Cardionerds: A Cardiology Podcast

CardioNerds (Daniel Ambinder), ACHD series co-chairs,  Dr. Josh Saef (ACHD fellow, University of Pennsylvania) Dr. Daniel Clark (ACHD fellow, Vanderbilt University), and ACHD FIT lead Dr. Jon Kochav (Columbia University) join Dr. Eric Krieger (Director of the Seattle Adult Congenital Heart Service and the ACHD Fellowship, University of Washington) to discuss multimodality imaging in congenital heart disease. Audio editing by CardioNerds Academy Intern, Dr. Maryam Barkhordarian. Special introduction to CardioNerds Clinical Trialist Dr. Shiva Patlolla (Baylor University Medical Center). In this episode we discuss the strengths and weaknesses of the imaging modalities most commonly utilized in the diagnosis and surveillance of patients with ACHD.  Specifically, we discuss transthoracic and transesophageal echocardiography, cardiac MRI and cardiac CT. The principles learned are then applied to the evaluation of two patient cases – a patient status post tetralogy of Fallot repair with a transannular patch, and a patient presenting with right ventricular enlargement of undetermined etiology. The CardioNerds Adult Congenital Heart Disease (ACHD) series provides a comprehensive curriculum to dive deep into the labyrinthine world of congenital heart disease with the aim of empowering every CardioNerd to help improve the lives of people living with congenital heart disease. This series is multi-institutional collaborative project made possible by contributions of stellar fellow leads and expert faculty from several programs, led by series co-chairs, Dr. Josh Saef, Dr. Agnes Koczo, and Dr. Dan Clark. The CardioNerds Adult Congenital Heart Disease Series is developed in collaboration with the Adult Congenital Heart Association, The CHiP Network, and Heart University. See more Disclosures: None Pearls • Notes • References • Guest Profiles • Production Team CardioNerds Adult Congenital Heart Disease PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls – Cardiovascular Multimodality Imaging in Congenital Heart Disease Transthoracic echocardiography (TTE) is the first line diagnostic test for the diagnosis and surveillance of congenital heart disease due to widespread availability, near absent contraindications, and ability to perform near comprehensive structural, functional, and hemodynamic assessments in patients for whom imaging windows allow visualization of anatomic areas of interest. Transesophageal echocardiography (TEE) use in ACHD patients is primarily focused on similar indications as in acquired cardiovascular disease patients: the assessment of endocarditis, valvular regurgitation/stenosis severity and mechanism, assessment of interatrial communications in the context of stroke, evaluation for left atrial appendage thrombus, and for intraprocedural guidance. When CT or MRI are unavailable or contraindicated, TEE can also be used when transthoracic imaging windows are poor, or when posterior structures (e.g. sinus venosus, atrial baffle) need to be better evaluated. Cardiac MRI (CMR) with MR angiography imaging is unencumbered by imaging planes or body habitus and can provide comprehensive high resolution structural and functional imaging of most cardiac and extracardiac structures. Additional key advantages over echocardiography are ability to reproducibly quantify chamber volumes, flow through a region of interest (helpful for quantifying regurgitation or shunt fraction), assess for focal fibrosis via late gadolinium enhancement imaging, and assess the right heart. Cardiac CT has superior spatial resolution in a 3D field of view which makes it useful for clarifying anatomic relationships between structures, visualizing small vessels such as coronary arteries or collateral vessels, and assessing patency of larger vessels (e.g branch pulmonary arteries) through metallic stents which may obscure MR imaging. Downsides relative to CMR include requirement of nephrotoxic contrast for imaging of intracardiac/intravascular structures, and while gated images can be obtained throughout the cardiac cycle similarly to CMR, this is particularly costly from an ionizing radiation standpoint. When working up an unknown congenital lesion, it is critical to communicate the differential diagnosis when ordering a test so that the imager can protocol the study accordingly. Not all echocardiograms, CT or MRI scans are the same. Show notes – Cardiovascular Multimodality Imaging in Congenital Heart Disease What are the key strengths and weaknesses of transthoracic echocardiography? STRENGTHS: (1) “Most important ability is availability”: Transthoracic echocardiography is the first line imaging modality in the assessment of patients with congenital heart disease because it is widely available at significantly lower cost wit

CardioNerds (Amit Goyal and Daniel Ambinder), join Dr. Kara Denby (Interventional cardiology fellow, Cleveland Clinic), Dr. Tony Pastor (ACHD fellow, Harvard Medical School), Dr. Katie Berlacher (Cardiology program director, UPMC), and Dr. Stephen Cook (ACHD cardiologist, Indiana University) to discuss empowering the LGBTQIA+ community of cardiovascular patients & professionals and more in this installment of the Narratives in Cardiology Series. This episode features the Indiana ACC Chapter. Episode introduction and audio editing by CardioNerds Academy Intern, Pace Wetstein. This discussion was inspired by this perspective piece on ACC.org titled: Finding Our Voices: Building an LGBTQIA+ Community Within Cardiology. To learn more about diversity and equity among the LGBTQIA+ population, check out this webinar organized by the ACC. The PA-ACC & CardioNerds Narratives in Cardiology is a multimedia educational series jointly developed by the Pennsylvania Chapter ACC, the ACC Fellows in Training Section, and the CardioNerds Platform with the goal to promote diversity, equity, and inclusion in cardiology. In this series, we host inspiring faculty and fellows from various ACC chapters to discuss their areas of expertise and their individual narratives. Join us for these captivating conversations as we celebrate our differences and share our joy for practicing cardiovascular medicine. We thank our project mentors Dr. Katie Berlacher and Dr. Nosheen Reza. Video Version • Notes • Production Team Claim free CME just for enjoying this episode! There are no relevant disclosures for this episode. The PA-ACC & CardioNerds Narratives in Cardiology PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Tweetorial – Empowering the LGBTQIA+ Community of Cardiovascular Patients & Professionals https://twitter.com/Gurleen_Kaur96/status/1526334939830034432?s=20&t=wMk75ORn1_KJtMTOY1IAdw Video version – Empowering the LGBTQIA+ Community of Cardiovascular Patients & Professionals Coming soon Production Team Dr. Gurleen Kaur Amit Goyal, MD Daniel Ambinder, MD

CardioNerds (Amit Goyal and Daniel Ambinder) join Dr. Sonu Abraham (Cardiology fellow, Lahey Hospital and Medical Center), Dr. Amitoj Singh (Internal Medicine Resident, Lahey Hospital and Medical Center), Dr. Ahmed Ghoneem (Internal Medicine Resident, Lahey Hospital and Medical Center, CardioNerds Academy Chief) and Dr. Aanika Balaji (Internal Medicine Resident, Johns Hopkins) for a scrumptious meal on the Boston Harbor as they discuss a case of a young woman with metastatic melanoma on immune checkpoint inhibitors presenting with dyspnea. The presentation, risk factors, work up and management of patients with immune checkpoint inhibitor induced myocarditis are described. The E-CPR segment is provided by Dr. Sarju Ganatra, the founding director of the cardio-oncology program at Lahey Clinic. CardioNerds Clinical Trialist Dr. Carrie Mahurin (University of Vermont Medical Center) is introduced at the beginning of the episode. A 41-year-old woman presented with mild dyspnea on exertion and non-productive cough. She had a history of Hashimoto thyroiditis, nodular thyroid s/p resection on levothyroxine, and metastatic melanoma on immune checkpoint inhibitor therapy with ipilimumab and nivolumab. She also had a history of obesity and underwent gastric bypass surgery several years prior. Though she lost weight after the surgery, she regained a significant amount and was 244 lbs with a BMI of 42. Her exam findings were remarkable for tachycardia, bilateral pulmonary rales, elevated JVP, and symmetric pedal edema. Investigations revealed a mild troponin elevation, non-specific EKG changes, and TTE with severely reduced left ventricular function (EF 15%) and a low GLS. Cardiac MRI showed patchy delayed myocardial enhancement in a non-ischemic distribution with marked global hypokinesis and EF of 11%. Endomyocardial biopsy confirmed the diagnosis of immune checkpoint inhibitor (ICI) associated myocarditis. The ICI therapy was discontinued and she was treated with high dose intravenous corticosteroids followed by a prolonged oral steroid taper with clinical improvement and complete recovery of left ventricular function. 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 – immune checkpoint inhibitor myocarditis Episode Schematics & Teaching CardioNerds Myocarditis, updated 1.20.21 Pearls – immune checkpoint inhibitor myocarditis ICI-associated myocarditis has a high mortality rate necessitating a high degree of clinical suspicion. When in doubt, check it out! The initial 4 diagnostic pillars include EKG, troponin, BNP and TTE. Cardiac MRI and endomyocardial biopsy help to confirm the diagnosis. Left ventricular function is normal in 50% of these patients with ICI-associated myocarditis, so the ejection fraction is not a sensitive test for ruling this out. Endomyocardial biopsy should be considered in patients with a high clinical suspicion but negative or ambiguous non-invasive imaging. Early initiation of corticosteroids within 24 hours of presentation is associated with better outcomes. ICIs should be discontinued indefinitely in those with Grade 3 or 4 disease. Notes – immune checkpoint inhibitor myocarditis 1. Immune checkpoint inhibitors – What are they and why should we as cardiologists know about them? Immune checkpoint inhibitors (ICI) boost the host immune response against tumor cells by inhibiting the intrinsic brakes of the immune response. There are currently 7 FDA approved drugs in this group: one CTLA-4-blocking antibody called ipilimumab; three PD-1-blocking antibodies [nivolumab, pembrolizumab, and cemiplimab]; and three PD-L1-blocking antibodies [atezolizumab, avelumab, and durvalumab]. Like a car, T-cells have an ignition switch, gas pedals, and brakes. T-cells become activated when receptors on the surface of the T-cell bind to an antigen on the surface of the invading cells like cancer cells. Think of the T-cell receptor as the ignition switch and the antigen as the key. Antigen presenting cells patrol the body and pick up evidence of foreign antigens like cancer which they present to T-cells in the lymph nodes via the T-cell receptor. Like gas pedals, there are co-stimulatory signals like CD 28 which interact with proteins on the antigen presenting cells. With these “gas pedal” stimuli, T-cells get activated, multiply, and hunt for the cancer and finally kill the cancer cells. The T-cells also have “breaks” or “checkpoints” to down-regulate the immune response. The Cytotoxic T-lymphocyte antigen 4, also called the CTLA-4, acts to slow down the activation of T-cells. Further down the line, there is another checkpoint called the Programmed cell death 1 or PD-1. PD-1 is a molecule on the surface of T-cells which acts as another set of brakes. W

The CardioNerds Academy Class of 2021 graduation ceremony kicked off the inaugural Sanjay V Desai Lecture: Growth Mindset, Power of Yet, & Pursuit of Mastery. Join us as Dr. Tommy Das (CardioNerds Academy Program Director), and Dr. Saman Nematollahi (CardioNerds Academy Director of Research) discuss Growth Mindset with Dr. Keri Shafer and Dr. David Hirsh. Terrific acting by Dr. Patrick Zakka, Dr. Teodora Donisan, Dr. Ahmed Ghoneem, and Dr. Jessie Holtzman. Dr. Sanjay V Desai serves as the Chief Academic Officer, The American Medical Association and is the former Program Director of the Osler Medical Residency at The Johns Hopkins Hospital. Dr. Keri Shafer is an adult congenital heart disease specialist at Boston Children’s Hospital, and an assistant professor of pediatrics within Harvard Medical School. She completed internal medicine residency at Beth Israel Deaconess Medical Center, before completing cardiology fellowship at UT Southwestern and Adult Congenital and Pulmonary Hypertension subspecialty training at Boston Children’s and BWH.    Dr. David Hirsh is an associate professor of Medicine within Harvard Medical School, as well as the director of the HMS Academy fellowship in medical education and the associate dean of undergraduate medical education. Relevant disclosures: None CardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron!

