Podcasts about Circulation

1 - Uccelli - Flicker 2 - Steve Parry - Freeze 3 - Quivver - Moonlight Pools (Cruz Vittor Remix) 4 - Circulation, Cass (UK) - Nuke the Site From Orbit (Cass Skunkworks Remix) 5 - Gai Barone - Macula (Extended Mix) 6 - Thaddeus X - Life in Wave (Noel Barbeito Edit) 7 - UNWA - Lonely (Katrin Souza Remix) 8 - Nick Stoynoff - Strawberry Fields 9 - Calcou - Closer 10 - HVOB - The Blame Game (Roman & Juan Ibáñez Bootleg) Download episode on MP3 (Right click, save link as...) Help me support NGO Alegría Intensiva, Hospital Clown, in Argentina. Donate now by clicking here!!! Donar desde Argentina haciendo click aquí!!!

CardioNerds (Dr. Jenna Skowronski [Heart Failure Council Chair], Dr. Shazli Khan, and Dr. Josh Longinow) are joined by renowned leaders in the field of AHFTC (Advanced Heart Failure and Transplant Cardiology) and mechanical circulatory support, Dr. Jeff Teuteberg and Dr. Mani Daneshmand to continue the discussion of advanced heart failure therapies by taking a deep dive into the world of durable LVADs (Left Ventricular Assist Devices). In this episode, we will review the history of ventricular assist devices, the basics of LVAD function, selection criteria for LVAD therapy, and surgical nuances of LVAD implantation. Audio Editing by CardioNerds intern, Joshua Khorsandi. 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 There have been significant advances in the field of MCS/LVAD therapy since the first implanted LVAD in the 1960s, to the first FDA approved device in the early 2000's, to now the HM3 LVAD, with the most important change being a centrifugal flow/magnetically levitated design that led to minimized hemocompatibility-related adverse events (HRAE's) (MOMENTUM 3 trial comparing HM2 and HM3).  The REMATCH trial in 2001 was a pivotal trial for LVAD therapy, demonstrating that in a population of patients with advanced HF (70% IV inotrope dependent), LVAD therapy significantly improved survival at both 1 and 2 years as compared to medical therapy alone.    MOMENTUM 3 trial was a landmark trial for the HM3 device, showing that in a population of end stage HF patients (86% inotrope dependent, 32% INTERMACS 1-2, and 60% DT strategy), 5-year survival with HM3 was 58% and HM3 had lower HRAE's compared with HM2.  There are both patient-specific factors and surgical considerations when it comes to candidacy for LVAD therapy.  RV function prior to LVAD is a key determinant for success post-LVAD  Many patients being considered for LVAD may not have robust RV function, however, predicting RV failure after LVAD is exceedingly difficult.   In general, it doesn’t matter how bad the RV may look on imaging; we care more about the pre-LVAD hemodynamics (look at the PAPi and RA/wedge ratio).   What happens in the OR may be the most important determinant of how the RV will do with the LVAD!  Notes Notes drafted by Dr. Josh Longinow.  1. Historical background of heart pumps and LVADs  LVAD Evolution   FDA approval year  2001  2008  2012  2017  Pump  HeartMate XVE   HeartMate II  Heartware HVAD  HeartMate III  Flow/Design Features  Pulsatile Technology   Continuous flow Axial design  Continuous flow  Centrifugal design  Continuous flow   Full MagLev + Centrifugal design  The 1960's ushered in the first ‘LVADs', when the first air-powered ‘LVAD' was implanted. It kept the patient alive for four days before the patient expired.   The first generation of LVADs were pulsatile pumps   The first nationally recognized, FDA approved LVAD was the HeartMate XVE (late 1990s to early 2000s, REMATCH trial). The XVE pump used compressed air (pneumatically driven) to power the pump.   Prior to the XVE, OHT was the standard of care for patients with advanced, end-stage heart failure.   The second and third generations of LVADs were non-pulsatile, continuous flow devices and included the HVAD, HM2, and HM3 devices.   MOMENTUM 3 was a landmark trial for the HM3 device, showing that in a population of sick patients with end stage HF (86% inotrope dependent, 32% INTERMACS 1-2, and 60% DT strategy), 5-year survival with HM3 was 58% and HM3 had lower HRAE's compared with HM2.   The only pump that is currently FDA approved for implant is the HM3, although other pumps are in clinical trials (BrioVAD system, INNOVATE Trial).  2. What are LVADs, and how do they work?   In simplest terms, the LVAD is a heart pump comprised of several key mechanistic components:   Inflow cannula  Mechanical pump   Outflow cannula  Driveline  Controller/Power source  The HM3 differs from its predecessors (HM2 and HVAD) in several key ways;   HM3 is placed intrapericardial whereas the HM2 was placed pre-peritoneal.   Perhaps most importantly, the HM3 is a fully magnetically levitated, centrifugal flow pump, whereas the HM2 is an axial flow device.  Axial flow pumps are not magnetically levitated, leading to more friction produced between the ruby bearing's contact with the pump rotors, and higher rates of hemocompatibility related adverse events (HRAEs, i.e. pump thrombosis) and the HM2 was ultimately discontinued in favor of the HM3 (MOMENTUM 3 trial).  3. What do the terms ‘Destination Therapy' (DT) or ‘Bridge to Transplant' (BTT) mean when it comes to LVADs?   When LVADs first came on the stage, EVERYONE was a BTT; these early pumps weren't designed for long term use (I.e. REMATCH Trial, Heartmate XVE)  Destination therapy means the LVAD was placed in leu of transplant because there are contraindications to transplant   REMATCH trial brought about the concept of “Destination therapy”, comparing outcomes in patients (with contraindications for transplant) who received an LVAD vs optimal medical therapy  Bridge to transplant means we are placing the LVAD in a patient who may not be a transplant candidate at this moment in time (is too sick, or conversely, not sick enough), but may be down the line   Bridge to recovery is another term used when the LVAD is being placed for a patient we think may have a recoverable cardiomyopathy  4. What are some factors we should consider when assessing a patient’s candidacy for LVAD, in general, and from a surgical perspective?   Patient factors   Older age might push us towards thinking LVAD rather than transplant  In general, age > 70 is the cutoff for transplant, but this is not a hard cut off and varies institution to institution    In general, think about things that help predict recovery after a major surgery; Frailty and Nutritional status are important, we try to optimize these prior to LVAD implant   Right ventricular function remains the Achilles heel of LV support  We know that needing temporary RV support post LVAD puts you on a different survival curve than patients who don’t need RVAD support  Studies have not been able to successfully predict who will develop RV failure after LVAD implantation  What happens in the time between when the patient goes to the OR and when they get back to the ICU is an important determinant who might develop RV failure post LVAD   Surgical techniques such as implanting the HM3 in the intra-thoracic cavity, rather than intra-pericardial may help maintain LV/RV geometry to help optimize the RV post LVAD   Surgical considerations for LVAD candidacy  Small, hypertrophied LV: HM3 inflow cannula is small, but small hypertrophied ventricles tend towards chamber collapse during systole causing suction, needing to run slower with lower flow rates  Chest size/diameter: pumps have gotten so small now, that for adults, these have become less of a consideration  BMI: low BMI used to be more of a concern with the older pumps due to where they were placed, and the relative size of the pump itself, not so much now with the smaller HM 3 pumps  Calcified LV apex: would increase risk of stroke, bleeding   Driveline tunneling becomes a concern in the super obese population, higher risk for driveline infections (might tunnel these driveline's shorter, and to a less fatty region of the abdomen, could even tunnel out the thoracic cavity in the super obese to limit skin motion)    5. Is there a role for MCS (i.e. temporary LVAD such as Impella) in pre-habilitation of patients prior to LVAD surgery?   The theory of being able to improve systemic perfusion, decongest the organs, and make the patient feel better prior to surgery makes sense, but becomes problematic due to the lack of a hard end point/time for prehabilitation which might risk delays in surgery   More likely that it can lead to delay in the surgery, with less-than-optimal benefit; you don't want to prolong the wait for surgery and increase the risk for complications prior to surgery    An Impella 5.5 is currently FDA approved for 2 weeks of support, not 2 months so timing is important to keep in mind  It’s unlikely that you will take a patient and convert them from a malnourished, cachectic person in 2 weeks’ time   6. Is there a role for LVAD therapy in the younger patient population? Should we be thinking of LVAD up front for these patients, with the goal of transplanting down the line?   Recovery may be more likely in certain populations, particularly younger females with smaller LV's; in those populations, perhaps bridge to recovery should be the focus, optimizing them on GDMT etc.   The replacement of transplant, with MCS (LVAD) in young patients has become a topic of discussion, because these pumps have become better and better, with the thinking that an LVAD could bridge a patient for 10 years or so, and they could get a transplant later   It is still a big unknown, but several concerns exist  Patients who get LVADs might end up with complications that become contraindication to transplant down the line (stroke, sensitization etc)   Patients and providers are more hesitant because of the more recent iteration for the UNOS criteria for OHT listing which no longer gives patients with an uncomplicated LVAD higher priority, and therefore they could end up waiting a longer time for a heart after undergoing LVAD  References Rose EA, Gelijns AC, Moskowitz AJ, et al. Long-term use of a left ventricular assist device for end-stage heart failure. N Engl J Med. 2001;345(20):1435-1443. doi:10.1056/NEJMoa012175  Mehra MR, Uriel N, Naka Y, et al. A Fully Magnetically Levitated Left Ventricular Assist Device – Final Report. N Engl J Med. 2019;380(17):1618-1627. doi:10.1056/NEJMoa1900486  Mancini D, Colombo PC. Left Ventricular Assist Devices: A Rapidly Evolving Alternative to Transplant. J Am Coll Cardiol. 2015;65(23):2542-2555. doi:10.1016/j.jacc.2015.04.039  Mehra MR, Goldstein DJ, Cleveland JC, et al. Five-Year Outcomes in Patients With Fully Magnetically Levitated vs Axial-Flow Left Ventricular Assist Devices in the MOMENTUM 3 Randomized Trial. JAMA. 2022;328(12):1233-1242. doi:10.1001/jama.2022.16197  Rose EA, Moskowitz AJ, Packer M, et al. The REMATCH trial: rationale, design, and end points. Randomized Evaluation of Mechanical Assistance for the Treatment of Congestive Heart Failure. Ann Thorac Surg. 1999;67(3):723-730. doi:10.1016/s0003-4975(99)00042-9  Kittleson MM, Shah P, Lala A, et al. INTERMACS profiles and outcomes of ambulatory advanced heart failure patients: A report from the REVIVAL Registry. J Heart Lung Transplant. 2020;39(1):16-26. doi:10.1016/j.healun.2019.08.017  Mehra MR, Netuka I, Uriel N, et al. Aspirin and Hemocompatibility Events With a Left Ventricular Assist Device in Advanced Heart Failure: The ARIES-HM3 Randomized Clinical Trial. JAMA. 2023;330(22):2171-2181. doi:10.1001/jama.2023.23204  Mehra MR, Nayak A, Morris AA, et al. Prediction of Survival After Implantation of a Fully Magnetically Levitated Left Ventricular Assist Device. JACC Heart Fail. 2022;10(12):948-959. doi:10.1016/j.jchf.2022.08.002  Bhardwaj A, Salas de Armas IA, Bergeron A, et al. Prehabilitation Maximizing Functional Mobility in Patients With Cardiogenic Shock Supported on Axillary Impella. ASAIO J. 2024;70(8):661-666. doi:10.1097/MAT.0000000000002170 

