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Hosts Mitsuaki Sawano, MD, Kentaro Ejiri, MD, and Nobuhiro Ikemura, MD, welcome Yuki Obayashi, MD, of Leiden University Medical Center, to discuss findings from the STOPDAPT-3 trial. Dr. Obayashi highlights that, among ACS patients—including those with HBR or STEMI—aspirin and clopidogrel monotherapy after 1 month of DAPT resulted in similar rates of ischemic and bleeding events. These results support flexible, patient-centered antiplatelet strategies beyond the acute phase.
JACC's June 10 dedicated issue on the ACS guidelines, author and former JACC Editor-in-Chief Valentin Fuster, MD, PhD, MACC, speaks with current JACC Deputy Editor Rasha Al-Lamee, MD concerning the recent ACC/AHA ACS guidelines. Dr. Fuster speaks to this comprehensive update aligning more closely with international (especially ESC) standards in acute coronary syndrome care. The interview and accompanying commentary publishing in the June 10 issue speaks to the importance of improved methodological rigor, global stakeholder inclusion, and alignment in key recommendations (e.g., DAPT duration), while also allowing greater transparency in controversial decisions and envisioning the potential for a future universal ACS guideline.
Darshan H. Brahmbhatt, Podcast Editor of JACC: Advances, discusses a recently published original research paper on Sex Differences in the Safety and Efficacy of Different Durations of DAPT After PCI
Será que a recomendação clássica de 12 meses de DAPT após SCA ou angioplastia ainda faz sentido? Neste episódio, exploramos as evidências mais recentes que questionam essa prática tradicional.✅ O que você vai ouvir: • Diferenças entre os principais inibidores do P2Y12 (clopidogrel, prasugrel e ticagrelor) • Quando encurtar, descalonar ou estender a DAPT com base nos principais Trials • Como avaliar o risco de sangramento (Scores PRECISE-DAPT e DAPT)• Terapia tripla em pacientes com fibrilação atrial e necessidade de anticoagulaçãoVamos discutir de forma prática e baseada em evidências quando a DAPT pode ser encurtada ou estendida — e o impacto direto dessas decisões nos desfechos do paciente.
This episode covers: Cardiology This Week: A concise summary of recent studies Dual antiplatelet therapy in 2025 Optimal communication with patients Snapshots Host: Emer Joyce Guests: Carlos Aguiar, Michelle Kittleson, Gilles Montalescot Want to watch that episode? Go to: https://esc365.escardio.org/event/1798 Disclaimer ESC TV Today is supported by Bristol Myers Squibb. This scientific content and opinions expressed in the programme have not been influenced in any way by its sponsor. This programme is intended for health care professionals only and is to be used for educational purposes. The European Society of Cardiology (ESC) does not aim to promote medicinal products nor devices. Any views or opinions expressed are the presenters' own and do not reflect the views of the ESC. Declarations of interests Stephan Achenbach, Emer Joyce, Michelle Kittleson and Nicolle Kraenkel have declared to have no potential conflicts of interest to report. Carlos Aguiar has declared to have potential conflicts of interest to report: personal fees for consultancy and/or speaker fees from Abbott, AbbVie, Alnylam, Amgen, AstraZeneca, Bayer, BiAL, Boehringer-Ingelheim, Daiichi-Sankyo, Ferrer, Gilead, GSK, Lilly, Novartis, Pfizer, Sanofi, Servier, Takeda, Tecnimede. Davide Capodanno has declared to have potential conflicts of interest to report: Bristol Myers Squibb, Daiichi Sankyo, Sanofi Aventis, Novo Nordisk, Terumo. Gilles Montalescot has declared to have potential conflicts of interest to report: research funds for Action Groupe or honoraria from Abbott, Amgen, AstraZeneca, Bayer, BMS, Boehringer-Ingelheim, Celecor, CSL Behring, Hexacath, Idorsia, Lilly, Novo Nordisk, Pfizer, SMT, Terumo. Steffen Petersen has declared to have potential conflicts of interest to report: consultancy for Circle Cardiovascular Imaging Inc. Calgary, Alberta, Canada. Emma Svennberg has declared to have potential conflicts of interest to report: Abbott, Astra Zeneca, Bayer, Bristol-Myers, Squibb-Pfizer, Johnson & Johnson.
Host: Emer Joyce Guest: Gilles Montalescot Want to watch that extended interview? Go to: https://esc365.escardio.org/event/1798?resource=interview Disclaimer ESC TV Today is supported by Bristol Myers Squibb. This scientific content and opinions expressed in the programme have not been influenced in any way by its sponsor. This programme is intended for health care professionals only and is to be used for educational purposes. The European Society of Cardiology (ESC) does not aim to promote medicinal products nor devices. Any views or opinions expressed are the presenters' own and do not reflect the views of the ESC. Declarations of interests Stephan Achenbach, Emer Joyce and Nicolle Kraenkel have declared to have no potential conflicts of interest to report. Carlos Aguiar has declared to have potential conflicts of interest to report: personal fees for consultancy and/or speaker fees from Abbott, AbbVie, Alnylam, Amgen, AstraZeneca, Bayer, BiAL, Boehringer-Ingelheim, Daiichi-Sankyo, Ferrer, Gilead, GSK, Lilly, Novartis, Pfizer, Sanofi, Servier, Takeda, Tecnimede. Davide Capodanno has declared to have potential conflicts of interest to report: Bristol Myers Squibb, Daiichi Sankyo, Sanofi Aventis, Novo Nordisk, Terumo. Gilles Montalescot has declared to have potential conflicts of interest to report: research funds for Action Groupe or honoraria from Abbott, Amgen, AstraZeneca, Bayer, BMS, Boehringer-Ingelheim, Celecor, CSL Behring, Hexacath, Idorsia, Lilly, Novo Nordisk, Pfizer, SMT, Terumo. Steffen Petersen has declared to have potential conflicts of interest to report: consultancy for Circle Cardiovascular Imaging Inc. Calgary, Alberta, Canada. Emma Svennberg has declared to have potential conflicts of interest to report: Abbott, Astra Zeneca, Bayer, Bristol-Myers, Squibb-Pfizer, Johnson & Johnson.
N Engl J Med 2016;375:1242-1252Background: The first drug-eluting stent (DES) was approved by the FDA in 2003 following the publication of the RAVEL trial. Since then, newer generations of DES were developed and were tested in clinical trials. The majority of trials comparing DES to bare-metal stents (BMS) showed reduction in repeat revascularization with DES but no significant reduction in death or myocardial infarction. Following these publications, the use of DES grew rapidly and was used in more than two thirds of percutaneous coronary interventions (PCI) by 2010.Cardiology Trial's Substack is a reader-supported publication. To receive new posts and support our work, consider becoming a free or paid subscriber.These trials, however, were very selective, had short follow up time (TAXUS-IV followed patients for 9 months and SPRIT IV followed patients for 12 months), and had limited power to assess hard outcomes.The NORSTENT trial investigators sought to compare DES to BMS in a more pragmatic design and follow patients for longer time.Patients: All patients who were undergoing PCI in Norway were assessed for enrollment. Patients had stable angina or acute coronary syndrome. Lesions were in native coronary arteries or bypass grafts.Patients were excluded if they had prior coronary stents, bifurcating lesions requiring a two-stent technique or life expectancy less than 5 years due to a medical condition other than coronary artery disease. Patients were also excluded if they had contraindications to dual antiplatelets or were taking warfarin.Baseline characteristics: The trial randomized 9,013 patients – 4,504 randomized to receive a DES and 4,509 to receive a BMS.The average age of patients was 63 years and 75% were men. Approximately 42% had hypertension, 54% had hyperlipidemia, 10% had prior myocardial infarction, 7% had prior CABG, 12% had diabetes, and 35% were current smokers.The indication for PCI was stable angina in 29% of the patients, unstable angina in 12% and STEMI or NSTEMI in 58%.Procedures: The study was open-label but outcomes assessment was blinded. Patients were randomly assigned in a 1:1 ratio to receive DES or BMS. Patients could receive several stents as clinically indicated but can only receive the assigned stent type during the index procedure.In all patients, aspirin 75 mg daily was given indefinitely while clopidogrel 75 mg daily was given for 9 months.Follow up visits were done as clinically appropriate without specification from the study protocol. Similarly, no routine follow up coronary angiography was performed.Endpoints: The primary outcome was a composite of all-cause death or spontaneous myocardial infarction. Secondary outcomes included repeat revascularization, stent thrombosis, major bleeding and health status based on the Seattle Angina Questionnaire.Clinical outcomes were collected by linking each patient unique national identification number to the Norwegian national patient registry.Analysis was performed based on the intention-to-treat principle. The study planned to enroll 8,000 patients to be followed for a median of 5 years. Assuming the 5-year event rate of the primary outcome to be 17%, the study would provide 93% power to detect 3% absolute risk difference between the study groups (rate ratio: 1.18). Due to lower than expected mortality, the sample size was increased to 9,000 patientsResults: Among the 20,663 patients who were assessed for eligibility, 12,425 met inclusion criteria. Among patients who met inclusion criteria, 9,013 were randomized. Figure 1 in the manuscript provides details for excluding patients and for not randomizing patients who met eligibility criteria. The most common reason for exclusion was prior PCI.The number of stents implanted per patient was 1.7 and more than 98% received the assigned stent type. The median follow up time was 5 years.The primary composite outcome of all-cause death or nonfatal spontaneous myocardial infarction was not significantly different between both treatment arms (16.6% with DES vs 17.1% with BMS, HR: 0.98; 95% CI: 0.88 - 1.09; p= 0.66).For the secondary outcomes – Hospitalization for unstable angina was similar between treatment groups (5.2% vs. 5.7%; p= 0.21). Stent thrombosis was lower with DES (0.8% vs 1.2%; p= 0.05). Target-lesion revascularization was also lower with DES (5.3% vs 10.3%; p< 0.001). Bleeding Academic Research Consortium (BARC) 3, 4 or 5 was similar between groups (5.5% vs 5.6%; p= 0.88).There was no significant difference in health status based on the Seattle Angina Questionnaire.There were no significant subgroup interactions.Conclusion: In patients undergoing PCI, the use of DES did not reduce the composite endpoint of death or spontaneous myocardial infarction compared to BMS. Target-lesion revascularization was reduced with DES with a number needed to treat of 20 patients.The findings of this study align with the results of other trials comparing DES to BMS. We have reviewed several key trials and included links to additional studies in this field below. Overall, DES significantly reduce target-lesion revascularization without significant effect on all-cause mortality or myocardial infarction.An important consideration in this and other related trials is that both stent types were studied using similar durations of dual antiplatelet therapy (DAPT) following PCI. For patients with stable angina, BMS typically require only one month of DAPT, while DES often necessitate three to twelve months. Since shorter durations of DAPT are generally safer for patients, a trial comparing DES with three to twelve months of DAPT compared to BMS with one month of DAPT would be insightful.A final teaching point is that less than 50% of screened patients were ultimately enrolled in this pragmatic trial, which had minimal exclusion criteria. It's not uncommon for trials to enroll less than 5% of screened patients which limits their external validity.* Other trials of DES vs BMShttps://pubmed.ncbi.nlm.nih.gov/21080780/https://pubmed.ncbi.nlm.nih.gov/22951305/Cardiology Trial's Substack is a reader-supported publication. To receive new posts and support our work, consider becoming a free or paid subscriber. Get full access to Cardiology Trial's Substack at cardiologytrials.substack.com/subscribe
What if the future of dual antiplatelet therapy (DAPT) could be shorter, safer, and more effective? Uncover the latest insights into drug-eluting stents and how they are transforming how we think about dual-antiplatelet therapy. Join us as we examine the game-changing recommendations from top cardiology societies, which suggest that newer-generation stents can significantly reduce the duration of DAPT, particularly for patients with a high bleeding risk. Listen in as we dissect the innovative tools like the PRECISE-DAPT score and ARC-HBR criteria used to determine bleeding risk, ensuring patient safety without compromising on the efficacy of treatment. We delve into pivotal studies, including the Global Leader Study and the STOP-DAPT trial, that back these groundbreaking changes.Our conversation takes an intriguing turn as we explore the intersection of cardiology advancements with anesthesia practices. Discover how these developments are influencing preoperative settings, potentially altering surgical timing and decision-making in anesthesia care. We bring you exclusive insights from contributor, Janak Chandrasoma, featured in the October 2024 APSF newsletter. We urge you to explore further resources, share the knowledge with your peers, and join us in promoting patient safety in perioperative environments. Don't forget to rate, review, and share the episode with colleagues keen on staying at the forefront of anesthesia patient safety advancements.For show notes & transcript, visit our episode page at apsf.org: https://www.apsf.org/podcast/229-revolutionizing-anesthesia-care-for-cardiac-patients/© 2024, The Anesthesia Patient Safety Foundation
Masahiro Natsuaki and C. Michael Gibson discuss this latest randomized comparison of prasugrel monotherapy and DAPT with aspirin for patients undergoing PCI.
