Podcasts about sglt2

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 zespół sercowo-nerkowo-metaboliczny.Nowe wytyczne ACC/AHA dotyczące zespołu sercowo-nerkowo-metabolicznego (CKM) rozwijają koncepcję przedstawioną wcześniej przez AHA i polskich ekspertów, traktując choroby serca, nerek i zaburzenia metaboliczne jako jedno kontinuum, a nie trzy odrębne jednostki chorobowe (https://www.ahajournals.org/doi/10.1161/CIR.0000000000001184, https://journals.viamedica.pl/nadcisnienie_tetnicze_w_praktyce/article/view/90302/68962). W praktyce oznacza to odejście od myślenia o pacjencie wyłącznie przez pryzmat niewydolności serca, cukrzycy czy przewlekłej choroby nerek na rzecz rozpoznania jednego zespołu CKM. Kluczowym markerem staje się albuminuria (UACR), która obok eGFR pozwala wcześnie wykryć uszkodzenie nerek i jednocześnie precyzyjnie ocenia ryzyko sercowo-naczyniowe. Wytyczne wyróżniają cztery stadia choroby – od nadwagi i otyłości, przez zaburzenia metaboliczne i subkliniczną chorobę serca, aż do jawnych powikłań narządowych – przy czym leczenie powinno rozpoczynać się już w stadium 1, zanim pojawią się objawy kliniczne. Największą zmianą filozofii jest przesunięcie akcentu z leczenia rozwiniętej choroby na ochronę serca i nerek poprzez wczesne zastosowanie inhibitorów SGLT2, agonistów GLP-1 oraz finerenonu u odpowiednio dobranych pacjentów. Dokument integruje wyniki najnowszych badań i proponuje spójną strategię terapii narządowej zamiast wybierania pojedynczych leków zależnie od specjalizacji. Jednocześnie pozostawia otwarte pytanie, kto powinien prowadzić takich chorych – kardiolog, nefrolog, diabetolog czy lekarz rodzinny – co w praktyce wymaga ścisłej współpracy wszystkich specjalności. Autor zwraca również uwagę na wyzwania organizacyjne, obejmujące konieczność powszechnego oznaczania UACR, wcześniejszego rozpoznawania nadwagi i otyłości oraz szerszego stosowania nowoczesnych terapii, co wiąże się ze wzrostem kosztów ochrony zdrowia. Nadal nie wiadomo, czy tak szeroki model prewencji okaże się w pełni opłacalny ekonomicznie, choć intuicyjnie zapobieganie niewydolności serca i przewlekłej chorobie nerek wydaje się korzystniejsze niż leczenie ich zaawansowanych powikłań. Zdaniem autora wytyczne wyznaczają kierunek rozwoju kardiologii, nefrologii, diabetologii i medycyny rodzinnej na najbliższe lata, a ich znaczenie pokaże również to, czy podobną filozofię przejmą kolejne wytyczne ESC dotyczące niewydolności serca, przewlekłej choroby nerek i prewencji sercowo-naczyniowej. Szczegółowy TRANSKRYPT do odcinka.Podcast jest przeznaczony wyłącznie dla osób z profesjonalnym wykształceniem medycznym.

New, Advanced Therapies in Gout explores the rapidly evolving therapeutic landscape beyond conventional urate-lowering therapy. Join our expert panel as they discuss emerging approaches—including cytokine inhibition, uricase therapies, NLRP3 and URAT-1 inhibitors, and the potential role of GLP-1 receptor agonists and SGLT2 inhibitors—while addressing which patients are most likely to benefit, how these agents fit into current treatment algorithms, and whether novel mechanisms of action have the potential to transform gout management. Panelists: Dr. Herbert Baraf Dr. Ken Saag Dr. Naomi Schlesinger Dr. Jack Cush (moderator)

ASN Kidney Translation explores advances in Cardiovascular-Kidney-Metabolic syndrome, including building a cardio-nephrology service (Kidney360), cardiorenal benefits of SGLT2 inhibitors & GLP-1 receptor agonists (JASN), & PREVENT risk prediction (CJASN).

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 najnowszą definicję niewydolności serca. Nowa definicja niewydolności serca (AHA/ACC/ESC/WHF 2026) została opublikowana 29 czerwca 2026 i aktualizuje definicję z 2021 roku, uwzględniając postęp diagnostyki, biomarkerów i nowych terapii, bez zmiany podstawowego rozpoznania niewydolności serca jako zespołu objawów wynikających z nieprawidłowej budowy lub funkcji serca, potwierdzonych podwyższonymi peptydami natriuretycznymi lub obiektywnymi cechami zastoju (https://www.ahajournals.org/doi/10.1161/CIR.0000000000001455). Najbardziej widoczną zmianą jest odejście od sztywnych progów frakcji wyrzutowej – zamiast HFrEF, HFmrEF i HFpEF autorzy proponują bardziej elastyczny podział na niewydolność serca z obniżoną, zachowaną oraz poprawioną frakcją wyrzutową, podkreślając, że pojedyncza wartość EF nie powinna decydować o fenotypie chorego. Jednocześnie zwracają uwagę na paradoks współczesnej kardiologii – większość badań klinicznych i zaleceń terapeutycznych nadal opiera się właśnie na wartościach LVEF, dlatego praktyka nie jest jeszcze gotowa na całkowite odejście od dotychczasowych progów. Po raz pierwszy wprowadzono również kompleksową klasyfikację etiologiczną niewydolności serca obejmującą m.in. przyczyny niedokrwienne, nadciśnieniowe, zastawkowe, zapalne, genetyczne, toksyczne, metaboliczne oraz choroby rzadkie, takie jak amyloidoza czy choroba Fabry'ego, co ma znaczenie ze względu na rosnącą liczbę terapii przyczynowych. Dokument mocno akcentuje także znaczenie trajektorii choroby – poprawa frakcji wyrzutowej nie oznacza wyleczenia, a leczenie o udowodnionej skuteczności powinno być kontynuowane mimo poprawy funkcji serca. Znacznie większy nacisk położono na wykrywanie stadium pre-HF, wykorzystując nie tylko NT-proBNP, ale również troponiny, wskaźnik albumina/kreatynina (ACR), zaawansowane obrazowanie oraz algorytmy sztucznej inteligencji analizujące zapis EKG. Profilaktyka staje się integralną częścią opieki nad pacjentem – autorzy wskazują na rolę inhibitorów SGLT2, agonistów receptora GLP-1 oraz finerenonu w ograniczaniu ryzyka rozwoju niewydolności serca u odpowiednio dobranych chorych. Dokument podkreśla także rosnące znaczenie sztucznej inteligencji w identyfikacji pacjentów z nierozpoznaną niewydolnością serca oraz zwraca uwagę na nierówności w dostępie do nowoczesnej opieki kardiologicznej. Największym wyzwaniem pozostaje jednak pogodzenie nowoczesnego biologicznego podejścia do niewydolności serca z obowiązującymi dowodami naukowymi, które nadal opierają kwalifikację do farmakoterapii, ICD czy CRT głównie na wartościach frakcji wyrzutowej. Szczegółowy TRANSKRYPT do odcinka.Podcast jest przeznaczony wyłącznie dla osób z profesjonalnym wykształceniem medycznym.