What would I actually do if I had to start over? No brand. No supplements to sell. No trends to chase. No social media theatrics. Just me, in 2026, building my health from the ground up. In this stripped-down solo episode, Darin lays out the foundational pillars he would implement immediately if he were starting fresh today. This is not about extremes. It's not about perfection. It's not about viral biohacks. It's about alignment. Infrastructure. Sovereignty. From water filtration and mineral balance to plant-dominant nutrition, strength training, sleep timing, nervous system regulation, purpose, and community, this is the grounded, research-backed roadmap to a Super Life. In This Episode Why reverse osmosis water filtration is step one The importance of remineralizing filtered water Eliminating PFAS, agrochemicals, and heavy metals from daily exposure Why non-toxic cookware is a non-negotiable A plant-dominant, whole-food strategy backed by longevity research Protein distribution and muscle protein synthesis science The truth about B12, the microbiome and supplementation Why algae-based omega-3s may be smarter than fish oil Resistance training as a longevity lever Why sleep timing consistency may matter more than duration Breathwork, meditation and nervous system training Community as biological medicine Limiting social media for mental health Purpose as a predictor of mortality risk Why you need a functional medical practitioner in your corner Nurturing creativity in a productivity-obsessed culture Chapters 00:00:00 – Welcome to SuperLife 00:00:33 – NAD supplement fraud & the importance of verification 00:02:23 – The question: If I started over in 2026, what would I do? 00:04:08 – No trends, no hype, just grounded science 00:05:15 – Step 1: Clean up your water 00:06:28 – PFAS, heavy metals & agrochemical contamination 00:07:59 – Reverse osmosis as the gold standard 00:08:35 – Re-mineralizing filtered water 00:09:40 – Mineral strategy & electrolyte balance 00:10:35 – Eliminating toxic cookware exposure 00:12:52 – Plant-dominant nutrition as foundational strategy 00:14:45 – Protein distribution & muscle protein synthesis 00:17:22 – Longevity Blue Zones & daily legumes 00:18:06 – B12 nuance & microbiome research 00:20:15 – Omega-3s: chia, flax & algae-based oils 00:22:39 – Strength training as the longevity switch 00:23:05 – Resistance training & reduced all-cause mortality 00:24:24 – Sleep timing consistency & mortality research 00:25:40 – Darkness, eye masks & sleep quality 00:26:20 – Nervous system regulation: meditation & somatic work 00:27:05 – Breathwork protocols & inflammation research 00:28:27 – Community as biological medicine 00:29:05 – Limiting social media & reducing depression risk 00:29:24 – Purpose & lower mortality association 00:30:12 – Functional medicine practitioners vs primary care 00:32:21 – Nurturing yourself in a productivity culture 00:34:22 – Closing: Build alignment, not perfection Thank You to Our Sponsors Our Place – Non-toxic cookware that keeps harmful chemicals out of your food. Get 10% off at fromourplace.com with code DARIN. Tru Niagen – Boost NAD+ levels for cellular health and longevity. Get 20% off with code Darin20 at truniagen.com. Key Takeaway If I were starting today, I wouldn't chase perfection. I would build alignment. Clean water. Plant-dominant nutrition. Strength. Sleep consistency. Nervous system regulation. Community. Purpose. And nurturing creativity. No hacks. No drama. Just infrastructure. That's how you build a Super Life. Bibliography/Sources British Journal of Sports Medicine. (2022). Muscle-strengthening activities and risk of cardiovascular disease, cancer, diabetes, and all-cause mortality: a systematic review and meta-analysis of prospective cohort studies. https://bjsm.bmj.com/content/56/13/757 Sleep. (2023). Sleep regularity is a stronger predictor of mortality risk than sleep duration: A prospective cohort study. https://academic.oup.com/sleep/article/47/2/zsad253/7280431 NIH Office of Dietary Supplements. (2024). Vitamin B12 Fact Sheet for Consumers. Provides guidance on necessary B12 sources for those on plant-based diets. https://ods.od.nih.gov/factsheets/VitaminB12-Consumer/ Nutrients. (2019). Dietary Protein and Amino Acids in Vegetarian Diets—A Review. Authored by Mariotti and Gardner, examining protein adequacy in plant-based eating. https://www.mdpi.com/2072-6643/11/11/2661 Circulation. (2021). Effect of omega-3 fatty acids on cardiovascular outcomes: A systematic review and meta-analysis. https://www.ahajournals.org/doi/10.1161/CIRCULATIONAHA.121.055656 Journal of Social and Clinical Psychology. (2018). No More FOMO: Limiting Social Media Decreases Loneliness and Depression. A randomized controlled trial on limiting social media use. https://guilfordjournals.com/doi/10.1521/jscp.2018.37.10.751 NHMRC. (2015). NHMRC Statement on Homeopathy. A comprehensive review of the evidence for the effectiveness of homeopathy. https://www.nhmrc.gov.au/about-us/publications/homeopathy