New Season is starting off with our selection for the month and an exclusive mix from Y-DAPT!Your Monthly House Music Sandwich! In the mix every month with our favourite Electronic Dance Music releases + a guest mix from our DJs. Disco Pastrami: Your Monthly Dance Music Sandwich!
Welcome to Season 6 of the Hot Topics podcast with Dr Neal Tucker. The summer holidays are over and it's back to work so time for a new podcast. In this episode, we look at research on whether SGLT2i might prevent dementia, on if it is safer to de-escalate sooner rather than later from dual anti-platelet therapy post-MI, and how effective is the new RSV vaccine at preventing hospitalisation in older people.ReferencesBMJ - SGLT2i & dementiaLancet - De-escalation of DAPT post-MIJAMA - RSV Vaccination Efficacy in Older Peoplewww.nbmedical.com/podcast
In the September 3, 2024, issue of JACC, Dr. Samuel Reinhart and team find that using direct oral anticoagulants alone is associated with fewer adverse events compared to combining them with aspirin after left atrial appendage occlusion. Their large-scale study suggests this streamlined approach might be optimal, though further randomized trials are needed to address limitations and refine long-term antithrombotic strategies.
This week, join Kate, Henry, Gary and Mark as they discuss same-day start contraception, krill oil for adults with knee DJD, misdiagnosis of community-acquired pneumonia, and ticagrelor + placebo VS ticagrelor + ASA after PCI. Plus some book recommendations: Whalefall, The Demon of Unrest, and the Commissario Brunetti novels by Donna Leon
Welcome back Rounds Table Listeners!We are back today with our Classic Rapid Fire Podcast!This week, Drs. Mike and John Fralick discuss two recent papers exploring the role of ticagrelor with aspirin versus ticagrelor alone after percutaneous coronary intervention in acute MI and the efficacy of empagliflozin after acute MI. Two papers, here we go!Ticagrelor alone versus ticagrelor plus aspirin from month 1 to month 12 after percutaneous coronary intervention in patients with acute coronary syndromes (ULTIMATE-DAPT) (0:00 – 9:22). Empagliflozin after Acute Myocardial Infarction (9:22 – 16:00).And for the Good Stuff:Impact of presentation at conference with timed release of academic publication (16:00 – 17:32).Top spot in the PWHL and attendance record at stake in latest Montreal-Toronto showdown (17:32 – 19:59).Questions? Comments? Feedback? We'd love to hear from you! @roundstable
Rapha e Joanne conversam sobre dúvidas no manejo de pacientes com dengue: quando suspender DAPT? Quando suspender anticoagulantes? Quando internar por plaquetopenia? Quanto transfundir plaquetas? Devo usar coloide ou cristaloide? Referências: 1. Brasil. Ministério da Saúde. Secretaria de Vigilância em Saúde e Ambiente. Departamento de Doenças Transmissíveis. Dengue : diagnóstico e manejo clínico : adulto e criança [recurso eletrônico] / Ministério da Saúde, Secretaria de Vigilância em Saúde e Ambiente, Departamento de Doenças Transmissíveis.– 6. ed. – Brasília : Ministério da Saúde, 2024. 81 p.: il. Acesso: http://bvsms.saude.gov.br/bvs/publicacoes/dengue_diagnostico_manejo_clinico_6ed.pdf 2. Guidelines for the Clinical Diagnosis and Treatment of Dengue, Chikungunya, and Zika. Washington, D.C.: Pan American Health Organization; 2022. License: CC BY-NC-SA 3.0 IGO. https://doi.org/10.37774/9789275124871.
This week, Kate, Henry, Mark and Gary discuss antiplatelet medications to prevent dementia, post-stroke blood pressure control, the latest guideline for managing patients with chronic cardiac disease, and probiotics for patients with irritable bowel syndrome.
Special guest Dave L. Dixon, PharmD, FACC, FAHA, FCCP, FNLA, BCACP, CDCES, CLS, the Nancy L. and Ronald H. McFarlane Professor of Pharmacy and Chair of the Department of Pharmacotherapy & Outcomes Science at the Virginia Commonwealth University School of Pharmacy, joins us to talk about chronic coronary disease.Listen in as he discusses the management of chronic coronary disease with a focus on the new American College of Cardiology/American Heart Association guidelines.You'll also hear practical advice from panelists on TRC's Editorial Advisory Board:Anthony A. Donato, Jr., MD, MHPE, Associate Program Director, Tower Health System Internal Medicine Residency Program and Professor of Medicine at the Drexel University College of MedicineSteven E. Nissen, MD, MACC, the Chief Academic Officer at the Heart and Vascular Institute and the Lewis and Patricia Dickey Chair in Cardiovascular Medicine Professor of Medicine at the Cleveland Clinic Lerner School of Medicine at Case Western Reserve UniversityCraig D. Williams, PharmD, FNLA, BCPS, Clinical Professor of Pharmacy Practice at the Oregon Health and Science UniversityFor the purposes of disclosure, Dr. Dixon reports a relevant financial relationship [GLP-1 agonists, SGLT2 inhibitors] with Boehringer Ingelheim (grants/research support). Dr. Steven Nissen reports relevant financial relationships [cardiology] with AbbVie, Amgen, AstraZeneca, Bristol-Myers Squibb, Eli Lilly, Esperion, Medtronic, MyoKardia, New Amsterdam Pharma, Novartis, Pfizer, Silence Therapeutics (grants/research support).The other speakers have nothing to disclose. All relevant financial relationships have been mitigated.TRC Healthcare offers CE credit for this podcast. Log in to your Pharmacist's Letter or Prescriber's Letter account and look for the title of this podcast in the list of available CE courses.The clinical resources mentioned during the podcast are part of a subscription to Pharmacist's Letter and Prescriber's Letter: Toolbox: Optimizing Care of Patients with Coronary Artery DiseaseChart: Dual Antiplatelet Therapy for Coronary Artery DiseaseChart: Treatment of HypertensionIf you're not yet a Pharmacist's Letter or Prescriber's Letter subscriber, find out more about our product offerings at trchealthcare.com. Follow or subscribe, rate, and review this show in your favorite podcast app. You can also reach out to provide feedback or make suggestions by emailing us at ContactUs@trchealthcare.com.
Marco Valgimigli and C. Michael Gibson discuss the long-term follow-up results from MASTER DAPT, which compared the outcomes of high bleeding risk patients randomized to either abbreviated or standard antiplatelet therapy.
ESC 2023: STOP-DAPT 3
Thrombolytics are the standard of care for acute stroke yet are not without risk. Join host, Geoff Wall, with guest, Jake Galdo, as they discuss combination aspirin and clopidogrel versus thrombolytics in mild stroke. The GameChangerThrombolytic use in mild stroke is common due to the time factor of administration, but data is mixed. New research has shown DAPT to be non-inferior to TPA. HostGeoff Wall, PharmD, BCPS, FCCP, BCGPProfessor of Pharmacy Practice, Drake UniversityInternal Medicine/Critical Care, UnityPoint HealthJake Galdo, PharmD, MBA, BCPS, BCGPCourse Content and Developer, CEimpactManaging Network Facilitator, CPESN Health EquityCEO, Seguridad ReferenceChen H, Cui Y, Zhou Z, et al. Dual Antiplatelet Therapy vs Alteplase for Patients With Minor Nondisabling Acute Ischemic Stroke: The ARAMIS Randomized Clinical Trial. JAMA. 2023;329(24):2135–2144. doi:10.1001/jama.2023.7827https://jamanetwork.com/journals/jama/article-abstract/2806532 Pharmacist Members, REDEEM YOUR CPE HERE! Not a member? Get a Pharmacist Membership & earn CE for GameChangers Podcast episodes! (30 mins/episode)CPE Information Learning ObjectivesUpon successful completion of this knowledge-based activity, participants should be able to:1. Discuss how the inclusion and exclusion criteria impact the interpretation of the ARIMIS study 2. Describe the potential benefits of DAPT therapy compared to thrombolytic therapy in mild stroke0.05 CEU/0.5 HrUAN: 0107-0000-23-249-H01-PInitial release date: 7/31/2023Expiration date: 7/31/2024Additional CPE details can be found here.Follow CEimpact on Social Media:LinkedInInstagramDownload the CEimpact App for Free Continuing Education + so much more!