CardioNerds, Amit Goyal, Dr. Tommy Das (Program Director of the CardioNerds Academy and Cardiology fellow at Cleveland Clinic), Dr. Rick Ferraro (Director of CardioNerds Journal Club and Cardiology fellow at the Johns Hopkins Hospital), Dr. Patrick Zakka (CardioNerds Academy Chief fellow of House Jones and Cardiology fellow at UCLA) discuss omega-3 fatty acids & the battle of the oils with Dr. Pam Taub, Director of Step Family Foundation Cardiovascular Rehabilitation and Wellness Center and Professor of Medicine at UC San Diego. Learn all about the different types of omega-3 fatty acids and the differences between prescription omega-3 fatty acids and dietary supplement fish oils. Audio editing by CardioNerds Academy Intern, Shivani Reddy. This episode is part of the CardioNerds Lipids Series which is a comprehensive series lead by co-chairs Dr. Rick Ferraro and Dr. Tommy Das and is developed in collaboration with the American Society For Preventive Cardiology (ASPC). Relevant disclosures: None Pearls • Notes • References • Guest Profiles • Production Team CardioNerds Cardiovascular Prevention PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls – Omega-3 Fatty Acids & The Battle Of The Oils Coming soon! Show notes – Omega-3 Fatty Acids & The Battle Of The Oils Coming soon! References – Omega-3 Fatty Acids & The Battle Of The Oils Arnett DK, Blumenthal RS, Albert MA, et al. 2019 ACC/AHA Guideline on the Primary Prevention of Cardiovascular Disease: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines [published correction appears in Circulation. 2019 Sep 10;140(11):e649-e650] [published correction appears in Circulation. 2020 Jan 28;141(4):e60] [published correction appears in Circulation. 2020 Apr 21;141(16):e774]. Grundy SM, Stone NJ, Bailey AL, et al. 2018 AHA/ACC/AACVPR/AAPA/ABC/ACPM/ADA/AGS/APhA/ASPC/NLA/PCNA Guideline on the Management of Blood Cholesterol: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines [published correction appears in Circulation. 2019 Jun 18;139(25):e1182-e1186]. Circulation. 2019;139(25):e1082-e1143. Authors/Task Force Members; ESC Committee for Practice Guidelines (CPG); ESC National Cardiac Societies. 2019 ESC/EAS guidelines for the management of dyslipidaemias: Lipid modification to reduce cardiovascular risk [published correction appears in Atherosclerosis. 2020 Jan;292:160-162] [published correction appears in Atherosclerosis. 2020 Feb;294:80-82]. Atherosclerosis. 2019;290:140-205. Bhatt D, Steg P, Miller M et al., 2019. Cardiovascular Risk Reduction with Icosapent Ethyl for Hypertriglyceridemia. The New England journal of medicine, 380(1), pp.11–22. Budoff M, Bhatt D, Kinninger A et al. Effect of icosapent ethyl on progression of coronary atherosclerosis in patients with elevated triglycerides on statin therapy: final results of the EVAPORATE trial. Eur Heart J. 2020;41(40):3925-3932. Nicholls S, Lincoff A, Garcia M et al. Effect of High-Dose Omega-3 Fatty Acids vs Corn Oil on Major Adverse Cardiovascular Events in Patients at High Cardiovascular Risk: The STRENGTH Randomized Clinical Trial. JAMA. 2020;324(22):2268-2280. Guest Profiles Dr. Pam Taub Dr. Pam Taub, Professor of Medicine, is the founding director of the StepFamily Foundation Cardiac Rehabilitation and Wellness Center at the University of California, San Diego. Dr. Taub is a leader in preventive cardiology and has authored over one hundred publications, abstracts and book chapters. Dr. Taub is a leader in multiple professional societies, including board membership for the American Society of Preventive Cardiology. Dr. Patrick Zakka Dr. Patrick Zakka completed his medical school at the American University of Beirut in Lebanon, followed by internal medicine residency and a chief resident year at Emory University. He is currently a first year cardiology fellow at UCLA and graduated as a CardioNerds fellow in House Taussig and is now the Chief Fellow of House Jones. CardioNerds Lipids Production Team Tommy Das, MD Dr. Rick Ferraro Amit Goyal, MD Daniel Ambinder, MD

In this episode we discuss cardiogenic shock due to valvular heart disease. Join Dr. Pranoti Hiremath (Interventional cardiology fellow, Johns Hopkins), Dr. Karan Desai (CN Critical Care Series Co-Chair, Cardiology fellow, University of Maryland), Dr. Yoav Karpenshif (CN Critical Care Series Co-Chair, Chief cardiology fellow, University of Pennsylvania), and Amit Goyal (CardioNerds Co-Founder) as they interview Dr. Paul Cremer (Associate Director of the Cardiac Intensive Care Unit and Associate Director of the Cardiovascular Fellowship at the Cleveland Clinic) in this broad overview of valvular shock. We discuss the nuances in diagnosis, differing presentations and how physical exam, multi-modality imaging, and invasive hemodynamics can inform management. Audio editing by Dr. Gurleen Kaur (Director of the CardioNerds Internship and CardioNerds Academy Fellow). The CardioNerds Cardiac Critical Care Series is a multi-institutional collaboration made possible by contributions of stellar fellow leads and expert faculty from several programs, led by series co-chairs, Dr. Mark Belkin, Dr. Eunice Dugan, Dr. Karan Desai, and Dr. Yoav Karpenshif. Pearls • Notes • References • Guest Profiles • Production Team CardioNerds Cardiac Critical Care PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls and Quotes – Cardiogenic Shock and Valvular Heart Disease Shock due to valve disease is the result of a structural abnormality that may be temporized with medical therapy and circulatory support devices. However, it is ultimately best treated with a structural solution in the form of either percutaneous valvular therapies or cardiac surgery. When treating a patient with cardiogenic shock with normal or hyperdynamic ventricular function, we should keep a high index of suspicion for valvular disease. The cardiac output may be reduced due to a stenotic lesion “blocking” forward flow or regurgitant lesion causing backward flow. Acute mitral and aortic regurgitation will typically not manifest as a loud murmur on physical exam. The combination of hypotension and rapid flow of regurgitant blood on an “unprepared” cardiac chamber results in rapid equalization of chamber pressures, shortening the intensity and duration of the murmur. On transthoracic echocardiogram, for instance with acute MR, color Doppler may not show a large turbulent jet, and thus the MR may be underestimated or not appreciated at all. Echocardiography is critical to understand the etiology and severity of valvular shock, and invasive hemodynamics are often needed to guide medical and mechanical interventions. In multi-valve disease with severe aortic stenosis and functional mitral regurgitation, we typically treat the aortic stenosis first, since the mitral regurgitation may improve from the reduction in afterload associated with treating aortic stenosis. Show notes – Cardiogenic Shock and Valvular Heart Disease 1. Shock due to valve disease arises due to a structural problem that may be temporized with medical therapy and circulatory support devices, but is ultimately best treated with a structural solution in the form of either percutaneous valvular therapies or cardiac surgery. Stabilizing therapies for acute mitral regurgitation include afterload reduction with vasodilators, diuresis as needed to reduce pulmonary edema, and mechanical circulatory support including intra-aortic balloon pumps. Therapies for acute aortic regurgitation are typically more limited and include vasopressors such as epinephrine.  Bradycardia should be avoided with agents such as dobutamine or temporary pacing to reduce time in diastole. Temporary mechanical circulatory support options are limited in the setting of acute AR, though case reports of techniques such as LAVA ECMO (left atrial venoarterial extracorpeal membrane oxygenation) as a bridge to definitive therapy have been reported. There are several factors to consider in patients with aortic stenosis and cardiogenic shock. In some patients with aortic stenosis and LV dysfunction, the shock is a result of LV pressure overload potentially leading to congestion, the high afterload introduced on the LV by the stenotic aortic valve, and increased systemic vascular resistance (compensatory for the failing LV). In these patients, acute vasodilators (specifically nitroprusside) can relieve the additive afterload on the LV imposed by increased SVR as a bridge to definitive therapy. In other patients with severe AS, the LV faces high afterload at the level of the aortic valve but the SVR is relatively low (as well as the pressures in the aortic root which can reduce coronary perfusion), and thus these patients may require a pure alpha agonist (e.g., phenylephrine) to reduce the afterload mismatch and reduce myocardial ischemia. Furthermore, when patients have high L