CardioNerds (Drs. Apoorva Gangavelli, Jenna Skowronski, and Hannah Every) discuss the continuum of prevention and heart failure with Drs. Anu Lala and Martha Gulati. Grounded in a clinical case of a 55-year-old woman with uncontrolled hypertension, type 2 diabetes, and obesity who is on the trajectory toward heart failure, this episode unpacks a paradigm-shifting framework from a joint HFSA/ASPC Scientific Statement. The discussion explores how prevention should not be siloed from heart failure management but rather integrated across a patient’s lifespan—from primary prevention in at-risk individuals, to secondary prevention in those with established heart failure, to tertiary prevention in patients with advanced therapies such as LVADs and heart transplantation. The experts highlight the importance of aggressive risk factor management, biomarker-guided screening, the AHA’s Life’s Essential 8, and the need for multidisciplinary collaboration and systems-level change to shift heart failure care from reactive to proactive. Audio editing for this episode was performed by CardioNerds Intern, Dr. Julia Marques Fernandes. Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. US Cardiology Review is now the official journal of CardioNerds! Submit your manuscript here. CardioNerds Prevention PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls Systemic inflammatory diseases are associated with an elevated CVD risk that has significant implications for early detection, risk Heart failure prevention is a continuum, not a checkpoint. Prevention applies at every stage—from at-risk (Stage A) through advanced/post-transplant care—and every clinical encounter is an opportunity to intervene. The AHA’s Life’s Essential 8 (diet, physical activity, nicotine exposure, sleep, BMI, blood lipids, blood glucose, blood pressure) forms the foundation at every stage. Hypertension carries the highest population-attributable risk for heart failure of any modifiable risk factor. In the Framingham Heart Study, 91% of patients with newly diagnosed HF had pre-existing hypertension. The SPRINT trial demonstrated a 38% reduction in HF incidence with intensive blood pressure targets (30 ng/L or NT-proBNP >125 ng/L) identify individuals at heightened risk for progression to symptomatic HF. The ACC/AHA/HFSA guidelines give a Class IIa recommendation for natriuretic peptide screening in at-risk patients. Urine albumin-to-creatinine ratio (UACR) is an underutilized screening tool that provides additional insight into CKM risk. The heart failure label does not close the prevention window—it accentuates it. Secondary prevention through GDMT optimization (quadruple therapy in HFrEF) and continued risk factor management remains critical. Tertiary prevention extends to post-LVAD and post-transplant patients, where hypertension, diabetes, obesity, and CKD management remain essential to long-term outcomes. Show notes For a comprehensive review, please review the full HFSA/ASPC Joint Scientific Statement: Lala A, Beavers C, Blumer V, et al. The Continuum of Prevention and Heart Failure in Cardiovascular Medicine. J Card Fail. 2026;32:75-105. doi:10.1016/j.cardfail.2025.06.013 1. What is the “continuum of prevention” framework, and how does it differ from traditional approaches to heart failure prevention? Historically, prevention and heart failure management have been treated as separate disciplines—primary prevention handled by preventive cardiologists and treatment managed by heart failure specialists. This joint HFSA/ASPC Scientific Statement reframes prevention as a dynamic, continuous process that spans a patient’s entire lifespan, regardless of HF stage or ejection fraction. The framework maps onto the ACC/AHA HF staging system: Primary prevention targets Stage A (“at risk”) and Stage B (“pre-HF”) patients to reduce the burden of incident HF. Secondary prevention targets Stage C (symptomatic) and Stage D (advanced) patients to reduce the impact of established HF through GDMT optimization and ongoing risk factor management. Tertiary prevention encompasses risk factor management in patients with LVADs or heart transplants—populations where hypertension, diabetes, and obesity still drive outcomes. The Central Figure of the statement illustrates that Life’s Essential 8 (blood pressure and lipid control, diabetes management, exercise, sleep, smoking cessation, weight management, and diet/nutrition counseling) forms the foundation at every stage, with pharmacologic and device-based therapies layered on top as disease progresses (Figure) 2. How do traditional risk factors drive heart failure, and what should clinicians prioritize? Hypertension carries the greatest population-attributable risk for HF. In the Framingham Heart Study (N=5,143), HTN was associated with a 2- to 3-fold increased risk of HF, with a population-attributable risk of 39% in men and 59% in women. The SPRINT trial showed a 38% reduction in HF incidence and 25% reduction in the primary composite outcome with intensive BP targets (30 ng/L or NT-proBNP >125 ng/L) are associated with heightened risk for progression to symptomatic HF. In the ARIC study, incorporating NT-proBNP reclassified 20% of older adults without HF into Stage B. Factors that affect interpretation include age, sex, obesity (lower values), and CKD (higher values). High-sensitivity cardiac troponin (hs-cTn): Concentrations above the 99th percentile are now included in the definition of Stage B HF. Troponin testing may complement natriuretic peptides, particularly when BNP/NT-proBNP values are ambiguous. Risk scores: The PCP-HF equation predicts 10-year HF risk using traditional risk factors plus QRS duration. The AHA PREVENT score incorporates HF risk calculation and includes markers of kidney function (albuminuria, eGFR), though it may underestimate risk in men and Black adults. The CKM syndrome staging framework (Stages 0–4) provides a holistic approach to assessing systemic cardiovascular-kidney-metabolic risk. 4. What are the key nontraditional risk factors and cross-cutting themes in heart failure prevention? Genetics: Pathogenic cardiomyopathy variants exist in ~1 in 200 individuals in the general population. The HFSA and ACMG recommend cascade testing to identify at-risk family members. Polygenic risk scores for dilated cardiomyopathy show a 3.8-fold risk for DCM in the top 10th percentile compared with the median. Sex-specific considerations: Women have 2.8 times the odds of developing HFpEF, while men have similarly increased odds of HFrEF. A complete obstetric/gynecologic history is essential—preeclampsia is associated with a 4-fold increased risk of HF. Peripartum cardiomyopathy requires intentional screening in high-risk populations. Cardiotoxic exposures: Clinicians should be aware of medications that cause direct myocardial toxicity (e.g., anthracyclines, trastuzumab, tyrosine kinase inhibitors). A team-based approach with pharmacists can help optimize medication selection and risk factor modification. Social determinants of health: Environmental exposures (air pollution, arsenic, lead, cadmium), food insecurity, financial instability, and limited healthcare access contribute to HF risk and progression. Equity-focused, risk-based prevention strategies are needed. Psychological health: Depression is common in HF and independently associated with worse outcomes. Screening with brief questionnaires (e.g., PHQ-2) is recommended. Meditation, spirituality, and holistic wellness approaches remain underutilized. 5. What systems-level and policy changes are needed to move the needle on heart failure prevention? Multidisciplinary HF prevention clinics that bring together preventive cardiologists, HF specialists, endocrinologists, nephrologists, dietitians, pharmacists, exercise physiologists, and genetic counselors are advocated by the statement. EHR-embedded risk stratification could proactively flag patients on a trajectory toward HF—analogous to sepsis alerts or fall risk flags—enabling earlier intervention, particularly for patients who may not reach a cardiologist. Cardiac rehabilitation remains underutilized, particularly in HFrEF (Class 2b recommendation) and HFpEF (not yet covered by Medicare). The HF-ACTION trial showed quality-of-life benefits, and the REHAB-HF trial showed particular benefit in older patients with HFpEF. Policy priorities include expanding insurance coverage for preventive screening and novel therapies (SGLT2i, GLP-1 RAs, nsMRAs), reducing clinical inertia through team-based care models with closer follow-up intervals, and ensuring equitable access to evidence-based therapies across diverse populations. Digital health and AI hold promise for personalized risk prediction, remote monitoring (e.g., wearable devices, implantable PA pressure monitors), and virtual cardiac rehabilitation to overcome access barriers. Figure  Lala A, Beavers C, Blumer V, et al. The continuum of prevention and heart failure in cardiovascular medicine: a joint scientific statement from the Heart Failure Society of America and the American Society for Preventive Cardiology. J Card Fail. 2026;32(1):75-105. doi:10.1016/j.cardfail.2025.06.013) References Key references are bolded. Lala A, Beavers C, Blumer V, et al. The continuum of prevention and heart failure in cardiovascular medicine: a joint scientific statement from the Heart Failure Society of America and the American Society for Preventive Cardiology. J Card Fail. 2026;32(1):75-105. doi:10.1016/j.cardfail.2025.06.013 Heidenreich PA, Bozkurt B, Aguilar D, et al. 2022 AHA/ACC/HFSA guideline for the management of heart failure: a report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. Circulation. 2022;145(18):e895-e1032. doi:10.1161/CIR.0000000000001063 Lloyd-Jones DM, Allen NB, Anderson CAM, et al. Life’s Essential 8: updating and enhancing the American Heart Association’s construct of cardiovascular health: a presidential advisory from the American Heart Association. Circulation. 2022;146(5):e18-e43. doi:10.1161/CIR.0000000000001078 SPRINT Research Group, Wright JT Jr, Williamson JD, et al. A randomized trial of intensive versus standard blood-pressure control. N Engl J Med. 2015;373(22):2103-2116. doi:10.1056/NEJMoa1511939 Levy D, Larson MG, Vasan RS, Kannel WB, Ho KK. The progression from hypertension to congestive heart failure. JAMA. 1996;275(20):1557-1562. doi:10.1001/jama.1996.03530440037034 Major outcomes in high-risk hypertensive patients randomized to angiotensin-converting enzyme inhibitor or calcium channel blocker vs diuretic: the Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT). JAMA. 2002;288(23):2981-2997. doi:10.1001/jama.288.23.2981 Yusuf S, Sleight P, Pogue J, et al. Effects of an angiotensin-converting-enzyme inhibitor, ramipril, on cardiovascular events in high-risk patients. N Engl J Med. 2000;342(3):145-153. doi:10.1056/NEJM200001203420301 Zinman B, Wanner C, Lachin JM, et al. Empagliflozin, cardiovascular outcomes, and mortality in type 2 diabetes. N Engl J Med. 2015;373(22):2117-2128. doi:10.1056/NEJMoa1504720 Anker SD, Butler J, Filippatos G, et al. Empagliflozin in heart failure with a preserved ejection fraction. N Engl J Med. 2021;385(16):1451-1461. doi:10.1056/NEJMoa2107038 Solomon SD, McMurray JJV, Claggett B, et al. Dapagliflozin in heart failure with mildly reduced or preserved ejection fraction. N Engl J Med. 2022;387(12):1089-1098. doi:10.1056/NEJMoa2206286 Filippatos G, Anker SD, Agarwal R, et al. Finerenone reduces risk of incident heart failure in patients with chronic kidney disease and type 2 diabetes: analyses from the FIGARO-DKD trial. Circulation. 2022;145(6):437-447. doi:10.1161/CIRCULATIONAHA.121.057983 Solomon SD, McMurray JJV, Vaduganathan M, et al. Finerenone in heart failure with mildly reduced or preserved ejection fraction. N Engl J Med. 2024;391(16):1475-1485. doi:10.1056/NEJMoa2407107 Lincoff AM, Brown-Frandsen K, Colhoun HM, et al. Semaglutide and cardiovascular outcomes in obesity without diabetes. N Engl J Med. 2023;389(24):2221-2232. doi:10.1056/NEJMoa2307563 Deanfield J, Verma S, Scirica BM, et al. Semaglutide and cardiovascular outcomes in patients with obesity and prevalent heart failure: a prespecified analysis of the SELECT trial. Lancet. 2024;404(10454):773-786. doi:10.1016/S0140-6736(24)01498-3  Kosiborod MN, Abildstrøm SZ, Borlaug BA, et al. Semaglutide in patients with heart failure with preserved ejection fraction and obesity. N Engl J Med. 2023;389(12):1069-1084. doi:10.1056/NEJMoa2306963 Ndumele CE, Neeland IJ, Tuttle KR, et al. A synopsis of the evidence for the science and clinical management of cardiovascular-kidney-metabolic (CKM) syndrome: a scientific statement from the American Heart Association. Circulation. 2023;148(20):1636-1664. doi:10.1161/CIR.0000000000001175 Khan SS, Matsushita K, Sang Y, et al. Development and validation of the American Heart Association’s PREVENT equations. Circulation. 2024;149(6):430-449. doi:10.1161/CIRCULATIONAHA.123.067626 Khan SS, Ning H, Shah SJ, et al. 10-year risk equations for incident heart failure in the general population. J Am Coll Cardiol. 2019;73(19):2388-2397. doi:10.1016/j.jacc.2019.02.057 Bozkurt B, Fonarow GC, Goldberg LR, et al. Cardiac rehabilitation for patients with heart failure: JACC expert panel. J Am Coll Cardiol. 2021;77(11):1454-1469. doi:10.1016/j.jacc.2021.01.030 Packer M. Leptin-aldosterone-neprilysin axis: identification of its distinctive role in the pathogenesis of the three phenotypes of heart failure in people with obesity. Circulation. 2018;137(15):1614-1631. doi:10.1161/CIRCULATIONAHA.117.032474 Lala A, Tayal U, Hamo CE, et al. Sex differences in heart failure. J Card Fail. 2022;28(3):477-498. doi:10.1016/j.cardfail.2021.10.006 Bozkurt B, Coats AJS, Tsutsui H, et al. Universal definition and classification of heart failure. Eur J Heart Fail. 2021;23(3):352-380. doi:10.1002/ejhf.2115 Hershberger RE, Givertz MM, Ho CY, et al. Genetic evaluation of cardiomyopathy—a Heart Failure Society of America practice guideline. J Card Fail. 2018;24(5):281-302. doi:10.1016/j.cardfail.2018.03.004 Levine GN, Cohen BE, Commodore-Mensah Y, et al. Psychological health, well-being, and the mind-heart-body connection: a scientific statement from the American Heart Association. Circulation. 2021;143(10):e763-e783. doi:10.1161/CIR.0000000000000947 Ezekowitz JA, Colin-Ramirez E, Ross H, et al. Reduction of dietary sodium to less than 100 mmol in heart failure (SODIUM-HF): an international, open-label, randomised, controlled trial. Lancet. 2022;399(10333):1391-1400. doi:10.1016/S0140-6736(22)00369-5

