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Your Hormones Are Killing You: Oxytocin, FSH, and the Anti-Aging Protocol Most Doctors Ignore Your hormones are running your love life, your intuition, your longevity, and your brain, and most doctors are getting it completely wrong. Host Dave Asprey sits down with triple board-certified OBGYN Dr. Anna Cabeca to break down the clinical science of oxytocin, female pleasure, hormonal optimization, and why fixing your hormones can make your 70s the best decade of your marriage. Dr. Anna Cabeca is a triple board-certified OBGYN and fellow of gynecology and obstetrics, integrative medicine, and anti-aging and regenerative medicine, with additional board certifications in functional medicine, sexual health, and bioidentical hormone replacement therapy. She is the bestselling author of The Hormone Fix, Keto-Green 16, and MenuPause, and has spent decades researching the clinical intersection of oxytocin, cortisol, estrogen, and progesterone on women's hormonal health, metabolism, and longevity. Her work on keto-green nutrition, vaginal and bladder microbiome health, and bioidentical hormone replacement has made her one of the most credentialed and clinically experienced voices in women's functional medicine practicing today. Dave and Dr. Anna break down the real pharmacology of oxytocin, including its role in muscle regeneration, cortisol suppression, mitochondrial signaling, and vagal tone optimization. They expose the toxic ingredients hiding in mainstream lubricants and vaginal hormone creams, including aspartame, parabens, and petroleum derivatives, and explain why the vaginal microbiome is a frontline organ for women's metabolism and anti-aging. They get into the neuroscience of orgasm, pineal gland activation, endogenous DMT release, and the neurochemical cascade behind peak altered states. Dr. Anna also breaks down the Women's Health Initiative disaster, the FDA's recent reversal on bioidentical hormone replacement, and why FSH is a critical and widely overlooked longevity biomarker. High post-menopausal FSH drives neuroinflammation, accelerates bone loss, and degrades brain optimization outcomes, and most physicians are not testing for it. This is essential listening for anyone serious about biohacking, longevity, anti-aging, functional medicine, human performance, brain optimization, and taking full ownership of their biology. You'll Learn: Why oxytocin functions as a regenerative hormone that rebuilds muscle, suppresses cortisol, and supports mitochondria signaling What toxic chemicals are hiding in standard lubricants and vaginal hormone creams and what to use instead How orgasm activates the pineal gland and triggers endogenous DMT release and altered neurological states Why female intuition may be directly linked to mitochondrial density concentrated in the ovaries How elevated FSH drives neuroinflammation, bone loss, and accelerated brain aging in post-menopausal women Why the FDA reversed 30 years of flawed guidance on bioidentical hormone replacement therapy How four days of sensory deprivation supercharges melatonin, oxytocin, and endogenous DMT production Why oxytocin combined with ketamine is being used clinically to break trauma patterns and rewire neural pathways How polyphenols, CoQ10, carnitine, and vagal tone training protect cardiovascular health and support longevity Why polypharma accelerates decline and what functional medicine does differently Thank you to our sponsors! - KILLSwitch | If you're ready for the best sleep of your life, order now at https://www.switchsupplements.com/and use code DAVE for 20% off - Gatlan | Book your free consultation at www.gatlan.com/DAVE - Redmond Real - Leaf Toothpaste | Go to https://redmond.com/asprey and use code ASPREY for 15% off your first order. - Neuronic | Go to www.neuronic.online Code DAVE for $100 off Dave Asprey is a four-time New York Times bestselling author, founder of Bulletproof Coffee, and the father of biohacking. With over 1,000 interviews and 1 million monthly listeners, The Human Upgrade brings you the knowledge to take control of your biology, extend your longevity, and optimize every system in your body and mind. Each episode delivers cutting-edge insights inhealth, performance, neuroscience, supplements, nutrition, biohacking, emotional intelligence, and conscious living. New episodes are released every Tuesday, Thursday, Friday, and Sunday (BONUS). Dave asks the questions no one else will and gives you real tools to become stronger, smarter, and more resilient. Keywords: Dr. Anna Cabeca, The Girlfriend Doctor, oxytocin, bioidentical hormone replacement, FSH, follicle-stimulating hormone, vaginal microbiome, Velve lubricant, Julva, Mighty Maca, cortisol suppression, pineal gland, DMT, neuroinflammation, broken heart syndrome, NT-proBNP, vagal tone, dark retreat, orgasmic meditation, Women's Health Initiative, perimenopause, postmenopause, yoni massage, oxytocin nasal spray, cabergoline, prolactin, Pitocin, CoQ10, carnitine, Arterosil, polypharma, keto-green, The Hormone Fix Resources: • Get An Exclusive Offer On Dr. Anna's Products At: dranna.com/tribe • Get My 2026 Clean Nicotine Roadmap | Enroll for free at https://daveasprey.com/2026-clean-nicotine-roadmap/ • Dave Asprey's Latest News | Go to https://daveasprey.com/ to join Inside Track today. • Danger Coffee: https://dangercoffee.com/discount/dave15 • My Daily Supplements: SuppGrade Labs (15% Off) • Favorite Blue Light Blocking Glasses: TrueDark (15% Off) • Dave Asprey's BEYOND Conference: https://beyondconference.com • Dave Asprey's New Book – Heavily Meditated: https://daveasprey.com/heavily-meditated • Join My Substack (Live Access To Podcast Recordings): https://substack.daveasprey.com/ • Upgrade Labs: https://upgradelabs.com Timestamps: 00:00 – Trailer 01:37 – What Is Oxytocin? 07:38 – Clean Lube Launch 09:11 – Toxic Lube Ingredients 17:08 – Oxytocin Prescribing 18:58 – FDA Reverses HRT Warning 26:50 – Dark Retreat & DMT 32:15 – Orgasmic Meditation 42:06 – Female Intuition 46:21 – Broken Heart Syndrome 51:15 – FSH & Hormone Monitoring See Privacy Policy at https://art19.com/privacy and California Privacy Notice at https://art19.com/privacy#do-not-sell-my-info.
This episode is part of our comprehensive Decipher the Guidelines Series covering the 2025 ACC/AHA/ACEP/NAEMSP/SCAI Guideline for the Management of Patients With Acute Coronary Syndromes. The following question refers to Section 5.2.1 of the 2025 ACS Guidelines. The question is asked by Thomas Jefferson medical student and CardioNerds Academy Intern Dr. Grace Qiu, answered first by Henry Ford Interventional cardiology fellow and member of the CardioNerds Interventional Cardiology Council Dr. Li Pang, and then by expert faculty Dr. Michelle O'Donoghue. Dr. O'Donoghue is a cardiologist, senior investigator with the TIMI Study Group, and Associate Professor of Medicine at Harvard Medical School who holds the McGillycuddy-Logue Endowed Chair in Cardiology at Brigham and Women's Hospital. She was the Vice Chair of the Writing Committee for the 2025 ACS Guidelines. Question #2 A 63-year-old woman presented to the emergency room for chest pain. She described having exertional chest pain for the past two months and had an episode of severe pain after dinner 3 days ago. She went to bed and slept it off. She told her children today at a family gathering, and was immediately brought to the ED by her daughter. She has a history of hypertension and hyperlipidemia. She was asymptomatic and normotensive in the ED. Labs show a down-trending troponin and an elevated NT-proBNP but are otherwise unremarkable. Her ECG showed Q waves with ST elevation in V2-V4. She was treated with aspirin and heparin drip, and taken to the cath lab. Coronary angiogram showed complete proximal LAD occlusion with right-to-left collaterals, without significant residual disease elsewhere. She remains asymptomatic and is stable, both hemodynamically and electrically. What is the next best step with regard to reperfusion and anti-thrombotic management? A Proceed with primary PCI to LAD B Medical management with aspirin and enoxaparin C Medical management with aspirin and clopidogrel D Medical management with aspirin and ticagrelor Answer #2 Explanation The Correct answer is D In patients who are stable with STEMI and have a totally occluded infarct-related artery >24 hours after symptom onset and are without evidence of ongoing ischemia, acute severe HF, or life-threatening arrhythmia, PPCI should not be performed due to lack of benefit. (Class 3, LOE B-R) The benefit of PPCI begins to diminish after >12 hours from symptom onset, but there appears to be continued benefit through approximately 24 hours. In stable asymptomatic patients with an occluded artery >48 hours after symptom onset, routine PCI has not been shown to be beneficial in the absence of ongoing ischemia. The relative utility of routine PCI for asymptomatic patients with STEMI between 24 and 48 hours from symptom onset is less rigorously tested. PCI is not recommended for an occluded infarct-related artery if the patient is asymptomatic and has a completed infarct. MACE outcomes were similar in those with an occluded infarct-related artery who underwent medical therapy versus those who underwent PCI 3 to 28 days after an MI (Occluded Artery Trial [OAT]), and results were no different at 7-year follow-up. Similar findings were noted in the DECOPI (Desobstruction Coronaire en Post-Infarctus) trial, which enrolled patients with an occluded artery and Q waves on the ECG presenting 2 to 15 days after symptom onset. However, coronary revascularization should be considered for patients with late presentations with continued signs and symptoms of ischemia, including cardiogenic shock, acute severe HF, persistent angina, and life-threatening arrhythmias. Main Takeaway In patients who are stable with STEMI who have a totally occluded infarct-related artery >24 hours after symptom onset and are without evidence of ongoing ischemia, acute severe HF, or life-threatening arrhythmia, PPCI should not be performed due to lack of benefit. Guideline Loc. Section 5.2.1
The shift from purely clinical heart failure diagnosis to biomarker-guided management unfolded over decades of incremental evidence, institutional skepticism, and a handful of pivotal decisions by a small number of physician-scientists willing to champion tools before their adoption became mainstream.In this episode of Moving the Needle in Medicine, host Alexander Hajduczok, MD, a cardiologist and heart failure specialist at Oklahoma Heart Institute, interviews Jim Januzzi, MD, the Adolph Hutter Professor of Medicine at Harvard Medical School, chief scientific officer and Gibson chair at the Baim Institute for Clinical Research, and a cardiologist at Massachusetts General Hospital, to explore the formative experiences, clinical innovations, and leadership principles that shaped his career and, more broadly, the evolution of modern cardiology.Januzzi described nearly declining the opportunity to conduct the first US-based clinical studies with NT-proBNP in 2002, having positioned himself primarily as a troponin and acute coronary syndrome researcher. The foundational diagnostic and prognostic work he ultimately led at MGH established the NT-proBNP cutoffs now used internationally, and the test has since evolved from an emergency department dyspnea-evaluation tool into a biomarker applied across all phases of heart failure management. He noted sacubitril/valsartan as a particularly meaningful convergence of therapeutic and biomarker science, consistently producing substantial reductions in NT-proBNP regardless of baseline value, a finding he has incorporated as a practical signal for adequacy of neurohormonal blockade.On the broader arc of guideline-directed medical therapy (GDMT), Januzzi reflected on witnessing the introduction of beta-blockers for heart failure as a fellow, a shift once considered counterintuitive, and tracing the subsequent addition of each pillar as a reminder that even well-established treatment paradigms remain open to displacement by rigorous evidence. He described his involvement in the endpoint committee for the EMPA-REG OUTCOME trial as the entry point for his work with SGLT2 inhibitors in heart failure, another opportunity initially approached with ambivalence. Despite four-pillar GDMT, he noted residual event rates underscore the continued need for novel therapeutics, and he expressed enthusiasm for gene-editing approaches and RNA-silencing therapies now entering cardiovascular development pipelines.Across the conversation, Januzzi returned to the role of mentorship and deliberate career planning, including maintaining clinical trial involvement from early protocol design rather than joining established programs at the phase three stage, advocating for sponsorship alongside mentorship, and structuring academic evolution in intentional five-year increments. The discussion positions biomarker-guided heart failure care not as a completed project but as a framework still being refined as the disease's diagnostic boundaries and therapeutic options continue to expand.