The following question refers to Section 4.8 of the 2021 ESC CV Prevention Guidelines. The question is asked by CardioNerds Academy Intern student Dr. Christian Faaborg-Andersen, answered first by UCSF resident Dr. Jessie Holtzman, and then by expert faculty Dr. Melissa Tracy. Dr. Tracy is a preventive cardiologist, echocardiographer, Director of Cardiac Rehabilitation, and solid organ transplant cardiologist at Rush University. 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. Question #6 A 62-year-old man with a history of non-obstructive coronary artery disease, heart failure with reduced ejection fraction (EF 30-35%), stage III chronic kidney disease, and type II diabetes mellitus presents to your clinic to establish care. His only medications are aspirin 81 mg daily and metformin 1000 mg BID, which he has taken since being diagnosed with diabetes mellitus 5 years ago. His hemoglobin A1c is 6.8%. What changes would you recommend to his medications at this time? A. Start glipizideB. Start saxagliptinC. Start empagliflozinD. No changes Answer #6 The correct answer is C – start empagliflozin. The Trials involving SGLT-2 inhibitors and GLP-1R agonists have shown cardiovascular benefits independent of glycemic control and metformin use. The ADA recommends metformin as a first-line therapy for all patients with type 2 DM. The ESC also recommends metformin as first-line therapy but only in patients without ASCVD, CKD, or HF (Class I, LOE B). If a patient has ASCVD, metformin can be considered (Class IIa, LOE B). Rather, for those patients with type 2 DM and ASCVD, the ESC recommends the use of GLP-1R agonist or SGLT-2 inhibitors with proven outcome benefits to reduce CV and/or cardiorenal outcomes (Class I, LOE A). Additionally, for those with type 2 DM and either CKD or HFrEF, the ESC recommends the use of SGLT-2 inhibitor to improve outcomes (Class I, LOE A). In contrast to the ADA, the view of the ESC is that metformin should be considered but is not mandatory first-line treatment in patients with diabetes and ASCVD or evidence of target organ damage. The initiation of metformin in such patients should not forego or delay the initiation of evidence-based SGLT2 inhibitors or GLP-1RAs. Therefore, the next best step for our patient is to start an SGLT-2 inhibitor given his history of CAD, HF, and CKD. While this patient’s A1c goal is within the range recommended for patients with Type 2 DM and ASCVD (<7%), given his CAD, HF, and CKD an SGLT-2 inhibitor should still be added. Saxagliptin is a DPP-4 inhibitor, a class of drugs that showed no effect of MACE but increased risk of HF hospitalization in patients with DM and existing. Lifestyle management is a top priority for ASCVD prevention and management of DM. Lifestyle intervention lowers future microvascular and macrovascular risks as well as mortality in the longer term. Intensive lifestyle changes with low-calorie diets and mean weight losses in the region of 10 kg leads to remission of type 2 DM in around 46% of cases at 1 year and 36% by 2 years. Smoking cessation, a diet low in saturated fat and high in fiber, aerobic physical activity, strength training, and reduction in energy intake for weight optimization are all recommended for patient with diabetes mellitus (Class I). Main Takeaway In patients with Type 2 DM and ASCVD or end organ dysfunction, SGLT-2 inhibitors or GLP-1R agonists should be recommended regardless of background therapy or glycemic control. For patients with type 2 diabetes mellitus and CKD or HFrEF, SGLT-2 inhibitor is recommended. Guideline Location Section 4.8.1, Pages 3289-90. CardioNerds Decipher the Guidelines – 2021 ESC Prevention SeriesCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron!

The following question refers to Section 4.10 of the 2021 ESC CV Prevention Guidelines. The question is asked by CardioNerds Academy Intern student Dr. Christian Faaborg-Andersen, answered first by UCSD fellow Dr. Patrick Azcarate, and then by expert faculty Dr. Laurence Sperling. Dr. Laurence Sperling is the Katz Professor in Preventive Cardiology at the Emory University School of Medicine and Founder of Preventive Cardiology at the Emory Clinic. Dr. Sperling was a member of the writing group for the 2018 Cholesterol Guidelines, serves as Co-Chair for the ACC’s Cardiometabolic and Diabetes working group, and is Co-Chair of the WHF Roadmap for Cardiovascular Prevention in Diabetes. 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. Question #5 The European Society of Cardiology Prevention guidelines currently recommend that low-dose colchicine (0.5mg/day) may be considered for the primary prevention of cardiovascular disease. A. TrueB. False Answer #5 The correct answer is False. The correct answer is False. The European Society of Cardiology recommends that low-dose colchicine may be considered as an adjunctive therapy for secondary rather than primary prevention of cardiovascular disease in individuals whose risk factors are otherwise insufficiently controlled (Class IIb, LOE A). A broad evidence base currently supports that inflammation has pro-atherosclerotic effects and that reducing inflammation may reduce atherogenesis in high-risk patients. The initial LoDoCo trial in 2013 first demonstrated a 10.7% absolute risk reduction in acute coronary syndrome, out of hospital cardiac arrest, and non-cardioembolic ischemic stroke with daily low-dose colchicine; however, results were clouded by small sample size. Subsequently, the CANTOS trial in 2017 demonstrated a 15% relative reduction in non-fatal myocardial infarction, non-fatal stroke, and cardiovascular death with Canakinumab, an anti-inflammatory monoclonal antibody inhibitor of interleukin-1. More recently, the COLCOT trial in 2019 studying patients with recent AMI and LoDoCo2 trial in 2021 studying patients with stable chronic CAD both demonstrated reductions in myocardial infarction, cardiovascular mortality, CVA, and ischemia-driven revascularization with colchicine 0.5mg/day. In the LoDoCo2 trial, stable CAD was defined either angiographically, by coronary CT, CAC >400, or history of CABG >10 years prior with evidence of failed grafts or angioplasty since that time. In high-risk individuals with stable ischemic heart disease, the most recent evidence suggests that once daily low dose colchicine may reduce myocardial infarction and other ischemic events. Future studies may assess the biochemical markers including the trend of lipids and inflammatory markers to identify subpopulations that may benefit most from this therapy. Main Takeaway: Based upon the 2021 ESC Prevention Guidelines, clinicians may consider initiating low-dose colchicine (0.5mg/day) for secondary prevention of cardiovascular disease, particularly if other risk factors are insufficiently controlled or if recurrent CVD events occur despite optimal therapy. Guideline Location: Section 4.10, page 3291. CardioNerds Decipher the Guidelines – 2021 ESC Prevention SeriesCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron!

The following question refers to Section 4.7 and figure 16 of the 2021 ESC CV Prevention Guidelines. The question is asked by CardioNerds Academy Intern Student Dr. Shivani Reddy, answered first by Fellow at Johns Hopkins Dr. Rick Ferraro, and then by expert faculty Dr. Roger Blumenthal. Dr. Roger Blumenthal is professor of medicine at Johns Hopkins where he is Director of the Ciccarone Center for the Prevention of Cardiovascular Disease. He was instrumental in developing the 2018 ACC/AHA CV Prevention Guidelines. Dr. Blumenthal has also been an incredible mentor to CardioNerds from our earliest days. 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. Question #4 Ms. K.M. is a 40-year-old woman presenting to the outpatient clinic for a routine physical exam required for her employment as an airline stewardess. She states she has been in her usual good health but does experience occasional headaches and lightheadedness while in flight. On exam her BP was noted to be 170/90. The diagnosis of hypertension is confirmed during a subsequent clinic visit. What would be the most appropriate initial therapy recommendation(s) for Ms. K.M.? A. Initiate single drug therapy with a beta-blocker.B. Discuss and initiate lifestyle interventionsC. Initiate two-drug combination therapy with a thiazide-like diuretic, BB, CCB, or an ARB.D. Both B and C Answer #4 The correct answer is D. Both B (lifestyle interventions) and C (initial combination therapy) are appropriate at this time. Lifestyle interventions are indicated for all patients with high-normal BP or hypertension because they can delay the need for drug treatment or complement the BP-lowering effect of drug treatment (Class 1). Moreover, most lifestyle interventions have health benefits beyond their effect on BP. Single-drug therapy will rarely achieve optimal BP control. Therefore, initial antihypertensive therapy with a combination of two drugs, preferably as a single-pill combination, is recommended for the management of HTN (Class 1). The only exceptions would be patients with a baseline BP close to the recommended target, who might achieve that target with a single drug, or very old (>80 years) or frail patients who may better tolerate a gentler reduction of BP. Five major classes of BP-lowering drug therapy have shown benefit in reducing CV events; angiotensin-converting enzyme (ACE) inhibitors, angiotensin receptor blockers (ARBs), beta-blockers, calcium channel blockers (CCBs), and thiazide or thiazide-like diuretics. A combination of an ACE inhibitor or ARB with a CCB or thiazide/thiazide-like diuretic is the preferred initial therapy for most patients with hypertension (Class 1). For those in whom treatment requires escalation to three drugs, a combination of an ACE inhibitor or ARB with a CCB and a thiazide/thiazide-like diuretic should be used (Class 1). Resistant hypertension is defined as BP being uncontrolled despite treatment with optimal or best-tolerated doses of three or more drugs including a diuretic, and confirmed by ABPM or HBPM. Spironolactone is the most effective drug for lowering BP in resistant hypertension when added to existing treatment; however, the risk of hyperkalaemia is increased in patients with CKD. When spironolactone is not tolerated, amiloride, alpha-blockers, beta-blockers, or centrally acting drugs, such as clonidine, have evidence supporting their use. Renal denervation and device-based therapy may be considered for specific cases. Beta-blockers should be used when there is a specific indication (e.g. angina, post myocardial infarction, arrythmia, HFrEF, or as an alternative to an ACE inhibitor or ARB in women of child-bearing potential). Combinations of an ACE inhibitor and an ARB are not recommended because of no added benefit on outcomes and increased risk of harm (Class III). The diagnosis and treatment of hypertension in women is similar to that in men, except for women of child-bearing potential or during pregnancy, because of potential adverse effects of some drugs on the fetus, especially in the first trimester. In addition, the effect of oral contraceptive pills on the risk of developing or worsening hypertension should be considered. Main Takeaway: Combination drug therapies are more effective in lowering BP than monotherapy. BP management in women is similar to men with the exception of child-bearing potential given potential teratogenicity of some agents. Guideline Location: 4.7.5.1-4, Page 3288 Figure 16, pg. 3287 CardioNerds Decipher the Guidelines – 2021 ESC Prevention SeriesCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron!