Have you heard of Farxiga (dapagliflozin), Jardiance (empagliflozin), Ozempic, Wegovy, Mounjaro, or finerenone, but aren't quite sure what they do or whether they're right for people living with kidney disease?   In this episode of Diary of a Kidney Warrior Podcast, host Dee Moore is joined by Professor Alex, Consultant Nephrologist and researcher, for an essential conversation about some of the biggest breakthroughs in kidney medicine in recent years.   Originally developed for diabetes, SGLT2 inhibitors have transformed kidney care and are now helping to protect kidney function, reduce protein in the urine and improve outcomes for many people living with chronic kidney disease (CKD). We also explore the growing role of GLP-1 receptor agonists and finerenone, and explain what patients need to know about these treatments.   Whether you're living with chronic kidney disease, caring for someone who is, or you're a healthcare professional wanting a patient-friendly explanation, this episode is packed with practical, evidence-based information.   In this episode, you'll learn:   ✅ What SGLT2 inhibitors are and how they protect the kidneys ✅ Why medications developed for diabetes are now transforming kidney care ✅ How GLP-1 receptor agonists (including Ozempic, Wegovy and Mounjaro) may benefit kidney health ✅ What finerenone is and who may benefit from it ✅ Why your eGFR may temporarily fall after starting treatment—and why this isn't always a cause for concern ✅ The benefits and possible side effects of these medications ✅ Which kidney patients may be suitable for these treatments ✅ The latest developments in kidney research and future treatments   This episode shares expert insight designed to educate, empower and inspire people living with kidney disease and those who support them.  

New insights into PPID and EMS, including risk factors, hyperinsulinemia-associated laminitis, and the role of SGLT2 inhibitors in managing insulin dysfunction.Read the article here: https://equimanagement.com/research-medical/metabolic/updates-on-equine-endocrinological-disorders-ppid-and-ems/This article was transformed for your listening pleasure using AI resources.Mentioned in this episode:EquiManagement on Audio All the articles you have come to love in EquiManagement Magazine are now available in this podcast for free. Each article is released as its own separate episode to make them quick and easy to listen to. EquiManagement always has the latest insights on equine health, veterinary practice management, and veterinarian wellness.

In the July open access episode of Chattering With iCatCare, Yaiza Gómez-Mejías is joined once again by feline specialist Nicki Reed to continue navigating the high-pressure world of feline medical emergencies. This second part shifts focus towards managing other challenging, high-stakes medical crises frequently encountered in general practice.They explore how to optimise positioning for the seizuring patient, why certain clinical markers can predict severe hyperkalemia in blocked cats before catheterisation, and how to spot the elusive signs of antifreeze toxicity. Nicki also breaks down the unique challenges of managing euglycaemic DKA following the rise of SGLT2 inhibitors and shares essential steps for making emergency referral transport as safe as possible.For further reading material please visit:Rational approach to feline medical emergencies: part 22024 RECOVER GuidelinesHost:Yaiza Gómez-Mejías, LdaVet MANZCVS (Medicine of Cats), RCVS CertAP (Feline Medicine), iCatCare Veterinary Community Co-ordinatorSpeaker:Nicki Reed, BVM&S CertVR CertSAM DipECVIM-CA DSAM(Feline) FRCVS, Internal Medicine & Feline Specialist

Welcome to the Hot Topics podcast from NB Medical with Dr Neal Tucker. In this episode, we have three new pieces of research and a special interview later on discussing the recommendations of the National Screening Committee on prostate cancer screening in the UK.First up for research: nasal sprays versus the common cold. The BJGP reports on longer-term findings through this simple intervention. Can it help this age-old problem?Second, new kid on the block, orforglipron - could it replace SGLT2 inhibitors for management of type 2 diabetes?Third, home-based hypnotherapy. Can it help children struggling with functional abdominal pain or IBS? We have a RCT to tell us. Finally, our interview with Dr Liz Bancroft, consultant nurse in oncogentics research, and Natalia Norori, interim Head of Data and Evidence at Prostate Cancer UK join us to discuss the new recommendations from the National Screening Programme with targeted screening of men with BRCA2, why they made this recommendation and how this affects us in general practice, plus what we need to know for our patients about the government-backed trial, TRANSFORM.ReferencesProstate Cancer UK Information on NSC decisionProstate Cancer UK Health Professional NSC FAQsNational Screening Committee report on prostate cancer screeningBJGP Nasal sprays for the common coldLancet Nasal Sprays original paperLancet Orforglipron vs dapagliflozin and T2DMBJGP Hypnotherapy in children for abdo painNational Screening Committee report on prostate cancer screeningwww.nbmedical.com/podcast

Randomized evidence suggests that routinely used mucoactive therapies may no longer have a role in mechanically ventilated ICU patients, while a large comparative effectiveness study indicates GLP-1 receptor agonists may offer superior cardiovascular and atrial fibrillation outcomes compared with SGLT2 inhibitors in patients with both AF and type 2 diabetes. We also highlight a promising blood-based RNA biomarker panel that may predict Alzheimer's symptom onset several years before cognitive decline, potentially improving patient selection for emerging disease-modifying therapies.

Drs. Witteles and Alexander discuss emerging data in transthyretin amyloid cardiomyopathy, highlighting durable survival benefits with long-term transthyretin-stabilizing therapy and the prognostic impact of atrial arrhythmias. They also review sex-related differences in phenotype that may contribute to under-recognition in women and emphasize earlier diagnosis with more nuanced, holistic management strategies.

➡️ Ouça o novo episódio do UroCast ABC!