From the World Congress of Anesthesiologists in Marrakech, TopMedTalk hosts Mike Grocott and Kate Leslie discuss perioperative cardiac risk assessment with Hilary Grocott, Professor and Head of, The Department of Anesthesiology, Pharmacology & Therapeutics (University of British Columbia) and Michelle Chew Professor of Anesthesiology and Intensive Care Medicine at Karolinska Institutet, Stockholm, Sweden, and editor for the British Journal of Anaesthesia. The conversation reviews perioperative cardiac biomarkers, noting abundant prognostic data but limited evidence for biomarker-led management. The discussion emphasizes that elevated troponins can reflect non-cardiac complications (AKI, PE, sepsis) as well as myocardial injury or heart failure, requiring context-specific follow-up pathways. The group highlights NT-proBNP as a specific marker for heart failure and useful for screening and optimization. The podcast then focuses on pulmonary hypertension and failing right ventricle: detect via history, exam, echo, and biomarkers; prioritize preemptive preparation, arterial beat-to-beat monitoring, modest fluids, early vasopressors/inotropes (norepinephrine, low-dose epinephrine), ventilatory optimization, and vigilant, rapid intervention. If you enjoyed this piece there's a fantastic Perioperative Profile with Michelle Chew you can hear here: https://topmedtalk.libsyn.com/perioperative-profiles-professor-michelle-chew-on-seizing-opportunities-in-anaesthesia-research-editing-and-guideline-work -- Join us at Evidence Based Perioperative Medicine (EBPOM) World Congress 2026 in London. Be part of a global conversation as clinicians from around the world gather between 7-9th July at the British Library in London. Three days of evidence-based perioperative medicine, global insights, and expert debate—featuring speakers including Michael Marmot and Ken Rockwood. Register here - https://ebpom.org/product/ebpom-world-congress-2026/
Witam Państwa, nazywam się Jarosław Drożdż, pracuję w Centralnym Szpitalu Klinicznym Uniwersytetu Medycznego w Łodzi, skąd nagrywam podcast Kardio Know-How. W tym odcinku omawiam drugą część badań opublikowanych podczas kongresu ACC 2026. Moja praca habilitacyjna dotyczyła prognostycznej roli oceny rezerwy kurczliwości w idiopatycznej kardiomiopatii rozstrzeniowej i została opublikowana w Chest: https://journal.chestnet.org/article/S0012-3692(15)34303-8/abstract, ale od tamtej pory świat kardiomiopatii zmienił się całkowicie. Najlepiej było to widać podczas III Międzynarodowego Kongresu Kardiomiopatii w Warszawie 30 marca 2026 roku, organizowanego przez I Klinikę i Katedrę Kardiologii WUM pod kierunkiem prof. Marcina Grabowskiego, prof. Krzysztofa Ozierańskiego i doc. Agaty Tymińskiej, a wszystkie wykłady dostępne są tutaj: https://remedium.md/wideo/iii-miedzynarodowy-kongres-kardiomiopatii-237/otwarcie-konferencji-875. Dziś kardiomiopatie leczymy zupełnie innymi lekami, coraz większą rolę odgrywa diagnostyka genetyczna, nowoczesna ocena ryzyka oraz terapie celowane, dzięki którym rokowanie pacjentów jest znacznie lepsze niż jeszcze dekadę temu. Szczególną uwagę podczas ACC zwróciła kardiomiopatia przerostowa u młodocianych pacjentów, ponieważ pojawiła się realna szansa zatrzymania niekorzystnej przebudowy mięśnia sercowego już na bardzo wczesnym etapie choroby. Kluczową rolę odgrywa tu mavacamten — doustny inhibitor miozyny sercowej stosowany w objawowej kardiomiopatii przerostowej z zawężeniem drogi odpływu lewej komory, wymagający jednak ścisłego monitorowania frakcji wyrzutowej lewej komory i bezpieczeństwa terapii. Badanie SCOUT-HCM wykazało, że u pacjentów w wieku 12–18 lat mavacamten znacząco obniża gradient w drodze odpływu lewej komory, zmniejsza grubość przegrody, poprawia klasę NYHA oraz redukuje NT-proBNP bez istotnych działań niepożądanych. To przełomowe podejście pokazuje, że doświadczenia kardiologii dorosłych coraz szybciej trafiają do kardiologii dziecięcej i zaczynamy leczyć choroby dorosłych już od 12 roku życia nowoczesnymi terapiami znanymi z praktyki dorosłych pacjentów. Drugim ważnym tematem ACC była amyloidoza transtyretynowa i lek acoramidis, którego skuteczność potwierdzono w wieloletnich obserwacjach opublikowanych w NEJM: https://www.nejm.org/doi/abs/10.1056/NEJMoa2601103 oraz w JAMA Cardiology: https://jamanetwork.com/journals/jamacardiology/fullarticle/2847055. Długotrwałe leczenie acoramidisem redukowało śmiertelność całkowitą o 45% i ryzyko pierwszej hospitalizacji sercowo-naczyniowej o 47%, pokazując jak ogromne znaczenie ma wczesne i nieprzerwane leczenie chorób kardiomiopatycznych. Przyszłość należy jednak także do terapii genowych, czego przykładem jest HEROIC-PKP2 w kardiomiopatii arytmicznej, gdzie leczenie ukierunkowane na mutację genu PKP2 może radykalnie ograniczyć ryzyko groźnych arytmii i nagłych zgonów sercowych. Szczegółowy TRANSKRYPT do odcinka.Podcast jest przeznaczony wyłącznie dla osób z profesjonalnym wykształceniem medycznym.
Witam Państwa, nazywam się Jarosław Drożdż, pracuję w Centralnym Szpitalu Klinicznym Uniwersytetu Medycznego w Łodzi, skąd nagrywam podcast Kardio Know-How. W tym odcinku omawiam drugą część badań opublikowanych podczas kongresu ACC 2026. Nadciśnienie płucne rozpoznajemy przy średnim ciśnieniu powyżej 20 mmHg, a kluczowa jest grupa I WHO związana z przebudową tętnic płucnych. Choroba wynika m.in. z zaburzenia równowagi między aktywiną a BMP, prowadząc do wzrostu oporu, przeciążenia prawej komory i zgonu w ciągu kilku lat.Objawem dominującym jest duszność wysiłkowa, często niewidoczna w spoczynku, ale nasilona nawet przy krótkim marszu. Przełomem okazał się sotatercept, który w badaniu STELLAR poprawił dystans marszu, parametry biochemiczne i znacząco zmniejszył śmiertelność (https://www.nejm.org/doi/full/10.1056/NEJMoa2213558). W badaniu ZENITH u pacjentów wysokiego ryzyka wykazano szybkie i wyraźne zmniejszenie ryzyka zgonu, przeszczepu płuc i hospitalizacji (https://www.nejm.org/doi/abs/10.1056/NEJMoa2415160).Nowe dane dotyczą także grupy II nadciśnienia płucnego w HFpEF, szczególnie postaci mieszanej CpcPH o wysokiej śmiertelności. Sotatercept działa jako inhibitor sygnalizacji aktywiny i jako pierwszy lek nie opiera się na rozszerzaniu naczyń, lecz wpływa na przebudowę naczyń. W badaniu CADENCE poprawiał opór płucny, ciśnienie, NT-proBNP i wydolność wysiłkową przy dobrej tolerancji (https://www.ahajournals.org/doi/10.1161/CIRCULATIONAHA.126.079918). To podejście wpisuje się w nową koncepcję HFpEF Miltona Packera, opisaną m.in. tutaj: https://open.spotify.com/episode/23WzUWHSoF1lZoiE130nEW?si=f12fe0e345e54111 oraz https://www.sciencedirect.com/science/article/pii/S1071916426002289. Szczegółowy TRANSKRYPT do odcinka.Podcast jest przeznaczony wyłącznie dla osób z profesjonalnym wykształceniem medycznym.