The following question refers to Section 4.3 of the 2021 ESC CV Prevention Guidelines. The question is asked by CardioNerds Academy Intern Dr. Maryam Barkhordarian, answered first by medicine resident CardioNerds Academy House Chief Dr. Ahmed Ghoneem, and then by expert faculty Dr. Kim Williams. Dr. Williams is Chief of the Division of Cardiology and is Professor of Medicine and Cardiology at Rush University Medical Center. He has served as President of ASNC, Chairman of the Board of the Association of Black Cardiologists (ABC, 2008-2010), and President of the American College of Cardiology (ACC, 2015-2016). 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. Question #3 Mrs. B is a 56-year-old African American woman with a past medical history significant for type 2 diabetes (HbA1C 7.6) and hypercholesterolemia. Her calculated ASCVD risk score today is 12.5% and her BMI is 24kg/m2. She is concerned about her high cholesterol levels despite being on a statin and feels that her diet is “not healthy enough.” She is interested in making dietary changes to help reduce her ASCVD risk. Which of the following recommendations is appropriate? A. Sodium restriction to <3g /day will be of no benefit because she is not hypertensive.B. Isocaloric substitution of saturated fat with polyunsaturated fat is associated with reduction of CHD risk.C. Dietary fiber intake is associated with GI benefits but has no CV risk reduction benefit.D. Supplementing diet with vitamins A, B, C and E helps reduce ASCVD risk. Answer #3 The correct answer is B. Risk of CHD is reduced when dietary saturated fats are replaced with other foods having similar caloric values. The greatest reduction was observed when saturated fats were isocalorically replaced with polyunsaturated fats (↓25%), followed by monounsaturated fats (↓15%) and carbohydrates from whole grains (↓9%). This is a class 1a recommendation in the ESC guidelines and a class IIa recommendation in the 2019 ACC/AHA guidelines. Conversely, increased trans fatty acid intake is associated with increased CHD risk. A regulation of the European Union (EU) Commission has set the upper limit of trans fats to 2 g per 100 g of fat. The ACC/AHA guidelines recommend that the intake of trans fats should be avoided (a class III: harm). Choice A is incorrect because dietary sodium restriction is recommended not only for control of blood pressure, but also for reduction of ASCVD risk. In a meta-analysis, salt reduction of 2.5 g/day resulted in a 20% reduction of ASCVD events (RR 0.80). Reduction of salt intake is a class 1 recommendation in the ESC guidelines compared to a class IIa recommendation in the 2019 ACC/AHA guidelines. Choice C is incorrect because a 10 g/day higher fiber intake was associated with a 16% lower risk of stroke (RR 0.84) and a 6% lower risk of type 2 DM (RR 0.94). A high fiber intake may reduce postprandial glucose responses after carbohydrate-rich meals and also lower triglyceride levels. The Mediterranean diet is rich in fiber (it includes high intakes of fruits, vegetables, pulses and wholegrain products) and is a class I recommendation. Choice D is incorrect because while vitamin supplementation has been associated with reduction in ASCVD risk in observational studies, intervention trials have failed to show any benefit. Main Takeaway: A healthy diet is recommended as a cornerstone of CVD prevention in all individuals, independent of their underlying co-morbidities. Replacing saturated with unsaturated fats, reducing salt intake, and choosing a more plant-based diet that is rich in fiber can lower risk of CVD. Guideline LocationSection 4.3.2, Page 3270 CardioNerds Decipher the Guidelines – 2021 ESC Prevention SeriesCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron!

The following question refers to Section 3.3 of the 2021 ESC CV Prevention Guidelines. The question is asked by CardioNerds Academy Intern student Dr. Adriana Mares, answered first by Brigham & Women’s medicine intern & Director of CardioNerds Internship Dr. Gurleen Kaur, and then by expert faculty Dr. Allison Bailey. Dr. Bailey is an advanced heart failure and transplant cardiologist at Centennial Heart. She is the editor-in-chief of the American College of Cardiology’s Extended Learning (ACCEL) editorial board and was a member of the writing group for the 2018 American Lipid Guidelines. 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. Question #2 Mr. Early M. Eye is a 55-year-old man with a history of GERD who is seeing you in clinic as he is concerned about his family history of early myocardial infarction and would like to discuss if he should be taking a statin for cardiovascular prevention. He has never smoked tobacco. His 10-year CVD risk is estimated to be 8%. Which imaging modality is recommended by the ESC guidelines to reclassify his CVD risk? A. Coronary Artery Calcium (CAC) scoringB. Echocardiography C. Ankle brachial index D. Contrast enhanced computed tomography coronary angiography (CCTA)E. None of the above Answer #2 The correct answer is A. Coronary artery calcium (CAC) scoring can reclassify CVD risk upwards and downwards and should specifically be considered in patients with calculated risk scores that are around decision thresholds. CAC scores which are high-than-expected for age and sex increase estimated future CVD risk. Notably, CAC scoring may also be used to “de-risk” if CAC is absent or lower-than-expected. The 2021 ESC Prevention Guidelines give a Class IIb (LOE B) recommendation to consider CAC scoring to improve risk classification around treatment decision thresholds. However, one limitation of CAC is that it does not provide direct information on total plaque burden or stenosis severity. In addition, there is also a Class IIb (LOE B) recommendation to use plaque detection by carotid ultrasound as an alternative when CAC scoring is unavailable or not feasible. Plaque assessed through carotid ultrasound is defined as presence of wall thickening that is >50% greater than the surrounding vessel wall or a focal region with intima-media thickness measurement >1.5mm that protrudes into the lumen. Similar to the ESC Prevention Guidelines, the 2019 ACC/AHA guidelines on primary prevention of CVD also have a Class IIa recommendation for using CAC score, and explicitly mention its use for adults at intermediate risk (>7.5% to <20% 10-year ASCVD risk) with cut-offs including >100 Agatson units to reclassify risk upwards and CAC of 0 to reclassify risk downwards. However, the guidelines also mention that clinicians should not down-classify risk in patients who have CAC of 0 if they are current smokers, have diabetes, have a family history of ASCVD, or have chronic inflammatory conditions. Furthermore, the 2018 ACC/AHA Cholesterol guidelines have a Class IIa recommendation that if CAC is 0, it is reasonable to withhold statin therapy and reassess risk in 5 to 10 years, as long as higher risk conditions that we just discussed are absent. If CAC is 1-99, it is reasonable to initiate statin therapy for patients ≥ 55 years of age. Choice B is incorrect. Echocardiography is not recommended to improve CV risk prediction due to lack of convincing evidence that it improves CVD risk reclassification. Choice C is incorrect. While the 2013 ESC guidelines mentioned that ABI may be considered as a risk modifier in CVD risk estimation, the newer 2021 guidelines state that ankle brachial index has limited potential in terms of reclassification risk, though an individual patient data meta-analysis showed there may be utility for women at intermediate risk. 12-27% of middle-aged individuals can have an abnormal ankle brachial index, defined as less than 0.9, of which 50-89% may not have typical claudication symptoms. Conversely, the 2019 ACC/AHA guidelines include ABI <0.9 as a risk-enhancing factor. Choice D is incorrect. Coronary computed tomographic angiography (CCTA) has been shown in studies such as SCOT-HEART to have utility in predicting cardiac events in patients with stable chest pain and can identify coronary stenosis. It is not currently recommended by ESC guidelines for prognostic value or risk classification in asymptomatic patients. According to the ESC guidelines, routine vascular testing or imaging other than CAC scoring or carotid ultrasound for plaque determination are not recommended (Class III, LOE B). In terms of this patient’s family history of premature CVD, the ESC guidelines describe that even though family history is significantly associated with CVD in stud

This question refers to Sections 3.2 and 3.3 of the 2021 ESC CV Prevention Guidelines. The question is asked by CardioNerds Academy Intern, student Dr. Hirsh Elhence, answered first by Ohio State University Cardiology Fellow Dr. Alli Bigeh, and then by expert faculty Dr. Eugene Yang. Dr. Yang is professor of medicine of the University of Washington where he is medical director of the Eastside Specialty Center and the co-Director of the Cardiovascular Wellness and Prevention Program. Dr. Yang is former Governor of the ACC Washington Chapter and current chair of the ACC Prevention of CVD Section. 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. Question #1 A 48-year-old Pakistani woman with rheumatoid arthritis comes to your clinic asking how she can reduce her risk of ASCVD. Her mother died of an MI at age 45, her father is healthy at age 79. Her calculated 10-year risk based on SCORE2 is 3%. SBP is 120 mmHg, LDL is 120 mg/dL. What is the next best step? A. Order an echocardiogram B. Schedule a follow-up appointment in 1 year C. Discuss initiating a statin D. Repeat lipid panel in 3-5 years Answer #1 Answer: C. Discuss Initiating a statin The absolute benefit derived from risk factor modification depends on the absolute risk of CVD and the absolute improvements in each risk factor category. Risk factor treatment recommendations are based on categories of CVD risk (“low-to-moderate”, “high”, and “very high”). The cut-off risk levels for these categories are numerically different for various age groups to avoid undertreatment in the young and to avoid overtreatment in the elderly. As age is a major driver of CVD risk, but lifelong risk factor treatment benefit is higher in younger people, the risk thresholds for considering treatment are lower for younger people as per the ESC guidelines. Treatment decisions should be made with shared decision-making valuing patient preference. Option A is INCORRECT- there is a lack of convincing evidence that echocardiography improves CVD risk reclassification, and it is NOT recommended to improve CV risk prediction. (Class III, LOE B) Option B is INCORRECT- simply doing nothing is not appropriate for this patient with elevated CVD risk. Option C is CORRECT- This patient has a seemingly low 10-year CVD risk based on SCORE 2 of 3% and her SBP is controlled; however, given her age she is considered as having high CVD risk, therefore treatment should be considered. Stepwise approach involves targeting LDL <100 (class IIa) so initiating a statin would be appropriate. This patient also carries several risk enhancing modifiers including Pakistani ethnicity, family history of premature CVD, and inflammatory comorbidity. All patients should be counseled on smoking cessation, lifestyle modifications, and target SBP <160 mmHg. Option D is INCORRECT- repeating a lipid panel without risk factor modification will not change treatment recommendations for this patient with elevated CVD risk. Main Takeaway In summary, when a patient <50 years old without established ASCVD has an estimated 10-year risk 2.5 to <7.5% they are considered high CVD risk and risk factor treatment should be considered. Risk modifiers should also be taken into consideration. *Of note- ACC/AHA guidelines recommend the ASCVD risk calculator to estimate 10-year risk and do not restructure CVD risk groups according to age groups. High risk in the ACC/AHA guidelines is considered to be >20%. Guideline Location Table 5 and Figure 5, Page 3251 3.2.3.4, Page 3253 3.2.3, Figure 6 page 3252 3.3, Pages 3258-3259 CardioNerds Decipher the Guidelines – 2021 ESC Prevention SeriesCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron!