It's In the News - a look at the top diabetes headlines and stories happening now. Our top stories: More information about type 1 and COVID, including the vaccine, why is the latest GLP-1 medication, not yet FDA approved, showing up all over the place, what table sugar and vinegar could mean for drug costs, a new inhaled insulin study and much more  I'll see you at Friends for Life next week. Come find me at Table T18 Learn more about our in-person events here: https://diabetes-connections.com/events/ Announcing Community Commericals! Learn how to get your message on the show here. Learn more about studies and research at Thrivable here Please visit our Sponsors & Partners - they help make the show possible! Omnipod - Simplify Life All about Dexcom  All about VIVI Cap to protect your insulin from extreme temperatures The best way to keep up with Stacey and the show is by signing up for our weekly newsletter: Sign up for our newsletter here Here's where to find us: Facebook (Group) Facebook (Page) Instagram Check out Stacey's books! Learn more about everything at our home page www.diabetes-connections.com  Transcript & links:    Okay.. our top story this week: XX A large Swedish study found that the increased risk of being diagnosed with type 1 diabetes after COVID-19 infection is mostly limited to the first 30 days after infection and does not continue long term. Researchers followed nearly the entire Swedish population under age 80 from 2020 through 2023 and found that while SARS-CoV-2 infection was linked to a temporary rise in new type 1 diabetes diagnoses, the risk declined over time. The study also found no evidence that COVID-19 vaccination increases the long-term risk of developing type 1 diabetes. Vaccination did not significantly change the relationship between COVID-19 infection and diabetes risk, and any small increase in diagnoses seen among adults shortly after a first vaccine dose was not seen after later doses or during longer follow-up. The researchers concluded that their findings do not support changing current COVID-19 vaccination recommendations because of concerns about type 1 diabetes risk. https://www.infectiousdiseaseadvisor.com/news/covid19-infection-may-increase-short-term-type-1-diabetes-risk/ XX Two new studies are challenging the traditional view that type 1 diabetes develops solely because the immune system attacks insulin-producing beta cells. Researchers from Indiana University found evidence that beta cells themselves may play an active role in determining whether they survive or succumb to the stresses that lead to type 1 diabetes. In the first study, scientists discovered that some healthy human beta cells can quickly activate an antiviral defense system when exposed to interferon-alpha, an immune signal often produced during viral infections. This response relies on molecules called reactive oxygen species (ROS), which are usually associated with cell damage but, in this case, appeared to help switch on protective antiviral genes. Researchers found this defense program in healthy cells and in people at risk for type 1 diabetes, but not in beta cells from people who already had the disease. The findings suggest that losing this built-in defense mechanism may make beta cells more vulnerable during the development of type 1 diabetes. The second study focused on autophagy, the process cells use to recycle damaged or worn-out components. Using a new imaging technique, researchers observed that beta cells in a mouse model of type 1 diabetes showed defects in autophagy before blood sugar levels began to rise and even before a full immune attack was underway. This suggests that problems inside the beta cells may occur early in the disease process rather than being caused entirely by the immune system. Together, the studies point to a more complex picture of type 1 diabetes. While they do not show that beta-cell defects cause the disease, they suggest that differences in how beta cells respond to stress, viral signals, and cellular damage may influence who develops type 1 diabetes and how the disease progresses. https://medicalxpress.com/news/2026-06-beta-cells-players-diabetes.html XX Researchers have created the most detailed map yet of how the human pancreas develops during childhood, offering new clues about why children are especially vulnerable to developing diabetes. The study, published in Nature Communications, examined pancreatic tissue from 123 children without diabetes, ranging from newborns through age 10. Using advanced imaging techniques, scientists tracked how insulin-producing islet cells grow and mature during the first decade of life. The researchers found that pancreas size varies dramatically at birth, with some infants having pancreases nearly four times larger than others. They also discovered that insulin-producing beta cells grow more slowly after birth than previously thought, suggesting that much of a person's lifelong beta cell capacity may be established before birth and during early childhood. Other findings showed that insulin-producing cells mature earlier than glucagon-producing cells and that new hormone-producing cells may continue to form after birth. The researchers hope this new understanding of pancreas development will help scientists identify diabetes risk earlier and develop better strategies for prevention and treatment in children. https://news.vumc.org/2026/06/29/unlocking-diabetes-secrets-pediatric-organ-donors-help-map-a-path-to-a-cure-and-prevention/   XX At the American Diabetes Association annual meeting, 2-year results from the SUPPRESS-EARLY trial showed that initiating tirzepatide (Mounjaro, Zepbound) early in the course of type 2 diabetes led to substantially higher rates of near-normal glycemic control and also led to broader metabolic improvements compared with intensive conventional therapy.   In this MedPage Today video, investigator Stefano Del Prato, MD, of the University of Pisa in Italy, discusses the findings.     Following is a transcript of his remarks:   What happened is that in the tirzepatide-treated arm, 85% of the population at the end of the second year was on the maximum dose of tirzepatide 15 mg. And then the remaining 15 with the different doses.   Interestingly, in the population that had been treated with the intensive conventional approach, 85% of them ended up to have, on top of metformin, a GLP-1 receptor agonist, mainly represented by subcutaneous semaglutide [Ozempic, Wegovy], 60+%, another 15% on oral semaglutide [Rybelsus], and the remaining on dulaglutide [Trulicity].   And I have to say that maybe the recommendation to really push along the line to try to achieve and to strive to achieve [glycemic] control was successful in these individuals. Because the population that had been recruited in the study started off with a baseline A1C of 7.8% and it went down to 6.3% in the conventionally intensive treatment, which is not bad at all, on average is below the target of 6.5%.     However, when we look at the effect of tirzepatide, the final level of A1C at the end of the second year was 5.6%, which is on average below the upper limit of the normal range for A1C, 5.7%. This also translates into more people not only achieving normal glycemia, if we can define normal glycemia as A1C below 5.7%, greater than what we observed in conventionally treated individuals. So it was around three times more people achieving an A1C of 5.7%, in the range of around 65%, as compared to 28% with people on a conventional optimized treatment.   Now, this is not surprising knowing the potency of tirzepatide. But again, going back to the rationale of the design, can we change what is the natural history of the disease? This seems to be at least of interest and it's possibly changing the trajectory of the disease for glycemic control, as I mentioned, but also in terms of the body weight and waist circumference because both body weight and waist circumference went much lower with tirzepatide compared to the conventional treatment.   Tirzepatide also was associated with an improvement in the lipid profile, in particular with the LDL, triglycerides, and the triglyceride concentration and non-HDL cholesterol, and also with a statistically significantly lower systolic blood pressure with a numerical reduction in the diastolic blood pressure.   And also the other thing that probably will ... become more apparent with the study continuing is that the investigators were allowed to add on any other treatment ... needed to achieve their target. So tirzepatide was just metformin and tirzepatide. In the control group, there was already 10% of people who were receiving two drugs on top of the metformin.   So another potential result of the trial is that it's possible to achieve and maintain better glycemic or better metabolic control over the time without really needing to increase the number of medications in order to achieve that goal. And we know that type 2 diabetes is a progressive condition often requiring intensification of the treatment.   So these initial results really stand for a great opportunity with tirzepatide. Of course, we need to wait for the 4 years just to confirm that this is indeed the case, but the initial result seems to point along that line. https://www.medpagetoday.com/meetingcoverage/adavideopearls/121967 XX A study from the University of Virginia found that high blood pressure is extremely common among people with diabetes, even among those who believe their blood pressure is under control. Researchers measured blood pressure in 172 adults with type 1 or type 2 diabetes during routine eye clinic visits and found that only 8% had normal readings. About half had stage 2 hypertension, and more than 10% had blood pressure levels high enough to be considered a medical emergency. The study also revealed that many patients were unaware of how serious their blood pressure problems were. Among those who thought their hypertension was well controlled, more than half still had stage 2 hypertension. Nearly 60% of participants were advised to contact their primary care provider, and one patient required an emergency department referral. Most patients supported blood pressure screening during eye exams, leading researchers to suggest that routine blood pressure checks in ophthalmology clinics could help identify undiagnosed or poorly controlled hypertension before it leads to serious complications such as heart attack, stroke, or worsening diabetic eye disease. https://medicalxpress.com/news/2026-06-routine-eye-exams-reveal-stage.html XX What is going on with retatrutide? This is the next generation GLP-1 but it's not authorized outside of clinical trials. Big investigation by CBS shows retatrutide is for sale all over the internet, a phenomenon they say has no modern precedent. CBS News identified more than 120 websites selling or promoting retatrutide, including more than 50 clinics staffed by licensed medical professionals. After being contacted by CBS News, at least 21 clinics abruptly removed retatrutide from their websites or changed the language to state they don't offer it. Others defended prescribing it, saying they're confident enough in results from clinical trials sponsored by drugmaker Eli Lilly that they didn't need to wait for the FDA's independent, rigorous review. An FDA spokesperson said retatrutide "has not been found safe or effective for any condition," adding that it "cannot be manufactured or distributed except for investigational use." The Justice Department is prosecuting two cases – in Utah and Florida – involving the sale and prescription of retatrutide. But the first line of enforcement is often at the state level. Ohio's Board of Pharmacy has taken action against several pharmacies and clinics providing retatrutide, and just last month, Alabama's Medical Board warned physicians against prescribing research-grade medications. The FDA has sent 14 warning letters to companies that have advertised retatrutide since 2024. Of these, at least six have continued to offer it online, including a business called Pink Pony Peptides. A TikTok account associated with the firm responded to the warning in April by taunting the FDA, boasting that the business "just had the best 24 hours ever." In May, Eli Lilly announced that participants in a large clinical trial taking the highest dose of retatrutide lost an average of 28% of their body weight over 80 weeks. Side effects – including nausea, diarrhea, constipation and vomiting – were comparable to similar therapies, the company said. "Anyone purporting to sell retatrutide to consumers is breaking the law," an Eli Lilly spokesperson said https://www.cbsnews.com/projects/2026/experimental-weight-loss-drug/ XX Pioneering research has developed a new way of creating carbohydrate-based medicines, which could ultimately replace costly drugs for common health conditions, using two cheap basic ingredients – table sugar and vinegar. These medications include SGLT2 inhibitors, widely prescribed drugs used to treat type 2 diabetes, heart failure and chronic kidney disease. Co-lead author Professor Phil Baran, Dr. Richard A. Lerner Endowed Chair at Scripps Research, in San Diego, California, said: "The point of this is to show that anyone in a garage can make an SGLT2 inhibitor with reagents that are widely available. We have not patented this method, so we welcome any generic drug company – or anyone else – who wants to use it to help bring costs down for patients." https://www.newswise.com/articles/new-study-shows-table-sugar-could-hold-a-cheaper-quicker-key-to-making-vital-drugs-for-diabetes-heart-failure-and-chronic-kidney-disease XX England and Wales approve teplizumab to slow progression of T1D. At the moment, the Scottish Medicines Consortium does not have an appraisal of Tzield on the go, so, there is likely to be a disparity in access within the UK for the time being. In Northern Ireland, access will depend on a review and adoption of NICE guidance.  Sanofi is expecting to see an uptick in momentum thanks to two subsequent FDA approvals, one in children as young as one with stage 2 T1D, and a second to delay the decline in endogenous insulin production in children aged eight to 17 years recently diagnosed with stage 3 T1D. btw you might here more people referring to stage 4 diabetes. They've added that to include people diagnosed with type 1 who've been on insulin for a longer period of time – basically long enough to not be eligible for the current guidelines for Tzield. https://www.bbc.com/news/articles/ce8mzd94r76oXX XX Obesity Association, a division of the American Diabetes Association® (the association), announced the next section in the Standards of Care in Overweight and Obesity, "Screening, Diagnosis, Evaluation, and Staging of Obesity in Adults," published in Diabetes, Obesity, and CardioMetabolic CARE® and BMJ Open Diabetes Research & Care.  Key highlights of the guidance: Early screening: Annual BMI screening with emphasis on tracking weight trends to identify risk earlier, including a longitudinal life-event weight graph tool for standardized assessment. Enhanced diagnosis: Combines BMI with waist measurements and population-specific thresholds to improve accuracy. Notably, the guidelines recommend that BMI in the overweight range together with central adiposity measurements warrant a formal obesity diagnosis. Comprehensive evaluation: Holistic assessment including medical, behavioral, and social factors. Offers a fully integrated obesity diagnostic algorithm. Risk stratification: Use of tools like the Edmonton Obesity Staging System to guide care. Chronic care approach: Ongoing monitoring and follow-up to support long-term management. Reducing bias: Promotes person-centered, non-stigmatizing care and system-level improvements at the clinical workflow level and encourages screening for prior weight bias/stigma experiences. https://www.prnewswire.com/news-releases/new-standards-of-care-in-overweight-and-obesity-section-screening-diagnosis-evaluation-and-staging-of-obesity-in-adults-302809670.html XX Dexcom (Nadsaq:DXCM) today announced the launch of its fully reimagined Stelo over-the-counter (OTC) sensor app experience. San Diego-based Dexcom plans to formally begin the new app rollout in July for Apple iPhone and Android users in the U.S. Dexcom said its reimagined app aims to make glucose insights easier to understand and act on. It hopes to help build awareness of how food, activity, sleep and stress influence overall wellbeing.   The company also reiterated plans to launch Stelo internationally. It expects to bring the sensor to the UK, Australia, New Zealand and South Korea later this year, continuing into 2027. https://www.drugdeliverybusiness.com/dexcom-launches-enhanced-stelo-app/ XX MannKind Corporation recently announced it received a grant from Breakthrough T1D to support the INHALE-1 clinical study of Afrezza, its ultra rapid-acting inhaled insulin, in newly diagnosed pediatric type 1 diabetes patients aged 10 to under 18 years. This external funding for a trial focused on early use of Afrezza in children highlights growing third-party support for inhaled insulin in pediatric diabetes care. https://simplywall.st/stocks/us/pharmaceuticals-biotech/nasdaq-mnkd/mannkind/news/afrezza-pediatric-trial-grant-might-change-the-case-for-inve XX Alexander Zverev heads into Wimbledon with plenty of momentum. The French Open champion returns to the All England Club looking to build on his first Grand Slam title and gain ground on Carlos Alcaraz in the race for the No. 2 spot in the ATP rankings. Zverev has an opportunity to make up points quickly after a first-round exit at Wimbledon last year. But his final tune-up before Wimbledon came with an unexpected challenge. During his semifinal loss to Taylor Fritz at the Halle Open, Zverev said a malfunctioning glucose sensor led to serious diabetes management issues on court. The sensor incorrectly showed his blood sugar was high when it was actually low, causing him to take more insulin than needed. "I had huge problems with the sugar because the sensor I use gave me a completely incorrect reading," Zverev said after the match. "During the match, or rather during the first 45 minutes, I had to consume about 350 grams of sugar. I felt absolutely terrible." Despite feeling unwell, Zverev pushed the match to three sets before falling 6-7(4), 6-4, 7-5 to Fritz. He credited his opponent with playing the better match and said the diabetes-related issue was not an excuse for the result. Zverev, who was diagnosed with type 1 diabetes at age 4, uses Medtronic diabetes technology to help manage his glucose levels while competing on the ATP Tour. He said the sensor error was the first major problem he has experienced after nearly a decade of using the technology. The German said the incident should not affect his Wimbledon preparations. With the sensor issue behind him, Zverev will begin his Wimbledon campaign focused on adding another strong result to what has already been a breakthrough season.   https://www.reuters.com/sports/tennis/zverev-says-glucose-sensor-malfunction-affected-halle-semi-final-loss-fritz-2026-06-21/