BUFFALO, NY — April 7, 2026 — A new #research paper was #published in Volume 18 of Aging-US on March 26, 2026, titled “Effects of intravenous furosemide plus small-volume hypertonic saline solutions on inflammatory, remodelling markers and epigenetics signatures of patients with congestive acute decompensated heart failure (ADHF).” Led by first author Mario Daidone from University Hospital, Policlinico, Paolo Giaccone, and the University of Palermo, with corresponding author Antonino Tuttolomondo from University Hospital, Policlinico, Paolo Giaccone, and University of Palermo, the randomized trial compared i.v. furosemide plus small-volume hypertonic saline solution (HSS) with i.v. furosemide alone in patients with acute decompensated heart failure due to reduced ejection fraction. The study enrolled 200 subjects, randomly assigning 107 to furosemide plus HSS and 93 to furosemide alone. The authors found that patients treated with i.v. furosemide plus HSS showed lower increases in inflammatory and remodeling biomarkers after saline load, including IL-6, hsTnT, sST2, galectin-3, and NT-proBNP, and the intervention was associated with reduced miR181b expression compared with furosemide alone. These findings suggest that adding small-volume hypertonic saline to loop diuretic therapy may influence both circulating biomarkers and miRNA-related epigenetic signatures in acute heart failure. “Nevertheless, the possible effects of the i.v. furosemide + HSS treatment on natriuretic and inflammatory markers of heart failure deserve further confirmation, whereas the effects of this type of treatment on epigenetic signatures of pathologic mechanisms involved in the left ventricular dysfunction involved in AHF pathogenesis seem to be still not studied.” The authors note that this was a randomized trial in a specific ADHF population, so additional studies will be needed to confirm the durability of the biomarker changes, define the optimal patient groups, and determine whether these molecular effects translate into improved clinical outcomes. Future work may also clarify how the saline strategy interacts with cardiac remodeling and miRNA regulation in larger and more diverse heart failure cohorts. DOI - https://doi.org/10.18632/aging.206364 Corresponding author - Antonino Tuttolomondo - bruno.tuttolomondo@unipa.it Abstract video - https://www.youtube.com/watch?v=EG65XlcDJ3U Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206364 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, heart failure, acute decompensated heart failure, furosemide, hypertonic saline solution To learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at: Bluesky - https://bsky.app/profile/aging-us.bsky.social ResearchGate - https://www.researchgate.net/journal/Aging-1945-4589 X - https://twitter.com/AgingJrnl Facebook - https://www.facebook.com/AgingUS/ Instagram - https://www.instagram.com/agingjrnl/ LinkedIn - https://www.linkedin.com/company/aging/ Reddit - https://www.reddit.com/user/AgingUS/ Pinterest - https://www.pinterest.com/AgingUS/ YouTube - https://www.youtube.com/@Aging-US Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM
En este episodio del podcast "ACHO TNE: entre la evidencia y la práctica", el Dr. Heliberto Páez, oncólogo clínico, conversa con el Dr. José Patricio López, cardiólogo e internista, ambos de Colombia, sobre los tumores neuroendocrinos y sus complicaciones cardíacas, con énfasis en el síndrome carcinoide cardíaco. La dinámica del episodio se centra en analizar la fisiopatología, el seguimiento y el manejo de estos pacientes, abordando tanto aspectos teóricos como recomendaciones prácticas para la detección temprana y el control de la enfermedad.Durante la conversación, los especialistas explican cómo las sustancias vasoactivas liberadas por los tumores neuroendocrinos afectan las válvulas cardíacas, provocando fibrosis, principalmente en el lado derecho del corazón, lo que se traduce en síntomas de insuficiencia cardíaca derecha como fatiga, disnea y edema. Se enfatiza la importancia del diagnóstico temprano mediante biomarcadores como el NT-proBNP y el seguimiento con ecocardiograma, así como la necesidad de un manejo multidisciplinario que incluya control de síntomas, intervención quirúrgica con prótesis biológicas y recomendaciones dietéticas para limitar alimentos que puedan exacerbar los síntomas. Además, se destaca que la complicación cardiovascular constituye un determinante pronóstico clave en estos pacientes.Preguntas abordadas durante la grabación:¿Cuál es la causa de la enfermedad cardíaca en el síndrome neuroendocrino?¿Qué síntomas se esperan en pacientes con corazón carcinoide y falla cardíaca derecha?¿Existe la posibilidad de tamizaje o recomendaciones para pacientes asintomáticos con tumores neuroendocrinos?¿Cuáles son las recomendaciones de manejo interdisciplinario en pacientes sintomáticos, más allá del tratamiento oncológico habitual?¿Qué pautas alimentarias se pueden seguir para limitar la serotonina y prevenir síntomas en pacientes con enfermedad cardíaca carcinoide? Fecha de grabación: 11 de marzo de 2026. El podcast “ACHO Tumores Neuroendocrinos: entre la evidencia y la práctica" es una iniciativa de ACHO.Referencia:Este contenido se basa en la interpretación crítica de la evidencia científica disponible, así como en la experiencia clínica del o los ponentes como profesionales de la salud en instituciones de referencia.Para profundizar en los conceptos discutidos, se recomienda al profesional de la salud consultar literatura científica vigente, guías clínicas internacionales y la normatividad aplicable en su país.
BUFFALO, NY — March 23, 2026 — A new #research paper was #published in Volume 18 of Aging-US on March 12, 2026, titled “Blood biochemical and gut microbiotic neural network models forecasting human biological age.” Led by Anastasia A. Kobelyatskaya from the Russian Clinical Research Center for Gerontology, Pirogov Russian National Research Medical University, and the Institute of Biology of Aging and Healthy Longevity Medicine with Preventive Medicine Clinic, Petrovsky Russian Research Centre of Surgery — with corresponding author Alexey Moskalev from the Institute of Biology of Aging and Healthy Longevity Medicine with Preventive Medicine Clinic, Petrovsky Russian Research Centre of Surgery — the study builds a gender-specific biochemical model (seven routine clinical markers, e.g., cystatin-C, IGF-1, DHEAS, plus sex-specific sets) and a microbiota model (45 species measured by full-length 16S sequencing). Both models were trained and tested on the same 637-person dataset and achieved mean absolute errors of around six years and R² values above 0.8. The team emphasised interpretability: they applied SHapley Additive exPlanations (SHAP) to convert each model from a “black box” into a more interpretable tool, showing how individual predictors (for example, DHEAS, cystatin-C, NT-proBNP in the blood model, and species such as Blautia obeum in the microbiota model) shift predicted age in years for a given individual. The biochemical clock yielded a small (clinically accessible) predictor set (7 markers) to ease clinical translation, while the microbiota clock used a 45-species signature and highlighted microbiome taxa whose abundance gradients correlate with predicted microbiotic age. “As the proposed models possess both global and local explainability, they hold future potential for application in monitoring the effectiveness of various interventions in clinical trials.” The authors note limitations and next steps: the cohort was restricted to a Caucasian population, and the microbiota model requires sequencing resources that may limit immediate clinical rollout. They call for external validation in larger, ethnically diverse cohorts, prospective testing to link model predictions to health outcomes, and application of the explainable models to monitor responses in intervention trials (for example, lifestyle, diet, or drug studies) where a change in predicted biological age would be an early, interpretable signal of benefit. DOI - https://doi.org/10.18632/aging.206360 Corresponding author - Alexey Moskalev - amoskalev@med.ru Abstract video - https://www.youtube.com/watch?v=wg3YEwXMKWY Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206360 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, biological age, blood biochemistry, gut microbiome, neural network To learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at: Bluesky - https://bsky.app/profile/aging-us.bsky.social ResearchGate - https://www.researchgate.net/journal/Aging-1945-4589 X - https://twitter.com/AgingJrnl Facebook - https://www.facebook.com/AgingUS/ Instagram - https://www.instagram.com/agingjrnl/ LinkedIn - https://www.linkedin.com/company/aging/ Reddit - https://www.reddit.com/user/AgingUS/ Pinterest - https://www.pinterest.com/AgingUS/ YouTube - https://www.youtube.com/@Aging-US Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM
METs and VA Disability Ratings — What Veterans Should Know About Heart ClaimsHosted by: Leah Bucholz, Founder & CEO of Prestige Veteran Medical Consulting
CME credits: 0.75 Valid until: 13-02-2027 Claim your CME credit at https://reachmd.com/programs/cme/gdmt-is-working-fine-why-add-more-therapies-the-clinical-rationale-for-layering-therapies-in-patients-with-hfref/54632/ Patients with heart failure with reduced ejection fraction (HFrEF) who have not experienced a recent worsening event pose a major clinical challenge: persistent and under-recognized cardiovascular (CV) risk. Recent findings show that these patients carry significant annual rates of CV death and heart failure (HF) hospitalization, despite adherence to quadruple guideline-directed medical therapy (GDMT) and device support. For cardiologists, the challenge is twofold: accurately identifying high-risk individuals without overt clinical deterioration and knowing when and how to intensify therapy in patients who appear stable but remain vulnerable. Recent data show that soluble guanylate cyclase (sGC) may provide significant reductions in CV death and all-cause mortality, particularly in individuals with moderately elevated NT-proBNP (≤6,000 pg/mL). These findings are especially important because this population is far more common in routine cardiology practice and has historically been overlooked in discussions of additional therapy. However, cardiologists often underestimate risk in these ambulatory patients and may hesitate to add therapies when GDMT appears to be working well. Tune in to learn best practices for patient selection and the implementation of added sGC therapy.
CME credits: 0.75 Valid until: 13-02-2027 Claim your CME credit at https://reachmd.com/programs/cme/when-gdmt-isnt-enough-understanding-residual-risk-in-patients-with-hfref/51036/ Patients with heart failure with reduced ejection fraction (HFrEF) who have not experienced a recent worsening event pose a major clinical challenge: persistent and under-recognized cardiovascular (CV) risk. Recent findings show that these patients carry significant annual rates of CV death and heart failure (HF) hospitalization, despite adherence to quadruple guideline-directed medical therapy (GDMT) and device support. For cardiologists, the challenge is twofold: accurately identifying high-risk individuals without overt clinical deterioration and knowing when and how to intensify therapy in patients who appear stable but remain vulnerable. Recent data show that soluble guanylate cyclase (sGC) may provide significant reductions in CV death and all-cause mortality, particularly in individuals with moderately elevated NT-proBNP (≤6,000 pg/mL). These findings are especially important because this population is far more common in routine cardiology practice and has historically been overlooked in discussions of additional therapy. However, cardiologists often underestimate risk in these ambulatory patients and may hesitate to add therapies when GDMT appears to be working well. Tune in to learn best practices for patient selection and the implementation of added sGC therapy.
CME credits: 0.75 Valid until: 13-02-2027 Claim your CME credit at https://reachmd.com/programs/cme/safety-clinical-integration-and-the-emerging-fifth-pillar-in-hf-practice/54635/ Patients with heart failure with reduced ejection fraction (HFrEF) who have not experienced a recent worsening event pose a major clinical challenge: persistent and under-recognized cardiovascular (CV) risk. Recent findings show that these patients carry significant annual rates of CV death and heart failure (HF) hospitalization, despite adherence to quadruple guideline-directed medical therapy (GDMT) and device support. For cardiologists, the challenge is twofold: accurately identifying high-risk individuals without overt clinical deterioration and knowing when and how to intensify therapy in patients who appear stable but remain vulnerable. Recent data show that soluble guanylate cyclase (sGC) may provide significant reductions in CV death and all-cause mortality, particularly in individuals with moderately elevated NT-proBNP (≤6,000 pg/mL). These findings are especially important because this population is far more common in routine cardiology practice and has historically been overlooked in discussions of additional therapy. However, cardiologists often underestimate risk in these ambulatory patients and may hesitate to add therapies when GDMT appears to be working well. Tune in to learn best practices for patient selection and the implementation of added sGC therapy.