CardioNerds (Amit Goyal and Daniel Ambinder) and guest host, Dr. Priya Kothapalli (UT Austin fellow and CardioNerds Ambassador), join SUNY Downstate cardiology fellows, Dr. Eric Kupferstein and Dr. Gautham Upadhya to discuss a case about a patient who had coronary artery bypass grafting that was complicated by a LIMA grafted to the great cardiac vein. Dr. Alan Feit (Professor of Medicine, SUNY Downstate) provides the E-CPR for this episode. Dr. Moritz Wyler von Ballmoos (Director, robotic cardiac and vascular surgery for Houston Methodist Cardiovascular Surgery Associates) provides a special perspective regarding coronary artery bypass grafting as it relates to this case. Episode introduction with CardioNerds Clinical Trialist Dr. Jana Lovell (Johns Hopkins). Left Internal Mammary Artery (LIMA) to Left Anterior Descending (LAD) artery anastomosis is the cornerstone of Coronary Artery Bypass Graft (CABG) surgery. Anastomosis of the LIMA to the Great Cardiac Vein (GCV) is a known but rare complication of the surgery. Currently there are no clear guidelines in regard to further management. We report a case of a LIMA to GCV anastomosis managed with a drug eluting stent (DES) to the mid LAD after ruling out a significant left to right heart shunt. 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 – Coronary Artery Bypass Grafting: An Iatrogenic Left to Right Cardiac Shunt Angiography Episode Schematics & Teaching – Coronary Artery Bypass Grafting: An Iatrogenic Left to Right Cardiac Shunt Pearls – Coronary Artery Bypass Grafting: An Iatrogenic Left to Right Cardiac Shunt Listen to the patient’s story. The patient determines when the angina is no longer stable angina. The placebo effect of our interventions should not be discounted. LIMA to GCV anastomosis creates a left to right cardiac shunt. A Qp:Qs greater than 1.5 signifies a significant shunt. Increasing the pressure in the coronary sinus may actually be beneficial to the patient. LIMA-LAD is remains the most efficacious and long lasting graft but why not other arterial grafts? Notes – Coronary Artery Bypass Grafting: An Iatrogenic Left to Right Cardiac Shunt Iatrogenic anastomosis of the LIMA to the GCV is a rare but noted complication of CABG surgery. Review of the literature has reported under 40 such cases of arteriovenous fistula formation in the coronary system. Detection of the anastomosis generally stems from recurrent angina which can be attributed to unresolved ischemia or coronary steal syndrome but also can be detected with new heart failure (namely right sided heart failure due to left to right shunting). Diagnosis is usually made with coronary angiography, but CT coronary angiography has also been reported. Due to the rarity of this complication, no clear guidelines are in place directing the management leaving it to the discretion of the various Heart Teams. Evaluating for signs of heart failure and/or ischemia, and measuring the Qp:Qs have been the most common signs directing management. Various options are available for closing the fistula and include coil or balloon embolization, vascular plugs, venous ligation or a covered stent. Redoing the surgery is also an option. Spontaneous closure of the fistula has also been reported. Lastly, if redo surgery is not performed then regardless of fistula closure, coronary intervention for the native diseased artery may be pursued to relieve symptoms. References Boden et al; COURAGE Trial Research Group. Optimal medical therapy with or without PCI for stable coronary disease. N Engl J Med. 2007 Apr 12;356(15):1503-16. doi: 10.1056/NEJMoa070829. Epub 2007 Mar 26. PMID: 17387127. Maron et al; ISCHEMIA Research Group. Initial Invasive or Conservative Strategy for Stable Coronary Disease. N Engl J Med. 2020 Apr 9;382(15):1395-1407. doi: 10.1056/NEJMoa1915922. Epub 2020 Mar 30. PMID: 32227755; PMCID: PMC7263833. Klocke et al; ACC/AHA/ASNC guidelines for the clinical use of cardiac radionuclide imaging–executive summary: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (ACC/AHA/ASNC Committee to Revise the 1995 Guidelines for the Clinical Use of Cardiac Radionuclide Imaging). J Am Coll Cardiol. 2003 Oct 1;42(7):1318-33. doi: 10.1016/j.jacc.2003.08.011. PMID: 14522503. Chow et al; Diagnostic accuracy and impact of computed tomographic coronary angiography on utilization of invasive coronary angiography. Circ Cardiovasc Imaging. 2009 Jan;2(1):16-23. doi: 10.1161/CIRCIMAGING.108.792572. PMID: 19808560. Sheiban et al; Iatrogenic left internal mammary artery-coronary vein anastomosis treated with covered stent deployment via retrograde percutaneous coronary sinus approach. Cathe

CardioNerds (Daniel Ambinder), ACHD series co-chair, Dr. Josh Saef (ACHD fellow at University of Pennsylvania), and ACHD FIT lead Dr. Charlie Jain (Mayo Clinic) join ACHD expert Dr. George Lui (Medical Director of The Adult Congenital Heart Program at Stanford and Program Director for the ACGME adult congenital heart disease fellowship at Stanford) to discuss Tetrology of Fallot. Audio editing by CardioNerds Academy Intern, Dr. Leticia Helms. Tetralogy of Fallot (ToF) is the most common cyanotic heart disease and one of the most common congenital heart diseases that we see in adults overall. The anatomy includes a ventricular septal defect (VSD), an overriding aorta, and infundibular hypertrophy with subpulmonic +/- pulmonic valvular +/- supravalvular stenosis, which causes severe RV outflow obstruction and subsequent RV hypertrophy. Patients require surgery during childhood, which includes patching the VSD and relieving RV outflow obstruction. This results in pulmonic regurgitation (usually severe) and patients can live with this for decades. Adults with ToF commonly will require pulmonic valve replacement, potential relief of subvalvular or supravalvular stenoses, and tricuspid valve repair (for functional tricuspid regurgitation caused by RV dilation). These patients are at increased risk of atrial and ventricular arrhythmias and may warrant prophylactic ICDs. The CardioNerds Adult Congenital Heart Disease (ACHD) series provides a comprehensive curriculum to dive deep into the labyrinthine world of congenital heart disease with the aim of empowering every CardioNerd to help improve the lives of people living with congenital heart disease. This series is multi-institutional collaborative project made possible by contributions of stellar fellow leads and expert faculty from several programs, led by series co-chairs, Dr. Josh Saef, Dr. Agnes Koczo, and Dr. Dan Clark. The CardioNerds Adult Congenital Heart Disease Series is developed in collaboration with the Adult Congenital Heart Association, The CHiP Network, and Heart University. See more Disclosures: None Pearls • Notes • References • Guest Profiles • Production Team CardioNerds Adult Congenital Heart Disease PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls – Tetralogy of Fallot Tetralogy of Fallot is the most common cyanotic heart disease and the 4 anatomic features are: VSD, infundibular hypertrophy (with RVOT obstruction), overriding aorta, and RV hypertrophy. The most common lesion you will see in adults with repaired Tetralogy of Fallot is pulmonic regurgitation. Pulmonic regurgitation (PR) can be easy to miss on exam as the murmur is brief and even shorter when the PR is severe. In patients with PR and aortic regurgitation, remember PR is clearest when laying supine, in comparison to aortic regurgitation which is loudest while leaning forward. Patients with ToF may also have coronary anomalies (e.g. LAD off RCA), right-sided aortic arches, and also left-sided heart disease (LV diastolic or systolic dysfunction). Patients with ToF are at risk for atrial and ventricular arrhythmias, and clinicians should consider prophylactic ICD for those with multiple risk factors for sudden death (e.g. QRS >180ms, scar on MRI). In all patients with congenital heart disease, inspection is a key part of the physical exam (e.g. right thoracotomy could clue you into a prior BTT shunt) and in patients with prior BTT shunts and/or prior brachial cut-downs (look in the antecubital fossa for scars), radial arterial access is discouraged. Show notes – Tetralogy of Fallot Lesion TTE TEE Cardiac MRI Cardiac CT Tetralogy of Fallot (1) Routine assessment of RV and LV size and function (2) Routine semiquantitative assessment of pulmonic valve regurgitation (3) Evaluation of PVR/conduit gradients, and RV pressure via tricuspid regurgitation gradient (4) Evaluation of proximal aortic dilation, proximal pulmonary artery branch stenosis (5) Identification of residual intracardiac shunts (1) Intraoperative management (pre- and post- bypass imaging). (2) Comprehensive echocardiographic evaluation when transthoracic windows are limited, and advanced imaging modalities are unavailable.   (1) Quantitative evaluation of PR severity (phase contrast MRI) when echo-derived severity is inconclusive (2) Serial quantitative assessment of RV volume and ejection fraction to evaluate indications for PVR or conduit replacement in patients with pulmonary insufficiency. (3) MR angiography of aorta and pulmonary artery/branches to assess for dilation or stenosis. (4) Quantitative flow assessment of differential pulmonary arterial blood flow in the setting of branch PA stenosis (phase contrast MRI). (5) Late gadolinium enhancement imaging to assess for RV fibrosis in arrhythmia risk stratification.  