Editor's Summary by Karen E. Lasser, MD, MPH, Senior Editor of JAMA, the Journal of the American Medical Association, for the June 27, 2023, issue. Related Content: Audio Highlights
The following question refers to Section 6.3 of the 2021 ESC CV Prevention Guidelines. The question is asked by Dr. Christian Faaborg-Andersen, answered first by UCSD cardiology fellow Dr. Harpreet Bhatia, and then by expert faculty Dr. Jaideep Patel.Dr. Patel recently graduated from Virginia Commonwealth University cardiology fellowship and is now a preventive cardiologist at the Johns Hopkins Hospital.The CardioNerds Decipher The Guidelines Series for the 2021 ESC CV Prevention Guidelines represents a collaboration with the ACC Prevention of CVD Section, the National Lipid Association, and Preventive Cardiovascular Nurses Association.Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. Question #24 A 65-year-old man with a history of ischemic stroke 6 months ago presents to cardiology clinic to establish care. An event monitor was negative for atrial fibrillation and TTE with agitated saline study was negative for a patent foramen ovale. Therefore, his ischemic stroke was presumed to be non-cardioembolic in origin. He is currently taking lisinopril 5 mg daily for hypertension (BP in clinic is 115/70) and atorvastatin 40 mg daily. He has no history of significant gastrointestinal or other bleeding. What do you recommend next?AStart apixaban 5 mg BIDBIncrease lisinopril to 10 mg dailyCStart aspirin 81 mg dailyDStart aspirin 81 mg daily and clopidogrel 75 mg dailyEStart aspirin 81 mg daily and ticagrelor 90 mg BID Answer #24 ExplanationThe correct answer is C – start aspirin 81mg daily.For the secondary prevention of non-cardioembolic ischemic stroke or TIA, anti-platelet therapy is recommended with aspirin only (75-150 mg/day), dipyridamole + aspirin (slightly superior to aspirin), or clopidogrel alone (slightly superior to aspirin) (Class I, LOE A).DAPT with aspirin and clopidogrel or aspirin and ticagrelor should be considered in the immediate period after a minor ischemic stroke or TIA (3 weeks after event, Class IIa), but not 6 months after an ischemic stroke. Dual antiplatelet therapy with aspirin and clopidogrel increases bleeding risk without a significant benefit over either agent alone. Dual antiplatelet therapy with aspirin and ticagrelor increases bleeding risk, but does not improve disability incidence.Oral anticoagulation would be recommended for a cardioembolic stroke, which does not fit the clinical picture.His BP is well controlled so increasing lisinopril is not necessary.Main TakeawayFor the secondary prevention of an ischemic stroke or TIA, anti-platelet therapy with aspirin, aspirin + dipyridamole, or clopidogrel alone is recommended.Guideline Loc.6.3, page 3296-3297 CardioNerds Decipher the Guidelines - 2021 ESC Prevention SeriesCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor RollCardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron!
DozeNews PRIME: as melhores e mais didáticas revisões de cardiologia direto na sua caixa de entrada! Assine agora e tenha acesso à todo material já produzido! - https://dozeporoito.substack.com/
In this episode, host Dr. Sabeen Dhand speaks with neurosurgeons Drs. David Altschul and Omar Tanweer about updates on cerebral aneurysms, including device innovation, risk stratification, and the importance of the doctor-patient relationship in decision-making. --- CHECK OUT OUR SPONSOR MicroVention FRED X https://www.microvention.com/emea/product/fred-x --- SHOW NOTES Dr. Omar Tanweer is the director of cerebrovascular and endovascular neurosurgery at Baylor College of Medicine. He works in a multidisciplinary group of neurologists, radiologists, and neurosurgeons. He trained at NYU and has been at Baylor for 2 years, where he does 100% neurovascular work. Dr. David Altschul is also from New York and is the division chief of neurovascular surgery at Montefiore. He completed an endovascular fellowship in Manhattan and has now been back at Monteriore since 2014. Both physicians have an 80 to 20 endovascular to open case ratio. In the case of ruptured cerebral aneurysms, Dr. Altschul describes a rule of threes. Around one third of patients pass away before reaching a hospital, another third arrive with significant neurologic deficits, the final third simply endure a headache. The severity of symptoms on presentation is generally predictive of outcome. They use the Hunt and Hess score, as well as the Modified Fisher Scale in their workup. They will generally only put in a ventriculostomy if a patient is lethargic and has a Hunt and Hess grade of at least 3. Both physicians use viz.ai to review their aneurysm cases at their home institutions, as well as at all local referring hospitals, as they are all connected via the viz platform. For unruptured aneurysms, they implement the PHASES score and rely on patient preference. Some patients are comfortable monitoring the growth of very small aneurysms, while others prefer the risk of treating it over the risk of monitoring due to the fear of having a known aneurysm. The two agree that developing a good doctor-patient relationship is important in these cases, because getting to know your patient can help you decide which of these small aneurysms to treat. Finally, we discuss new technology in the treatment of cerebral aneurysms. Coils have improved by becoming smaller, containing biologic agents, and coming in different shapes. Dr. Tanweer discusses the difference between balloon and stent assisted techniques. Balloon assisted is great for wide neck aneurysms or patients who can't be on dual anti-platelet therapy (DAPT) and are better in the case of re-rupture. Stent assisted, when tolerated, increases efficacy and reduces recurrence by keeping coils in place, as well as providing a scaffold for endothelial cells to heal across. The Flow Diverter, a vessel preservation device, is less porous and good for internal carotid and anterior circulation aneurysms. The downside is that it requires DAPT. There is also the Web device, an intrasaccular device that diverts flow across the metal in the aneurysm and at the base of the neck, but does not leave any metal in the normal part of the artery. These are mainly used for wide neck bifurcation aneurysms at the internal carotid, basilar, anterior communicating, and middle cerebral artery bifurcations. --- RESOURCES Twitter: @DavidAltschulMD @omar_tanweer Viz.aneurysm: https://www.viz.ai/aneurysm
Commentary by Dr Davide Capodanno
ESC TV Today brings you concise analysis from the world's leading experts, so you can stay on top of what's happening in your field quickly. This episode covers: Cardiology This Week: A concise summary of recent studies Cardiac involvement in Fabry's Disease Anti-thrombotic therapy post PCI: DAPT in 2023 Mythbusters: Powernap for heart health Host: Rick Grobbee Guests: Perry Elliott, Nicolle Kraenkel, Roxana Mehran and Franz Weidinger Want to watch that episode? Go to: https://esc365.escardio.org/event/896 Disclaimer This programme is intended for health care professionals only and is to be used for educational purposes. The European Society of Cardiology (ESC) does not aim to promote medicinal products nor devices. Any views or opinions expressed are the presenters' own and do not reflect the views of the ESC. Declarations of interests Stephan Achenbach, Rick Grobbee, Nicolle Kraenkel and Franz Weidinger have declared to have no potential conflicts of interest to report. Carlos Aguiar has declared to have potential conflicts of interest to report: personal fees for consultancy and/or speaker fees from Abbott, Alnylam, Amgen, AstraZeneca, Bayer, Boehringer-Ingelheim, Daiichi-Sankyo, Ferrer, Gilead, Lilly, Novartis, Pfizer, Sanofi, Servier, Tecnimede. Davide Capodanno has declared to have potential conflicts of interest to report: Sanofi, Daiichi Sankyo, Terumo, Medtronic, Chiesi. Perry Elliott has declared to have potential conflicts of interest to report: consultancies for Sanofi. Roxana Mehran has declared to have potential conflicts of interest to report: institutional research payments from Abbott, Abiomed, Alleviant Medical, Amgen, AM-Pharma, Arena, AstraZeneca, Atricure, Bayer, Biosensors, Biotronik, Boston Scientific, Bristol-Myers Squibb, CardiaWave, CeloNova, Chiesi, Concept Medical, CSL Behring, Cytosorbents, Daiichi Sankyo, Element Science, Faraday, Filterlex Medical, Humacyte, Idorsia Pharmaceuticals, Janssen, Mediasphere, Medtelligence, Medtronic, Novartis, OrbusNeich, Penumbra, PhaseBio, Philips, Pi-Cardia, PLx Pharma, Protembis, RenalPro, RM Global, Shockwave, Vivasure, Zoll; personal fees from Cine-Med Research, Ionis Pharmaceuticals, Novartis, Novo Nordisk, Vectura, WebMD; Equity
Merriam-Webster's Word of the Day for January 30, 2023 is: adapt • uh-DAPT • verb To adapt is to make or become fit (as for a new use) often by modification. // When people move to a new country, it can take them a while to adapt. // The teachers adapted the curriculum so that students of all abilities will benefit from it. See the entry > Examples: "Isaac Asimov's [Foundation] novels are collections of short stories and novellas spanning thousands of years, which makes them hard to adapt as a continuous story." — Belen Edwards, Mashable.com, 22 Dec. 2021 Did you know? "Nothing in this world is as reliable as change" is a common aphorism and one we can certainly attest to as lexicographers. English speakers adapted adapt, for example, in the 15th century from the Middle French adapter, which was itself an adaptation of Latin adaptāre. That source traces back to Latin aptus, meaning "fit" or "apt." Other adaptations of aptus in English include aptitude, inept, and of course apt itself, as well as unapt and inapt.