CME credits: 0.75 Valid until: 13-02-2027 Claim your CME credit at https://reachmd.com/programs/cme/do-not-delay-timing-triggers-and-identifying-the-right-patient-for-additional-therapies-in-hfref/54633/ Patients with heart failure with reduced ejection fraction (HFrEF) who have not experienced a recent worsening event pose a major clinical challenge: persistent and under-recognized cardiovascular (CV) risk. Recent findings show that these patients carry significant annual rates of CV death and heart failure (HF) hospitalization, despite adherence to quadruple guideline-directed medical therapy (GDMT) and device support. For cardiologists, the challenge is twofold: accurately identifying high-risk individuals without overt clinical deterioration and knowing when and how to intensify therapy in patients who appear stable but remain vulnerable. Recent data show that soluble guanylate cyclase (sGC) may provide significant reductions in CV death and all-cause mortality, particularly in individuals with moderately elevated NT-proBNP (≤6,000 pg/mL). These findings are especially important because this population is far more common in routine cardiology practice and has historically been overlooked in discussions of additional therapy. However, cardiologists often underestimate risk in these ambulatory patients and may hesitate to add therapies when GDMT appears to be working well. Tune in to learn best practices for patient selection and the implementation of added sGC therapy.
CME credits: 0.75 Valid until: 13-02-2027 Claim your CME credit at https://reachmd.com/programs/cme/evidence-at-a-glance-the-totality-of-evidence-impacting-clinical-decision-making-in-patients-with-hfref-without-a-recent-worsening-event/54634/ Patients with heart failure with reduced ejection fraction (HFrEF) who have not experienced a recent worsening event pose a major clinical challenge: persistent and under-recognized cardiovascular (CV) risk. Recent findings show that these patients carry significant annual rates of CV death and heart failure (HF) hospitalization, despite adherence to quadruple guideline-directed medical therapy (GDMT) and device support. For cardiologists, the challenge is twofold: accurately identifying high-risk individuals without overt clinical deterioration and knowing when and how to intensify therapy in patients who appear stable but remain vulnerable. Recent data show that soluble guanylate cyclase (sGC) may provide significant reductions in CV death and all-cause mortality, particularly in individuals with moderately elevated NT-proBNP (≤6,000 pg/mL). These findings are especially important because this population is far more common in routine cardiology practice and has historically been overlooked in discussions of additional therapy. However, cardiologists often underestimate risk in these ambulatory patients and may hesitate to add therapies when GDMT appears to be working well. Tune in to learn best practices for patient selection and the implementation of added sGC therapy.
CME credits: 0.25 Valid until: 10-02-2027 Claim your CME credit at https://reachmd.com/programs/cme/gdmt-is-working-fine-so-why-add-more-therapies-for-patients-with-hfref/48811/ Contemporary trial data and global registries consistently show that ambulatory patients with heart failure with reduced ejection fraction (HFrEF) who have not experienced a recent worsening event still carry residual risk of cardiovascular death and heart failure hospitalizations. These annual rates have been estimated to exceed 10%–20%, despite adherence to quadruple guideline-directed medical therapy (GDMT) and device support. This paradox of clinical stability on the surface, yet significant residual risk underneath, creates a critical blind spot in the management of chronic HFrEF. Recent data show that the addition of soluble guanylate cyclase (sGC) stimulators provides significant reductions in CV death and all-cause mortality, particularly in individuals with moderately elevated NT-proBNP (≤6,000 pg/mL). These findings are especially important because this population is far more common in routine cardiology practice and has historically been overlooked in discussions of additional therapy. Tune in to explore a case to better understand which patients can derive the most benefit from added therapy.=
CME credits: 0.25 Valid until: 30-01-2027 Claim your CME credit at https://reachmd.com/programs/cme/missing-the-window-in-ambulatory-patients-with-hfref-on-gdmt-strategies-for-cv-risk-reduction/48813/ For ambulatory patients with heart failure with reduced ejection fraction (HFrEF) who have not experienced a recent worsening event, cardiologists continue to face a major clinical challenge: persistent and under-recognized cardiovascular (CV) risk. Despite adherence to quadruple guideline-directed medical therapy (GDMT) and device support, these “stable,” guideline-treated patients carry residual risk for CV death. Recent evidence shows that the addition of soluble guanylate cyclase (sGC) stimulators provides significant reductions in CV death and all-cause mortality, particularly in individuals with moderately elevated NT-proBNP (≤6,000 pg/mL). However, cardiologists often underestimate risk in these ambulatory patients and may hesitate to add therapies when GDMT appears to be working well. Our experts break down a case to illustrate how and when to employ recent data regarding the use of additional sGC in appropriate patients with HFrEF.=
In this episode, host Alyssa Watson, DVM, welcomes Andrea C. Eriksson De Rezende, DVM, DACVIM (Cardiology), to discuss her recent Clinician's Brief article, “Hypertrophic Cardiomyopathy in a Cat.” Dr. Eriksson De Rezende covers a variety of presentations, the full list of diagnostics including NT-proBNP, the virtues of sedation, and therapies ranging from the mainstays to that new sirolimus drug. Following this case-based exercise, they go well beyond the basics when it comes to HCM and thromboembolic disease in cats.Resource:https://www.cliniciansbrief.com/article/hypertrophic-cardiomyopathy-catContact:podcast@instinct.vetWhere To Find Us:Website: CliniciansBrief.com/PodcastsYouTube: Youtube.com/@clinicians_briefFacebook: Facebook.com/CliniciansBriefLinkedIn: LinkedIn.com/showcase/CliniciansBrief/Instagram: @Clinicians.BriefX: @CliniciansBriefThe Team:Alyssa Watson, DVM - HostAlexis Ussery - Producer & Multimedia Specialist
Send us a textCould a simple blood test help identify chronic pulmonary hypertension when echo access is limited? This week on The Incubator Podcast, Ben and Daphna explore this question and others relevant to daily NICU practice. A Toronto study examines NT-proBNP as a practical diagnostic tool in extremely preterm infants.They also examine a puzzling finding from Italy and Belgium: despite near-universal antibiotic use in neonates with HIE undergoing cooling, actual culture-positive sepsis rates are surprisingly low. What does this mean for our approach to empiric antibiotics?Ben presents Norwegian data showing that serial physical exams cut antibiotic exposure in half for term and late preterm infants—without compromising safety. Daphna follows with research connecting NICU capacity strain to patient outcomes, underscoring why adequate staffing isn't just about comfort, but about survival.The episode concludes with Ben, Daphna, and Eli discussing the recent CDC changes to Hepatitis B birth dose recommendations. With federal guidance now diverging from AAP recommendations, how do we navigate conversations with families? They explore transmission risks parents may overlook and share approaches to shared decision-making when expert opinions conflict. A full week of neonatal medicine research and real-world clinical challenges, all in one episodeSupport the showAs always, feel free to send us questions, comments, or suggestions to our email: nicupodcast@gmail.com. You can also contact the show through Instagram or Twitter, @nicupodcast. Or contact Ben and Daphna directly via their Twitter profiles: @drnicu and @doctordaphnamd. The papers discussed in today's episode are listed and timestamped on the webpage linked below. Enjoy!
Send us a textIn this Journal Club episode of the Incubator Podcast, Ben Courchia and Daphna Yasova-Barbeau review a study from the Journal of Perinatology evaluating NT-proBNP as a diagnostic tool for chronic pulmonary hypertension in extremely preterm infants. The discussion walks through the clinical burden of pulmonary hypertension in babies with bronchopulmonary dysplasia, the limitations of echocardiography, and the appeal of accessible biomarkers. Using data from a SickKids Toronto cohort, the hosts unpack sensitivity, specificity, cutoff values, and real-world applicability, while exploring how NT-proBNP could support screening, risk stratification, and bedside decision-making in everyday NICU practice.----Can N-terminal pro-brain natriuretic peptide accurately diagnose chronic pulmonary hypertension among extremely low gestational age neonates: A Retrospective Cohort Study. Garcia-Gozalo M, Jain A, Weisz DE, Jasani B.J Perinatol. 2025 Nov 13. doi: 10.1038/s41372-025-02462-3. Online ahead of print.PMID: 41233504Support the showAs always, feel free to send us questions, comments, or suggestions to our email: nicupodcast@gmail.com. You can also contact the show through Instagram or Twitter, @nicupodcast. Or contact Ben and Daphna directly via their Twitter profiles: @drnicu and @doctordaphnamd. The papers discussed in today's episode are listed and timestamped on the webpage linked below. Enjoy!
Message our hosts, Kieran and Jose.Cardiology is one of the more accessible disciplines for primary care vets, but still poses a number of important challenges for the clinician. Join Jose and Kieran as they host an amazing panel of guests: Rory Cowlam, Cat Henstridge, James Greenwood, and Louisa Graham - experienced GP vets with different levels of enthusiasm for cardiology! Our excellent panel share their perspectives on the utility of NT-proBNP in cats with a heart murmur, how vets can use staging systems for heart disease, and a number of other primary-care focused topics - live from the London Vet Show in 2025.Held each November at the London ExCel, the London Vet Show is the biggest event in the calendar of the UK vet profession. This year, LVS debuted their new showcase for talent, The Studio.