To begin the episode, cohosts Diana Isaacs, PharmD, and Natalie Bellini, DNP, discuss the rapidly evolving landscape of wearable insulin delivery, focusing on recent developments in patch pump technology and the growing number of tubeless insulin delivery systems entering the market. The conversation centers on the recent FDA clearance of the Pivot patch pump from Modular Medical, which the hosts describe as an important addition to a field that has historically been dominated by a single tubeless option.Isaacs reviews the design of the Pivot system, explaining that while it is a tubeless insulin pump, it differs from current automated insulin delivery (AID) systems because it does not communicate with a continuous glucose monitor (CGM) or use an insulin-dosing algorithm. Instead, the device delivers programmable basal insulin with ≤2 selectable basal rates and allows users to administer manual bolus doses. The hosts note its 300-unit insulin reservoir, highlighting the larger capacity as a potential advantage for individuals with higher daily insulin requirements.Bellini discusses where Pivot may fit into current clinical practice, suggesting it could provide an option for people who are unwilling or unable to use CGM technology but would still benefit from wearable insulin delivery. She also points to the possibility of future partnerships with commercially available AID algorithms, which could allow the platform to evolve into a more automated system. The hosts acknowledge that current diabetes guidelines generally favor AID for individuals with type 1 diabetes but recognize that simplified technologies continue to have an important role for select patient populations.The discussion expands to the broader pipeline of tubeless insulin pumps currently under development. Isaacs and Bellini review anticipated products from Tandem, Beta Bionics, and Medtronic, noting that virtually every major insulin pump manufacturer is now investing in patch pump technology. They compare reservoir capacities, expected timelines, and device designs while emphasizing the increasing demand for tubeless systems that improve convenience and reduce many of the practical challenges associated with traditional tubing.The hosts also examine several practical design considerations. They discuss Pivot's reusable and disposable components, explaining that many newer patch pumps incorporate reusable elements because of existing intellectual property surrounding fully disposable tubeless systems. While reusable components may lower manufacturing costs, they also introduce considerations such as the potential for patients to misplace components or inadvertently lose them during hospitalizations. Isaacs adds that the simplified design and absence of an onboard algorithm may ultimately make the device more affordable, although real-world pricing remains to be determined.Attention then shifts to recent updates from CeQur Simplicity, which recently announced a 7-day bolus-only patch featuring an expanded 240-unit insulin reservoir and a new one-unit dosing option for individuals requiring smaller mealtime insulin doses. The hosts discuss how these enhancements could broaden the device's applicability while maintaining its emphasis on simplicity, requiring neither smartphone connectivity nor a dedicated mobile application.Bellini highlights the potential synergy between the 7-day patch and emerging once-weekly basal insulin formulations, suggesting that synchronizing weekly basal insulin administration with weekly patch replacement could simplify treatment routines and improve adherence. She emphasizes that insulin therapy should continue to complement guideline-directed pharmacologic management, including GLP-1 receptor agonists, SGLT2 inhibitors, and other glucose-lowering therapies when appropriate.The episode concludes with an optimistic assessment of the future of insulin delivery technology. Isaacs and Bellini emphasize that increasing competition among manufacturers is likely to expand patient choice, improve affordability, and accelerate innovation. They express particular enthusiasm for the continued growth of tubeless insulin delivery, broader pharmacy benefit coverage, and the next generation of AID systems, all of which they believe will further individualize diabetes management and improve outcomes for people requiring insulin therapy.Editors' Note: Isaacs reports disclosures with Dexcom, Abbott, Lilly, Novo Nordisk, Medtronic, Insulet, and others. Bellini reports disclosures with Abbott Diabetes Care, MannKind, Povention Bio, and others.

Darshan H. Brahmbhatt, Podcast Editor of JACC: Advances, discusses a recently published original research paper on SGLT2 Inhibitors in Cardio-Oncology: A Systematic Review and Meta-Analysis.

Commentary by Dr. Jian'an Wang.

CME credits: 0.25 Valid until: 23-06-2027 Claim your CME credit at https://reachmd.com/programs/cme/translating-evidence-into-action-nonsteroidal-mras-in-patients-with-hf/49259/ In this panel discussion from the ESC Heart Failure Congress 2026, Drs. Muthu Vaduganathan, Michael Böhm, and Koichiro Kinugawa discuss the role of nonsteroidal MRAs in patients with HFmrEF and HFpEF. Using a clinical case, the faculty review evolving recommendations supporting finerenone as part of guideline-directed medical therapy, along with evidence from FINEARTS-HF and related analyses. The discussion highlights considerations for early initiation, use in combination with SGLT2 inhibitors, patient selection, dosing and monitoring, and management of potassium and renal function changes in clinical practice.=

Check out the video version of this episode on HCPLive!Finerenone's expansion into non-diabetic kidney disease is prompting a broader rethink of how chronic kidney disease is measured, mechanistically understood, and treated across its many causes.On an episode of Don't Miss a Beat recorded at the 10th Annual Heart in Diabetes Meeting, hosts Stephen Greene, MD, meeting co-chair and heart failure specialist at Duke University School of Medicine, and Muthiah Vaduganathan, MD, MPH, codirector of the Center for Cardiometabolic Implementation and cardiologist at Brigham and Women's Hospital, spoke with Katherine Tuttle, MD, professor of medicine at the University of Washington, about the phase 3 FIND-CKD trial and how it informs on the overall role of finerenone (Kerendia) in management of cardiovascular-kidney-metabolic syndrome.FIND-CKD showed finerenone slowed total estimated glomerular filtration rate (eGFR) slope by 0.7 mL/min/1.73 m² per year versus placebo, irrespective of diagnosis. Much of the discussion focused less on the number and more on why it counts as clinically meaningful.Drawing on CKD Prognosis Consortium data from hundreds of thousands of patients, Tuttle explained why eGFR slope reliably predicts kidney failure when a trial runs at least 2 years. CKD progresses rather than striking as a discrete event, so the field has moved toward endpoints measurable without waiting for organ failure or death.On safety, hyperkalemia occurred more often with finerenone than placebo, about 12% versus 3%, though fewer than 1% of patients discontinued. The framing was practical, with background SGLT2 inhibition expected to lower the risk.Mechanism anchors much of the conversation between Tuttle, Greene, and Vaduganathan.Tuttle highlighted how glomerular diseases, like IgA nephropathy, are immunologic disorders needing disease-specific therapy, yet all CKD converges on shared final common pathways of inflammation and fibrosis. Broad agents like finerenone target those pathways, making combination therapy the emerging model, pairing treatment of the inciting disease with control of progression.The group also discussed the field's trend toward precision nephrology. Protocol biopsies from the Kidney Precision Medicine Project showed only about half of patients labeled as diabetic CKD had classic diabetic nephropathy. A parallel to oncology followed, where deep phenotyping replaced uniform regimens, suggesting not every patient will need every drug.Tuttle positioned finerenone alongside renin-angiotensin system inhibitors and SGLT2 inhibitors as an emerging pillar for non-diabetic CKD, with GLP-1 receptor agonists and endothelin antagonists possibly to come. A pooled analysis of FIDELIO-DKD, FIGARO-DKD, and FIND-CKD showed roughly 30% reductions in kidney and cardiovascular outcomes and an 11% drop in all-cause mortality. The closing point held the cardiorenal patient often arrives through either specialty's door, making preservation of organ function and quality of life the shared aim.Relevant disclosures for Tuttle include Alnylam, AstraZeneca, Bayer, Boehringer Ingelheim, Eli Lilly, GSK, Novo Nordisk, Roche, and Travere Therapeutics. Relevant disclosures for Vaduganathan include Amgen, AstraZeneca, Bayer AG, Boehringer Ingelheim Pharmaceuticals, Cytokinetics, Lexicon, and others. Relevant disclosures for Greene include Amgen, AstraZeneca, Bayer Healthcare Pharmaceuticals, Boehringer Ingelheim Pharmaceuticals, Cytokinetics, and others.References: Heerspink HJL, Neuen BL, Agarwal R, et al. Finerenone in Persons with Chronic Kidney Disease without Diabetes. N Engl J Med. Published online June 4, 2026. doi:10.1056/NEJMoa2604625 Bayer. Bayer to Present First Full FIND-CKD Results Investigating KERENDIA® (finerenone) in Non-Diabetic Chronic Kidney Disease at ERA 2026. Bayer.com. Published June 2, 2026. Accessed June 21, 2026. https://www.bayer.com/en/us/news-stories/kerendia-in-non-diabetic-chronic-kidney-disease

The new 2026 AHA/ACC/ADA/ASN Cardiovascular–Kidney–Metabolic (CKM) Guideline reframes chronic disease through a unified lens connecting obesity, diabetes, chronic kidney disease, and cardiovascular disease. Key themes: ✅ CKM staging across the life course ✅ PREVENT risk assessment for personalized care ✅ Early detection of kidney and cardiometabolic risk ✅ Lifestyle and weight management as foundational therapy ✅ Evidence-based use of SGLT2 inhibitors and GLP-1–based therapies ✅ Team-based, patient-centered care A landmark step toward integrated prevention and better long-term outcomes. #Cardiology #Nephrology #Diabetes #Obesity #CKM #PreventiveCardiology #MedicalPodcasts #PrecisionMedicine #HeartFailure #KidneyDisease

Fontes do episódio aqui: https://portal.afya.com.br/podcasts/afya-news/25-05-2026Nesta segunda-feira, analisamos alertas de biossegurança internacional, ampliações importantes no acesso a tratamentos crónicos no Brasil e a evolução digital da saúde. Começamos com a confirmação de novos casos de Ebola em Uganda envolvendo a cepa rara Bundibugyo, que acende o alerta para a proteção das equipas de saúde. Detalhamos a aprovação pela Anvisa do primeiro genérico da associação entre dapagliflozina e metformina para o diabetes tipo 2, uma medida que promete expandir o acesso e a adesão ao tratamento com inibidores de SGLT2. Por fim, abordamos no Radar a expansão do atendimento virtual e dos hospitais conectados suportados por IA. Afya News. Informação médica confiável e atualizada no seu tempo.