Please join author Pieter Martens and Associate Editor Justin Grodin as they discuss the article "Decongestion With Acetazolamide in Acute Decompensated Heart Failure Across the Spectrum of Left Ventricular Ejection Fraction: A Prespecified Analysis From the ADVOR Trial." Dr. Greg Hundley: Welcome listeners to this January 17th issue of Circulation on the Run. And I am Dr. Greg Hundley, Director at the Pauley Heart Center at VCU Health in Richmond, Virginia. Dr. Peder Myhre: And I'm Dr. Peder Myhre from Akershus University Hospital and University of Oslo, in Norway. And today, Greg, we have such an exciting feature paper. It comes to us from the ADVOR trialists. And the ADVOR trial examined the effect of acetazolamide in acute decompensated heart failure. And in this paper we're going to discuss how that treatment effect was across the left ventricular ejection fraction, across the spectrum. Greg, what do you think? Dr. Greg Hundley: Oh, wow. Sounds very interesting. But we might have some other articles in the issue. How about we grab a cup of coffee and Peder maybe this week, I'll go first and we'll start with preclinical science. How about that? Dr. Peder Myhre: Let's do preclinical science, Greg. Dr. Greg Hundley: Well, Peder, this particular paper focuses on the relationship between cardiac fibroblasts and cardiomyocytes. Remember that myocytes sit on a lattice of network of fibroblasts. And when the myocytes die, the fibroblasts then proliferates, secrete collagen and form this thick scar. Now, if we're going to try to regenerate, how are we going to get myocytes to get back into that thick scar when there's really a complete absence? And so as adult cardiomyocytes have little regenerative capacity, resident cardiac fibroblasts synthesize extracellular matrix, post myocardial infarction to form fibrosis, leading to cardiac dysfunction and heart failure. And therapies that can regenerate the myocardium and reverse fibrosis in the setting of a chronic myocardial infarction are lacking. Now, these investigators led by Professor Masaki Ieda from University of Tsukuba, were going to evaluate this process. The overexpression of cardiac transcription factors, including Mef2c, Gata4, Tbx5, Han2, all combined as MGTH. They can directly reprogram cardiac fibroblasts into induced cardiomyocytes and improve cardiac function in and under the setting of an acute myocardial infarction. However, the ability of an in vivo cardiac reprogramming to repair chronic myocardial infarction with established scars, well, that is really undetermined. Dr. Peder Myhre: Oh, what a wonderful introduction, Greg. And the way you described to us how cardiomyocytes and fibroblasts interact was really fascinating. Thank you. And now let's hear what the authors found and don't forget the clinical implications. Dr. Greg Hundley: Thanks, Peder. So these authors developed a novel transgenic mouse system where cardiac reprogramming and fibroblasts lineage tracing could be regulated spatiotemporally with tamoxifen treatment to analyze in vivo cardiac reprogramming in the setting of chronic MI. Then with this new model, the authors found in vivo cardiac reprogramming generates new induced cardiomyocytes from resident cardiac fibroblasts that improves cardiac function and reduces fibrosis in chronic myocardial infarction in mice. Wow. And additionally, they found that overexpression of cardiac reprogramming factors converts profibrotic cardio fibroblasts to a quiescent state, and that reverses fibrosis in chronic myocardial infarction. And therefore, Peder, direct cardiac reprogramming may be a promising therapy for chronic ischemic cardiomyopathies and heart failure. Really exciting work, converting scar tissue to actual functional cardiomyocytes. Dr. Peder Myhre: That was such a fantastic summary, Greg, and a very interesting paper. And I'm now going to take us back to clinical science and epidemiology. Because Greg, we all know that social and psychosocial factors are associated with cardiovascular disease risk. But the relative contributions of these factors to racial and ethnic differences in cardiovascular health has not been quantified. So these authors, led by the corresponding author, Nilay Shah from Northwestern University Feinberg School of Medicine in Chicago, used data from NHANES to examine the contributions of individual level social and psychosocial factors to racial and ethnic differences in population cardiovascular health. And that was measured by something called the cardiovascular health score, CVH score, which ranges from zero to 14, and it counts for diet, smoking, physical activity, body mass index, blood pressure, cholesterol, and blood glucose. Dr. Greg Hundley: Wow, really interesting, Peder. So what did they find here? Dr. Peder Myhre: So Greg, among males, the mean cardiovascular health score was 7.5 in Hispanic, 8.7 in non-Hispanic Asian, 7.5 in non-Hispanic black, and 7.6 in non-Hispanic white adults. And the authors found that the education explained the largest component of cardiovascular health differences among males. And now what about females? In females, the mean score was 8.0 in Hispanic, 9.3 in non-Hispanic Asian, 7.4 in non-Hispanic black, and 8.0 in non-Hispanic white adults. And for women, education explained the largest competence of cardiovascular health difference in non-Hispanic black. And place of birth, and that is US born versus born outside the US, explained the largest component of cardiovascular health difference in Hispanic and non-Hispanic Asian females. So Greg, the authors conclude that education and place of birth conferred the largest statistical contributions to the racial and ethnic differences in cardiovascular health among US adults. Dr. Greg Hundley: Very nice, Peder. What a beautiful description and outline that so well highlighting the differences in men versus women. Well, now we're going to turn back to the world of preclinical science, listeners. And we will continue with the paper by Dr. Amit Khera from Verve Therapeutics. Now, Peder, VERVE-101, this is an investigational in vivo CRISPR base editing medicine designed to alter a single DNA base in the PCSK9 gene. And that permanently turns off hepatic protein production and thereby, durably lowers LDL cholesterol. In this study, the investigators tested the efficacy, durability, tolerability, and potential for germline editing of VERVE-101 in studies of non-human primates and also in a murine F1 progeny study. Dr. Peder Myhre: So more on PCSK9s, and this time CRISPR technology. Very exciting. Greg, what did they find? Dr. Greg Hundley: Right, Peder. So VERVE-101 was well tolerated in non-human primates and led to, listen to this, an 83% lower blood PCSK9 protein and 69% lowering of LDL-C with durable effects up to 476 days following the dosing. These results have supported initiation of a first inhuman clinical trial. That's what needs to come next in patients with heterozygous familial hypercholesterolemia and atherosclerotic cardiovascular disease. Wow. Dr. Peder Myhre: Even greater reductions from this therapy on PCSK9 than the previous PCSK9 inhibitor therapies. Wow. Okay, Greg, and now we go from one fascinating study to another. And this time we actually have the primary results from a large randomized clinical trial, Greg. Isn't that exciting? Dr. Greg Hundley: Yes. Dr. Peder Myhre: And this paper describes the primary results of a trial testing in Indobufen versus aspirin on top of clopidogrel in patients undergoing PCI with drug-eluting stent DES who did not have elevated troponin. So that is patients without mycardial infarction. And in fact, fact, this is the first large randomized control trial to explore the efficacy and safety of aspirin replacement on top of P2Y12 inhibitor in patients receiving PCI with death. And Greg, I suppose you like I wonder what Indobufen is, and I just learned that that is a reversible inhibitor of platelet Cox-1 activity and it has comparable biochemical and functional effects to dose of aspirin. And previous data indicate that Indobufen could lessen the unwanted side effects of aspirin and that includes allergy intolerance and most importantly, aspirin resistance, while it retains the antithrombotic efficacy. Dr. Greg Hundley: Wow, Peder. Really interesting and great explanation. Indobufen. So how did they design this trial and what were the primary results? Dr. Peder Myhre: So Greg, the investigators of this trial, called OPTION, led by corresponding authors, Drs. Ge, Quian, and Wu from Fudan University in Shanghai, randomized 4,551 patients from 103 center to either indobufen based DAPT or conventional, and that is aspirin based DAPT for 12 months after DES implementation. And the trial was open label and with a non-inferiority design, which is important to keep in mind. And the primary endpoint was a one year composite of cardiovascular death, non-fatal MI, ischemic stroke, definite or probable stent thrombosis or bleeding, defined as BARC criteria type 2, 3, or 5. And now Greg, the primary endpoint occurred in 101, that is 4.5% of patients in the indobufen based DAPT group compared to 140, that is 6.1% patients, in the conventional DAPT group. And that yields an absolute difference of 1.6%. And the P for non-inferiority was less than 0.01. And the hazard ratio was 0.73 with confidence intervals ranging from 0.56 to 0.94. And Greg, the occurrence of bleeding was particularly interesting and that was also lower in the indobufen based DAPT group compared to the conventional DAPT group. And that was 3.0% versus 4.0% with the hazard ratio of 0.63. And that was primarily driven by a decrease in BARC type two bleeding. So Greg, the authors conclude that in Chinese patients with negative cardiac troponin undergoing DES implementation, indobufen plus clopidogrel DAPT compared with aspirin plus clopidogrel DAPT significantly reduced the risk of one year net clinical outcomes, which was mainly driven by reduction in bleeding events without an increase in ischemic events. Dr. Greg Hundley: Very nice, Peder. So another reversible inhibitor of platelet COX-1 activity, indobufen. And seems to be very, have high utility in individuals of Chinese ethnicity and Asian race. Well, perhaps more to come on that particular drug. Peder, how about we dive into some of the other articles in the issue? And I'll go first. So first, there's a Frontiers article by Professor Beatty entitled “A New Era and Cardiac Rehabilitation Delivery: Research Gaps, Questions, Strategies and Priorities.” And then there's a Research Letter by Professor Zuurbier entitled, “SGLT-2 inhibitor, Empagliflozin, reduces Infarct Size Independent of SGLT-2.” Dr. Peder Myhre: And then Greg, we have a new ECG challenge by Drs. Haghighat, Goldschlager and Oesterle entitled, “AV Block or Something Else?” And then there is a Perspective piece by Dr. Patrick Lawler entitled, “Models for Evidence Generation During the COVID-19 Pandemic: New Opportunities for Clinical Trials in Cardiovascular Medicine.” And Greg, there's definitely so much to learn from all the research that has been done through the pandemic. And finally, we have our own Molly Robbins giving us Highlights from the Circulation Family of Journals. And first, there is a paper describing the characteristics of postoperative heart block in patients undergoing congenital heart surgery described in Circulation: Arrhythmia Electrophysiology. Next, the impact of socioeconomic disadvantages on heart failure outcomes reported in Circulation: Heart Failure. Then there is social and physical barriers to healthy food explored in circulation, cardiovascular quality and outcomes. And then there is the association of culprit-plaque morphology with varying degrees of infarct, myocardial injury size reported in Circulation: Cardiovascular Imaging. And finally, the impact of optical coherence tomography on PCI decisions reported in circulation cardiovascular interventions. Dr. Greg Hundley: Fantastic, Peder. Well, how about we get off to that feature discussion? Dr. Peder Myhre: Let's go. Dr. Mercedes Carnethon: Well, thank you and welcome to this episode of the Circulation on the Run Podcast. I'm really excited today to host this show. My name is Mercedes Carnethon. I'm an associate editor at Circulation and Professor and Vice Chair of Preventive Medicine at the Northwestern University Feinberg School of Medicine. I'm really excited to learn from the lead author of a new study on decongestion with Acetazolamide and acute decompensated heart failure across the spectrum of LV ejection fraction. And I've got the lead author with me today, Pieter Martens, as well as my colleague and associate editor Justin Grodin, who handled the paper. So I'd love to start off with just welcoming you, Dr. Martens. Dr. Pieter Martens: Thank you for having me. It's a pleasure to be here today. Dr. Mercedes Carnethon: Yes. And thank you so much for submitting your important work to the journal, Circulation. I'd