JCO Editorial Fellow Peter Li and author Dr. Jahanzaib Khwaja discuss the ASH 2025 Simultaneous Publication article, "A New Validated Staging System for AL Amyloidosis With Stage lllC Defining Ultra-Poor Risk: AL International Staging System." TRANSCRIPT The disclosures for guests on this podcast can be found in the show notes. Dr. Peter Li: Welcome to this episode of JCO Article Insights. I am Dr. Peter Li, JCO's Editorial Fellow, and today, I am joined by Dr. Jahanzaib Khwaja on a new validated staging system on AL amyloidosis with stage lllC defining ultra-poor risk, AL International Staging System. This is a simultaneous publication that will be presented at this year's ASH Conference. At the time of this recording, our guest has disclosures that will be linked in the transcript. So, Dr. Khwaja, let's start off first: What would you say is the significance of your study? Dr. Jahanzaib Khwaja: Thank you very much. This is an important study in that, in the current treatment era, we have really improved outcomes of patients with systemic AL amyloidosis. Traditionally, the staging systems that have been employed, which are the Mayo 2012 and the European modification 2016, have been founded in eras where there were historic treatment protocols. So the significance of this new staging system is looking at outcomes of patients in the modern treatment era. That is patients who are treated with daratumumab-based treatments in the first line. And this is kind of the largest study which is externally validating a new prognostic model in the current treatment era with modern outcomes. Dr. Peter Li: Can you tell our listeners what is different about your new staging system? Dr. Jahanzaib Khwaja: The traditional staging systems, the Mayo 2012 and the European modification of 2016, looked at outcomes of patients with systemic AL amyloidosis with historic treatment protocols. And we know that they looked at outcomes according to an NT-proBNP and troponin, and in the Mayo 2012, they looked at it with the addition of the dFLC, which is the difference in the involved and uninvolved free light chain. Over the years, we have seen that outcomes have improved, and over decades, actually, outcomes are much better when we compare them to the previous decade. If we look at current treatment approaches, those traditional staging systems inadequately determine the poorest prognostic risk. So they are unable to tell us those who are going to perform poorly. Our current new validated staging system looks at the traditional NT-proBNP and troponin but uses the addition of the longitudinal strain. This is an echocardiographic parameter, and it is used widely in treatment centers who treat amyloidosis. This really identifies those ultra-high risk patients, and these are the patients who will perform poorly in current treatment protocols. And why is that important? Well, we need a robust staging system in the current treatment era which can stratify patients who will do well but also stratify those patients who do not do well. Because that is important for counseling patients, for risk stratification, for treatment approaches, and in the future, for designing clinical trials. Dr. Peter Li: And that is referring to the longitudinal strain greater than -9% and NT-proBNP greater than 8,500 and then the high-sensitivity troponins greater than 50, which will define the new staging system. Can you talk more about how you picked these cutoffs and also what that alludes to in terms of the outcomes that you have discovered in this age of daratumumab-based therapy? Dr. Jahanzaib Khwaja: Yeah, that is a really excellent question because we have aimed to build upon traditional staging systems. So clinicians have used these traditional models for many, many years, and they have robustly underpinned our stratification of patients and how we counsel patients. So we didn't want to change some of these well-established thresholds, but we wanted to test them in the current treatment era. So the NT-proBNP of 8,500 and the high-sensitivity troponin of 50 were the traditionally used thresholds. And they actually stand the test of time. But we found that longitudinal strain additionally and independently predicts outcome independent of these other biomarkers. It is independent actually as a continuous variable, so you can cut this at a number of different stratification points and find independence. But we wanted to determine and discriminate those with the poorest outcomes. So we validated a longitudinal strain threshold of greater than -9% by deriving this from a dataset of patients with the traditionally highest risk. Those are with European stage lllB. And looked at the optimal threshold with time-dependent ROC analysis. So we did this in our derivation cohort and then validated this externally in our external validation cohort amongst a number of centers in Europe, in the US, and in the UK. And it is important to note because longitudinal strain is an echocardiographic parameter, and traditionally the limitations are considered to be inter-vendor and inter-operator variability and intra-operator variability, and there are challenges with reproducibility of some of these measurements. So that is often cited as a limitation. But we found, when we have externally validated this across different centers using different platforms, actually the threshold of -9% is independently predictive of poorer outcomes independent of the traditional NT-proBNP and troponin thresholds, and it is robustly predictive of poorest outcomes. We know that those with stage lllC have a median overall survival of 4 to 7 months in the modern treatment era. And if we sub-stratify these by patients treated with daratumumab, outcomes have improved, but still, even if we look at daratumumab-treated patients, one-year overall survival is still only around 50 percent. So these are a poor risk group in the modern treatment era. Dr. Peter Li: Which kind of makes sense in a way because this kind of predicts whether they have amyloid-related cardiomyopathy. So I think this all tracks with our listeners. But given the poor outcomes even with daratumumab-based therapies, do you think this new staging system would change practice, if at all? Dr. Jahanzaib Khwaja: Yeah, I think that is a really good point because I think it comes to the question of why we use a staging system. What are its applications? I think one of the key things we think about in the clinic is how do we counsel patients when we first talk to them about their diagnosis. So there is a lot of information, but predominantly people want to know, what is my outlook going to look like? And as I say, in the bortezomib treatment era, 2010 to 2020, we used to say you have stage lllB, you have very poor outcomes, median survival maybe around six months. We have shown here that actually those with lllB have much better outcomes definitely over 12 months, up to 24 months in those with daratumumab-based therapies. So we need to counsel them in a different way. We then also need to say, "Well, who are the ultra-high risk?" So we said those with the longitudinal strain of greater than -9% with the traditional NT-proBNP and troponin cutoffs. And those patients will have poor outcomes. We need to talk about palliation. We need to talk about alternate treatment approaches. And then importantly for the community is about treatment and clinical trial design. So again, traditionally the traditional high-risk group lllB used to be considered an exclusion for all major trials. So these were excluded in the ANDROMEDA study, which led to the approval of daratumumab-based therapy, and multiple other trials. And we show here that actually patients with lllB should not be excluded from these studies because they do have good outcomes. And I think we make the important point that those with lllC, who do have poor outcomes, they need a different treatment approach, and we need to think about stratifying these patients differently. So perhaps the next modality of treatment will be the anti-fibril antibodies or a mode of treatment which can clear antibodies or clear the amyloid fibrils from the organs and reduce the organ toxicity early on. We know that those with lllC have poor outcomes particularly within the first year, and organ dysfunction really predominates here. So a different treatment approach is required, and we need to design trials specifically for these patients which look beyond anti-plasma cell clone therapy but also look at clearing the amyloid fibrils and improving organ function as this is predominantly the cause of death in these patients. Dr. Peter Li: That's an excellent point right there. Do you foresee any limitations to this new staging system, or can you comment on is there potentially a better way to refine this staging criteria in the future? Dr. Jahanzaib Khwaja: Yeah, I think that is a really excellent point to consider, that staging systems always need refining across treatment eras. So we have looked at the bortezomib era, and then we have validated this in the daratumumab-based era. We know that amongst different countries access to treatment varies. We know that there are a number of factors which determine your health-related outcomes. That's access to healthcare, speed of diagnosis, access to tertiary diagnostics, ability to biopsy, and then supportive care. And I think our staging system highlights the importance of organ dysfunction predominantly causing death early on. And I think that as treatments improve this should be refined. So the expectation I think is, as we have better anti-plasma cell directed therapies, and as we hopefully develop anti-fibril antibodies and anti-fibril clearance drugs, that we will need to revalidate new models to effectively prognosticate in this treatment era. And I also think that as we become a bit more sophisticated with our approaches, we know that this can be refined in the future looking at other prognostic factors with regards to healthcare outcomes. I would say one of the strengths, however, of this model is that it builds on the traditional model, and it's quite simple to use. You just have the NT-proBNP and the troponin, and then longitudinal strain, which is used quite frequently in amyloid centers, and an echocardiogram is used in essentially all patients for diagnosis. So I think it will certainly be quite practical. But certainly I think, as you say, as treatment approaches change over time, and as we have further options in the future, we will need to refine prognostication. Dr. Peter Li: For the listeners out there, let's say someone comes in our clinic and we diagnose them with stage lllC amyloidosis. Can you comment on what clinical trials are out there that potentially they can refer their patients to? You mentioned anti-fibril therapy, which I think would be the way of the future. Can you kind of comment what you know at this current stage and point listeners in the right direction? Dr. Jahanzaib Khwaja: This is the challenge in amyloidosis. We don't have specific trials that are looking at those with the highest risk. And at present, even the ISA International Guidelines talk about risk according to the old treatment approaches and discuss attenuating our current chemotherapy approaches. And I think that for clinicians out there who identify those at the highest risk, it is really important to have a multidisciplinary approach, to consider palliation and palliative services early, and really work with your fellow cardiologists and renal physicians and neurologists to enable the best supportive care you have in order to deliver this anti-plasma cell directed therapy. We know that actually you only need for most patients small amounts of doses of chemotherapy to get good clonal responses, and we have seen that even in the bortezomib era that actually they have good CR rates and more impressive CR rates with daratumumab. But because of the organ dysfunction, it can be really challenging to deliver these doses. And supportive care is going to be really important particularly for these challenging patients. The future will be designing clinical trials that are appropriate for these patients. At present, we currently don't have available options, but I think the more we gather this data, the more we work collaboratively as a community, we will be able to mobilize our resources and get the best outcomes for these patients. Dr. Peter Li: First build the field of dreams and then hopefully more therapies will arrive in the future. Thank you so much, Dr. Khwaja, for speaking about the JCO article, "A New Validated Staging System for AL Amyloidosis With Stage lllC Defining Ultra-Poor Risk: AL International Staging System," and for all your valuable input today. Dr. Jahanzaib Khwaja: Thank you very much. Dr. Peter Li: Make sure to check out the presentation at this year's ASH Conference taking place from December 6 to December 9. Thank you for listening to JCO Article Insights. Please come back for more interviews and article summaries and be sure to leave us a rating and review so others can find our show. For more podcasts and episodes from ASCO, please visit asco.org/podcast. The purpose of this podcast is to educate and to inform. This is not a substitute for professional medical care and is not intended for use in the diagnosis or treatment of individual conditions. Guests on this podcast express their own opinions, experience, and conclusions. Guest statements on the podcast do not express the opinions of ASCO. The mention of any product, service, organization, activity, or therapy should not be construed as an ASCO endorsement.