Partielles dans Chicoutimi: une victoire pour le PQ, mais une victoire aux yeux des conservateurs aussi | Crise au Mexique: la reprise des vols, le signal d’envoi d’un retour imminent vers la tranquillité | Commerces ouverts jusqu’à 21h: le Québec est la seule province qui impose des heures d’ouverture et de fermeture aux entrepreneurs! | 4 ans de guerre en Ukraine: un conflit banalisé qui ne risque pas de se régler… | Un acteur d’ici a obtenu un rôle en anglais: un rôle qui le fait rêver Dans cet épisode intégral du 24 février, en entrevue : Gilles Baril, ancien ministre péquiste et spécialiste de l’Amérique Latine. Éric Duhaime, chef du Parti conservateur du Québec. Samuel Poulin, ministre délégué à l’Économie et aux Petites et Moyennes Entreprises. Justin Massie, professeur titulaire de science politique à l’Université du Québec à Montréal et co-directeur du Réseau d’analyse stratégique. Henri Picard, acteur. Une production QUB Février 2026Pour de l'information concernant l'utilisation de vos données personnelles - https://omnystudio.com/policies/listener/fr

L’aspirante première ministre du Québec se prononce sur le fiasco SAAQclic, affirme que Santé Québec est là pour rester et confirme qu’elle se voit comme première ministre | 4 ans depuis le début de la guerre en Ukraine : un triste anniversaire… | Christian Page met la lumière sur deux phénomènes paranormaux | Le PLC affirme que le projet Cúram est un succès ! Dans cet épisode intégral du 24 février, en entrevue : Christine Fréchette, candidate à la direction de la Coalition avenir Québec (CAQ) et députée de Sanguinet. Michael Shwec, président du Congrès des Ukrainiens Canadiens au Québec. Christine Normandin, députée de St-Jean, leader parlementaire du Bloc Québécois. Une production QUB Février 2026Pour de l'information concernant l'utilisation de vos données personnelles - https://omnystudio.com/policies/listener/fr

This week, join author Moritz J. Hundertmark and Associate Editor Vlad Zaha as they discuss their article "IMPROVE-DiCE, a 2-Part, Open-Label, Phase 2a Trial Evaluating the Safety and Effectiveness of Ninerafaxstat in Patients With Cardiometabolic Syndromes." For the episode transcript, visit: https://www.ahajournals.org/do/10.1161/podcast.20260223.163027

Ça brasse au Mexique: les cartels prennent Puerto Vallarta d’assaut, la plupart des vols annulés | La Cour suprême invalide les tarifs de Donald Trump | Défaite crève-coeur pour le Canada aux Jeux olympiques | René Lajoie en duo avec Romy: synergie instantanée pour les deux chanteurs Dans cet épisode intégral du 23 février, en entrevue : Gilles Baril, ancien ministre péquiste et spécialiste de l’Amérique Latine. Clément Gignac, sénateur et économiste. Maxime Lapierre, ancien joueur professionnel canadien de hockey et analyste sportif chez TVA Sports. René Lajoie, candidat à La Voix - Équipe Mario Pelchat. Une production QUB Février 2026Pour de l'information concernant l'utilisation de vos données personnelles - https://omnystudio.com/policies/listener/fr

#3 part of best progressive house 00:00:00 Gai Barone - Macula (Extended Mix) 00:06:02 Guy J - Worlds Apart (Original Mix) 00:13:23 HAFT - Traverse (Original Mix) 00:19:09 Seesko - Carousel of Time (Original Mix) 00:25:25 Hicky & Kalo - Rise (Extended Mix) 00:31:22 Circulation, Cass (UK) - Nuke the Site From Orbit (Original Mix) 00:38:35 Stereo Underground - Above the Clouds (Original Mix) 00:44:33 Matan Caspi, Luis M - Groovy Beach (Extended Mix) 00:50:42 Ruben Karapetyan - Cycling Through Amsterdam (Original Mix) 00:56:31 DAVI - Self CNTRL (Original Mix) 01:04:00 Ilias Katelanos, Plecta, Anonimat - Coaster (Durante Remix)

Un médecin de famille veut continuer de traiter des patients en télémédecine et… Santé Québec refuse | Les artistes devraient éviter de nous faire la leçon dans leurs chansons… | Ça brasse au Mexique | Rapport sur l’immigration: quand même le ministre Roberge est sous le choc… Dans cet épisode intégral du 23 février, en entrevue : Dr Gaby Zagury, médecin de famille retraité. Lino Zambito, entrepreneur. Jean-François Roberge, ministre de l’Immigration, de la Francisation et de l’Intégration. Une production QUB Février 2026Pour de l'information concernant l'utilisation de vos données personnelles - https://omnystudio.com/policies/listener/fr

«C’est dégueulasse»: elle abandonne son chien… en plein aéroport! | Tarifs invalidés: «Pour tous ceux qui craignaient une dictature aux États-Unis…» | «J’ai beaucoup de souffrance que mon fils soit décédé dans la peur!» | Ovnis: «Ça ne va rien donner, on va juste continuer à alimenter les théories du complot» | Itinérance: «Montréal est à un carrefour pour ne pas devenir San Francisco ou Vancouver!», prévient Soraya Martinez Ferrada Dans cet épisode intégral du 20 février, en entrevue : Jennifer Maccarone, députée de Westmount–Saint-Louis pour le Parti libéral du Québec. Christopher Skeete, ministre responsable de la Lutte contre le racisme. Jacinthe-Ève Arel, co-animatrice de l’émission Arel-Villemure le samedi au 99.5 FM. Susie Langlois, maman de feu Gabriel Robillard. Une production QUB Février 2026Pour de l'information concernant l'utilisation de vos données personnelles - https://omnystudio.com/policies/listener/fr

Dan Dicks just obliterated the veil on this show—Canada's forcing SOGI gender perversion on kindergarten babies, mutilating confused kids through affirmation mills, then herding the broken straight into MAiD government-assisted suicide with over 100,000 already executed since 2016 in this demonic harvest.  