love to start to hear a little bit about what was your rationale for carrying out this trial and tell us a little bit about what you found. Dr. Pieter Martens: So the ADVOR trial was a double blind placebo controlled randomized trial, which was performed in Belgium. And it set out to assess the effect of acetazolamide in acute decompensated heart failure and this on top of standardized loop diuretic therapy and patients with heart failure. And the goal of the current analysis was to assess whether the treatment effect of acetazolamide in acute heart failure differs amongst patients with a different ejection fraction at baseline at randomization. So we looked specifically at patients with heart failure, reduced, mildly reduced and preserved ejection fraction to determine whether acetazolamide works equally well in those patients. Dr. Mercedes Carnethon: Well, thank you so much. Tell me a little more. What did you find? Did your findings surprise you? Dr. Pieter Martens: All patients that were randomized in the ADVOR trial, we registered a baseline left ventricular ejection fraction at baseline. And what we saw was at the multiple endpoints that we collected in the ADVOR trial, that randomization towards acetazolamide was associated with a pronounced and preserved treatment effect. And different endpoints that we looked at was a primary endpoint which was successful, which is an important endpoint, which we all strive towards in acute decompensated heart failure. And we saw that irrespective of what your baseline ejection fraction was, that randomization towards acetazolamide was associated with a higher odds ratio for having successful decongestion. And also looking at other endpoints which we find important in the treatment of patients with acute compensated heart failure, such as renal endpoints such as the diuresis, the amount of urine that they make, or the natruresis, the amount of sodium that they excrete, we again saw that randomization towards acetazolamide was associated with a higher treatment effect, so more diuresis, more natruresis, which was not effective, whether you had heart failure, reduced, mildly reduced or preserved eject fraction. We did see a slight increase in the creatinine, which was a little bit more pronounced in patients with heart failure with reduced ejection fraction. Dr. Mercedes Carnethon: Thank you so much for that excellent summary. I'm an epidemiologist, so I'm certainly aware that of the cardiovascular diseases and their changes over time, heart failure is one that is going up over time and affecting more of the population. So I know I really enjoyed hearing about an additional therapy that helps to improve quality of life and improve clinical outcomes in individuals who are experiencing heart failure. And I'm really curious as I turn to you, Justin, what attracted you to this particular article and why did you find it to be such a good fit for our audience here at Circulation? Dr. Justin Grodin: Well, Mercedes, I mean, I think you hit the nail on the head with your comment. And clearly when we look at Medicare beneficiaries in the United States, hospitalization for decompensated heart failure is the number one or most common cause for hospitalization. And up to this time, we really haven't had any multi-center randomized control clinical trials that have really informed clinical care with a positive result or a novel strategy that says, "Hey, this might be a better way to treat someone in comparison with something else." And so when we have a clinical trial like ADVOR, one of the crucial things that we want to understand is how does this work and does it work for everybody? And now when we look at the population hospitalized with heart failure, we know that approximately half of them have a weak heart or low ejection fraction, and the other half have a stiff heart, a normal ejection fraction. And so since we've got this 50/50 makeup, it is a crucially important question to understand if we have an important study like ADVOR, does this apply? Are these benefits enjoyed by all these individuals across the spectrum? Dr. Mercedes Carnethon: Thank you so much for really putting that in context. And I believe you had some additional questions for Dr. Martens. Dr. Justin Grodin: Yes. Yeah, thank you. So Pieter, I mean obviously this was a terrific study. One question I had for you guys is, you and your colleagues and the ADVOR research team is whether you had expected these results. Because we know at least historically, that there might be different cardiorenal implications for individuals that have a weak heart or heart failure with reduced ejection fraction in comparison with a stiff heart or heart failure with preserved ejection fraction. Dr. Pieter Martens: Thank you for that comment. And thank you also for the nice feedback on the paper. I think we were not really completely surprised by the results. I think from a pathophysiologic perspective, we do wonder whether heart failure with reduced ejection fraction from a kind of renal perspective is different from heart failure with preserved ejection fraction. Clearly, there are a lot of pathophysiological differences between heart failure with reduced, mildly reduced and preserved ejection fraction. But when it comes to congestion and acute heart failure, they seem to behave, or at least similarly in terms of response to acetazolamide, which was very interesting. We do think there are neurohormonal differences between heart failure reduced ejection fraction, preserved ejection fraction. But at least how acetazolamide works seems relatively unaffected by the ejection fraction. Dr. Justin Grodin: And Pieter, another question that comes to mind, and this is getting a little bit technical, but there have been studies that have shown that people that present to the hospital with decompensated heart failure, that have HFpEF, have a very different perhaps congestion phenotype where they might not have as much blood volume expansion. And so I, for one, was pretty curious as to how these results were going to play out. And I wonder what your thoughts are on that, or maybe that's perhaps more niche and less widely applicable than what you observed. Dr. Pieter Martens: Now, I can completely agree that when we are thinking about congestion, the congestion itself is a sort of pressure based phenomenon. And the pressure based phenomenon is based on what your volume is and the compliance within your cardiovascular system. But I think one of the important things to remember is that how we enrolled patients in the ADVOR trial was that we enrolled patients who had clear signs of volume overload. Remember, we used a volume score to assess clinical decongestion or actually getting rid of the volume. Volume assessment isn't really necessarily a pressure based assessment. And pressures might be the genesis of elevated pressures might be different amongst heart failure with reduced versus preserved ejection fraction. But what was really clear was that all these patients were volume overloaded. And when you think about the volume axis, then it's really about getting rid of that additional sodium, water, and that's where really acetazolamide works. So I do think we differ a little bit from historical acute decompensated heart failure trials in which they sometimes use signs and symptoms of more congestion, a pressure based phenomenon, where our endpoint was truly at volume endpoint. And we do believe that diuretics work really on a volume component of heart failure. Dr. Mercedes Carnethon: Thank you so much, especially for explaining that in a way that even non-clinicians such as myself can understand the potential implications. A big picture question that I have, and I really enjoy these discussions because they give us an opportunity to speculate beyond what we read in the paper. And that question is we do clinical trials and we identify effective therapies. And one of the bigger challenges we often face is getting those therapies out to the people who need them. Do you perceive any barriers in uptake of the use of acetazolamide in clinical practice? Dr. Pieter Martens: That's an excellent question. So one of the, I think beauties about acetazolamide is that this drug has been on the market for about 70 years. So I think everybody has access to it. This is not a novel compound which needs to go through different steps of getting marketing approval and getting a sort of reimbursement before it becomes available in clinical practice. And in theory, everybody should have access to this relatively cheap agent and can use it in its clinical practice. And I think it was very interested when we came out with the initial paper. I think already the day afterwards, we were getting messages from across the world that people have been using acetazolamide. So I think it is an agent which is available in current clinical practice and should not be too many barriers to its current implementation and clinical practice. Dr. Mercedes Carnethon: Well, that's fantastic to hear. So I hope Justin, that you will certainly help to ring the bell to get the information out about this wonderful study. I do want to turn to you, Pieter, to find out whether or not there are any final points that you didn't have an opportunity to discuss with us today. Dr. Pieter Martens: Think some of the other end points we didn't discuss were the effect, for instance, on length of stay. I think length of stay is a very important endpoint because hospital admissions, like Justin said, heart failure is the number one reason why elderly patients are being admitted. And just shortening the length of stay from a financial perspective might be important. So it was also very interesting to see that the use of acetazolamide in the study also translated into a shorter length of stay, which was also was unaffected, whether you had heart failure, reduced, mildly reduced or preserved ejection fraction, Dr. Mercedes Carnethon: Well, I certainly know people appreciate being in their own homes and being able to discharge is certainly a major benefit. So thank you so much for sharing that final point. I really want to thank you so much for a stimulating discussion today. I know that I learned a lot from you, Pieter, and the hard work of your research team as well as from you, Justin, for putting these findings in context and really helping our listeners and the readers of our journal understand why this paper is so important and how it's really moving the field forward for a clinically important problem. So thank you both so much for joining us here today on Circulation on the Run. Dr. Justin Grodin: Thank you. Dr. Pieter Martens: Thank you for having me. Dr. Mercedes Carnethon: I really want to thank our listeners for joining us today for this episode of Circulation on the Run. I hope you will join us again next week for more exciting discussions with our authors. Dr. Greg Hundley: This program is copyright of the American Heart Association 2023. The opinions expressed by speakers in this podcast are their own and not necessarily those of the editors or of the American Heart Association. For more, please visit ahajournals.org.
Annnnnnnnd We are back. Sorry, but after Andor has finally finished we have now got time to discuss the old type 1 MI, aka STEMI aka Occlusive Myocardial Infarction. Come listen for all those basics and some nuances around myocardial infarction in critically unwell patients. We talk when to DAPT, who gets full anticoagulation, hemodynamic support, and when to wake our Cardiology friends up in the night.
#1005- Devo fazer DAPT após cirurgia de revascularização miocárdica no IAM? by Cardiopapers
ACCEL Lite: Featured ACCEL Interviews on Exciting CV Research
This subgroup analysis from the MASTER-DAPT trial demonstrates that in high-bleeding risk patients with acute or recent myocardial infarction it is safe to stop DAPT 1 month after stenting and that this strategy provides a reduction in bleeding risk. In this interview, Pieter C. Smits MD, PhD, FESC and Sidney C. Smith Jr. MD, MACC, with Jeffrey Hsu MD, PhD, discuss a recent piece from JACC: Abbreviated Antiplatelet Therapy after Coronary Stenting in Patients with Myocardial Infarction at High Bleeding Risk. Subscribe on Apple Podcasts | Subscribe on Google Play | Subscribe to ACCEL
Kyle A. Hess, PharmD (Twitter: @KyleHessPharmD ) describes current guideline recommendations for duration of dual antiplatelet therapy (DAPT) following percutaneous coronary intervention, compares and contrasts strategies for antiplatelet regimens for reduced duration DAPT and selects an appropriate duration of therapy when utilizing shortened DAPT. For more pharmacy content, follow Mayo Clinic Pharmacy Residency Programs @MayoPharmRes or the host, Garrett E. Schramm, Pharm.D., @garrett_schramm on Twitter! You can also connect with the Mayo Clinic's School of Continuous Professional Development online at https://ce.mayo.edu/ or on Twitter @MayoMedEd.