Witam Państwa, nazywam się Jarosław Drożdż, pracuję w Centralnym Szpitalu Klinicznym Uniwersytetu Medycznego w Łodzi, skąd nagrywam podcast Kardio Know-How. W tym odcinku rozpoczynam omawianie doniesień z tegorocznego kongresu AHA.Koncepcja polypil ma długą historię — od klasycznych projektów Salima Yusufa, przez rewolucję w leczeniu nadciśnienia dzięki SPC, aż po nowsze dane dotyczące statyny z ezetymibem (https://www.jacc.org/doi/10.1016/j.jacc.2023.05.042). W prewencji wtórnej szybkie wdrożenie statyny + ezetymibu w jednej tabletce zmniejsza ryzyko zgonów, zawałów i rewaskularyzacji o około 25% w porównaniu z terapią sekwencyjną. Najnowsza, czwarta odsłona dotyczy niewydolności serca, gdzie teoretycznie idealnie pasuje model polypil obejmujący 4 filary terapii, choć dotąd utrudniały to liczne dawki β-blokerów i ACE-I. W badaniu POLY-HF (https://www.ahajournals.org/doi/10.1161/CIRCOUTCOMES.125.012834) sprawdzono SPC zawierającą empagliflozynę 10 mg, spironolakton 12,5 mg i metoprolol 25–150 mg u pacjentów z HFrEF. Po 6 miesiącach częstość stosowania pełnej terapii wzrosła o 50%, a samodzielne odstawianie leków spadło z 18% do 4%. Poprawiła się EF (+3,5%), NT-proBNP spadło o 35%, zmniejszyła się hiperkaliemia i redukowano spadek GFR. Odnotowano także poprawę jakości życia i łączną redukcję powikłań oraz zgonów o 59%, a hospitalizacji o 60%. To niewielkie, ale przełomowe badanie pokazuje, że polypil może zmienić praktykę w niewydolności serca poprzez uproszczenie terapii. Co więcej, najnowsze wytyczne AHA/ACC dotyczące nadciśnienia po raz pierwszy jednoznacznie zaleciły stosowanie SPC (https://www.ahajournals.org/doi/10.1161/CIR.0000000000001356).Szczegółowy TRANSKRYPT do odcinka.Podcast jest przeznaczony wyłącznie dla osób z profesjonalnym wykształceniem medycznym.
Host: Ryan Quigley Guest: Luigi Adamo, MD, PhD Guest: Andrea Fava, MD Fatigue and exercise intolerance in patients with systemic lupus erythematosus (SLE) may persist even when disease activity is controlled, and preload deficiency could be an overlooked cause. In this expert-led discussion, Drs. Luigi Adamo and Andrea Fava share insights from their research, highlighting diagnostic clues, the role of NT-proBNP, and emerging interventions aimed at improving quality of life. Dr. Adamo is an Associate Professor of Medicine and the Director of Cardiac Immunology, and Dr. Fava is an Assistant Professor of Medicine in the Division of Rheumatology and Director of Lupus Translational Research at Johns Hopkins Medicine.
Host: Ryan Quigley Guest: Luigi Adamo, MD, PhD Guest: Andrea Fava, MD Fatigue and exercise intolerance in patients with systemic lupus erythematosus (SLE) may persist even when disease activity is controlled, and preload deficiency could be an overlooked cause. In this expert-led discussion, Drs. Luigi Adamo and Andrea Fava share insights from their research, highlighting diagnostic clues, the role of NT-proBNP, and emerging interventions aimed at improving quality of life. Dr. Adamo is an Associate Professor of Medicine and the Director of Cardiac Immunology, and Dr. Fava is an Assistant Professor of Medicine in the Division of Rheumatology and Director of Lupus Translational Research at Johns Hopkins Medicine.
Message our hosts, Kieran and Jose.In the first part of our very special, two-part Animal Heartbeat Season 3 finale, Kieran and Jose are joined by Dr Mark Rishniw. Double-boarded in Cardiology and Internal Medicine, Mark works as a VIN Consultant and Research Associate of the Simpson Lab at Cornell University College of Veterinary Medicine. Through his numerous educational roles, lectures and publications, Dr Rishniw has become known as a critical thinker who is on a mission to bust myths and break down barriers to communication.In part one, join Mark as he dissects the topic of NT-proBNP screening for feline cardiomyopathy, and treatment for pets in stage B2...
When a cat is presented with acute dyspnea, differentiating heart from lung disease isn't just important—it's imperative. In this episode of the Partner Podcast, we sit down with Dr. Paul Zoyhofski to explore practical approaches for distinguishing cardiac from primary respiratory disease during feline emergencies. From physical examination cues to point-of-care biomarkers like NT-proBNP, get expert insights into making faster, more confident treatment decisions.Sponsored by BionoteContact us:Podcast@instinct.vetWhere to find us:Website: CliniciansBrief.com/PodcastsYouTube: Youtube.com/@clinicians_briefFacebook: Facebook.com/CliniciansBriefLinkedIn: LinkedIn.com/showcase/CliniciansBrief/X: @cliniciansbriefInstagram: @clinicians.briefThe Team:Beth Molleson, DVM - HostSarah Pate - Producer & Project Manager, Brief StudioTaylor Argo- Podcast Production & Sound Editing
When it comes to cardiac disease, early and accurate detection can make all the difference in providing the best patient care. In this episode of the Partner Podcast, Dr. Stacey Hendershott shares her real-world experience with using NT-proBNP testing in both healthy and sick patients—whether for routine screening, investigating new murmurs, or managing complex cases, all with the convenience of point-of-care technology.Sponsored by BionoteResource: bionote.comContact us:Podcast@instinct.vetWhere to find us:Website: CliniciansBrief.com/PodcastsYouTube: Youtube.com/@clinicians_briefFacebook: Facebook.com/CliniciansBriefLinkedIn: LinkedIn.com/showcase/CliniciansBrief/X: @cliniciansbriefInstagram: @clinicians.briefThe Team:Beth Molleson, DVM - HostSarah Pate - Producer & Project Manager, Brief StudioTaylor Argo - Podcast Production & Sound Editing
CardioNerds (Drs. Rick Ferraro and Georgia Vasilakis Tsatiris) discuss ATTR cardiac amyloidosis with expert Dr. Justin Grodin. This episode is a must-listen for all who want to know how to diagnose and treat ATTR with current available therapies, as well as management of concomitant diseases through a multidisciplinary approach. We take a deep dive into the importance of genetic testing, not only for patients and families, but also for gene-specific therapies on the horizon. Dr. Grodin draws us a roadmap, guiding us through new experimental therapies that may reverse the amyloidosis disease process once and for all. Audio editing by CardioNerds academy intern, Christiana Dangas. This episode was developed in collaboration with the American Society of Preventive Cardiology and supported by an educational grant from BridgeBio. Enjoy this Circulation Paths to Discovery article to learn more about the CardioNerds mission and journey. US Cardiology Review is now the official journal of CardioNerds! Submit your manuscripts here. CardioNerds Cardiac Amyloid PageCardioNerds Episode Page Pearls: You must THINK about your patient having amyloid to recognize the pattern and make the diagnosis. Start with a routine ECG and TTE, and look for a disproportionately large heart muscle with relatively low voltages on the ECG. Before you diagnose ATTR amyloidosis, AL amyloidosis must be ruled out (or ruled in) with serum light chains, serum/urine immunofixation, and/or tissue biopsy. Genetic testing is standard of care for all patients and families with ATTR amyloidosis, and the future is promising for gene-specific treatments. Current FDA-approved treatments for TTR amyloidosis are TTR stabilizers and TTR silencers, but TTR fibril-depleting agents are on their way. Early diagnosis of ATTR affords patients maximal benefit from current amyloidosis therapies. TTR amyloidosis patients require a multidisciplinary approach for success, given the high number of concomitant diseases with cardiomyopathy. Notes: Notes: Notes drafted by Dr. Georgia Vasilakis Tsatiris. What makes you most suspicious of a diagnosis of cardiac amyloidosis from the typical heart failure patient? You must have a strong index of suspicion, meaning you THINK that the patient could have cardiac amyloidosis, to consider it diagnostically. Some characteristics or “red flags” to not miss: Disproportionately thick heart muscle with a relatively low voltages on EKG Bilateral carpal tunnel syndrome – estimated that 1 in 10 people >65 years old will have amyloidosis Previously tolerated antihypertensive medications Atraumatic biceps tendon rupture Bilateral carpal tunnel syndrome Spinal stenosis Concomitant with other diseases: HFpEF, low-flow low-gradient aortic stenosis How would you work up a patient for cardiac amyloidosis? Start with a routine ECG (looking for disproportionally low voltage) and routine TTE (looking for thick heart muscle) CBC, serum chemistries, hepatic function panel, NT proBNP, and troponin levels NOTE: It is critical to differentiate between amyloid light chain (AL amyloidosis) and transthyretin ATTR amyloidosis, as both make up 95-99% of amyloidosis cases. Obtain serum free light chains, serum & urine electrophoresis, and serum & urine immunofixation to rule out AL amyloidosis. (See table below) AL Amyloidosis ATTR Amyloidosis → Positive serum free light chains and immunofixation (Abnormal M protein) → Tissue biopsy (endomyocardial, fat pad) to confirm diagnosis → Negative serum free light chains and immunofixation (ruled out AL amyloidosis) → Cardiac scintigraphy (Technetium pyrophosphate with SPECT imaging) What treatment options do we have to offer now for ATTR CM, and how has this compared to prior years? Before 2019, treatment options were limited outside of cardiac tr...
In this week's issue, Dr. Harlan Krumholz highlights new science with direct clinical implications: a randomized trial showing conduction system pacing outperforms RV pacing in AV block, a pragmatic study suggesting HEPA filtration may modestly lower blood pressure, and long-term data from FLAVOR comparing FFR and IVUS-guided PCI. Also featured are a state-of-the-art review on heart failure therapy implementation, a brief report refining NT-proBNP thresholds for pre–heart failure, and an updated JACC Report Card revealing persistent cardiovascular mortality disparities among Black Americans. The issue closes with reflections on equity, anatomy, and two complex case reports.