Gareth Icke rips into the Epstein files leak as elite mockery—Jewish-linked globalists parading taped child rape, torture, cannibalism, sacrifices, and transhuman experiments, daring us to either submit or end them for defiling our children.   BitChute's Ray Vahey details dodging Jewish-led globalist assaults—debanked in Europe, slammed by regimes, NGOs, and blacklists—delivering censorship-free video since 2017 with spy-free ops, honest trending, auto-monetization for creators, and a $10K shadowban bounty untouched.

What if the key to "getting" more in life isn't about trying harder—but about giving more freely? In this episode, we explore the the Law of Circulation and how it shapes everything from our relationships, finances, and even to our overall sense of abundance. Through insights from both science and spirituality, we look at how nature itself models this truth—nothing thrives by holding on, but by allowing energy to move. When we consciously choose to give—whether it's love, attention, generosity, or presence—we create space for something new to flow back into our lives.We also talk about how aligning with these universal laws can transform not just what we experience externally, but who we become internally. How might your life shift if you focused more on what you can contribute rather than what you can get? And what would happen if giving became less about obligation and more about expression? Join us for a heartfelt and practical conversation that invites us to step into a deeper level of abundance, fulfillment, and conscious living—by simply starting with what we already have to give.Chapters00:00 New Beginnings and Updates02:53 The Law of Circulation: Giving to Receive05:47 Nature's Examples of Giving and Receiving08:41 The Importance of Alignment with Universal Laws12:04 Concrete Examples of Giving in Life14:56 Financial Giving and Spiritual Nourishment17:51 Transformative Stories of Giving and Receiving20:47 Recommended Resource: The Go-Giver23:43 Closing Thoughts and Future Directions

Thomas English talks with a guest from the Nevada Public Library about the upcoming teen programs and events through the month of February. The guest is Library Circulation Supervisor of Teen Programs and Outreach Services Kevin Polo. He discusses the next TV Trivia Tuesday theme as well as the D&D events. He highlights some of the teen programs the library has including various craft events. Lastly, he explains how the technology grant has positively benefitted the library since its installment. 

Jake GTV joins Stew Peters live from Puerto Vallarta at Anarchapulco ripping open the Epstein files that nail Bill Gates in direct collusion with Jeffrey Epstein—the pedo financier who bankrolled the entire COVID bioweapon operation—complete with pre-planned depopulation, white fibrous clots yanked from corpses, and skyrocketing deaths that prove this was mass murder, not a pandemic. Max Igan live from Anarchapulco Genesis in Puerto Vallarta dropping hard truth: Trump was Epstein's best buddy sharing the Talmudic, Star of Moloch child-sacrifice fetish of the elite Jewish network running blackmail-free pedo rings, while Rothschild central banks control compliant governments and depopulate the world through wars for Greater Israel.

Aging is inevitable. Being misled about it isn't.In this episode of Plastic Surgery Uncensored, Dr. Rady Rahban breaks down the true biology of aging — and why it's far more complex than just “wrinkles.” Collagen and elastin decline. Fat shifts and disappears. Bone resorbs. Muscle thins. Circulation changes. Then you layer in sun exposure, stress, lifestyle, and genetics. Aging isn't one event — it's a cascade happening simultaneously.Dr. Rahban explains what can realistically slow the process — SPF, medical-grade skincare, retinoids, properly used Botox, disciplined lifestyle choices — and what's mostly marketing noise. He also dives into filler misuse, overpromised devices, social media illusions, and why “doing more” often makes people look worse, not better. Most importantly, he answers the question everyone eventually asks: When is it actually time to consider surgery?This episode is the foundation. If you want to manage aging with clarity instead of hype, start here.✨ If you enjoyed this episode of Plastic Surgery Uncensored:✔️ Subscribe on Apple Podcasts, Spotify, or wherever you listen.✔️ Rate & Review—your feedback helps more people find us.✔️ Follow Dr. Rady Rahban across all platforms for daily insights, behind-the-scenes, and patient education:Instagram: @drradyrahbanTikTok: @radyrahbanMDYouTube: @Rady RahbanFacebook: @Rady Rahban✔️ Share this episode with someone considering plastic surgery—the right knowledge can save a life.

This week, please join guest hosts Sana Al-Khatib and Mercedes Carnethon as first, they briefly introduce Circulation's annual Go Red for Women® issue. Then, our hosts welcome author Emilia Benjamin and Section Editor Maryjane Farr as they discuss the unique challenges women cardiologists have faced in the past and still encounter, and the importance of mentors and mentees in the field of cardiology. Finally, our hosts welcome Ju-Young (Judy) Shin to discuss her article "Association of Statin Discontinuation in Pregnancy With Maternal Cardiovascular Health and Birth Outcomes: A Nationwide Cohort Study." Don't miss this important podcast! For the episode transcript, visit: https://www.ahajournals.org/do/10.1161/podcast.20260213.424527

CardioNerds (Dr. Ramy Doss, Dr. Kelly Arps, and Dr. Naima Maqsood) dive into the nuances of atrial fibrillation (AF) ablation with Dr. Jon Piccini. They provide a high-yield overview of AF ablation, guiding listeners from patient selection through post-procedural management. We review appropriate candidacy for catheter ablation across AF phenotypes, key elements of pre-procedural evaluation including imaging and anticoagulation strategy, and the fundamental procedural steps with pulmonary vein isolation as the cornerstone. The discussion compares lesion set strategies in de novo ablation and reviews currently used energy sources—including radiofrequency, cryoablation, and pulsed-field ablation—highlighting differences in safety and efficacy. They also examine surgical and hybrid approaches for selected patients and outline essential components of post-ablation care, including rhythm monitoring, anticoagulation decisions, and management of complications. This episode integrates contemporary evidence with practical insights to support clinicians delivering comprehensive AF ablation care. Audio editing for this episode was performed by CardioNerds intern Dr. Bhavya Shah. NOTE: This episode was recorded in March 2025. Since then, the OCEAN trial showed that among patients who had had successful catheter ablation for atrial fibrillation at least 1 year earlier and had risk factors for stroke, treatment with rivaroxaban did not result in a significantly lower incidence of a composite of stroke, systemic embolism, or new covert embolic stroke than treatment with aspirin.  Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. CardioNerds Atrial Fibrillation PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron!

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/.

Marking 5 months since Charlie Kirk's execution on Sept 10, 2025, at Utah Valley University, Stew dismantles the Zionist cover-up shielding his killers. JD Sharp joins Stew to discuss the illusion of American democracy exposed by the latest Epstein files drop. Trump shows up over 38,000 times, linked to unspeakable crimes against kids, with survivors naming him directly in assaults.  

Trump's named 38,000+ times in the Epstein files he swore to release—yet he lies, obstructs, attacks Massie, and buries millions more pages to hide his pedophile accomplice role. Full truth exposes the child-sacrifice network he protects at all costs. They murdered Charlie Kirk with a military-grade exploding lavalier mic rigged by insiders who sold him out for rejecting Israel's blood money – forget the 30-06 fairy tale, John Bray is dismantling it piece by piece with motion mapping, explosive gas analysis, shrapnel forensics, and custom ballistic dummies that replicate the exact brain-stem-killing blast.  