This week, please join authors John McMurray and David Cherney, editorialist Kausik Umanath, as well as Associate Editors Ian Neeland and Brendan Everett as they discuss the original research articles "Initial Decline (Dip) in Estimated Glomerular Filtration Rate After Initiation of Dapagliflozin in Patients With Heart Failure and Reduced Ejection Fraction: Insights from DAPA-HF" and "Renal and Vascular Effects of Combined SGLT2 and Angiotensin-Converting Enzyme Inhibition" and editorial ""Dip" in eGFR: Stay the Course With SGLT-2 Inhibition." Dr. Carolyn Lam: Welcome to Circulation On the Run, your weekly podcast summary and backstage pass to the Journal and its editors. We're your co-hosts, I'm Dr. Carolyn Lam, Associate Editor from the National Heart Centre and Duke National University of Singapore. Dr. Greg Hundley: I'm Dr. Greg Hundley, Associate Editor and director of the Pauley Heart Center at VCU Health in Richmond, Virginia. Dr. Carolyn Lam: Greg, it's the season of double features. Except this time, we're having a forum discussion of two related articles and an editorial that discusses both. What is it on? SGLT2 inhibitors. In the first paper, an analysis from the DAPA-HF trial, looking specifically at that initial dip in GFR that follows initiation of dapagliflozin in patients with HFrEF. Then we will discuss further, in a mechanistic way, the renal and vascular effects of combining SGLT2 inhibition on top of ACE inhibition. Lots and lots of good learning and insights, but let's go on first to the other papers in today's issue. Shall we? Dr. Greg Hundley: You bet, Carolyn, and I'm going to grab a cup of coffee. Carolyn, in this issue, wow, so many exciting original articles. In fact, there are two more articles that were going to pair together, both clinical and pertaining to TAVR procedures. In the first one, it was a group of authors led by Dr. Duk-Woo Park from the Asan Medical Center at the University of Ulsan College of Medicine. They conducted a multicenter, open-label randomized trial comparing edoxaban with dual antiplatelet therapy or DAPT, aspirin plus clopidogrel, in patients who had undergone successful TAVR and did not have an indication for anticoagulation. Now in this study, Carolyn, the primary endpoint was an incidence of leaflet thrombosis on four-dimensional computed tomography, CT, performed at six months after the TAVR procedure. Key secondary endpoints were the number and volume of new cerebral lesions on brain magnetic resonance imaging or MRI and the serial changes of neurological and neurocognitive function between six months and that time immediately post the TAVR procedure. Dr. Carolyn Lam: Oh, interesting. What did they find? Dr. Greg Hundley: Right, Carolyn. In patients without an indication for long-term anticoagulation after successful TAVR, the incidence of leaflet thrombosis was numerically lower with edoxaban than with dual antiplatelet therapy, but this was not statistically significant. The effect on new cerebral thromboembolism and neurological or neurocognitive function were also not different between the two groups. Now because the study was underpowered, the results should be considered really as hypothesis generating, but do highlight the need for further research. Dr. Greg Hundley: Carolyn, there's a second paper pertaining to transcatheter aortic valve prosthesis. It's led by a group directed by Dr. Paul Sorajja from the Minneapolis Heart Institute Foundation and Abbott Northwestern Hospital. Carolyn, these authors prospectively examined 565 patients with cardiac CT screening for HALT, or what we would define as hypoattenuating leaflet thickening, at 30 days following balloon-expandable and self-expanding TAVR. Now, deformation of the TAVR prosthesis, asymmetric prosthesis leaflet expansion, prosthesis sinus volumes, and commissural alignment were analyzed on the post-procedural CT. For descriptive purposes, an index of prosthesis deformation was calculated, with values greater than 1 representing relative midsegment underexpansion. A time-to-event model was also performed to evaluate the association of HALT with the clinical outcomes. Dr. Carolyn Lam: Oh, interesting. What did they find? Dr. Greg Hundley: Right, Carolyn. Nonuniform expansion of TAVR prosthesis resulting in frame deformation, asymmetric leaflet, and smaller neosinus volume was related to the occurrence of HALT in patients who underwent TAVR. What's the take home here, Carolyn? These data may have implications for both prosthesis valve design and deployment techniques to improve clinical outcomes in these patients. Now, Carolyn, both of these articles are accompanied by an editorial from Dr. Raj Makkar from the Smidt Heart Institute at Cedars-Sinai's Medical Center. It's a very lovely piece entitled Missing Pieces of the TAVR Subclinical Leaflet Thrombosis Puzzle. Well, how about we check what else is in this issue? My goodness, this was a packed issue. First, Carolyn, there are three letters to the editor from Professors Ennezat, Dweck, and then a response from Dr. Banovic pertaining to a follow-up from a previously published study, the AVATAR study, in evaluating valve replacement in asymptomatic aortic stenosis. There's also a Perspective piece from Dr. Wells entitled “Treatment of Chronic Hypertension in Pregnancy: Is It Time For A Change?” There's a Global Rounds piece from Professor Berwanger entitled “Cardiovascular Care in Brazil: Current Status, Challenges, and Opportunities.” Then there's also a Research Letter from Professor Eikelboom entitled “Rivaroxaban 2.5 mg Twice Daily Plus Aspirin Reduces Venous Thromboembolism in Patients With Chronic Atherosclerosis.” Dr. Carolyn Lam: There's another Research letter by Dr. Borlaug on longitudinal evolution of cardiac dysfunction in heart failure with normal natriuretic peptide levels. There's also a beautiful Cardiology News piece by Bridget Kuehn on the post-COVID return to play guidelines and how they're evolving. Well, that was a great summary of today's issue. Let's hop on to our feature forum. Shall we? Dr. Greg Hundley: You bet, Carolyn. Can't wait. Dr. Carolyn Lam: Today's feature discussion is actually a forum because we have two feature papers in today's issue. They all surround the cardiorenal interaction, should I say, of the SGLT2 inhibitors. For the first paper, discussing that initial decline or that dip in the GFR following initiation of dapagliflozin would be Dr. John McMurray, who's the corresponding author of this paper from DAPA-HF. Dr. John McMurray's from the University of Glasgow. Now next, we have also the corresponding author of another paper, really going into the mechanistic insights of the renal and vascular effects of combined SGLT2 and ACE inhibition. Dr. David Cherney is from Toronto General Hospital, University of Toronto. Dr. Carolyn Lam: We have the editorial list of these two wonderful papers, Dr. Kausik Umanath from Henry Ford Health in Michigan. Finally, our beloved associate editors, Dr. Ian Neeland from Case Western Reserve and Dr. Brendan Everett from Brigham and Women's Hospital, Harvard Medical School. Thank you, gentlemen. Now with all of that, what an exciting forum we have in front of us. Could I start by asking, of course, the respective authors to talk a little bit about your papers? I think a good place to start would be with Dr. McMurray. John, please. Dr. John McMurray: Thanks, Carolyn. I think our paper had three key messages. The early dip in eGFR that we saw was, on average, very small in patients with heart failure, about 3 mLs/min or about 5%. Very few patients had a large reduction in the eGFR. It was around 3%. Dapagliflozin-treated patients had a 30% or greater decline compared to about 1% of placebo patients. Finally, very few of those patients had a decline in the eGFR below a critical threshold, which for cardiologists might be around 20 mLs/min. We saw that in only five patients; that's 0.2% of the dapagliflozin-treated patients. Second message was that that early decline partially reverses. The nadir in our study was about 14 days. But by 60 days, on average, eGFR had increased again. Hold your nerve if you see an early decline in eGFR. Dr. John McMurray: Maybe the most important message was that that decline in the eGFR is not associated with worse cardiovascular or renal outcomes. In fact, if anything, the opposite. If you look at the patients in the dapagliflozin group with a 10% or greater decline in eGFR, then compare it to patients who didn't have that decline, these individuals were about 27% less likely to experience the primary composite outcome of worsening heart failure and cardiovascular death. If you look at the placebo group, we saw exactly the opposite. Amongst those who had a greater than 10% decline in eGFR compared to those who didn't, those people with the early decline in eGFR were 45% more likely to experience the primary composite endpoint. The same is true for other cardiovascular outcomes for worsening kidney function. In the dapagliflozin group, decline in eGFR was not associated with more adverse events, not associated with more treatment discontinuation. That small decline in the eGFR is not a bad prognostic sign. If anything, it might be the opposite. Dr. Carolyn Lam: Thank you so much. That was really clear. David, are you going to tell us why this decline occurs? Dr. David Cherney: Yeah. Perhaps the paper that we published gives some insights into the mechanisms that are responsible for some of those changes in GFR that are thought to be acute hemodynamic effects. In the between trial, which is the trial that we published examining the effect of ACE inhibition followed by SGLT2 inhibition in patients with type 1 diabetes, we also saw that there was an expected effect of adding SGLT2 inhibition on top of an ACE inhibitor in people with uncomplicated type 1 diabetes. This acute dip in GFR was seen in this cohort of patients. We included only 30 patients in this small mechanistic study. At the same time, along with that dip in GFR, we also saw an increase in measures of proximal natriuresis. That proximal sodium loss is linked with changes in sodium handling in the kidney, which then causes changes in both probably afferent and efferent tone, which causes this dip in GFR primarily through natriuresis in this phenomenon called tubuloglomerular feedback. That was one major observation that gives insight into what we see in larger trials around the dip in GFR. Dr. David Cherney: In our mechanistic study, we also saw an additive effect on blood pressure. Blood pressure went down further with the addition of empagliflozin on top of an ACE inhibitor. In terms of the mechanisms that are responsible for the reduction in blood pressure, natriuresis certainly may be in part responsible, but we also saw a novel observation whereby there was a reduction in peripheral vascular resistance using noninvasive measures. There are likely several mechanisms that are responsible for the reduction in blood pressure. Then finally, we also saw reductions in markers of oxidative stress, which may also account for some of the effects that we see in blood pressure, as well as potentially some of the anti-inflammatory and anti-fibrotic effects that we see at least in experimental models that may have some clinical translatability to humans as well around the clinical benefits. I think the blood pressure, the renal hemodynamic effects, and some of the neurohormonal mechanisms are the major observations that we saw that may in part explain some of the really nice changes that were seen in Dr. McMurray's study. Dr. Carolyn Lam: Right. Thanks, David. But these were patients with type 1 diabetes and no heart failure. John, do you have any reflections or questions about how that may apply? By the way, what a beautiful study. Thank you, David. Dr. David Cherney: Pleasure. Thank you. Dr. John McMurray: Yes, David. I really enjoyed your study. In fact, I think, Carolyn, it does shed some insights perhaps to what's going on. As David pointed out, the reduction in peripheral arterial resistance, reduction in blood pressure, that may play some role in that early dip in eGFR as well as autoregulation in the kidney. Then the other interesting thing is that the distal nephron seems to adapt to that effect in the proximal tubule. Again, that may account for some of that recovery in eGFR, that reversal in the early dip that I spoke about, and which I think is very clinically important because, of course, physicians should make sure that they recheck eGFR if they see that early dip. Because they may find that few weeks later that that dip is much smaller and of much less concern. Dr. Carolyn Lam: Thank you, John. In fact, you're saying, stay the course, right- Dr. John McMurray: I have. Dr. Carolyn Lam: ... with the SGLT2 inhibitors. I'm actually stealing the words of the title of the editorial, a beautiful editorial by Kausik. I love that. Stay the course. Kausik, please, could you frame both papers and then with an important clinical take home message for our audience? Dr. Kausik Umanath: Sure. I think the analysis by John and his group was really relevant with the large sample size. What's impressive? Similar to a lot of these other SGLT2 studies that have come out, both in heart failure and in kidney disease progression and so on, it's remarkable how the other analysis, like the analysis of EMPA-REG and CREDENCE and so on, of similar dips. All show more or less the same magnitude, the same relative proportions of this GFR trajectory. I think the mechanistic study only highlights that though it's working with a slightly different population of type 1 patients and much earlier in their course in terms of where their GFRs are. Dr. Kausik Umanath: The other piece is that ultimately we need to understand this dip and know to monitor for it and so on. But I think the general clinician should really understand that a dip of greater than 10% really occurs in less than half the population that takes these agents. That dip, if it occurs, certainly doesn't do any harm. That said, if they see a bigger dip in the 30% range, monitor more closely and