Discover how dual sodium-glucose cotransporter 1/2 (SGLT1/2) inhibition can improve outcomes for your patients across the heart failure (HF) spectrum. Credit available for this activity expires: 05/15/27 Earn Credit / Learning Objectives & Disclosures: https://www.medscape.org/viewarticle/beyond-sglt2-emerging-role-dual-sglt1-2-inhibition-heart-2026a1000es7?ecd=bdc_podcast_libsyn_mscpedu

Send us Fan MailEver wonder why some people thrive on weekly semaglutide while others prefer daily dosing or a combo approach? We take you inside the GLP-1 playbook—how these medications mimic a natural hormone to calm appetite, smooth blood sugar, and make weight loss feel doable instead of punishing. Along the way, we compare short-acting and long-acting options in plain language, lay out when combination therapy with insulin or SGLT2 inhibitors makes sense, and share the small lifestyle edits that turn good results into great ones.We dig into the physiology that matters in real life: insulin up when you need it, glucagon down when you do not, slower gastric emptying that actually keeps you full, and what that means for cravings at 9 p.m. Then we connect the dots to daily choices—protein-forward meals, high-fiber staples, and low glycemic index foods that amplify GLP-1 signaling rather than fight it. You will also hear why the gut microbiome is not just a buzzword here, how fermented foods and prebiotic fibers can support endogenous GLP-1, and why a simple post-meal walk can be as strategic as your next dose adjustment.Safety is front and center. We outline common side effects like nausea and how to ease them with slower titration and smarter meal timing, plus the growing evidence for cardiovascular benefits when therapy is monitored well. Most importantly, we focus on personalization: picking a dosing rhythm you can stick with, integrating stress management and sleep, and keeping an ongoing dialogue with your clinician so the plan flexes as your life changes.If this helped clarify your options, follow the show, share it with a friend who is weighing GLP-1 therapy, and leave a quick review to tell us what you want to learn next. Support the showSponsor Affiliates Empowering Your Healthhttps://www.atecam.com/Get YOUR Own Joburg Protein Snacks Discount Code:  Damaris15 Or Damaris18Feeling need to Lose Weight & Become metabolically HealthyGET METABOLIC COURSE GLP 1 REseTThis course is designed for individuals looking to optimize their metabolic health through integrative and functional medicine approaches. Whether you're on a GLP-1 medication or seeking natural ways to enhance your metabolic function, this course provides actionable steps, expert insights, and a personalized roadmap sustainable wellness.Are you feeling stressed, tired, or Metabolism imbalanced? Take advantage of our free mindful steps to help improve your well-being.ENJOY ONE OF our Books Mindful Ways  Health Wealth & Life https://stan.store/MindfullyintegrativeJoin Yearly membership ALL IN ONE  FUNCTION HEALTHAsk Us for help with Medica...

In Part 2, Pranav Garimella discusses major advances in diabetic kidney disease management. Learn how sodium-glucose cotransporter 2 (SGLT2) inhibitors and novel therapies are reshaping disease progression, and why early intervention is critical to improving long-term outcomes. Timestamps: 01:07 – Practice-changing developments 05:10 – GLP-1 agonists 07:00 – Early intervention 08:43 – Unmet needs

In the final episode, Pranav Garimella explores glomerular and cystic kidney diseases, including IgA nephropathy and autosomal dominant polycystic kidney disease. Discover how personalised medicine, biomarkers, and earlier diagnosis are shaping the future of care in these complex conditions. Timestamps: 01:11 – Current treatment for IgA nephropathy 02:24 – SGLT2 inhibitors 03:38 – Cystic kidney disease diagnosis

This inaugural episode of Mind the Meds introduces neurology pharmacy practice through a discussion between 3 neurology pharmacists working across inpatient and outpatient settings at the University of Utah. Host Erica Marini, PharmD, meets with her colleagues, Sarah Dahoney, PharmD, and Tyler Kenny, PharmD, BCCCP, both of whom are clinical pharmacists at the University of Utah Health, to discuss the research presented at the 2026 American Academy of Neurology (AAN) Annual Meeting. After sharing their diverse professional “origin stories,” the conversation then shifts to the role of pharmacists in neurology care and highlights key updates from the American Academy of Neurology annual meeting. The hosts discuss advances in neuromuscular disease, particularly myasthenia gravis, where emerging therapies such as FcRn inhibitors and CAR T-cell therapies are reshaping treatment paradigms. They also explore rare neurological conditions like stiff person syndrome and Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD), where early-phase trials suggest promising but still preliminary therapeutic options. Finally, the episode reviews broader neurologic and systemic trends, including GLP-1 receptor agonists and SGLT2 inhibitors, noting potential but not yet definitive benefits in dementia prevention, stroke risk reduction, and migraine outcomes. Across all topics, the episode emphasizes the rapid evolution of neurological therapeutics and the expanding role of pharmacists in maneuvering complex, high-cost, and highly specialized treatments.Key Takeaways: Neurology pharmacy is highly collaborative and evolving, with non-linear career pathways. Pharmacists in neurology often enter the field through diverse experiences rather than a standardized training pipeline, and success depends heavily on adaptability, clinical curiosity, and initiative.  Pharmacists play a critical role in optimizing complex neurological therapies and care transitions. Their contributions span inpatient safety monitoring, outpatient medication access and affordability support, and ensuring continuity of care for high-risk, high-cost therapies.  Neurology therapeutics are rapidly advancing, but many emerging treatments remain early-stage. New therapies such as FcRn inhibitors, CAR T-cell approaches, and complement-targeting agents show promise across conditions like myasthenia gravis and rare neuroimmunologic diseases, while broader drug classes like GLP-1s are still under investigation for neurological benefits. 

Your cells start failing at 35. Dr Sandra Kaufmann reveals the 7 systems breaking down — and how to stop it. Your cells start failing at 35. Dr Sandra Kaufmann reveals the 7 systems breaking down — and how to stop it.

Chronic kidney disease (CKD) affects an estimated 37 million Americans, yet most cases go undiagnosed until the disease has significantly progressed. A urine albumin-to-creatinine ratio (uACR) test can detect kidney damage years before a decline in the estimated glomerular filtration rate (eGFR), but it remains underutilized. In the first episode of Beyond the Silo: Integrated Care Across the CRM Continuum, a podcast series from The American Journal of Managed Care®, Marc P. Bonaca, MD, MPH, moderates a discussion with Josephine Harrington, MD, on why uACR has not yet become a standard of care, how CKD fits into the broader cardio-renal-metabolic (CRM) disease continuum, and what changes are needed across specialties, systems, and workflows. Bonaca is a cardiologist and vascular medicine specialist at the University of Colorado Anschutz and the executive director of CPC Clinical Research. Harrington is also a cardiologist, specializing in advanced heart failure and transplant cardiology at UCHealth's Heart and Vascular Center at the University of Colorado Hospital. Throughout the conversation, they emphasize that CKD is an early integral part of the CRM continuum, as it is both a driver and consequence of cardiovascular risk, with uACR elevation often appearing before eGFR decline and signaling increased risk even at mild levels. Despite strong guideline support, uACR screening remains underused due to structural barriers. Therefore, the experts explained that the primary barrier is not the test itself but the lack of streamlined workflows that make screening routine and results actionable without adding clinician burden. They concluded that early detection is critical because it enables the timely use of therapies such as SGLT2 inhibitors, glucagon-like peptide-1 receptor agonists, and finerenone, which improve outcomes. To close the gap, the experts noted that uACR should be treated as a routine vital sign for cardiometabolic risk and embedded into health system quality metrics to ensure consistent, accountable use.

This podcast episode provides nurses with a clear, practical overview of non-insulin diabetes medications, focusing on how to safely and effectively manage patients with type 2 diabetes. It reviews key drug classes such as metformin, glipizide, empagliflozin, and semaglutide, emphasizing mechanisms of action, common side effects, and important monitoring parameters. Nurses will learn how to recognize risks like hypoglycemia with sulfonylureas, genitourinary infections with SGLT2 inhibitors, and gastrointestinal effects with GLP-1 agents, along with key patient counseling points. The episode also connects medication selection to real-world considerations such as weight impact, cardiovascular benefit, and kidney function, helping nurses feel more confident in supporting individualized diabetes care. Be sure to check out our free Top 200 study guide – a 31 page PDF that is yours for FREE!

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.

If you're managing patients with heart failure, you already know the medication landscape has evolved quickly over the past decade. From traditional volume management with furosemide to newer, guideline-driven therapies like sacubitril/valsartan and empagliflozin, staying up to date is essential—but not always easy. In this episode, we break down three cornerstone medication classes you'll encounter every day in practice: loop diuretics, ARNI therapy, and SGLT2 inhibitors. We start with the fundamentals of loop diuretics—how they work, when to use them, and key monitoring parameters—before shifting into the mortality-reducing benefits of ARNI therapy. Finally, we explore the rapidly expanding role of SGLT2 inhibitors, which have transformed both heart failure and chronic kidney disease management. Whether you're a pharmacist, nurse, or student, this episode focuses on practical, real-world application. We highlight clinical pearls, common pitfalls, and monitoring strategies to help you feel more confident when optimizing therapy. Tune in to sharpen your understanding of these essential therapies and walk away with actionable insights you can use right away in patient care. Be sure to check out our free Top 200 study guide – a 31 page PDF that is yours for FREE! Support The Podcast and Check Out These Amazing Resources! NAPLEX Study Materials BCPS Study Materials BCACP Study Materials BCGP Study Materials BCMTMS Study Materials Meded101 Guide to Nursing Pharmacology (Amazon Highly Rated) Guide to Drug Food Interactions (Amazon Best Seller) Pharmacy Technician Study Guide by Meded101