Tonight on The Stew Peters Show, Jeff Berwick joins me to expose how Bill Gates, Epstein, and their demonic cabal plotted pandemics since 2011 for trillion-dollar profits, laundered billions through the Gates Foundation, obsessed over gene-editing Africans while testing deadly jabs on black kids, and engineered COVID as a global blood sacrifice ritual. Joining me tonight is E. Michael Jones to blow the lid off the Zionist Super Bowl psyop that's erasing the Epstein files proving our leaders are kid-eating pedophiles dragging us into nuclear war for Israel against Iran, ready to wipe out our troops. Epstein's alive, still eating child jerky in hiding. Files prove PizzaGate, Zorro Ranch kid farms, human jerky shipments, and acid baths—this cannibal network runs bolder than ever.

What if the American Revolution was never just an American story? Historian Ronald Angelo Johnson helps us uncover the deep connections between the American and Haitian Revolutions to reveal how both revolutions emerged from the same Atlantic imperial struggle for empire, racialized power, and war. Using details from his book Entangled Alliances, Ron will guide us from the Treaty of Paris in 1763 to the Siege of Savannah in 1779, where hundreds of Black soldiers from French Saint Domingue landed on Georgia's shores—not as enslaved laborers, but as uniformed volunteers ready to fight for American Independence. Ron's Website | Book |Show Notes: https://www.benfranklinsworld.com/433 EPISODE OUTLINE00:00:00  Introduction00:01:08  Episode Overview00:04:50 The Treaty of Paris 1763 and its Impact00:09:09 Consequences of the Seven Years' War for Saint Domingue00:18:39 Saint Domingue Society Post-Seven Years' War00:24:32 French Imperial Reaction vs. Local Resentment00:28:36 Circulation of News Between British North America & Saint Domingue00:39:22 France's Strategy to Assist American Revolutionaries00:50:42 Reception of the Chasseurs Volontaires Regiment in Georgia00:54:42 Re-evaluating the American Revolution00:57:32 Time Warp01:05:38 ConclusionRECOMMENDED NEXT EPISODES

This week, join authors Shaan Khurshid and Julian S. Haimovich as they discuss their article "Incidence, Risk Factors, and Outcomes in Stressor-Associated Atrial Fibrillation: Insights From the VITAL-AF Trial." For the episode transcript, visit:  https://www.ahajournals.org/do/10.1161/podcast.20260209.180892

Owen Benjamin joins Stew to discuss Charlie Kirk's betrayal and murder, linking it to the Epstein files cover-up by elite international pedophiles.

Owen Benjamin joins Stew to discuss Charlie Kirk's betrayal and murder, linking it to the Epstein files cover-up by elite international pedophiles.

Gia Santos joins Stew to dismantle the myth of Trump's mass deportations. Over a year into his second term, less than 350,000 illegals deported in 2025—far from the promised 50 million. Instead, DHS, ICE, and Border Patrol, backed by Palantir, are building a facial recognition dystopia to track Americans. Jake GTV exposes Trump's sellout betrayal, buried Epstein child rape tapes, and the AI surveillance grid Talmudic perverts are forcing on Americans to destroy us while pushing Netanyahu's Iran war.