consider making sure that there aren't any other renal issues out there for that patient because they are a much smaller proportion of patients in these large trials that generate that level of dip. They should be monitored. Dr. Kausik Umanath: The other thought that we had, and thinking through this in a practical sense, is because you expect this dip, many of our cardiologists or even the nephrologists when we titrate these drugs, they're on a suite of other drugs. It's probably best to not adjust their Lasix or their loop diuretic, or their RAAS inhibitor at the same time as you're adjusting the SGLT2 inhibitor or starting it because then you may just introduce more noise into the GFR changes that you see over the next several weeks. It may be a sequential piece or at least holding those other agents constant while this gets titrated and introduced is a prudent course of action, so you don't misattribute changes. Dr. Carolyn Lam: Thanks so much. What clinically relevant points. In fact, that point about the diuretic especially applies in our heart failure world. You see the dip. Well, first, make sure the patient's not overdiuresed. Remember, there's more that the patient's taking. Thank you. That was a really great point. Brendan and Ian, I have to get you guys to share your views and questions right now. But before that, can I take a pause with you and just say, aren't you just so proud to be AEs of Circulation when we see papers like these and we just realize how incredible the data are and the clinical implications are? I just really had to say that. All right. But with that, please, what are your thoughts, Brendan? Dr. Brendan Everett: Yeah, sure. Thank you, Carolyn. Hats off to all three of our authors today for doing some amazing science. Thank you for sending it to Circulation. I think, in particular, I handled David's paper. I'm not a nephrologist and I'm probably the furthest thing from a nephrologist. Had to do my best to try and understand these concepts that I'm not sure I ever even was exposed to in medical school many years ago. I think it shows the breadth of the interest in our readership. The fact that these changes in eGFR have become a primary focus for our cardiovascular patients and that the clinical implications are really important. I guess my question, David, is... In your paper, you talked a little bit about this hypothesis of hyperfiltration and the role that hyperfiltration plays in setting patients with diabetes up for kidney disease. Is that playing a role in John's observation or not? Again, as a non-nephrologist, I have trouble connecting the dots in terms of that hypothesis and John's observation of the clinical benefit for patients that have a reduction in eGFR as opposed to no change. Dr. David Cherney: Yeah. It's a great question. It's very difficult to know with certainty in a human cohort because we can't measure the critical parameter, which is intraglomerular pressure, which we think these changes in GFR are a surrogate for. But if we go along with that train of thought, along reductions in glomerular hypertension, it very much makes sense that the patients who dip are those who have the... They're taking their medication, number one. Number two, they respond physiologically in the way that you expect them to, which is that their GFR dips at least transiently and then goes back up again through some of the compensatory mechanisms that John mentioned earlier. As was mentioned not only in this paper, but also in previous analyses from CREDENCE and previous analyses from VERTIS CV and others have shown that indeed that dip in GFR is linked with longer term renal benefits, at least. That is reflected in a reduction in the loss of kidney function over time. Dr. David Cherney: The patients who are on an SGLT2 inhibitor and those who dip by around 10% or less, those patients tend to do the best over time in terms of preserving GFR, not losing kidney function compared to patients who are on an SGLT2 inhibitor but do not dip, or those patients who actually have an increase in GFR. That is consistent with this idea that there may be a reduction in glomerular pressure, which is protective over the long term. That ties back into your question around hyperfiltration that this may indeed be due to a reduction in glomerular pressure, which is linked with risk over the long term. Dr. Carolyn Lam: Ian? Dr. Ian Neeland: I wanted to echo Brendan's comments about the excellent science. When I read these papers, it really speaks to the existential struggle that cardiologists have between kidney function and these medications that we know have cardiovascular benefits. How do we manage that practically? It's so clinically relevant, both the observation that John's paper made about the dip in the DAPA-HF trial as well as, David, your mechanistic insights. Dr. Ian Neeland: I wanted to ask John potentially about the most fascinating aspect to me of this paper was that patients with a dip of 10% or more actually ended up doing better in terms of cardiovascular outcomes, specifically hospital heart failure and hospitalizations than people on placebo with a greater than 10% dip. It speaks to the fact that... Is the physiology going on here different between those individuals whose GFR went down on placebo versus those who are on SGLT2 inhibitors? All the mechanistic insight that David's paper had in terms of blood pressure and intraglomerular pressure, how does that feedback and speak to why heart failure is strongly linked to this mechanism? We see this not just with SGLT2 inhibitors, but there are other medications now coming out showing that there's a relationship between this dip in GFR and heart failure. Can you speak to why this heart failure-kidney connection is so important and becoming greater and greater in terms of our understanding? Dr. John McMurray: Well, thank you for asking me the hardest question and one that I truly don't think I have a good answer to. I think it's obvious to all of us that the kidney is central in heart failure and perhaps cardiologists have neglected that fact, focusing more on the other organ. But by definition, almost the fluid retention that characterizes heart failure in terms of signs, and probably is the primary cause of symptoms, that clearly is a renally-mediated phenomenon. The kidney must be central to all of this. I think David right. I think the decline in eGFR that you see with this drug is simply a marker that the drug is having its physiological effect or effects. Whatever those are, they're beneficial. Clearly, patients who have an eGFR decline on placebo are different and they reflect, again, the patients that we see all the time. As our patients with heart failure deteriorate, one of the things that we commonly see, in fact becomes one of the biggest problems that we have to deal with, is that their kidney function declines. As their symptoms get worse, as their cardiac function gets worse, their kidney function also declines. Dr. John McMurray: I think you're seeing two contrasting effects here. One is the background change in eGFR, which is the placebo patients, and we've always known that that's a bad thing. Then we're seeing that early within 14 days marker of the pharmacological or physiological action of the drug. I hope you don't ask me how SGLT2 inhibitors work in heart failure. That's the other most difficult question I can think of, but I think this is just a marker of the fact that they are working. Dr. David Cherney: Yeah. Just to add to that briefly, there is this difficulty in sorting out the mechanisms that are relevant around the acute effects in the kidney that the dip in GFR reflects natriuresis that could keep patients out of heart failure; that the reduction in glomerular pressure reduces albuminuria. Albuminuria reduction is linked with kidney protection. It's linked with heart failure and ASCVD protection. Then there's also this concept of if you dip and then you stay stable afterwards, your GFR stays stable afterwards, those patients with stable kidney function that's not declining, the dippers in other words, those patients are probably able to maintain salt and water homeostasis better than someone who's declining more rapidly. All these things probably tie together in order to reflect, of course, there's a renal protective effect, but that some of those mechanisms may also tie into the heart failure mechanisms that John was mentioning. Dr. John McMurray: But, David, it's hard to imagine if we don't protect the kidney, we won't protect patients with heart failure given how fundamental, as I said, the kidney is, and how fundamentally important worsening kidney function is. Not only because it is a marker of things going badly, but also because it often results in discontinuation or reduction in dose of other life-saving treatments. To Kausik's point, it was very important about the risk of changing background life-saving disease modifying therapy. Actually, we didn't see that in DAPA-HF, which was very intriguing. There was no reduction in use of renin-angiotensin system blockers or mineralocorticoid receptor antagonists. Dr. Carolyn Lam: Thank you so much, gentlemen. Unfortunately, we are running out of time, but I would really like to ask one last question to the guests, if possible. Where do you think the field is heading? What next? What's the next most important thing we need to know? David, do you want to start? Then John, then Kausik. Dr. David Cherney: I think one of the aspects that we need to know in the future is where else can we extend these therapies into novel indications and extend the boundaries of where we currently work with these therapies. People with type 1 diabetes, for example, with either heart failure or with significant kidney disease, patients with kidney transplantation, is there a renal or cardiovascular protective effect? Then another high risk cohorts who have not been included in trials, those on immunosuppressants, for example, who were excluded from the trials. I think those are some of the areas that we need to extend into now that we understand how these therapies work in even very sick patients and that we also know that they likely have at least some benefit through suppressing inflammation, and possibly reducing infectious risks. That would provide a rationale for extending into some of these new areas. I think that's certainly, hopefully on the horizon for us. Dr. Carolyn Lam: John? Dr. John McMurray: Carolyn, obviously I think looking at post myocardial infarction population, that's an obvious place to go. There are a couple of trials there. I suppose the trial that I would love to see, and which I think would address the core question that we've been discussing today, which is: Is this all about the effect in the kidney and how important is the diuretic and natriuretic action of these drugs in heart failure? I think the key study that would address this would be doing a study in patients on dialysis. Because in those patients we could, I think, separate the issue of natriuresis, diuresis, and maybe even the dip in EGR that we've been talking about. If these drugs prove to be effective in end-stage kidney disease, patients on dialysis, that would be really fascinating. Dr. Carolyn Lam: Kausik? Dr. Kausik Umanath: That is a very interesting point. I don't know that we know necessarily outcomes, but I think from working with the DAPA-CKD, we do have a little bit of the safety data because we did continue it. I was the US MLI for that study and we did continue the SGLT2 passed into renal failure. There is a little bit of safety data there. But I don't think once you've declared an outcome, you're not collecting outcomes data after that point. That's a very interesting area to look into. Dr. Kausik Umanath: I also think the other place where this field's heading is trying to better tier and layer the multitude of agents. I think we've been waiting for about 20 to 30 years, at least in the kidney field, for something new to affect the progression of kidney disease after the ACE/ARB trials and so on. This one we've got SGLT2 inhibitors. We've got the new MRA, finerenone, and so on, which also have very beneficial cardiovascular effects. The question becomes: How do we layer these therapies? Which sequence to go in? Some of the others that are in pipeline as well that are out there that have very beneficial cardiovascular effects that may indeed also help kidney function and diabetes control, which do you go with first and so on? Dr. Carolyn Lam: Wow! Thank you so much. We really could go on forever on this topic, but it has been tremendous. Thank you once again. On behalf of Brendan, Ian, Greg, thank you so much for joining us today in the audience. You've been listening to Circulation On the Run. Don't forget to tune in again next week. Dr. Greg Hundley: This program is copyright of the American Heart Association 2022. The opinions expressed by speakers in this podcast are their own and not necessarily those of the editors or of the American Heart Association. For more, please visit ahajournals.org.
Dr. Josh Belfer continues his discussion with his high school classmate and good friend Dr. Levi Mulladzhanov, an anesthesiologist in Philadelphia. In part two of an ongoing series of discussions between the two, the pair talk about Dr. Levi's path to anesthesia, how they manage the pressures of high intensity medical situations, and begin to explore the challenges of residency. Check out more of the Doctors Are People Too podcast on https://instagram.com/doctorsarepeopletoopodcast (Instagram) and https://www.tiktok.com/@daptpodcast (TikTok)!
Dr. Josh Belfer speaks with his high school classmate and good friend Dr. Levi Mulladzhanov, an anesthesiologist in Philadelphia. In part one of an ongoing series of discussions between the two, the pair reminisce about the beginnings of their friendship, why they chose to go into medicine, and the hardships of medical school. Check out more of the Doctors Are People Too podcast on https://instagram.com/doctorsarepeopletoopodcast (Instagram) and https://www.tiktok.com/@daptpodcast (TikTok)!