We have covered Low Dose Aspirin (LDA) for pre-natal preeclampsia prevention MANY times before. But here's a good clinical question: Since preeclampsia can also pop-up in the first 6 weeks postpartum (pp), should we continue it in the immediate pp interval? There is a new publication, an RCT, in the AJOG that looked to answer this- and we will highlight that publication in this episode. PLUS, we will briefly summarize a separate publication from the American J Perinatology back in 2023 that also provided some clinical insights on this topic. Listen in for details.1. The association between postpartum aspirin use and NT-proBNP levels as a marker for maternal cardiac health: a randomized-controlled trial; July 2025 (AJOG): https://www.sciencedirect.com/science/article/pii/S00029378250047522. Christenson E, Stout MJ, Williams D, Verma AK, Davila-Roman VG, Lindley KJ. Prenatal Low-Dose Aspirin Use Associated with Reduced Incidence of Postpartum Hypertension among Women with Preeclampsia. Am J Perinatol. 2023 Mar;40(4):394-399. doi: 10.1055/s-0041-1728826. Epub 2021 May 3. PMID: 33940641.3. Mendoza M, Bonacina E, Garcia-Manau P, et al. Aspirin Discontinuation at 24 to 28 Weeks' Gestation in Pregnancies at High Risk of Preterm Preeclampsia: A Randomized Clinical Trial. JAMA. 2023;329(7):542–550. doi:10.1001/jama.2023.0691
With Kevin Damman, University Medical Center Groningen, Groningen - The Netherlands, Floran Sahiti, University Hospital of Wurzburg, Wurzburg - Germany, Joao Pedro Ferreira, University of Porto, Porto - Portugal, Novi Yanti Sari, Siloam Hospitals Group, Jakarta - Indonesia, Marat Fudim, Duke University Medical Center, Durham, NC - USA, Gregorio Tersalvi, Mayo Clinic, Rochester, MN - USA, Jose Luis Morales Rull, University Hospital Arnau de Vilanova, Lleida - Spain and Cornelia Margineanu, Bucharest - Romania. In this episode, we discuss four late-breaking clinical trials presented at the Heart Failure Congress 2025 in Belgrade, Serbia. First, Kevin Damman presents the results of FUTURE-HF, a first-in-human study evaluating the long-term safety, accuracy, and clinical utility of a novel implantable IVC sensor for remote heart failure management. Next, Joao Pedro Ferreira highlights the key findings of SOGALDI-PEF, a crossover trial comparing SGLT2 inhibitor monotherapy versus combination therapy with an SGLT2 inhibitor and a mineralocorticoid receptor antagonist (MRA) in reducing NT-proBNP levels. Third, Marat Fudim reports on the MUSIC-HFpEF phase 1/2a trial, which explores the safety and preliminary efficacy of a novel gene therapy using adeno-associated virus vectors in patients with HFpEF. Finally, Jose Luis Morales Rull shares insights from PREFER-HF, a study assessing the effects of intravenous or oral iron therapy versus placebo in patients with HFpEF and iron deficiency anemia. FUTURE-HF: Long-term safety, accuracy, and utility of a novel implantable IVC sensor for remote HF management - Kevin Damman, University Medical Center Groningen, Groningen, The Netherlands. Host: Floran Sahiti, University Hospital of Wurzburg, Wurzburg, Germany doi: 10.1016/j.jchf.2025.01.019. SOGALDI-PEF: SOdium-Glucose cotransporter 2 inhibitor with and without an ALDosterone AntagonIst for heart failure with preserved ejection fraction – Joao Pedro Ferreira, University of Porto, Porto, Portugal. Host: Novi Yanti Sari, Siloam Hospitals Group, Jakarta (Indonesia). MUSIC-HFpEF: Gene therapy in Heart Failure with Preserved Ejection Fraction – Marat Fudim, Duke University Medical Center, Durham, NC, USA. Host: Gregorio Tersalvi, Mayo Clinic, Rochester, MN, USA PREFER¬-HF: Effects intravenous iron or oral iron therapy compared to placebo in HFpEF with iron deficiency anemia - Jose Luis Morales Rull, University Hospital Arnau de Vilanova, Lleida, Spain. Host: Cornelia Margineanu, Bucharest, Romania. This 2025 HFA Cardio Talk podcast series is supported by Bayer AG in the form of an unrestricted financial support. The discussion has not been influenced in any way by its sponsor.
Darshan H. Brahmbhatt, Podcast Editor of JACC: Advances, discusses a recently published original research paper on Third-Trimester NT-proBNP for Pre-eclampsia Risk Prediction: A Comparison With sFlt-1/PlGF in a Population-Based Cohort.
Hosts Mitsuaki Sawano, MD, and Nobuhiro Ikemura, MD, welcome Yuichiro Mori, MD, MPH, a physician-scientist at Kyoto University, to discuss his ACC.25 poster presentation on biomarker-based pre-heart failure screening using NT-proBNP, conducted in a rural Japanese city in Hokkaido. Drawing from a screening cohort of 1,585 individuals aged 40–74 in Furano, the study integrated NT-proBNP testing into Japan's routine general health checkups. Dr. Mori shares key takeaways from the study and emphasizes how even single-site efforts, when well-structured and strategically communicated, can gain recognition at major global meetings like ACC.
Watch here for a video interview with JACC Associate Editor Michelle Kittleson, MD, FACC, and author Mathew S. Muarer, MD, FACC, as they discuss Dr. Maurer's study published in JACC and presented at ACC.25. This exploratory analysis of HELIOS-B assessed the efficacy of vutrisiran versus placebo in patients with transthyretin amyloidosis with cardiomyopathy (ATTR-CM) by subgroups of baseline heart failure severity (primarily by NYHA class and NT-proBNP levels). Vutrisiran showed evidence of benefit vs placebo on mortality, cardiovascular events, functional capacity, quality of life, and cardiac biomarkers across the range of baseline disease severities in patients enrolled in HELIOS-B, with greatest benefit observed in patients with earlier, less severe disease.
Heart failure is a clinical diagnosis with specific signs. If unsure, N-terminal pro b-type natriuretic peptide (NT-proBNP) levels can help rule it out Differences between brain natriuretic peptide (BNP) and NT-proBNP, and how to apply each of them to your heart failure patients In patients with chronic kidney disease, NT-proBNP levels should be within context of renal dysfunction Serial measurements of NT-proBNP are associated with prognosis, guidance and response to heart failure treatment Only one NT-proBNP test per patient per year is reimbursed; additional tests must be self-funded Host: Dr David Lim | Total Time: 39 mins Experts: Prof Andrew Sindone, Cardiologist A/Prof Ralph Audehm, General Practitioner Register for our fortnightly FREE WEBCASTSEvery second Tuesday | 7:00pm-9:00pm AEDT Click here to register for the next oneSee omnystudio.com/listener for privacy information.
Welcome to the first episode in a special three-part series of the Diabetes Core Update podcast, focused on heart screening in people with diabetes. Sponsored by Roche, this series explores "heart failure with preserved ejection fraction" (HFpEF), providing primary care clinicians and healthcare professionals with essential insights into screening, diagnosis, and management of this increasingly recognized condition. Episode Summary In this episode, host Dr. Neil Skolnik introduces the growing importance of HFpEF in diabetes care and is joined by two esteemed experts: Rodica Busui, MD, PhD, professor and chief of the division of endocrinology at the Oregon Health and Science University and past president of the American Diabetes Association for Medicine and Science. James Jannuzzi, MD, professor of medicine at Harvard Medical School, staff cardiologist at Massachusetts General Hospital, and senior cardiometabolic faculty at Baim Institute for Clinical Research. The discussion explores: HFpEF Basics: Definition, prevalence, and how it differs from heart failure with reduced ejection fraction (HFrEF). Pathophysiology: The multifactorial causes of HFpEF, including aging, obesity, diabetes, and more. Diabetes and HFpEF: Why HFpEF should be considered a major complication of diabetes alongside atherosclerotic and microvascular diseases. Screening Recommendations: Insights from the 2022 ADA/ACC Consensus Report, emphasizing early detection through biomarkers like NT-proBNP and annual testing for at-risk patients. Key Takeaways Epidemiology: HFpEF affects at least half of heart failure patients and is increasingly prevalent due to aging, obesity, and diabetes. Screening Guidelines: Every person with diabetes, especially those with chronic kidney disease, hypertension, or obesity, should be considered for HFpEF screening. Biomarkers: NT-proBNP thresholds are key tools for early diagnosis, with tailored considerations for obesity and other conditions. Prevention and Collaboration: Effective risk factor management and team-based care can prevent HFpEF progression and improve outcomes. Thank you for joining us on this first of a multipart series on early detection and treatment of heart failure with preserved ejection fraction. In the first part of this series, we focused on basics—epidemiology, pathophysiology, and staging—as well as the critically important new recommendations around screening people with diabetes for heart failure. In the second part of the series, we'll explore treatment strategies for HFpEF. This special edition of Diabetes Core Update is sponsored by Roche.
This week, please join authors Amil Shah and our own Peder Myhre, as well as Guest Editor Allan Jaffe as they discuss the article "NT-proBNP and Cardiac Troponin I, but Not Cardiac Troponin T, Are Associated With 7-Year Changes in Cardiac Structure and Function in Older Adults: The ARIC Study." For the episode transcript, visit: https://www.ahajournals.org/do/10.1161/podcast.20241202.603271
JACC Associate Editor Muthiah Vaduganathan, MD speaks with author Ambarish Pandey, MD about the LookAHEAD trial published in JACC and presented at AHA. Among adults with T2D and overweight/obesity in the Look Action for Health in Diabetes (AHEAD) trial, an intensive lifestyle intervention targeting weight loss led to sustained reductions in hs-cTnT at 1- and 4-year follow-up, and a rise in NT-proBNP at 1 year that attenuated at 4 years. After accounting for baseline biomarker levels and baseline and changes in risk factors, longitudinal increase in NT-proBNP was associated with higher risk of ASCVD and incident HF. In contrast, increase in hs-cTnT was significantly associated with ASCVD but not incident HF.
In the October 15, 2024 issue of JACC, a study led by Dr. Paul Hayler investigates the use of biomarkers—NT-proBNP, high-sensitive cardiac troponin T, and GDF-15—to assess heart failure risk in patients with atrial fibrillation. The findings reveal that these biomarkers significantly enhance risk stratification, suggesting their potential to identify patients at varying risks for heart failure and improve clinical management.