Episode 211: Understanding HFpEF.  Hyo Mun and Jordan Redden (medical students) explain the pathophysiology of heart failure with preserved ejection fraction (HFpEF) and how it differentiates from HFrEF. Dr. Arreaza asks insightful questions and summarizes some key elements of HFpEF. Written by Hyo Mun, MS4, American University of the Caribbean; and Jordan Redden, MS4, Ross University School of Medicine. Comments and edits by Hector Arreaza, MD.You are listening to Rio Bravo qWeek Podcast, your weekly dose of knowledge brought to you by the Rio Bravo Family Medicine Residency Program from Bakersfield, California, a UCLA-affiliated program sponsored by Clinica Sierra Vista, Let Us Be Your Healthcare Home. This podcast was created for educational purposes only. Visit your primary care provider for additional medical advice.What is EF? Just imagine, the heart is a pump, blood gets into the heart through the veins, the ventricles fill up and then squeeze the blood out. So, the percent of blood that is pumped out is the EF. Let's start at the beginning. What is HFpEF?Mike: HFpEF stands for heart failure with preserved ejection fraction. Basically, these patients squeeze normally—their ejection fraction is 50% or higher—but here's the thing: the heart can't relax and fill the way it should. The muscle gets stiff, almost like a thick leather boot that just won't stretch. And because the ventricle can't fill properly, pressure starts backing up into the lungs and the rest of the body. That's when patients start experiencing shortness of breath, leg swelling, fatigue—all those classic symptoms.Dr. Arreaza: And this is where people get fooled by the ejection fraction.Mike: Exactly. The ejectionfraction tells you total left ventricular emptying, not just forward flow.Jordan: The classic example is severe mitral regurgitation. You can eject 60% of your blood volume and still be in cardiogenic shock because most of that blood is leaking backward into the left atrium instead of going into the aorta. So, you get pulmonary edema, hypotension, fatigue, all with a “normal” EF. Which is honestly terrifying if you're over-relying on echo reports without thinking clinically.Dr. Arreaza: And in HFpEF, functional mitral regurgitation often shows up later in the disease. It's not usually the primary cause; it's more of a marker of advanced disease. Moderate to severe MR in HFpEF independently predicts worse outcomes, including a higher risk of mortality or heart failure hospitalization. So, let's contrast this with HFrEF. How are these two different?Mike: HFrEF—heart failure with reduced ejection fraction—is a pumping problem. The heart muscle is weak and can't contracteffectively. Ejection fraction drops below 40%, and this is your classic systolic dysfunction.Jordan: HFpEF, on the other hand, is diastolic dysfunction. The heart muscle is thick, fibrotic, and noncompliant. It squeezes fine, but it just doesn't relax, even though the EF looks reassuring on paper.Mike: I like to explain it this way: HFrEF is a weak heart that can't squeeze. HFpEF is a stiff heart that can't relax. Totally different problems.Dr. Arreaza: And then there's the gray zone: heart failure with mildly reduced EF, or HFmrEF. That's an EF between 41 and 49% with evidence of elevated filling pressures. It really shares the features of both worlds. So, what actually causes HFpEF versus HFrEF?Jordan: HFpEF is basically what happens when all the problems of modern living catch up with you. You've got chronic hypertension, obesity, diabetes, metabolic syndrome, aging, systemic inflammation—all of these things slowly remodel the heart over years. The muscle gets thick and stiff, and eventually the ventricle just loses its ability to relax. So, HFpEF is really a disease of metabolic dysfunction and chronic stress in the heart. Mike: HFrEF is more about direct injury. Think about myocardial infarctions, ischemic cardiomyopathy, viral myocarditis, alcohol toxicity, chemotherapy like doxorubicin, genetic cardiomyopathies, or chronic uncontrolled tachycardia. These insults actually damage or kill heart muscle cells, leading to a dilated, weak ventricle that can't pump effectively.Dr. Arreaza: So the short version: HFpEF is caused by chronic metabolic and hypertensive stress, while HFrEF is caused mainly by myocardial damage. A question we get a lot: does HFpEF eventually turn into HFrEF? What do you guys think?Mike: In most cases, no. HFpEF patients usually stay HFpEF throughout their disease course. They don't just “burn out” and turn into HFrEF.Jordan: They're generally separate disease entities with different pathophysiology. A patient with HFpEF can develop HFrEF if they have a big myocardial infarction or ongoing ischemia that damages the muscle, but that's not the natural progression.Mike: Interestingly though, the opposite can happen. Some HFrEF patients actually improve their ejection fraction with good medical therapy—that's called HF with improved EF—and it's a great sign that treatment is working.Dr. Arreaza: Another question. How do HFpEF and HFrEF compare to restrictive cardiomyopathy and constrictive pericarditis?Jordan: Clinically, they can all look very similar: dyspnea, edema, fatigue, but the underlying mechanisms are completely different.Mike: In HFpEF, the myocardium itself is stiff from hypertrophy and fibrosis. The problem is intrinsic to the heart muscle, and EF stays preserved. Echoshows diastolic dysfunction with elevated filling pressures.Jordan: In HFrEF, the myocardium is weak. The ventricle is often dilated and contracts poorly, with a reduced EF.Mike: Restrictive cardiomyopathy is different. Here, the myocardium gets infiltrated by abnormal stuff—amyloid, iron, sarcoid—and that makes it extremely stiff. It can look like HFpEF on the surface, but it's usually more severe. On Echo You'll see biatrial enlargement, small ventricles, and preserved EF. And importantly, it's a pathologic diagnosis, so you need advanced imaging or biopsy to confirm it.Jordan: Constrictive pericarditis is another mimic, but here the myocardium is usually normal. The problem is that the pericardium is thickened, calcified, and rigid. This will physically prevent the heart from being filled. Imaging shows pericardial thickening, septal bounce, and respiratory variation in flow, and cath shows equalization of diastolic pressures, which is the hallmark of constrictive pericarditis.Dr. Arreaza: So the takeaway is: HFpEF is a clinical syndrome driven by common metabolic and hypertensive causes, while restrictive and constrictive diseases are specific pathologic entities. If “HFpEF” is unusually severe or not responding to treatment, you need to think beyond HFpEF. Which type of heart failure is more common right now?Mike: Good question, the answer is: HFpEF. It now accounts for up to 60% of all heart failure cases, and it's still rising.Dr. Arreaza: Why is that?Jordan: Because people are living longer, gaining weight, and developing more metabolic syndrome. HFpEF thrives in older, or people with obesity, hypertension, or diabetes: basically, the modern American population. At the same time, better treatment of acute MIs means fewer people are developing HFrEF from massive heart attacks.Mike: HFpEF is the heart failure epidemic of the 21st century. It's honestly the cardiology equivalent of type 2 diabetes.Dr. Arreaza: Let's talk aboutCOVID-19. (2025 and still talking about it) Does it actually increase heart failure risk?Mike: Yes, absolutely. COVID increases both acute and long-term heart failure risk.Jordan: During acute infection, COVID can cause myocarditis, trigger massive inflammation, and precipitate acute decompensated heart failure, especially in patients with pre-existing disease. It also causes microthrombi, which can injure the myocardium.Mike: And after infection, even mild cases are linked to a significantly higher risk of developing new heart failure within the following year. Both HFpEF and HFrEF rates go up.Dr. Arreaza: I remember seeing this in 2021, we had a patient with acute COVID and HFrEF, her EF was about 10%, I lost contact with the patient and at the end I don't know what happened to her. What's the pathophysiology of COVID and heart failure?Mike: COVID causes direct viral injury through ACE2 receptors, triggers massive inflammation that damages the endothelium and heart muscle, leads to microvascular clotting and fibrosis—all mechanisms that promote HFpEF.Jordan: Add autonomic dysfunction, persistent low-grade inflammation, and worsening metabolic syndrome, and you've got a perfect storm for heart failure.Dr. Arreaza: Bottom line: COVID is a cardiovascular disease as much as a respiratory one. If someone had COVID and now has unexplained dyspnea or fatigue, think about heart failure. Get an echo, get a BNP, start treatment. Last big question: why did we have so many therapies for HFrEF but essentially none for HFpEF for years?Mike: HFrEF is mechanistically straightforward. You've got a weak heart with excessive neurohormonal activation going on — so you block RAAS, block the sympathetic system, drop the afterload. The drugs make sense.Jordan: HFpEF is messy. It's not one disease. It's stiffness, fibrosis, inflammation, microvascular dysfunction, metabolic disease, atrial fibrillation, all overlapping. One drug can't fix all of that.Mike: And some drugs that worked beautifully in HFrEF actually made HFpEF worse. Take Beta blockers, for example.  They slow heart rate, which is a problem because HFpEF patients rely on heart rate to maintain their cardiac output.Jordan: The breakthrough came with SGLT-2 inhibitors: diabetes drugs that unexpectedly addressed multiple HFpEF mechanisms at once: volume, metabolism, inflammation, and myocardial energetics.Dr. Arreaza: The miracle drug for HFpEF! Alright, let's wrap up.Mike: Bottom line: HFpEF is common, complex, and dangerous: even if the EF looks “normal.”Jordan: And if you're relying on ejection fraction alone, HFpEF will humble you every time.Dr. Arreaza: If you liked this episode, share it with a friend or a colleague and rate us wherever you listen. This is Dr. Arreaza, signing off.Even without trying, every night you go to bed a little wiser. Thanks for listening to Rio Bravo qWeek Podcast. We want to hear from you, send us an email at RioBravoqWeek@clinicasierravista.org, or visit our website riobravofmrp.org/qweek. See you next week! _____________________References:Barzin A, Barnhouse KK, Kane SF. Heart Failure With Preserved Ejection Fraction. Am Fam Physician. 2025;112(4):435-440.Heidenreich PA, Bozkurt B, Aguilar D, et al. 2022 AHA/ACC/HFSA guideline for the management of heart failure. Circulation. 2022;145(18):e895-e1032.Kittleson MM, Panjrath GS, Amancherla K, et al. 2023 ACC expert consensus decision pathway on management of heart failure with preserved ejection fraction. J Am Coll Cardiol. 2023;81(18):1835-1878.Anker SD, Butler J, Filippatos G, et al. Empagliflozin in heart failure with a preserved ejection fraction. N Engl J Med. 2021;385(16):1451-1461.Solomon SD, McMurray JJV, Claggett B, et al. Dapagliflozin in heart failure with mildly reduced or preserved ejection fraction. N Engl J Med. 2022;387(12):1089-1098.Pitt B, Pfeffer MA, Assmann SF, et al. Spironolactone for heart failure with preserved ejection fraction. N Engl J Med. 2014;370(15):1383-1392.Yusuf S, Pfeffer MA, Swedberg K, et al. Effects of candesartan in patients with chronic heart failure and preserved left-ventricular ejection fraction. Lancet. 2003;362(9386):777-781.Solomon SD, McMurray JJV, Anand IS, et al. Angiotensin-neprilysin inhibition in heart failure with preserved ejection fraction. N Engl J Med. 2019;381(17):1609-1620.Kosiborod MN, Abildstrøm SZ, Borlaug BA, et al. Semaglutide in patients with heart failure with preserved ejection fraction and obesity. N Engl J Med. 2023;389(12):1069-1084.Xie Y, Xu E, Bowe B, Al-Aly Z. Long-term cardiovascular outcomes of COVID-19. Nat Med. 2022;28(3):583-590.Puntmann VO, Carerj ML, Wieters I, et al. Outcomes of cardiovascular magnetic resonance imaging in patients recently recovered from COVID-19. JAMA Cardiol. 2020;5(11):1265-1273.Basso C, Leone O, Rizzo S, et al. Pathological features of COVID-19-associated myocardial injury. Eur Heart J. 2020;41(39):3827-3835.Nalbandian A, Sehgal K, Gupta A, et al. Post-acute COVID-19 syndrome. Nat Med. 2021;27(4):601-615.Badve SV, Roberts MA, Hawley CM, et al. Effects of angiotensin-converting enzyme inhibitors and angiotensin receptor blockers in adults with estimated GFR less than 60 mL/min per 1.73 m². Ann Intern Med. 2024;177(8):953-963.Navis G, Faber HJ, de Zeeuw D, de Jong PE. ACE inhibitors and the kidney: a risk-benefit assessment. Drug Saf. 1996;15(3):200-211.Textor SC, Novick AC, Tarazi RC, et al. Critical perfusion pressure for renal function in patients with bilateral atherosclerotic renal vascular disease. Ann Intern Med. 1985;102(3):308-314.Hackam DG, Spence JD, Garg AX, Textor SC. Role of renin-angiotensin system blockade in atherosclerotic renal artery stenosis and renovascular hypertension. Hypertension. 2007;50(6):998-1003.Ronco C, Haapio M, House AA, et al. Cardiorenal syndrome. J Am Coll Cardiol. 2008;52(19):1527-1539.Prins KW, Neill JM, Tyler JO, et al. Effects of beta-blocker withdrawal in acute decompensated heart failure. JACC Heart Fail. 2015;3(8):647-653.Jondeau G, Neuder Y, Eicher JC, et al. B-CONVINCED: Beta-blocker CONtinuation Vs. INterruption in patients with Congestive heart failure hospitalizED for a decompensation episode. Eur Heart J. 2009;30(18):2186-2192.Theme song, Works All The Time by Dominik Schwarzer, YouTube ID: CUBDNERZU8HXUHBS, purchased from https://www.premiumbeat.com/. 