CardioNerds (Amit and Dan) join Dr. Omid Amidi (CardioNerds Academy Graduate) and Dr. Marwah Shahid from the UCLA Cardiology Fellowship program along with Dr. Evelyn Song (CardioNerds Academy House Faculty and Heart Failure Hospitalist at UCSF) to discuss a complex case focused on management of severe coronary artery disease in a patient with Glanzmann thrombasthenia. Dr. Rushi Parikh (Interventional cardiologist, UCLA) provides the ECPR for this episode. Audio editing by CardioNerds Academy Intern, student doctor Akiva Rosenzveig. Glanzmann Thrombasthenia is a bleeding disorder due to impairment of platelet aggregation secondary to a mutation in the GPIIB/IIIA receptor. This case is focused on work up of stable coronary artery disease followed by a discussion on duration of dual antiplatelet therapy post percutaneous coronary intervention in a patient with Glanzmann thrombasthenia. Check out this published case in JACC: Case Reports Jump to: Case media - Case teaching - References 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 See the published case in JACC: Case Reports Episode Schematics & Teaching Pearls 1. Patients with Glanzmann thrombocytopenia (GT) may have a higher risk of bleeding, depending on their disease phenotype. 2. It is unclear whether the mechanism of GT protects patient against stent thrombosis in the setting of PCI. Additionally, there is little data on the use of antiplatelet agents in patients with GT. 3. Short-term DAPT may be a reasonably safe option for patients with GT undergoing PCI. 4. We report a successful case of percutaneous coronary intervention in a patient with GT with no complications at a 1 year follow up. Notes 1. What is Glanzmann thrombasthenia? GT is an inherited platelet disorder that is characterized by spontaneous bleeding with phenotypic variability ranging from minimal bruising to potentially fatal hemorrhaging. GT is caused by autosomal recessive inheritance of quantitative or qualitative deficiencies of functional αIIbβ3 integrin coded by ITGA2B or ITGB3 genes for αIIb and β3, respectively. As a result, platelets may be stimulated, but the platelet glycoprotein IIb/IIIa receptor is unable to bind fibrinogen to cross-link platelets, rending them potentially ineffective. In platelet aggregation studies, there is lack of response to collagen, epinephrine, arachidonic acid, and ADP stimulation. Thus, platelet aggregation is impaired. 2. What is known about PCI and antiplatelet therapy in the setting of Glanzmann thrombasthenia? To the best of our knowledge, this is the first case report of percutaneous coronary intervention in the setting of GT. It is unclear if the mechanism of GT alone provides sufficient antiplatelet activity and whether antiplatelet therapy leads to significantly increased bleeding risk. The use of antiplatelet therapy is not well studied in the GT population. What we do know is that the mechanism of GT prevents platelet aggregation—the final step in platelet-related thrombosis—while oral antiplatelet therapy affects platelet activation, thus, in our patient we felt that short term DAPT was reasonable. It is important to note that in the event of an active bleed requiring platelet transfusion, donor platelets possess functional glycoprotein IIb/IIIa receptors and thus exponentially increase the risk of stent thrombosis. Therefore, unlike our case, if a patient is not maintained on chronic oral antiplatelet therapy, initiation of oral or intravenous antiplatelet therapy should be considered to prevent stent thrombosis at the time of platelet transfusion. Like any other patient with a high bleeding risk, it is important to have clear indications to conduct a coronary angiogram in patient...
Dr. Josh Belfer speaks with Olga Kudinenko, founder and chair of the board of the Tabletochki Charity Foundation. Tabletochki is the biggest childhood cancer charity in Ukraine, and helps to support pediatric patients and their families through every aspect of cancer treatment. Olga describes why she created the foundation, how it has grown exponentially over the last 10 years, and how the war in Ukraine has impacted the work that the foundation is doing. Learn more about Tabletochki, including opportunities to donate, https://tabletochki.org/en/ (here). Check out more of the Doctors Are People Too podcast on https://instagram.com/doctorsarepeopletoopodcast (Instagram) and https://www.tiktok.com/@daptpodcast (TikTok)! This week's episode is presented by FIGS. Use the code DAPT at https://www.wearfigs.com/ (wearFIGS.com) for 15% off your first order.
Dr. Josh Belfer continues his discussion with Dr. Tiffany Moon, an anesthesiologist, entrepreneur, and star of Bravo TV's The Real Housewives of Dallas. Dr. Moon talks about how she thinks it's time for a reality show about the world of anesthesia. She also speaks about her entrepreneurial pursuits and the secret to her success! Follow Dr. Moon on https://www.instagram.com/tiffanymoonmd/?hl=en (Instagram) and https://www.tiktok.com/@tiffanymoonmd?lang=en (TikTok). Use the code DAPT at checkout for a discount on Dr. Moon's https://www.tiffanymoonmd.com/ (Aroma-sthesia candles)! Follow the podcast on Instagram: https://instagram.com/doctorsarepeopletoopodcast (@doctorsarepeopletoopodcast) Have a question, comment, or guest recommendation? Message us on Instagram!
Dr. Josh Belfer speaks with Dr. Tiffany Moon, an anesthesiologist, entrepreneur, and star of Bravo TV's The Real Housewives of Dallas. Dr. Moon speaks about her decision to pursue anesthesia and reflects on being a frontline worker during COVID. She also speaks about how she decided to join The Real Housewives, and how her experience on reality television has impacted her medical career. Follow Dr. Moon on https://www.instagram.com/tiffanymoonmd/?hl=en (Instagram) and https://www.tiktok.com/@tiffanymoonmd?lang=en (TikTok). Use the code DAPT at checkout for a discount on Dr. Moon's https://www.tiffanymoonmd.com/ (Aroma-sthesia candles)! Follow the podcast on Instagram: https://instagram.com/doctorsarepeopletoopodcast (@doctorsarepeopletoopodcast) Have a question, comment, or guest recommendation? Message us on Instagram!
Dr. Brian Locke is back to talk about that "nonrandomized" proning trial. We also talk about the new oral carbapenem for UTI trial, whether 1-2 months of DAPT is non-inferior to 12 months of DAPT, whether less than 1500 mg of sodium reduces heart failure hospitalizations, the risk of anaphylaxis from IV iron, and whether pickle juice is effective for treating cramps in cirrhosis. Check it out! Oral Tebipenem vs IV Ertapenem for Complicated UTIAwake Proning for Hospitalized COVID-19 Patients1-2 Months of DAPT vs 12 months of DAPT vs ACSLow Sodium Diet for Heart FailureEstimating Excess Mortality due to COVID-19Risk of Anaphylaxis from IV Iron Pickle Juice for Cramps in CirrhosisMusic from Uppbeat (free for Creators!):https://uppbeat.io/t/soundroll/dopeLicense code: NP8HLP5WKGKXFW2R
Go online to PeerView.com/SPE860 to view the activity, download slides and practice aids, and complete the post-test to earn credit. The latest stroke statistics estimate that about 800,000 individuals in the United States experience a stroke each year. Furthermore, about 20% of all strokes are recurrent, and many of these patients previously experienced a minor stroke or transient ischemic attack (TIA). Recurrence is greatest within the first 24 to 48 hours, but the risk remains elevated for months, even years, after the initial event. The American Heart Association (AHA) and American Stroke Association (ASA) recently updated their guidelines for stroke prevention to include expanded and detailed recommendations for the use of dual antiplatelet therapy (DAPT), the combination of aspirin and clopidogrel or ticagrelor, to further reduce the risk of stroke. These guidelines also include specific recommendations for individuals with minor acute ischemic stroke (AIS) or a TIA. In this activity based on a recent satellite symposium in New Orleans, leading experts on stroke management highlight the current guideline recommendations and discuss the latest perspectives on DAPT before transitioning to patient case scenarios where each expert demonstrates how these advances can be translated into clinical practice to improve outcomes and reduce the risk of recurrent stroke, while accounting for bleeding risks, antiplatelet resistance, and patient adherence. Upon completion of this CE activity, participants will be able to: Identify individuals with AIS or TIA who are appropriate candidates for treatment with antiplatelet therapy to reduce the risk of recurrent stroke, Assess the benefits and risks of using P2Y12 inhibitors with aspirin as DAPT for the prevention of recurrent stroke, Apply DAPT with P2Y12 inhibitors in appropriate patients following symptom onset to reduce the risk of recurrent stroke, Employ patient-centered communication strategies to facilitate adherence to DAPT with P2Y12 inhibitors in appropriate patients with AIS or TIA to reduce the risk of recurrent stroke.
Go online to PeerView.com/SPE860 to view the activity, download slides and practice aids, and complete the post-test to earn credit. The latest stroke statistics estimate that about 800,000 individuals in the United States experience a stroke each year. Furthermore, about 20% of all strokes are recurrent, and many of these patients previously experienced a minor stroke or transient ischemic attack (TIA). Recurrence is greatest within the first 24 to 48 hours, but the risk remains elevated for months, even years, after the initial event. The American Heart Association (AHA) and American Stroke Association (ASA) recently updated their guidelines for stroke prevention to include expanded and detailed recommendations for the use of dual antiplatelet therapy (DAPT), the combination of aspirin and clopidogrel or ticagrelor, to further reduce the risk of stroke. These guidelines also include specific recommendations for individuals with minor acute ischemic stroke (AIS) or a TIA. In this activity based on a recent satellite symposium in New Orleans, leading experts on stroke management highlight the current guideline recommendations and discuss the latest perspectives on DAPT before transitioning to patient case scenarios where each expert demonstrates how these advances can be translated into clinical practice to improve outcomes and reduce the risk of recurrent stroke, while accounting for bleeding risks, antiplatelet resistance, and patient adherence. Upon completion of this CE activity, participants will be able to: Identify individuals with AIS or TIA who are appropriate candidates for treatment with antiplatelet therapy to reduce the risk of recurrent stroke, Assess the benefits and risks of using P2Y12 inhibitors with aspirin as DAPT for the prevention of recurrent stroke, Apply DAPT with P2Y12 inhibitors in appropriate patients following symptom onset to reduce the risk of recurrent stroke, Employ patient-centered communication strategies to facilitate adherence to DAPT with P2Y12 inhibitors in appropriate patients with AIS or TIA to reduce the risk of recurrent stroke.
Dr. Ebell and Dr. Wilkes discuss the POEM titled ' DAPT with aspirin plus clopidogrel for 30 days is the best option after minor stroke or TIA '
DAPT after ischemic stroke or TIA
A recent meta-analysis about antiplatelet therapy in stroke
The latest updates on DAPT
Dr. Ashley Schenk discusses the MASTER DAPT trial with co-host, Dr. Liz Wang.
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