CardioNerds Rounds Co-Chairs, Dr. Karan Desai and Dr. Natalie Stokes and CardioNerds Academy Fellow, Dr. Najah Khan, join Dr. Martha Gulati – President-Elect of the American Society for Preventive Cardiology (ASPC) and prior Chief of Cardiology and Professor of Medicine at the University of Arizona – to discuss challenging cases in cardiac prevention. As an author on numerous papers regarding cardiac prevention and women’s health, Dr. Gulati provides many prevention pearls to help guide patient care. Come round with us today by listening to the episodes now and joining future sessions of #CardsRounds! This episode is supported with unrestricted funding from Zoll LifeVest. A special thank you to Mitzy Applegate and Ivan Chevere for their production skills that help make CardioNerds Rounds such an amazing success. All CardioNerds content is planned, produced, and reviewed solely by CardioNerds. Case details are altered to protect patient health information. CardioNerds Rounds is co-chaired by Dr. Karan Desai and Dr. Natalie Stokes.  Speaker disclosures: None Cases discussed and Show Notes • References • Production Team CardioNerds Rounds PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Show notes – CardioNerds Rounds: Challenging Cases of Cardiovascular Prevention with Dr. Martha Gulati Case #1 Synopsis: A 55-year-old South Asian woman presents to prevention clinic for an evaluation of an elevated LDL-C. Her prior history includes hyperlipidemia, hypertension, obesity, and pre-eclampsia. She was told she had “high cholesterol” a few years prior and would need medication. She started exercising regularly and cut out sweets from her diet. Before clinic, labs showed: Total Cholesterol (mg/dL) of 320, HDL 45, Triglycerides 175, and (directly measured) LCL-C 180. Her Lipoprotein(a) is 90 mg/dL (ULN being ~ 30 mg/dL). Her HbA1C is 5.2% and her 10-year ASCVD Risk (by the Pooled Cohorts Equation) is 5.4%. Her recent CAC score was 110. She prefers not to be on medication and seeks a second opinion. Takeaways from Case #1 As Dr. Gulati notes, in the 2019 ACC/AHA Guideline on the Primary Prevention of Cardiovascular Disease, South Asian ethnicity is considered a “risk enhancing factor.” The pooled cohort equations (PCE) may underestimate risk in South Asians. Furthermore, risk varies within different South Asian populations, with the risk for cardiovascular events seemingly higher in those individuals of Bangladeshi versus Pakistani or Indian origin. There are multiple hypotheses for why this may be the case including cultural aspects, such as diet, physical activity, and tobacco use. A better understanding of these factors could inform targeted preventive measures. In the same 2019 ACC/AHA Guideline on the Primary Prevention of Cardiovascular Disease mentioned above, history of an adverse pregnancy outcome (APO) increases later ASCVD risk (e.g., preeclampsia) and is also included as a “risk-enhancing factor.” Studies have shown that preeclampsia is an independent risk factor for developing early onset coronary artery calcification. Recent data has shown that the risk for developing preeclampsia is not the same across race and ethnicity, with Black women more likely to develop preeclampsia. Black women also had the highest rates of peripartum cardiomyopathy, heart failure, and acute renal failure. After adjustment for socioeconomic factors and co-morbidities, preeclampsia was associated with increased risk of CVD events in all women, the risk was highest among Asian and Pacific Islander women. Listen to Episode #174. Black Maternal Health with Dr. Rachel Bond to learn more about race-based disparities in cardio-obstetric care and outcomes. Our patient thus has multiple risk-enhancing factors to help in shared decision making and personalize her decision for statin use. Another risk-enhancing factor for her is an elevated Lp(a), which is considered elevated when ≥ 50 mg/dL or ≥ 125 nmol/L. One other aspect that Dr. Gulati briefly covered was how CAC score may inform Aspirin use for primary prevention. There continues to be debate over when to prescribe aspirin when there is demonstrable calcium on imaging. In the MESA study, for individuals with CAC ≥ 100, the NNT (for 5 years to prevent an ASCVD event) was a 140 and NNH was 518. Case #2 Synopsis: A 58-year-old woman presents to establish care at a general cardiology clinic for shortness of breath. Her history includes hypertension, cutaneous lupus, and ongoing tobacco use. A year ago, she started having nausea, more common with stress or on exertion. She saw her PCP who obtained an EKG and GI evaluation. Endoscopy was unrevealing and EKG showed non-specific ST-T changes inferiorly. She was treated for GERD and then 6 months prior she developed dyspnea on exertion while exercising on her stationary bike

CardioNerds (Amit Goyal), Dr. Natalie Stokes (Cardiology Fellow at UPMC and Co-Chair of the Cardionerds Cardio-Ob series), and episode lead Dr. Priya Freaney (Northwestern University cardiology fellow) discuss “The Fourth Trimester” with Dr. Malamo Countouris and Dr. Alisse Hauspurg, from the University of Pittsburgh Departments of Cardiology and Obstetrics and Gynecology, respectively. We discuss the cardiovascular considerations after adverse pregnancy outcomes in the postpartum and long-term follow-up periods. The discussion is focused mainly on hypertensive disorders of pregnancy (HDP), guided by a series of clinical vignettes. We cover a wide range of topics from cardiovascular complications and management considerations in the immediate postpartum period after a HDP, postpartum outpatient follow-up, long term cardiovascular morbidity related to HDP and related preventive strategies, contraceptive considerations for the cardiologist, and interdisciplinary care management pearls for cardiologists working in a cardio-obstetrics team. Notes • References • Guest Profiles • Production Team CardioNerds Cardio-Obstetrics Series PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls – The Fourth Trimester Blood pressures >160/110 should be treated like a true emergency during pregnancy and the postpartum period, as the cerebrovascular circulation is more sensitive to hypertension, due to hormonal changes related to pregnancy. Women with pre-eclampsia are at higher risk for peripartum cardiomyopathy. Have a low threshold to do a clinical heart failure evaluation (i.e., natriuretic peptides, echocardiogram), and administer diuretics as appropriate to improve volume status and blood pressure. Women with HDP should have their blood pressures monitored closely after discharge, ideally with a home BP monitoring program, as they can have exacerbations of their HTN for up to 2 weeks postpartum. The American Rescue Plan Act of 2021 included a landmark policy to extend postpartum Medicaid coverage up to a year postpartum (from 60 days). Remember to take a reproductive history for every woman you see in cardiology clinic! This can be done in one minute. At a minimum, include obstetric history [number of pregnancies, outcome of each pregnancy, gestational age and weight at delivery, pregnancy complications (HDP, GDM, etc), and delivery method] and menopausal history (age at menarche, age at menopause). The Pooled Cohort Equations may underestimate ASCVD risk for a woman who has had pregnancy complications or premature menopause – consider obtaining a CAC score to aid in risk-stratification in middle-aged women who may have underestimated risk. Low dose aspirin during pregnancy in women who have risk factors for pre-eclampsia reduces the risk of development of HDP by 15-20%. Quotables – The Fourth Trimester “Some of our traditional approaches to caring for women in the postpartum period just aren’t realistic…we need to think about how we can improve care from a policy standpoint to ensure women have access to care and think about how we deliver care.” – Dr. Alisse Hauspurg “Silos are never good. Cardio-obstetrics is a space where you really want to have open communications, be truly collaborative – taking into consideration the expertise of multiple disciplines…because it’s really hard to do it alone.” – Dr. Malamo Countouris Show notes – The Fourth Trimester For more on hypertensive disorders of pregnancy enjoy: Episode #128: Cardio-Obstetrics: Hypertensive Disorders of Pregnancy with Dr. Jennifer Lewey Episode #66: Case Report: Severe Pre-eclampsia & Cardio-Obstetrics – UPMC Hypertensive Disorders of Pregnancy 1.     What are some of the immediate postpartum cardiovascular risks and complications following a hypertensive disorder of pregnancy (HDP) and how do you manage these? Persistent hypertension: there can be a spike in BP in the days following delivery, and clinicians should remember that preeclampsia may develop de novo intra- or early postpartum. BPs >160/110 are considered severe HTN and should be treated urgently with an aggressive rapid-acting anti-HTN regimen to prevent stroke. BPs should be monitored at least every 4 to 6 hours for at least 3 days postpartum.1 A return visit for BP monitoring should be arranged at 1 week following discharge; alternatively, a home BP monitoring program may be considered Pulmonary edema: Women with preeclampsia should be delivered if they develop pulmonary edema. This is more likely to occur in women who have more severe preeclampsia features. Clinical practice guidelines suggest limiting intrapartum fluid intake/replacement to 60-80mL/h to avoid risks of pulmonary edema, with a goal euvolemic fluid balance.1 Peripartum cardiomyopathy: Preeclampsia, gestational hypertension, and chron

CardioNerds (Amit Goyal & Karan Desai)  join Dr. Matthew Delfiner (Cardiology fellow, Temple University Hospital) and Dr. Katie Vanchiere (Internal medicine resident, Temple University Hospital) in the beautiful Fairmount Park in Philadelphia. They discuss a case of a 53-year-old man with an LVAD who presents with progressive dyspnea since LVAD implant due to right-to-left shunting due to a PFO. Dr. Val Rakita (Assistant professor of medicine and advanced heart failure and transplant specialist at Temple University Hospital) provides the E-CPR for this episode. Episode introduction by CardioNerds Clinical Trialist Dr. Anthony Peters (Duke Heart Center). This case has been published by Circulation: Heart failure. See Invasive Hemodynamic Study Unmasks Intracardiac Shunt With Ventricular Assist Device. Claim free CME just for enjoying this episode!  Disclosures: NoneJump to: Pearls – Notes – 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 Summary – Dyspnea with an LVAD: A Tale of Hypoxia and Hemodynamics A 53-year-old man with an LVAD placed 3 months prior presents with progressive dyspnea since LVAD implant, though it has acutely worsened over the past 2 weeks. Two weeks ago, he had a hemodynamic and echocardiographic ramp study, where the LVAD speed was increased. By increasing the speed, his LV was more adequately decongested, and flow improved. In the Emergency Department, he was hypoxic on room air, and remained so with escalation ultimately with intubation. Even then he remained severely hypoxic requiring cannulation to veno-venous ECMO. Chest imaging was normal, and LVAD parameters were normal without any alarms. An astute clinician noticed that when the patient became hypertensive, his oxygen saturation improved. A subsequent echocardiogram revealed a patent foramen ovale, with right to left shunting. The patient then went to the cath lab, where simultaneous right atrial and left atrial pressures and oxygen pressures were measured, along with trans-esophageal echocardiography, while adjusting LVAD speed. It became evident that right-to-left shunting occurred only when there was high LVAD speed and low peripheral blood pressure. Essentially, faster LVAD speeds (sucking blood from the LV) and low systemic blood pressure (reducing LV afterload) increased right to left shunting by decreasing the left atrial pressure relative to the right atrial pressure. The PFO was closed at that time, drastically improving oxygenation. He was decannulated and extubated the following day. Invasive Hemodynamic Study Unmasks Intracardiac Shunt With Ventricular Assist Device | Circulation: Heart Failure (ahajournals.org) Episode Teaching -Dyspnea with an LVAD: A Tale of Hypoxia and Hemodynamics Pearls PFOs are present in up to 25% of individuals, including those with LVADs. LV unloading, and therefore LA decompression, depends on both LVAD speed and systemic vascular resistance. Blood pressure dependent hypoxia may be suggestive of a right-to-left intracardiac shunt. Hypoxia refractory to mechanical ventilation should raise suspicion for intracardiac shunt. Patients with LVADs can suffer from the same diseases that anyone can. Notes – Dyspnea with an LVAD: A Tale of Hypoxia and Hemodynamics 1. What factors influence LVAD flow? Factors that influence LVAD flow include pump speed, blood pressure, volume status, RV function, cardiac rhythm, and some other variables. The faster the pump is spinning, the more flow you should provide (to an extent). However, if your LV is underfilled, either from systemic hypovolemia or an RV not providing the needed LV preload, then you have no blood to flow! If you have high systemic vascular resistance, then you will have less forward flow, just as a native heart would.  We must always think about the interaction between a patient and the LVAD, not just the machine settings. 2. What can cause dyspnea and hypoxia in LVAD patients? The same things that cause dyspnea in any other patient! But also… inadequate unloading of the LV due to the above factors in addition to possible suction events. Aortic regurgitation can cause an endless loop of flow from: LV > LVAD > aorta > AV > LV. Pump malfunction must always be considered, including inflow/outflow obstruction and pump thrombosis. Anemia may also contribute, as patients with LVAD are prone to both bleeding and hemolysis. 3. What are the ideal LVAD settings? There are no standard settings for LVADs, especially because there are different manufacturers. But most importantly, every patient is different, and therefore the patient-LVAD interaction is different. Overall, the ideal LVAD speed would decongest the heart while preserving RV function, maintaining the interventricular septum