Explore the fascinating world of muscle as an organ, delving into its roles beyond movement, including its secretory functions and impact on overall health. This episode uncovers the surprising influences muscles have on inflammation, vascular health, and more. Discover how muscles communicate with the body through myokines, manage blood flow, and contribute to heart health. 5 KEY TAKEAWAYS: 1.Muscles as Secretory Organs: Learn how skeletal muscles produce myokines like IL-6 and BDNF, affecting body functions both locally and systemically. 2.Vascular Health and Muscles: Understand how eNOS activity in muscles enhances vascular health through better blood flow and vascular relaxation. 3.Heart Health Insights: Discover the role of NT-proBNP in heart health, produced by the heart under stress and closely linked with muscle function. 4.Muscle Health and Systemic Effects: See how muscle health impacts systemic conditions like diabetes and inflammation through the production of myokines. 5.Nutritional Impacts on Muscle Function: Gain insights into how amino acids like glutamine support muscle function and overall metabolic health. FEATURED PRODUCT: Boost your muscle health with our advanced formula! Designed to enhance muscle function and support your body's natural processes, this product is perfect for anyone looking to improve their muscular system's overall health and efficiency, as discussed in today's episode. Gut: https://www.mswnutrition.com/products/gut?srsltid=AfmBOoqDiokc4Thnr44DyfkJYjwU-6zhP0aUWyx4Yu2kMccW20vbZfQ0 TIMESTAMPS: •00:00 START: Introduction to Muscle Health •02:00: Muscles as Secretory Organs •05:00: The Role of eNOS in Muscle Function •10:00: Heart Health and Muscle Interaction •15:00: Systemic Effects of Healthy Muscles •20:00: Nutritional Strategies for Muscle Support RESOURCES: 1.Myokines and Muscle Function: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3710002/ 2.eNOS and Vascular Health: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8774925/ 3.Heart Stress and BNP: https://my.clevelandclinic.org/health/diagnostics/22629-b-type-natriuretic-peptide 4.Nutritional Influence on Muscles: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7019684/
The following question refers to Section 5.1 of the 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure.The question is asked by University of Colorado internal medicine resident Dr. Hirsh Elhence, answered first by advanced heart failure faculty at the University of Chicago and Co-Chair for the CardioNerds Critical Care Cardiology Series Dr. Mark Belkin, and then by expert faculty Dr. Biykem Bozkurt.Dr. Bozkurt is the Mary and Gordon Cain Chair, Professor of Medicine, Director of the Winters Center for Heart Failure Research, and an advanced heart failure and transplant cardiologist at Baylor College of Medicine in Houston, TX. She is former President of HFSA, former senior associate editor for Circulation, and current Editor-In-Chief of JACC Heart Failure. Dr. Bozkurt was the Vice Chair of the writing committee for the 2022 Heart Failure Guidelines.The Decipher the Guidelines: 2022 AHA / ACC / HFSA Guideline for The Management of Heart Failure series was developed by the CardioNerds and created in collaboration with the American Heart Association and the Heart Failure Society of America. It was created by 30 trainees spanning college through advanced fellowship under the leadership of CardioNerds Cofounders Dr. Amit Goyal and Dr. Dan Ambinder, with mentorship from Dr. Anu Lala, Dr. Robert Mentz, and Dr. Nancy Sweitzer. We thank Dr. Judy Bezanson and Dr. Elliott Antman for tremendous guidance.Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. /*! elementor - v3.23.0 - 25-07-2024 */ .elementor-toggle{text-align:start}.elementor-toggle .elementor-tab-title{font-weight:700;line-height:1;margin:0;padding:15px;border-bottom:1px solid #d5d8dc;cursor:pointer;outline:none}.elementor-toggle .elementor-tab-title .elementor-toggle-icon{display:inline-block;width:1em}.elementor-toggle .elementor-tab-title .elementor-toggle-icon svg{margin-inline-start:-5px;width:1em;height:1em}.elementor-toggle .elementor-tab-title .elementor-toggle-icon.elementor-toggle-icon-right{float:right;text-align:right}.elementor-toggle .elementor-tab-title .elementor-toggle-icon.elementor-toggle-icon-left{float:left;text-align:left}.elementor-toggle .elementor-tab-title .elementor-toggle-icon .elementor-toggle-icon-closed{display:block}.elementor-toggle .elementor-tab-title .elementor-toggle-icon .elementor-toggle-icon-opened{display:none}.elementor-toggle .elementor-tab-title.elementor-active{border-bottom:none}.elementor-toggle .elementor-tab-title.elementor-active .elementor-toggle-icon-closed{display:none}.elementor-toggle .elementor-tab-title.elementor-active .elementor-toggle-icon-opened{display:block}.elementor-toggle .elementor-tab-content{padding:15px;border-bottom:1px solid #d5d8dc;display:none}@media (max-width:767px){.elementor-toggle .elementor-tab-title{padding:12px}.elementor-toggle .elementor-tab-content{padding:12px 10px}}.e-con-inner>.elementor-widget-toggle,.e-con>.elementor-widget-toggle{width:var(--container-widget-width);--flex-grow:var(--container-widget-flex-grow)} Question #33 A 63-year-old man with a past medical history of hypertension and type 2 diabetes mellitus presents for routine follow-up. He reports feeling in general good health and enjoys 2-mile walks daily. A review of systems is negative for any symptoms. Which of the following laboratory studies may be beneficial for screening?ANT-proBNPBCK-MBCTroponinDC-reactive proteinENone of the above Answer #33 ExplanationThe correct answer is A – NT-proBNP.This patient is at risk for HF (Stage A) given the presence of risk factors (hypertension and type 2 diabetes mellitus) but the absence of signs or symptoms of heart failure.Patients at risk for HF screened with BNP or NT-proBNP followed by collaborative care, diagnostic evaluation, and treatment in those with elevated levels can reduce combined rates of LV systolic ...
Dr. Amy Kaplan, DACVECC here today! In today's VETgirl online veterinary CE podcast, we're going to explore the various diagnostics tools available to us to workup nonhemorrhagic ascites in dogs beyond our initial physical examination. Now in the ER, when I tap an abdomen and it comes back as blood, I'm all over it – the majority of the time, it's often secondary to hemangiosarcoma or less common causes such as hemangiomas or hematomas (which DO happen!). Less commonly, I'll see patients present with abdominal effusion that is considered a nonhemorrhagic ascites (what we'll call NHA from now on) – this is fluid with a packed cell volume of < 10%). A variety of diseases can cause NHA including right-sided congestive heart failure, neoplasia, liver failure, hypoalbuminemia, pancreatitis, chyloabdomen, uroabdomen, or septic peritonitis. So, when it's NOT blood, how do you figure out the cause of the ascites?Sponsored By: Royal Canin
In today's VETgirl online veterinary CE podcast, we're going to review a study by Morey et al out of University of Missouri entitled “N-terminal brain natriuretic peptide, cardiac troponin-I, and point-of-care ultrasound in dogs with cardiac and noncardiac causes of nonhemorrhagic ascites.”
CardioNerds Dr. Josh Saef and Dr. Tommy Das join Dr. Omkar Betageri, Dr. Andrew Geissler, Dr. Philip Lacombe, and Dr. Cashel O'Brien from the Maine Medical Center in Portland, Maine to enjoy an afternoon by the famous Portland headlight. They discuss a case of a patient who presents with obstructive cardiogenic shock. Dr. Bram Geller and Dr. Jon Donnelly provide the Expert CardioNerd Perspectives & Review segment for this episode. Dr. Maxwell Afari, the Maine Medical Center cardiology fellowship program director highlights the fellowship program. Audio editing by CardioNerds Academy Intern, student doctor Tina Reddy. This is the case of a 42 year-old woman born with complicated Tetralogy of Fallot repair culminating in a 29mm Edwards Sapiens (ES) S3 valve placement within a pulmonary homograft for graft failure who was admitted to the cardiac ICU for progressive cardiogenic shock requiring vasopressors and inotropic support. Initial workup showed lactic acidosis, acute kidney injury, elevated NT-proBNP, and negative blood cultures. TTE showed at least moderate biventricular systolic dysfunction. She was placed on furosemide infusion, blood cultures were drawn and empiric antibiotics initiated. Right heart catheterization demonstrated elevated right sided filling pressures, blunted PA pressures with low PCWP, low cardiac index, and low pulmonary artery pulsatility index. Intracardiac echocardiography (ICE) showed a large mass within the ES valve apparatus causing restrictive valve motion with a low gradient across the pulmonic valve in the setting of poor RV function. Angiography revealed a large filling defect and balloon valvuloplasty was performed with immediate hemodynamic improvement. Blood cultures remained negative, she was gradually weaned off of inotropic and vasopressor support, and discharged. Despite empiric treatment for culture negative endocarditis and ongoing anticoagulation, she was readmitted for recurrent shock one month later at which time the pulmonic mass was revisualized on ICE. A valve-in-valve transcatheter pulmonary valve (29mm ES S3) was placed to compress what was likely pannus, with an excellent hemodynamic result and no visible mass on ICE. US Cardiology Review is now the official journal of CardioNerds! Submit your manuscript here. CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Case Media Pearls - Obstructive Cardiogenic ShocK Tetralogy of Fallot is the most common cyanotic defect and can lead to long term complications after surgical repair including chronic pulmonary insufficiency, RV dysfunction, residual RVOT obstruction and branch pulmonary artery stenoses. Chronic RV failure may be more indicative of a structural defect and therefore require interventional or surgical management. Valve thrombosis, infective endocarditis and obstructive pannus formation should be considered in the differential of a patient with obstructive shock with a prosthetic valve. Bioprosthetic pulmonic valve obstruction may be effectively managed with balloon valvuloplasty in patients who present in acute extremis but TCPV will likely provide a more lasting result. While valvular gradients are typically assessed via echocardiography, invasive hemodynamics can serve as a critical adjunctive tool in its characterization. Show Notes - Obstructive Cardiogenic ShocK Notes were drafted by Drs. Omkar Betageri, Philip Lacombe, Cashel O'Brien, and Andrew Geissler. What are the common therapies and management for Tetralogy of Fallot? Tetralogy of Fallot is the most common cyanotic defect in children beyond the age of one year Anatomic Abnormalities: Anterior and Superior deviation of the conal septum creating a SubAo VSD and encroachment on the RVOT.
Join Dr. Joel Kahn on this episode of Heart Doc VIP as he delves into the fascinating world of biomarkers, specifically focusing on one called BNP (B-type natriuretic peptide) or NT-proBNP. Biomarkers play a crucial role in providing diagnostic and prognostic information in clinical care, as well as in the realm of life insurance panels. Discover what BNP is and how it functions within the body, along with the conditions that can lead to elevated levels of this biomarker. Dr. Kahn expertly guides us through the evaluation process when abnormal results are observed, shedding light on the significance of such findings for patients' health. Moreover, in this episode, Dr. Kahn introduces a special supplement known as MitoQ, which shows promising potential in helping to lower BNP levels. If you're intrigued to learn more about MitoQ, you can find it at (https://shop.drjoelkahn.com/mitoq-pure-60-capsules.html). Once again, we extend our gratitude to our sponsor, healthycell.com, and invite you to take advantage of the exclusive 20% discount with the code KAHN during checkout. Tune in to this informative and empowering episode to stay ahead in your journey to a healthier heart!
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