learn more and schedule your free consultation at Panacea.Legal.

On this episode, we evaluate current guidelines and evidence-based treatment strategies for managing heart failure (primarily focusing on HFrEF). We compare and contrast the efficacy, safety profiles, and appropriate use of heart failure medications. We also review some of the landmark clinical trials that were used when developing the heart failure treatment guidelines.  Cole and I are happy to share that our listeners can claim ACPE-accredited continuing education for listening to this podcast episode! We have continued to partner with freeCE.com to provide listeners with the opportunity to claim 1-hour of continuing education credit for select episodes. For existing Unlimited (Gold) freeCE members, this CE option is included in your membership benefits at no additional cost! A password, which will be given at some point during this episode, is required to access the post-activity test. To earn credit for this episode, visit the following link below to go to freeCE's website: https://www.freece.com/ If you're not currently a freeCE member, we definitely suggest you explore all the benefits of their Unlimited Membership on their website and earn CE for listening to this podcast. Thanks for listening! If you want to support the podcast, check out our Patreon account. Subscribers will have access to all previous and new pharmacotherapy lectures as well as downloadable PowerPoint slides for each lecture. If you purchase an annual membership, you'll also get a free digital copy of High-Powered Medicine 3rd edition by Dr. Alex Poppen, PharmD. HPM is a book/website database of summaries for over 150 landmark clinical trials.You can visit our Patreon page at the website below:  www.patreon.com/corconsultrx We want to give a big thanks to Dr. Alex Poppen, PharmD and High-Powered Medicine for sponsoring the podcast..  You can get a copy of HPM at the links below:  Purchase a subscription or PDF copy - https://highpoweredmedicine.com/ Purchase the paperback and hardcover - Barnes and Noble website We want to say thank you to our sponsor, Pyrls. Try out their drug information app today. Visit the website below for a free trial: www.pyrls.com/corconsultrx We also want to thank our sponsor Freed AI. Freed is an AI scribe that listens, prepares your SOAP notes, and writes patient instructions. Charting is done before your patient walks out of the room. You can try 10 notes for free and after that it only costs $99/month. Visit the website below for more information: https://www.getfreed.ai/  If you have any questions for Cole or me, reach out to us via e-mail: Mike - mcorvino@corconsultrx.com Cole - cswanson@corconsultrx.com

Dr. K talks with cardiologist Cara Pellegrini, MD, to discuss the key aspects of heart failure, including its types (congestive, systolic, diastolic, HFrEF, and HFpEF), causes, symptoms, and treatment options. They also cover special considerations for frail older adults, heart failure and end of life issues, and much more.

The following question refers to Sections 7.3.3 and 7.3.6 of the 2022 ACC/AHA/HFSA Guideline for the Management of Heart Failure.The question is asked by Palisades Medical Center medicine resident & CardioNerds Academy Fellow Dr. Maryam Barkhordarian, answered first by UTSW AHFT Cardiologist & CardioNerds FIT Ambassador Dr. Natalie Tapaskar, and then by expert faculty Dr. Robert Mentz.Dr. Mentz is associate professor of medicine and section chief for Heart Failure at Duke University, a clinical researcher at the Duke Clinical Research Institute, and editor-in-chief of the Journal of Cardiac Failure. Dr. Mentz has been a mentor for the CardioNerds Clinical Trials Network as lead principal investigator for PARAGLIDE-HF and is a series mentor for this very Decipher the Guidelines Series. For these reasons and many more, he was awarded the Master CardioNerd Award during ACC22.The Decipher the Guidelines: 2022 AHA / ACC / HFSA Guideline for The Management of Heart Failure series was developed by the CardioNerds and created in collaboration with the American Heart Association and the Heart Failure Society of America. It was created by 30 trainees spanning college through advanced fellowship under the leadership of CardioNerds Cofounders Dr. Amit Goyal and Dr. Dan Ambinder, with mentorship from Dr. Anu Lala, Dr. Robert Mentz, and Dr. Nancy Sweitzer. We thank Dr. Judy Bezanson and Dr. Elliott Antman for tremendous guidance.Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. American Heart Association's Scientific Sessions 2024As heard in this episode, the American Heart Association's Scientific Sessions 2024 is coming up November 16-18 in Chicago, Illinois at McCormick Place Convention Center. Come a day early for Pre-Sessions Symposia, Early Career content, QCOR programming and the International Symposium on November 15. It's a special year you won't want to miss for the premier event for advancements in cardiovascular science and medicine as AHA celebrates its 100th birthday. Registration is now open, secure your spot here!When registering, use code NERDS and if you're among the first 20 to sign up, you'll receive a free 1-year AHA Professional Membership! Question #39 Ms. Kay Lotsa is a 48-year-old woman with a history of CKD stage 2 (baseline creatinine ~1.2 mg/dL) & type 2 diabetes mellitus. She has recently noticed progressively reduced exercise tolerance, leg swelling, and trouble lying flat. This prompted a hospital admission with a new diagnosis of decompensated heart failure. A transthoracic echocardiogram reveals LVEF of 35%. Ms. Lotsa is diuresed to euvolemia, and she is started on carvedilol 25mg BID, sacubitril/valsartan 49-51mg BID, and empagliflozin 10mg daily, which she tolerates well. Her eGFR is at her baseline of 55 mL/min/1.73 m2 and serum potassium concentration is 3.9 mEq/L. Your team is anticipating she will be discharged home in the next one to two days and wants to start spironolactone. Which of the following is most important regarding her treatment with mineralocorticoid antagonists?ASpironolactone is contraindicated based on her level of renal impairment and should not be startedBSerum potassium levels and kidney function should be assessed within 1-2 weeks of starting spironolactoneCEplerenone confers a higher risk of gynecomastia than does spironolactoneDThe patient will likely not benefit from initiation of spironolactone if her cardiomyopathy is ischemic in origin Answer #39 ExplanationThe correct answer is B – after starting a mineralocorticoid receptor antagonist (MRA), it is important to closely monitor renal function and serum potassium levels.MRA (also known as aldosterone antagonists or anti-mineralocorticoids) show consistent improvements in all-cause mortality, HF hospitalizations, and SCD across a wide range of patients with HFrEF.