CardioNerds, Daniel Ambinder and CardioNerds Academy Program Director, Dr. Tommy Das (Cardiology fellow, Cleveland Clinic), Dr. Jacqueline Latina (Structural heart fellow, Johns Hopkins) discuss aortic stenosis and the story of TAVR from both the historical perspective and in terms of future directions with Dr. Jon Resar, Professor of Medicine and Director of the Adult Catheterization Laboratory and Interventional Cardiology at the Johns Hopkins Hospital. This episode is brought to you for Heart Valve Disease Awareness Day. Audio editing by CardioNerds Academy Intern, Shivani Reddy. As many as 11 million Americans have heart valve disease (HVD)—a potentially disabling and deadly disease—yet 3 out of 4 Americans know little to nothing about heart valve disease. Learn more about valve disease. Pearls • Notes • References • Guest Profiles • Production Team CardioNerds Aortic Stenosis SeriesCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls and Quotes – Aortic Stenosis and the Story of TAVR In the previous century, patients with severe aortic stenosis who were treated “medically” had 50% mortality over 2 years after developing symptoms. Balloon aortic valvuloplasty was initially touted as extremely “efficacious” for aortic stenosis but follow-up studies showed that the improvement in symptoms were not durable, and long-term prognosis was dismal. The PARTNER Trial started enrolling in 2007 in extreme risk patients – patients who were not surgical candidates. In 2010, the PARTNER trial was published and TAVR blew away the “standard of care” in inoperable patients at the time, cutting outcomes in half (composite of death and repeat hospitalization). The PARTNER trial studied balloon expandable intra-annular valve implantation. The CoreValve trial studied self-expanding supra-annular valve implantation and was published in 2014. The “Heart Team” approach entails collaborative decision making between cardiologists and cardiac surgeons to personalize management for patients. Both intra-annular and supra-annular valves show non-inferior outcomes to surgery in intermediate and low risk patients. Revascularization prior to TAVR is an evolving arena; the trend has been interventionalists performing fewer PCIs prior to TAVR given the benefit is not clear if angina is not a prominent symptom. Show notes – Aortic Stenosis and the Story of TAVR (TAVR/TAVI are using interchangeably) CardioNerds Aortic Stenosis, updated 1.20.21 1. In the 1990s, patients with severe aortic stenosis (AS) who were deemed to be at high surgical risk would weigh the risks of surgery and prolonged recovery. Balloon Aortic Valvuloplasty (BAV) was first performed by Dr. Alain Cribier in 1986. The technique was based on the foundation of pulmonary valvuloplasty performed initially in 1982 by Drs. Jean Kan and Bob White, and mitral valvuloplasty in 1984. BAV was initially touted as an efficacious cure for aortic stenosis, but unfortunately it had a high restenosis rate as well as high risks for stroke and vascular complications (no closure devices at that time) with an overall poor long-term prognosis. Balloon aortic valvuloplasty was primarily used for decompensated Class IV heart failure in non-surgical candidates. 2. Transcatheter aortic valve replacement (TAVR/TAVI) was developed and first performed in human in 2002.(1) This was performed by Dr. Alain Cribier in France in 2002, initially by trans-septal approach and then by retroaortic approach. Here is a representative diagram of the procedure. Figure: Transcatheter Aortic-Valve Replacement. The transcatheter valve is positioned at the level of the native aortic valve during the final step of valve replacement, when the balloon is inflated within the native valve during a brief period of rapid ventricular pacing. The delivery system is shown after it has traversed the aorta retrograde over a guidewire from its point of insertion in the femoral artery (transfemoral placement). Before balloon inflation, the valve and balloon are collapsed on the catheter (dark blue) and fit within the sheath (blue). After balloon inflation, the calcified native valve (upper panel) is replaced by the expanded transcatheter valve (lower panel, shown in short-axis view from the aortic side of the valve). Smith CR et al. N Engl J Med 2011;364:2187-2198. 3. The PARTNER trial was first published in a landmark NEJM article in extreme surgical risk patients comparing TAVR (with a balloon-expandable aortic valve implant) versus stndard “medical” therapy of aortic stenosis. TAVR markedly reduced the composite outcome of all-cause mortality and repeat hospitalization in these patients.(2)  PARTNER then compared TAVR to aortic valve surgery in high risk patients, and TAVR performed quite well, though there were more strokes and vascular complications in the TAVR g

CardioNerds (Amit Goyal and Daniel Ambinder), Dr. Leticia Helms (Internal medicine resident at Columbia University), Dr. Silia DeFilippis (AHFT FIT at Columbia University), and Dr. Anu Lala (AHFT faculty and program director at Mount Sinai Hospital) to discuss diversity and inclusion in academic cardiology and more in this installment of the Narratives in Cardiology Series. The President of the New York ACC Chapter Dr. Hima Vidula discusses D&I initiatives at her chapter. Episode introduction and audio editing by CardioNerds Academy Intern, Shivani Reddy. Although women compose 50% of medical students in the United States, cardiology remains a male dominated field. Gender disparity is even more prominent when we look at leadership positions. In this episode we discuss why and how cardiology (and advanced heart failure) can be such a rewarding field for women. The episode reflects on the significant contributions women have made to the field in the past and how they continue to move the field with respect to clinical care and research. The PA-ACC & CardioNerds Narratives in Cardiology is a multimedia educational series jointly developed by the Pennsylvania Chapter ACC, the ACC Fellows in Training Section, and the CardioNerds Platform with the goal to promote diversity, equity, and inclusion in cardiology. In this series, we host inspiring faculty and fellows from various ACC chapters to discuss their areas of expertise and their individual narratives. Join us for these captivating conversations as we celebrate our differences and share our joy for practicing cardiovascular medicine. We thank our project mentors Dr. Katie Berlacher and Dr. Nosheen Reza. Video Version • Notes • Production Team Claim free CME just for enjoying this episode! There are no relevant disclosures for this episode. The PA-ACC & CardioNerds Narratives in Cardiology PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Tweetorial – Raising Women Leaders in Academic Cardiology with Dr. Anu Lala https://twitter.com/Gurleen_Kaur96/status/1509286469051031556?s=20&t=9BFDUXbSnWLcAc5-daXK2A Video version – Raising Women Leaders in Academic Cardiology with Dr. Anu Lala https://youtu.be/vVuhUCbqwYk Quotables – Raising Women Leaders in Academic Cardiology with Dr. Anu Lala “We all have multiple roles – and those roles don’t always have to be completely distinct and separate from one another. You know, our ability in one role, maybe it makes us better at another.” “I felt like being there was like in medical Disneyland for research.” – Anu Lala “Heart failure is unique in that it truly requires that cross disciplinary collaboration at the precipice of what is often life and death.” – Anu Lala “It points to the importance of seeing people do things before you who look like you.” – Anu Lala “All human beings want to feel heard. They want to feel seen and they want to feel like their voice matters.”  – Anu Lala “consciously deliberately disruptive” “I like the idea of calling it work-life harmony.” Show notes – Raising Women Leaders in Academic Cardiology with Dr. Anu Lala How do women compare to men in cardiology in 2022? Although nearly 50% of US medical graduates and more than 40% of internal medicine graduates are women, the field of cardiology remains male dominated. Approximately 20% of general cardiology fellows are women, which is comparable to women in surgical subspecialties like neurosurgery (17%), thoracic surgery (21%), and orthopedic surgery (15%) (Reza 2021). Additionally, women hold significantly fewer leadership positions and are less likely to be promoted to senior academic ranks. Out of LBCT presented at ACC 2021, zero had a female first author and zero were presented by women (Kaur 2021). What may make heart failure unique with respect to the recruitment of women? Heart failure is the only subspecialty of cardiology that was founded by a woman. Dr. Sharon Hunt is often described as the founder of the subspecialty. She posited a few reasons why heart failure may attract a higher proportion of women including presence of models and mentors for women, women have been included since the inception of the field, and one that requires collaboration (Hunt 2019). The number of women in HF training programs ranges between 26 to 36% which is much higher than that of women in other subspecialties like EP and interventional cardiology (Reza 2021). How can we increase diversity in clinical trial leadership? Women only represent 1 in 10 authors of cardiovascular trials in high impact journals (Van Spall 2021). Build diverse research team. Hold stakeholders accountable including academic institutions, professional societies, industry sponsors, funding agencies, and scientific journals (Van Spall 2