In this episode of 'Science of Slink,' Dr. Rosy Boa explains how often and how intensely recreational adult pole dancers should practice based on findings from exercise science. Dr. Boa shares the American College of Sports Medicine's guidelines for aerobic physical activity, which recommend either 150 minutes of moderate-intensity exercise spread over five days or 60 minutes of vigorous-intensity exercise across three days weekly. She discusses the importance of balancing exercise with proper rest and recovery and emphasizes that even short, less than 10-minute sessions can provide significant health benefits. Lastly, Dr. Boa introduces her Science of Slink membership options for those interested in structured, evidence-based pole dance training.Are you a pole nerd interested in trying out online pole classes with Slink Through Strength? We'd love to have you! Use the code “podcast” for 10% off the Intro Pack and try out all of our unique online pole classes: https://app.acuityscheduling.com/catalog/25a67bd1/?productId=1828315&clearCart=true Chapters:00:00 Introduction to Exercise Science for Pole Dancers01:00 Membership Options and Podcast Shoutout01:35 Caveats and Target Audience02:41 Top Line Recommendations for Pole Dance Frequency03:49 Understanding Exercise Intensity04:53 Practical Tips for Monitoring Intensity07:52 Importance of Rest and Recovery09:20 Cognitive Benefits of Physical Activity10:38 Consistency and Habit Formation12:37 Final Recommendations and ConclusionCitations: Erickson, K. I., Hillman, C., Stillman, C. M., Ballard, R. M., Bloodgood, B., Conroy, D. E., ... & Powell, K. E. (2019). Physical activity, cognition, and brain outcomes: a review of the 2018 physical activity guidelines. Medicine and science in sports and exercise, 51(6), 1242.Haskell, W. L., Lee, I. M., Pate, R. R., Powell, K. E., Blair, S. N., Franklin, B. A., ... & Bauman, A. (2007). Physical activity and public health: updated recommendation for adults from the American College of Sports Medicine and the American Heart Association. Circulation, 116(9), 1081.Jakicic, J. M., Kraus, W. E., Powell, K. E., Campbell, W. W., Janz, K. F., Troiano, R. P., ... & 2018 Physical Activity Guidelines Advisory Committee. (2019). Association between bout duration of physical activity and health: systematic review. Medicine and science in sports and exercise, 51(6), 1213.Kaushal, N., & Rhodes, R. E. (2015). Exercise habit formation in new gym members: a longitudinal study. Journal of behavioral medicine, 38(4), 652-663.

Fresh DOJ/FBI docs unleash nightmare: Epstein's trafficked teens strangled by Robin Leach during taped orgies, with bodies sold to cartels via Ghislaine Maxwell and buried at Trump's LA golf resort. EJ Prior tears apart Utah's sham trial: Rifle DNA hits 5 strangers (not Tyler), prosecutor's daughter is an eyewitness, and Erika Kirk's Epstein-linked lawyer rams fake speedy trial.

Block Therapy, Fascia & Flow: Why Your Body Can't Heal What It Can't Release with Deanna Hansen What if your pain, stiffness, poor recovery, hormone resistance, or "mystery inflammation" isn't coming from weak muscles, aging joints, or overtraining—but from dehydrated, compressed fascia? In this episode of The Coach Debbie Potts Show, I'm joined by Deanna Hansen, creator of Block Therapy®, to unpack the missing link in healing, performance, and longevity: your fascial system. Fascia is not just connective tissue—it's a sensory organ, communication highway, and drainage system. And when it becomes compressed from stress, repetitive training, injuries, sitting, or breath restriction, everything downstream suffers. That includes: Lymphatic flow Circulation and oxygen delivery Hormone signaling Nervous system regulation Detox and waste removal Pain-free movement and recovery In true FLOW Foundation™ fashion, we explore why you can't "train harder" or supplement your way out of a body that can't move, hydrate, and release. In this episode, we cover: What fascia really is—and why it's not passive tissue How chronic stress, endurance training, and aging compress fascia Why lymph has no pump (and how fascia is the pump) The connection between fascia, breath, vagal tone, and inflammation How Block Therapy® helps rehydrate tissues and restore flow Why aggressive workouts, detoxes, and even HRT can backfire when fascia is stuck How gentle, intentional decompression prepares your body to adapt, heal, and perform Why this matters for high performers and aging athletes: If you're: Doing "all the right things" but not seeing results Struggling with lingering pain, stiffness, or slow recovery Feeling inflamed, puffy, tight, or restricted Sensitive to supplements, training, or hormone therapies This conversation may completely change how you approach your health. Because nothing detoxes, heals, or adapts if it can't move first.