CardioNerds (Drs. Natalie Marrero, Shivani Reddy, and Rebecca S. Steinberg), discuss the role of SGLT2i in cancer therapy-related cardiac dysfunction (CTRCD) with Dr. Manu Murali Mysore. This episode was produced as part of the CardioNerds Academy curriculum by House Taussig under the guidance of House Chief, Dr. Natalie Marrero, and Academy Program Director, Dr. Gurleen Kaur. A matching review article will be published in US Cardiology Review, the official journal of CardioNerds. Audio editing for this episode was performed by CardioNerds Intern, Dr. Julia Marques Fernandes. Summary: Cancer therapy-related cardiac dysfunction (CTRCD) spans a spectrum from subclinical biomarker elevation to overt heart failure, with risk amplified by preexisting cardiovascular disease, diabetes, hypertension, obesity, and exposure to therapies, such as anthracyclines, HER2-targeted therapies, or radiation. This episode explores the emerging and promising role of SGLT2 inhibitors as a cardioprotective adjunct in cardio-oncology — examining mechanisms, clinical evidence, ongoing trials, and critical knowledge gaps — while affirming that guideline-directed medical therapy remains the cornerstone of prevention and treatment. Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. US Cardiology Review is now the official journal of CardioNerds! Submit your manuscript here. CardioNerds Cardio-Oncology PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls CTRCD is a spectrum — catch it early. CTRCD ranges from subclinical injury detected by imaging and biomarkers to overt heart failure. Early identification in high-risk patients (preexisting CVD, diabetes, HTN, obesity, anthracycline/HER2/radiation exposure) is essential, and early initiation of guideline-directed medical therapy — including ACE inhibitors/ARBs/ARNIs, mineralocorticoid receptor antagonists, and beta-blockers — remains the backbone of prevention and treatment to preserve LVEF and allow safe continuation of cancer therapy. SGLT2 inhibitors are a promising new pillar of cardioprotection in cardio-oncology. They act through a unique combination of mechanisms: renal effects, metabolic reprogramming of the myocardium, anti-inflammatory and antioxidant pathways, and vascular fibrosis modulation — making them a compelling complement to standard therapies rather than a replacement. Early clinical data is encouraging but not yet definitive. The 2024 EMPACARD-PILOT trial demonstrated preserved LVEF and reduced CTRCD in higher-risk patients with diabetes or kidney disease. Ongoing trials — EMPACT and PROTECT — are actively exploring SGLT2 inhibitors for primary prevention during anthracycline and HER2-targeted therapy. SGLT2 inhibitors are NOT yet indicated for ICI-related myocarditis. Immune checkpoint inhibitor (ICI)-related myocarditis is mechanistically immune-driven. While SGLT2 inhibitors have theoretically anti-inflammatory benefits, there is currently no clinical evidence to support their use in this specific setting. The use of SGLT2 inhibitors should be guided by patient risk, existing indications, and ongoing research. Large prospective trials, clarity on timing and patient selection, long-term safety data, and deeper mechanistic understanding in humans remain the most urgent gaps in the field before broader adoption can be recommended. References Theofilis P, Vlachakis PK, Oikonomou E, et al. Cancer therapy-related cardiac dysfunction: A review of current trends in epidemiology, diagnosis, and treatment. Biomedicines. 2024;12(12):2914. doi:10.3390/biomedicines12122914. https://pubmed.ncbi.nlm.nih.gov/39767820/ Lyon AR, Dent S, Stanway S, et al. Baseline cardiovascular risk assessment in cancer patients scheduled to receive cardiotoxic cancer therapies: a position statement and new risk assessment tools from the Cardio-Oncology Study Group of the Heart Failure Association of the European Society of Cardiology in collaboration with the International Cardio-Oncology Society. Eur J Heart Fail. 2020;22(11):1945-1960. doi:10.1002/ejhf.1920. https://pmc.ncbi.nlm.nih.gov/articles/PMC8019326/ Li X, Li Y, Zhang T, et al. Role of cardioprotective agents on chemotherapy-induced heart failure: A systematic review and network meta-analysis of randomized controlled trials. Pharmacol Res. 2020;151(104577):104577. doi:10.1016/j.phrs.2019.104577. https://pubmed.ncbi.nlm.nih.gov/31790821/ Lee YH, Lim S, Davies MJ. Cardiometabolic and renal benefits of sodium-glucose cotransporter 2 inhibitors. Nat Rev Endocrinol. 2025;21(12):783-798. doi:10.1038/s41574-025-01170-4. https://pubmed.ncbi.nlm.nih.gov/40935880/ Dabour MS, George MY, Daniel MR, Blaes AH, Zordoky BN. The cardioprotective and anticancer effects of SGLT2 inhibitors: JACC: CardioOncology state-of-the-art review. JACC CardioOncol. 2024;6(2):159-182. doi:10.1016/j.jaccao.2024.01.007. https://pubmed.ncbi.nlm.nih.gov/38774006/ Armillotta M, Angeli F, Paolisso P, et al. Cardiovascular therapeutic targets of sodium-glucose co-transporter 2 (SGLT2) inhibitors beyond heart failure. Pharmacol Ther. 2025;270(108861):108861. doi:10.1016/j.pharmthera.2025.10886. https://pubmed.ncbi.nlm.nih.gov/40245989/ Góes-Santos BR, Castro PC, Girardi ACC, Antunes-Correa LM, Davel AP. Vascular effects of SGLT2 inhibitors: evidence and mechanisms. Am J Physiol Cell Physiol. 2025;329(4):C1150-C1160. doi:10.1152/ajpcell.00569.2025. https://pubmed.ncbi.nlm.nih.gov/40908107/ Daniele AJ, Gregorietti V, Costa D, López-Fernández T. Use of EMPAgliflozin in the prevention of CARDiotoxicity: the EMPACARD – PILOT trial. CardioOncology. 2024;10(1):58. doi:10.1186/s40959-024-00260-y. https://pubmed.ncbi.nlm.nih.gov/39237985/ Clinicaltrials.gov. Clinicaltrials.gov. Accessed April 16, 2026. https://clinicaltrials.gov/study/NCT05271162 Greco A, Quagliariello V, Rizzo G, et al. SGLT2i Dapagliflozin in primary prevention of chemotherapy induced cardiotoxicity in breast cancer patients treated with neo-adjuvant anthracycline-based chemotherapy +/- trastuzumab: rationale and design of the multicenter PROTECT trial. CardioOncology. 2025;11(1):79. doi:10.1186/s40959-025-00368-9. https://pmc.ncbi.nlm.nih.gov/articles/PMC12400668/ Key Guideline Reference: Lyon AR, López-Fernández T, Couch LS, et al. 2022 ESC guidelines on cardio-oncology developed in collaboration with the European hematology association (EHA), the European society for therapeutic radiology and oncology (ESTRO) and the international cardio-oncology society (IC-OS). Eur Heart J Cardiovasc Imaging. 2022;23(10):e333-e465. doi:10.1093/ehjci/jeac106. https://pubmed.ncbi.nlm.nih.gov/36017575/ Be sure to check out the corresponding review article on the cardioprotective role of SGLT2 inhibitors in CTRCD that will be published in US Cardiology Review, the official journal of CardioNerds. Additionally, please reference CardioNerds Cardio-Oncology Episodes 261 and 274 for related content.

In this episode of the RCP Medicine Podcast, Professor Jeremy Levy, consultant nephrologist in London, joins Dr Alex Crowe, consultant physician in Liverpool, for an insightful and practical conversation about chronic kidney disease (CKD). Together, they explore why CKD is so common, and often silent. How to distinguish acute from chronic kidney problems, and which investigations matter most.The discussion also highlights the growing importance of cardiorenal metabolic medicine, offering clinicians a clear approach to assessing risk, optimising treatment, and supporting long‑term health. From EGFR trends to SGLT2 inhibitors, from lifestyle change to coding accuracy, this episode provides an essential, up‑to‑date guide for managing CKD in everyday practice.Resources For kidney sake podcast:  Home | ForKidneysSake.com Excellent resources on CKD here from NHS NW London:  Chronic kidney diseaseNICE guidelines: Overview | Chronic kidney disease: assessment and management | Guidance | NICE Hypertension in CKD from UK kidney association  FINAL UKKA NICE-KDIGO commentary December 2022.pdfExercise and Lifestyle in CKD from UK kidney association   Exercise and Lifestyle in CKD clinical practice guideline33_v4_FINAL_0.pdf SGLT2i in CKD  from UK kidney association  Sodium Glucose Co transporter 2 - UK Kidney Association.KDIGO (international) guidelines on CKD management   CKD Evaluation and Management – KDIGOKIDGO prognosis of CKD by Albuminuria Categories: KIDGO 2012 S126American Diabetes Association guidelines including CKD   Volume 48 Issue Supplement_1 | Diabetes Care | American Diabetes AssociationFor Kidneys SakeFor Kidneys Sake is a clinician-led podcast from Imperial College Healthcare NHS Trust and North West London Integrated Care Board, offering practical, evidence-based insight into chronic kidney disease and cardio-renal care. Through short, accessible conversations with experts across primary and secondary care, the series supports shared learning on CKD detection, risk management and integrated patient care. The podcast is for GPs, pharmacists, nurses and multidisciplinary teams, and is relevant for clinicians, patients and anyone interested in improving kidney health.Explore our CPD portfolio by your career stageRCP | Education and professional developmentRCP LinksEducationRCP Social MediaInstagramLinkedInFacebookBlueskyMusic Episode 50 onward - Bensound.com  Episodes 1 - 49 'Impressive Deals' - Nicolai Heidlas Any adverts within this podcast may use computer generated voices

Sodium-glucose cotransporter 2 (SGLT2) inhibitors transformed HF care. Meet SGLT1, a transporter that may unlock even greater CV protection. Credit available for this activity expires: 4/10/27 Earn Credit / Learning Objectives & Disclosures: https://www.medscape.org/viewarticle/science-sglt1-and-sglt2-unpacking-dual-inhibition-heart-2026a1000axj?ecd=bdc_podcast_libsyn_mscpedu

Dr. Matt Kaeberlein and Clinical Director Dr. Nicki Byrne tackle your most pressing supplement questions in this AMA episode, cutting through the hype to give you science-backed answers you can actually use. From CoQ10 and statins to sulforaphane influencer hype, creatine and kidney disease, and why a popular longevity doctor may be losing Matt's trust, this episode covers a lot of ground. If you've ever wondered which supplements are worth your money and which ones belong in the trash, this one's for you.Timestamps:00:00 — Cold open highlights01:18 — Episode intro: AMA focused on supplements01:57 — CoQ10: Does it help with statin-induced muscle pain?04:43 — Is there any reason to take CoQ10 on its own?05:23 — Taurine: Promising or overhyped?07:35 — Astaxanthin: What the evidence actually shows09:45 — Why supplement research is structurally flawed11:05 — Creatine for plant-based dieters12:22 — Creatine and kidney disease: What the data says15:48 — Matt, Nicki & Nick's current creatine doses17:00 — Vitamin D: Reference ranges vs. optimal ranges18:57 — Vitamin K2: Bone density, vascular calcification & dosing caution21:55 — Sulforaphane: Great biology, limited evidence, too much hype27:21 — Resveratrol, hormesis & plant defense chemicals27:58 — Fish oil & the omega index: Why Matt supplements even though he eats fish29:23 — Mark Hyman, sirtuins & the problem with longevity influencers32:08 — Lithium & SGLT2 inhibitors: Matt adjusts his dose live34:15 — Is lithium orotate safe? Addressing the liver carcinogen concern36:26 — Is there an OTC alternative to rapamycin?37:40 — Berberine vs. metformin: More similar than you think38:58 — What do Matt, Nicki & Nick actually take?41:48 — Wrap-up & teaser: Deep dive on magnesium coming soon