Kittleson Rules Outpatient Heart Failure Volume 1 Provide superb outpatient care for your patients with HFrEF. Identify underlying causes of heart failure and titrate medications with ease. Dr Michelle Kittleson @MKittlesonMD (Cedars Sinai) breaks down the nuances of treating this common cardiac condition.  Claim CME for this episode at curbsiders.vcuhealth.org! Patreon | Episodes | Subscribe | Spotify | YouTube | Newsletter | Contact | Swag! | CME Show Segments 00:00 Introduction  03:22 Case Presentation: Newly Diagnosed Heart Failure 07:26 Using Physical Exam Findings to Guide Diuresis 11:58 The Four Pillars of Guideline-Directed Medical Therapy for Heart Failure 15:07 Optimizing Therapy and Follow-Up in Heart Failure Patients 22:10 The Benefits of High-Intensity Initiation and Titration of Guideline-Directed Medical Therapy 28:02 Consideration of Other Medications 40:02 Referral to Advanced Heart Failure Specialist 49:11 Optimizing Therapy and Follow-Up 55:33 Conclusion and Book Recommendation Credits Writer and Producer: Deborah Gorth MD, PhD Infographic and Cover Art: Zoya Surani Hosts: Matthew Watto MD, FACP; Paul Williams MD, FACP    Reviewer: Emi Okamoto MD Showrunners: Matthew Watto MD, FACP; Paul Williams MD, FACP Technical Production: PodPaste Guest: Michelle Kittleson MD, PhD Sponsor: Freed You can try Freed for free right now by going to freed.ai. And listeners of Curbsiders can use code CURB50 for $50 off their first month.  Sponsor: Litter Robot Right now, Whisker is offering $75 off Litter-Robot bundles. AND, as a special offer to listeners, you can get an additional $50 off when you go to stopscooping.com/CURB. Sponsor: Beginly Health Ready to take control of your job search? Visit beginlyhealth.com/curbsiders to get started

Surgical clearance, NICM assessment, dueling perspectives on PCI as first-line therapy for angina, GDMT in HFrEF 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. New ACC Peri-operative Guidelines Released ACC Guideline document https://www.jacc.org/doi/10.1016/j.jacc.2024.06.013 J Vasc Surg https://www.jvascsurg.org/article/S0741-5214(21)00335-9/fulltext McFalls and colleagues; CARP https://www.nejm.org/doi/full/10.1056/NEJMoa041905 II. NICM – We may be doing it wrong in Selecting ICDs JAMA Meta-analysis https://jamanetwork.com/journals/jama/fullarticle/2823869/ German CMR ICD Trial https://www.clinicaltrials.gov/study/NCT04558723 BRITISH CMR trial https://www.hra.nhs.uk/planning-and-improving-research/application-summaries/research-summaries/britishusing-cmr-scar-as-risk-indication-tool-in-nicm-and-severe-lvsd/ III. When Should PCI be Used in Chronic Stable CAD?   Rajkumar and Al-Lamee; PCI First https://www.ahajournals.org/doi/10.1161/CIRCOUTCOMES.124.011201   Boden and De Caterina; Meds First https://www.ahajournals.org/doi/10.1161/CIRCOUTCOMES.124.011268 ORBITA 10.1016/S0140-6736(17)32714-9 ORBITA 2 trial https://www.nejm.org/doi/full/10.1056/NEJMoa2310610 IV. GDMT Underuse in HFrEF Greene and colleagues https://doi.org/10.1016/j.jchf.2024.08.002 DAPA HF https://www.nejm.org/doi/full/10.1056/NEJMoa1911303 RALES https://www.nejm.org/doi/full/10.1056/NEJM199909023411001 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

Diuretic therapy in HFrEF, AF ablation, TACT 2 and the story of subgroups, and SGLT2 inhibitor underuse 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. Diuretic Therapy in HF Dapa vs Metolazone Trial https://doi.org/10.1093/eurheartj/ehad341 ADVOR https://www.nejm.org/doi/10.1056/NEJMoa2203094 II. Rapid Medication Titration for Acute HF ACC Decision Pathway https://www.jacc.org/doi/10.1016/j.jacc.2024.06.002 III. SGLT2 Inhibitor Use in the US Shin and Colleagues; JACC  https://www.sciencedirect.com/science/article/abs/pii/S0735109724076332 Editorial  https://doi.org/10.1016/j.jacc.2024.07.001 IV. AF Ablation: General Anesthesia vs Conscious Sedation Da Riis-Vestergaard and Colleagues  https://doi.org/10.1093/europace/euae203 V. TACT 2 Published TACT 1 https://jamanetwork.com/journals/jama/fullarticle/1672238 TACT 1 DM https://www.ahajournals.org/doi/10.1161/CIRCOUTCOMES.113.000663 TACT 2 https://jamanetwork.com/journals/jama/fullarticle/2822472 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