CardioNerds (Dr. Shazli Khan, Dr. Jenna Skowronski, and Dr. Shiva Patlolla) discuss the management of patients post‑heart transplantation with Dr. Shelley Hall from Baylor University Medical Center and Dr. MaryJane Farr from UTSW. In this comprehensive review, we cover the physiology of the transplanted heart, immunosuppression strategies, rejection surveillance, and long-term complications including cardiac allograft vasculopathy (CAV) and malignancy. Audio editing for this episode was performed by CardioNerds intern Dr. Bhavya Shah. 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 Denervated Heart: The donor heart is surgically severed from the autonomic nervous system, leading to a higher resting heart rate (90-110 bpm) due to loss of vagal tone. Because the heart relies on circulating catecholamines rather than neural input to increase heart rate, patients experience a delayed chronotropic response to exercise and stress. Importantly, because afferent pain fibers are severed, ischemia is often painless. Rejection Surveillance: Rejection is classified into Acute Cellular Rejection (ACR), which is T-cell mediated, and Antibody-Mediated Rejection (AMR), which is B-cell mediated. While endomyocardial biopsy remains the gold standard for diagnosis, non-invasive surveillance using gene-expression profiling (e.g., AlloMap) and donor-derived cell-free DNA (dd-cfDNA) is increasingly utilized to reduce the burden of invasive procedures. The Infection Timeline: The risk of infection follows a predictable timeline based on the intensity of immunosuppression. The first month is dominated by nosocomial infections. Months one through six are the peak for opportunistic infections (Cytomegalovirus, Pneumocystis, Toxoplasmosis) requiring prophylaxis. After six months, patients are primarily at risk for community-acquired pathogens, though late viral reactivation can occur. Cardiac Allograft Vasculopathy (CAV): Unlike native coronary artery disease, CAV presents as diffuse, concentric intimal thickening that affects the entire length of the vessel, including the microvasculature. Due to denervation, patients rarely present with angina; instead, CAV manifests as unexplained heart failure, fatigue, or sudden cardiac death. Malignancy Risk: Long-term immunosuppression significantly increases the risk of malignancy. Skin cancers (squamous and basal cell) are the most common, followed by Post-Transplant Lymphoproliferative Disorder (PTLD), which is often driven by Epstein-Barr Virus (EBV) reactivation. Notes Notes: Notes drafted by Dr. Patlolla 1. What are the unique physiological features of the transplanted heart? The hallmark of the transplanted heart is denervation. Because the autonomic nerve fibers are severed during harvest, the heart loses parasympathetic or vagal tone, resulting in a resting tachycardia (typically 90-110 bpm). The heart also loses the ability to mount a reflex tachycardia; thus, the heart rate response to exercise or hypovolemia relies on circulating catecholamines, which results in a slower “warm-up” and “cool-down” period during exertion. 2. What are the pillars of maintenance immunosuppression regimen? The triple drug maintenance regimen typically consists of: Calcineurin Inhibitor (CNI): Tacrolimus is preferred over cyclosporine. Key side effects include nephrotoxicity, hypertension, tremor, hyperkalemia, and hypomagnesemia. Antimetabolite: Mycophenolate mofetil (MMF) inhibits lymphocyte proliferation. Key side effects include leukopenia and GI distress. Corticosteroids: Prednisone is used for maintenance but is often weaned to low doses or discontinued after the first year to mitigate metabolic side effects (diabetes, osteoporosis, weight gain). 3. How is rejection classified and diagnosed? Rejection is the immune system’s response to the foreign graft and is categorized by the arm of the immune system involved: Acute Cellular Rejection (ACR): Mediated by T-lymphocytes infiltrating the myocardium. It is graded from 1R (mild) to 3R (severe) based on the extent of infiltration and myocyte damage. Antibody-Mediated Rejection (AMR): Mediated by B-cells producing donor-specific antibodies (DSAs) that attack the graft endothelium. It is diagnosed via histology (capillary swelling) and immunofluorescence (C4d staining). Diagnosis has historically relied on endomyocardial biopsy. However, non-invasive tools are gaining traction. Gene Expression Profiling (GEP) assesses the expression of genes associated with immune activation to rule out rejection in low-risk patients. Donor-Derived Cell-Free DNA (dd-cfDNA) measures the fraction of donor DNA in the recipient’s blood. Elevated levels suggest graft injury which can occur in both ACR and AMR. 4. What is the timeline of infectious risk and how does it guide prophylaxis? Infectious risk correlates with the net state of immunosuppression. < 1 Month (Nosocomial): Risks include surgical site infections, catheter-associated infections, and aspiration pneumonia. 1 – 6 Months (Opportunistic): This is the period of peak immunosuppression. Patients are at risk for PJP, CMV, Toxoplasma, and fungal infections. Prophylaxis typically includes Trimethoprim-Sulfamethoxazole (for PJP/Toxo) and Valganciclovir (for CMV, dependent on donor/recipient serostatus). > 6 Months (Community-Acquired): As immunosuppression is weaned, the risk profile shifts toward community-acquired respiratory viruses (Influenza, RSV) and pneumonias. However, patients with recurrent rejection requiring boosted immunosuppression remain at risk for opportunistic pathogens. 5. How does Cardiac Allograft Vasculopathy (CAV) differ from native CAD? CAV is the leading cause of late graft failure. Unlike the focal, eccentric plaques seen in native atherosclerosis, CAV is an immunologically driven process causing diffuse, concentric intimal hyperplasia. It affects both epicardial vessels and the microvasculature. Because of this diffuse nature, percutaneous coronary intervention (PCI) is often technically difficult and provides only temporary palliation. The only definitive treatment for severe CAV is re-transplantation. Surveillance is critical and is typically performed via annual coronary angiography, often using intravascular ultrasound (IVUS) to detect early intimal thickening before it is visible on the angiogram. References Costanzo MR, Dipchand A, Starling R, et al. The International Society of Heart and Lung Transplantation Guidelines for the care of heart transplant recipients. J Heart Lung Transplant. 2010;29(8):914-956. doi:10.1016/j.healun.2010.05.034. https://www.jhltonline.org/article/S1053-2498(10)00358-X/fulltext Kittleson MM, Kobashigawa JA. Cardiac Allograft Vasculopathy: Current Understanding and Treatment. JACC Heart Fail. 2017;5(12):857-868. doi:10.1016/j.jchf.2017.07.003. https://www.jacc.org/doi/10.1016/j.jchf.2017.07.003 Velleca A, Shullo MA, Dhital K, et al. The International Society for Heart and Lung Transplantation (ISHLT) guidelines for the care of heart transplant recipients. J Heart Lung Transplant. 2023;42(5):e1-e141. doi:10.1016/j.healun.2022.10.015. https://www.jhltonline.org/article/S1053-2498(22)02187-5/fulltext

Trump dominates Epstein docs with 4,500+ hits—flight logs, assault claims, elite dirt—tied to the depraved Zionist Jewish rulers using child rape and sacrifices to control U.S. gov and military. Dr. Michael Rectenwald exposes it all. Ryan Matta breaks down the massive Epstein release—millions of pages exposing Jeffrey as Mossad's blackmail kingpin targeting politicians, tech giants, and fueling regime shifts like Ukraine 2014 to back Israel's wars and expansions. John Jubilee from Energized Health is dropping truth bombs today, revealing how inner cellular hydration reverses heart damage, gets patriots off dozens of deadly meds, and rebuilds real health from the cells up. Go to energizedhealth.com right now, smash the red Cellular Health Training button for the free live class this February, register, and arm yourself with the knowledge to survive their attack!

This week, join author Chao Jiang as he discusses the article "Dapagliflozin to Reduce Early Recurrence After Catheter Ablation for Atrial Fibrillation: The DARE-AF Randomized Clinical Trial." For the episode transcript, visit: https://www.ahajournals.org/do/10.1161/podcast.20260202.172048

Jimmy Dore and Stew Peters blow the lid off Charlie Kirk's suspicious “death”—insider leaks reveal Mossad puppets pulling strings at TPUSA, geo-fencing Christians for Zionist data theft, crocodile tears from fake trad-wives, mass staff firings to silence dissent, and Trump's bogus pardon on Zionist letterhead!