Feline diabetes management is evolving fast, and SGLT2 inhibitors are at the center of that conversation. In this deep-dive episode, Dr. Susan and Dr. Jolle are joined by Dr. Renee Rucinsky — board-certified feline specialist, owner of Mid Atlantic Cat Hospital and Mid Atlantic Feline Thyroid Center, and a key contributor to the AAHA diabetes management guidelines, including the upcoming updated edition. Dr. Rucinsky walks through the mechanism of action of oral SGLT2 inhibitors, their emerging role in feline diabetes management, patient selection criteria, and what the latest evidence is telling us about when and how to use them in practice. If you've been fielding questions from clients about these drugs — or wondering where they fit in your own protocols — this episode gives you the clinical clarity to move forward with confidence.Thanks for tuning in to the Purr Podcast with Dr. Susan and Dr. Jolle!If you enjoyed today's episode, don't forget to subscribe, rate, and leave us a review—it really helps other cat lovers and vet nerds find the show. Follow us on social media for behind-the-scenes stories, cat trivia, and the occasional bad pun. And remember: every day is better with cats, curiosity, and maybe just a little purring in the background. Until next time—stay curious, stay kind, and give your cats an extra chin scratch from us. The Purr Podcast – where feline medicine meets feline fun.

Dr. Abid Hussain is a triple board-certified cardiologist in cardiology, internal medicine, and functional medicine. After years in the traditional hospital system in New Jersey, he walked away to focus on what actually prevents disease — and now practices at the Boulder Longevity Institute, combining conventional medicine with peptides, HRT, and longevity protocols.This is one of the most important conversations we've had on the podcast. If you're using hormones, peptides, or GLPs — or you're thinking about it — you need to hear what a real cardiologist has to say about all of it.In this episode, Hunter and Dr. Abid cover why cholesterol alone is a terrible predictor of heart disease, what APOB and particle size actually tell you, and why the AI-powered cardiac imaging most people have never heard of is the real state of the art. They break down the testosterone and heart disease myth — fully debunked — along with hematocrit, blood clots, and what's actually dangerous on TRT. They cover the Women's Health Initiative, why bioidentical and synthetic hormones are not the same thing, and what women of any age need to know about HRT.Then the conversation shifts to peptides — how BPC-157, TB-500, and Thymosin Alpha-1 benefit the cardiovascular system, what the SELECT trial proved about GLPs and heart health, why synthetic growth hormone and secretagogues are completely different, and how to think about cancer risk before starting GH protocols. They close with SS-31, Humanin, MOTS-C, and why the order you use mitochondrial peptides in actually matters — plus a deep dive into SGLT2 inhibitors, the most underrated longevity drug almost nobody in this space is talking about.Episode 3 of The Hunter Williams Podcast.https://hunterwilliamshealth.com/Podcast───────────────────────────CONNECT WITH DR. ABID HUSSAIN───────────────────────────

Too busy to read the Lens? Listen to our weekly summary here! In this week's episode we discuss…Major complications after strabismus surgery are rare but often vision-threatening, with higher risk in older patients and complex procedures.Protective eyewear remains underused among professional and amateur pickleball players despite rising eye injury risk.Modern diabetes therapies, SGLT2 inhibitors and GLP-1 receptor agonists, may help reduce cataract risk.Estrogen signaling may help maintain intraocular pressure homeostasis via the trabecular meshwork.

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

In this episode, Allen Page, DVM, PhD, joined us to discuss some of his research on the metabolic effects of various intra-articular corticosteroids, as well as how ertugliflozin may influence horses' metabolic responses to these treatments. Page spoke about how differences among corticosteroids can inform veterinarians' choices when selecting intra-articular agents, key considerations when using SGLT2 inhibitors in horses that require joint injections, the limitations of the current research, and more.This episode of Disease Du Jour is brought to you by Equithrive.GUESTS AND LINKS - EPISODE 178:Host: Carly Sisson (Digital Content Manager) of EquiManagement | Email Carly (CSisson@equinenetwork.com)Guest: Allen Page, DVM, PhDPodcast Website: Disease Du JourThis episode of Disease Du Jour podcast is brought to you by Equithrive.Connect with the Host: Carly Sisson (Digital Content Manager) of EquiManagement | Email Carly (CSisson@equinenetwork.com)

Drs. Petri and Woolfson review the American College of Rheumatology Convergence 2025 data that suggest belimumab might lower mortality in SLE compared with traditional oral immunosuppressants, supporting earlier biologic use. They also discuss an observational study in lupus nephritis that links GLP-1 agonists to better kidney, survival, and cardiovascular outcomes than SGLT2 inhibitors, particularly in overweight patients.

In this 329th episode I welcome Dr. Tyler Jones, founder of the Anesthesia Thoughts Blog, to the show to discuss management of SGLT2 inhibitors and GLP1 receptor agonists. We discuss the evidence for and against holding them before surgery and what you need to know to manage patients on them.Our Sponsors:* Check out BetterHelp: https://www.betterhelp.com* Check out FIGS and use my code FIGSRX for a great deal: https://wearfigs.com* Check out Factor: https://factormeals.com/accrac50off* Check out Quince: https://quince.com/ACCRAC* Check out Truelearn and use my code ACCRAC for a great deal: https://Truelearn.comAdvertising Inquiries: https://redcircle.com/brandsPrivacy & Opt-Out: https://redcircle.com/privacy

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.     

New AHA/ACC guidelines overhaul pulmonary embolism management with a five-tier risk classification, endorsing ED discharge for low-risk patients and DOACs as first-line therapy. A JAMA trial confirms IV acetaminophen adds modest but real pain relief when combined with morphine. A large cohort study shows SGLT2 inhibitors dramatically reduce kidney, cardiovascular, and liver complications in diabetic cirrhosis patients.

Heart failure management has evolved dramatically, and nurses are central to optimizing outcomes and preventing hospital readmissions. In this episode, we break down the core medication classes used in heart failure, including ACE inhibitors, ARBs, beta blockers, mineralocorticoid receptor antagonists, diuretics, and newer agents like ARNIs and SGLT2 inhibitors. You'll learn how these medications improve symptoms and survival, key monitoring parameters such as blood pressure, potassium, and renal function, and common adverse effects to watch for. We'll also review practical bedside considerations and patient education pearls that improve adherence and safety. Your support helps me provide more free resources like this! Consider supporting and getting more amazing pharmacology content! Head on over to meded101.com/nurse

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/.

A JAMA Network Open consensus guide standardizes adult UTI triage for telehealth and in-person care. Nonpregnant women with classic cystitis symptoms and no resistance risks may receive empiric antibiotics without testing; men and higher-risk women require urinalysis with culture before treatment. Urine color or odor alone does not justify testing, and urgent evaluation is advised for suspected complicated infection or sepsis. A Danish registry study in JAMA Internal Medicine found SGLT2 inhibitors offer greater kidney protection than GLP-1 receptor agonists in type 2 diabetes. Long-term ASPREE follow-up in JAMA Oncology showed low-dose aspirin did not lower cancer incidence and increased cancer-related mortality in older adults.

View the Show Notes Page for This Episode Become a Member to Receive Exclusive Content Sign Up to Receive Peter's Weekly Newsletter In this “Ask Me Anything” (AMA) episode, Peter revisits the “proven, promising, fuzzy, noise, nonsense” scale and applies it to a variety of popular topics. He begins with a refresher on what each category represents before classifying a range of interventions based on the strength of their supporting evidence. The conversation spans three main areas: drugs for geroprotection (including GLP-1 receptor agonists, SGLT2 inhibitors, methylene blue, and telomere-lengthening supplements), the use of low-dose aspirin for cardiovascular disease prevention, and strategies to improve muscle mass through optimal protein intake and follistatin gene therapy. This episode provides a clear, evidence-based overview for listeners seeking to understand where these popular health and longevity interventions stand on the spectrum of scientific credibility. If you're not a subscriber and are listening on a podcast player, you'll only be able to hear a preview of the AMA. If you're a subscriber, you can now listen to this full episode on your private RSS feed or our website at the AMA #76 show notes page. If you are not a subscriber, you can learn more about the subscriber benefits here. We discuss: A scale for evaluating scientific claims: proven, promising, fuzzy, noise, or nonsense [1:30]; Strong convictions, loosely held: the mindset that separates great scientists from the rest [7:30]; GLP-1 receptor agonists: are there benefits beyond improving metabolic health and promoting weight loss? [12:45]; GLP-1 drugs and the brain: exploring the potential cognitive benefits [18:45]; GLP-1 drugs and lifespan: examining the evidence for potential geroprotective effects [23:00]; Rapamycin and geroprotection: why it remains in the “promising” category [25:45]; SGLT2 inhibitors and their potential geroprotective effect [27:30]; Methylene blue: examining the evidence of an anti-aging effect [34:45]; Methylene blue's potential neuroprotective effects: limited and inconsistent evidence in humans, and the challenges of dosing and safety [41:15]; Telomeres: what they are, how they relate to aging, and why telomere-lengthening supplements lack credible scientific evidence [43:45]; Does the idea of targeting telomere length to extend lifespan have scientific merit? [50:15]; Low-dose aspirin for cardiovascular disease prevention: weighing its clot-prevention benefits against bleeding risks across different populations [55:00]; Rethinking the protein RDA: why most people need twice the recommended amount for muscle health [1:00:45]; Debunking the protein–cancer myth: why higher protein intake doesn't promote tumor growth [1:06:15]; The biology of follistatin and myostatin, and why follistatin gene therapy has become an emerging topic of interest for muscle growth [1:13:15]; Follistatin gene therapy for muscle growth: state of the evidence in animals and humans, and the technical challenges and regulatory barriers [1:17:00]; Why injectable follistatin is theoretically possible but impractical for real-world use [1:23:15]; and More. Connect With Peter on Twitter, Instagram, Facebook and YouTube