CardioNerds Tommy Das (Program Director of the CardioNerds Academy and cardiology fellow at Cleveland Clinic), Rick Ferraro (Director of CardioNerds Journal Club and cardiology fellow at the Johns Hopkins Hospital), and CardioNerds Healy Honor Roll Ambassador Dr. Justice Oranefo (UConn cardiology fellow) discuss omega-3 fatty acids acid with Dr. Ty Gluckman, preventive cardiologist and medical director of the Center for Cardiovascular Analytics, Research, and Data Science (CARDS) at the Providence St. Joseph Heart Institute in Portland, Oregon. Audio editing by CardioNerds Academy Intern, Christian Faaborg-Andersen. In the recent years, purified omega 3 fatty acids and its esters have emerged as a potential new tool in our arsenal for management of hypertriglyceridemia and atherosclerotic coronary artery disease. In this episode we review the sources and basic structure of these compounds, as well as their metabolic effects as it pertains to cardiovascular disease. Using hypothetical patient cases, we also discuss scenarios in which these therapies can be useful. This episode is part of the CardioNerds Lipids Series which is a comprehensive series lead by co-chairs Dr. Rick Ferraro and Dr. Tommy Das and is developed in collaboration with the American Society For Preventive Cardiology (ASPC). Relevant disclosures: None Pearls • Notes • References • Guest Profiles • Production Team CardioNerds Lipid Series PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls Omega 3 (n-3) fatty acids are a class of polyunsaturated fatty acids [PUFA]. The most studied n-3 fatty acids include eicosapentaenoic acid [EPA], docosahexaenoic acid [DHA] and alpha linoleic acid [ALA]. ALA is found in certain vegetable oils while EPA and DHA are abundant in fish sources. Cardiovascular benefits of n-3 fatty acids include blood pressure reduction, enhanced diastolic function, triglyceride reduction, and immunomodulatory properties. Inflammation plays a major role in the atherogenic process and plaque rupture. Inflammatory marker hs-CRP is a risk enhancing factor for predicting future ASCVD risk. Ongoing trials are investigating therapy that target the inflammatory process in treatment of atherosclerotic heart disease. Prevention and management of ASCVD require aggressive lifestyle modifications and medical therapy addressing risk factors and underlying inflammatory conditions. Purified forms of n-3 fatty acids are approved for the treatment of severe hypertriglyceridemia and as an adjunct therapy to statins for reduction of coronary events in high-risk individuals. Show notes 1. What are omega 3 (n-3) fatty acids? What are the natural sources of n-3 fatty acids? n-3 fatty acids are class of polyunsaturated fatty acids [PUFA]. PUFA are types of unsaturated fats that have more than one double bond in their backbone. PUFAs are important constituents of the phospholipids of all cell membranes. The most studied n-3 fatty acids include eicosapentaenoic acid [EPA], docosahexaenoic acid [DHA] and alpha linoleic acid [ALA]. ALA is found in certain vegetable oils including walnuts, flaxseeds, chia seeds. EPA and DHA are abundant in cold water fish oils such as salmon, mackerel, tuna sardines. Interestingly, farm raised fish usually have higher levels of EPA and DHA than wild caught fish; however, this depends on what the fish are fed. Another important class of PUFAs are omega 6 (n-6) fatty acids, found in vegetable oils (1,2).  2. What are the metabolic effects of omega 3 fatty acids? Multiple early studies have demonstrated the anti-inflammatory properties of n-3 fatty acids. The typical Western diet with a high arachidonic acid (an n-6 fatty acid) content promotes atherogenesis leading to the high incidence of CAD in this population. Supplementation with diets rich in DHA and EPA has been associated with reduced arachidonic acid content as well as reduced markers of inflammation. The relative dietary ratios of n-6:n-3 fatty acids have major implications for cardiovascular health. Anti-inflammatory mechanism of n-3 fatty acids include cell membrane stabilization, anti-oxidant properties, reduced leukocyte chemotaxis. (1-3). Other studied cardiovascular benefits of n-3 fatty acids include triglyceride lowering properties (11, 12), blood pressure and heart rate reduction (13, 14), improved endothelial function and antithrombotic properties (15, 16). Importantly, EPA and DHA are distinct molecules (different hydrocarbon length and number of double bonds) with different biologic effects. EPA assumes an extended conformation in cellular membranes, allowing it to neutralize reactive oxygen species, facilitate membrane stabilization, and limit oxidation of LDL cholesterol more easily. In contrast, DHA has a longer carbon chain and has one additional double bond, resulting in less membrane stabili

CardioNerds (Amit Goyal and Daniel Ambinder) join Dr. Loie Farina (Northwestern University CardioNerds Ambassador), Dr. Josh Cheema, and Dr. Graham Peigh from Northwestern University for drinks along the shores of Lake Michigan at North Avenue Beach. They discuss a case of a 52-year-old woman with limited cutaneous systemic sclerosis who presents with progressive symptoms of heart failure and is found to have a severe, non-ischemic cardiomyopathy. The etiology of her cardiomyopathy is not clear until her untimely death. She is ultimately diagnosed with cardiac AL amyloidosis with isolated vascular involvement a real occam’s razor or hickam’s dictum conundrum. We discuss the work-up and management of her condition including a detailed discussion of the differential diagnosis, the underlying features of systemic sclerosis with cardiac involvement as well as cardiac amyloidosis, the role of a shock team in managing cardiogenic shock, and how to identify those with advanced or stage D heart failure. Advanced heart failure expert Dr. Yasmin Raza (Northwestern University) provides the ECPR segment. Episode introduction by CardioNerds Clinical Trialist Dr. Liane Arcinas. Audio editing by CardioNerds Academy Intern, Christian Faaborg-Andersen. Claim free CME just for enjoying this episode!  Disclosures: NoneJump to: Pearls – Notes – 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 Summary – Occam’s Razor or Hickam’s Dictum? This is a case of a 52-year-old woman with limited cutaneous systemic sclerosis who presented with progressive dyspnea on exertion and weight loss over the course of 1 year. Her initial work-up was notable for abnormal PFTs and finding of interstitial pneumonia on high-resolution CT, an ECG with frequent PVCs and normal voltage, a transthoracic echocardiogram with a mildly reduced ejection fraction of 40%, and a right/left heart catheterization with normal coronary arteries, filling pressures, and cardiac output. Scleroderma-related cardiac involvement is suspected. She is placed on GDMT, but her condition worsens over the next several months, and repeat echocardiogram shows severely reduced biventricular function, reduced LV global longitudinal strain (GLS) with apical preservation of strain, severely reduced mitral annular tissue Doppler velocities, and a normal left ventricular wall thickness. Scleroderma-related cardiac involvement remains highest on the differential, but because of some findings on the echo that are concerning for cardiac amyloidosis, an endomyocardial biopsy was obtained. It showed vascular amyloid deposition without interstitial involvement. The diagnosis of cardiac amyloid was discussed but deemed unlikely due to lack of interstitial involvement. However, a serologic work-up soon revealed a monoclonal serum lambda light chain and a follow-up bone marrow biopsy showed 20% plasma cells. She was discharged with very near-term follow-up in oncology clinic with a presumptive diagnosis of AL amyloidosis, but she unfortunately returned in shock and suffered a cardiac arrest. She initially survived and underwent emergent veno-arterial extracorporeal membrane oxygenation (VA ECMO) cannulation with subsequent left ventricular assist device placement (LVAD). However, she passed away due to post-operative hemorrhage. Autopsy was consistent with a final diagnosis of cardiac AL amyloidosis with isolated vascular involvement.  Case Media – Occam’s Razor or Hickam’s Dictum? EKG CXR TTE Pathology CMR Episode Teaching -Occam’s Razor or Hickam’s Dictum? Pearls Scleroderma causes repeated focal ischemia-reperfusion injuries which result in patchy myocardial fibrosis. Cardiac involvement in scleroderma is frequent but often not clinically evident; when symptomatic, it is associated with a poor prognosis.  Myocardial dysfunction in cardiac AL amyloidosis can result from myocardial infiltration, vascular deposition causing microvascular dysfunction and ischemia, and direct cardiotoxicity from circulating light chains.  While isolated vascular amyloid is very rare, it can occur and can be seen without key characteristics of interstitial amyloid deposition, namely left ventricular hypertrophy and low voltage on an ECG.   Cardiogenic shock outcomes are improved by multi-disciplinary discussions, commonly referred to as a “shock team call.”   Heart failure is a progressive, morbid, and potentially fatal condition. LVADs and heart transplantation improve life expectancy and decrease morbidity among patients with stage D heart failure. Identification of patients with advanced heart failure can be challenging – a helpful mnemonic is “I NEED HELP  Notes – Occam’s Razor or Hickam’s Dictum? 1. How does scleroderma affect the heart?  Scleroder

Approximately 350,000 adults per year in the US experienced out-of-hospital cardiac arrest (OHCA). Only about 10% of such patients survive their initial hospitalization. The key drivers of successful resuscitation from OHCA are bystander cardiopulmonary resuscitation (CPR) and public use of an automated external defibrillator (AED). Survival rates from OHCA vary dramatically between US regions. For instance, the extracorporeal CPR (eCPR) program at the University of Minnesota has over a 40% survival rate in patients with OHCA and refractory ventricular fibrillation (VF) based on data published in the ARREST trial. In this episode, we are joined by experts from the University of Minnesota, including Dr. Jason Bartos (Interventional and Critical Care Faculty) and Dr. Julie Power (Chief Fellow at University of Minnesota and CardioNerds Academy Fellow), along with Dr. Yoav Karpenshif (Co-Chair Critical Care Series, University of Pennsylvania) and CardioNerds Co-Founders (Amit Goyal and Dan Ambinder) to discuss cardiac arrest, E-CPR, & post-arrest care. This includes targeted temperature management, coronary angiography and revascularization, as well as the growing field of eCPR and VA ECMO.  Episode introduction by CardioNerds Clinical Trialist Dr. Jason Feinman. Audio editing by CardioNerds Academy Intern, Shivani Reddy. The CardioNerds Cardiac Critical Care Series is a multi-institutional collaboration made possible by contributions of stellar fellow leads and expert faculty from several programs, led by series co-chairs, Dr. Mark Belkin, Dr. Eunice Dugan, Dr. Karan Desai, and Dr. Yoav Karpenshif. Claim free CME for enjoying this episode! Disclosures: None Pearls • Notes • References • Guest Profiles • Production Team CardioNerds Cardiac Critical Care PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Abbreviations – Cardiac Arrest, E-CPR, & Post-Arrest Care eCPR- extracorporeal cardiopulmonary resuscitation VA ECMO- veno-arterial extracorporeal membrane oxygenation VT/VF- ventricular tachycardia/ventricular fibrillation ACLS- advanced cardiovascular life support ROSC- return of spontaneous circulation- OHCA- out-of-hospital cardiac arrest IHCA- in-hospital cardiac arrest TTM- targeted temperature management Pearls and Quotes – Cardiac Arrest, E-CPR, & Post-Arrest Care The ARREST trial showed early VA ECMO-facilitated resuscitation for patients with OHCA and refractory VF significantly improved survival to hospital discharge when compared to standard ACLS treatment. Coronary artery disease is common in the setting of cardiac arrest, with up to 96% of patients with STEMI on post resuscitation EKG and up to 85% of refractory out-of-hospital VT/VF arrests. Guidelines recommend emergent coronary angiography for patients with ST-segment elevation on the post-ROSC ECG. The role of timing of revascularization after ROSC in patients without STEMI or shock is unknown. The role of coronary angiography in cardiac arrest with nonshockable rhythms is also unclear. The current AHA guidelines recommend initiation of targeted temperature management between 32°C and 36°C for at least 24 hours for all patients who do not follow commands after ROSC in both OHCA and IHCA. Show notes – Cardiac Arrest, E-CPR, & Post-Arrest Care 1. What are early post arrest management considerations? The key drivers of successful resuscitations from OHCA: CPR and public use of AEDs in the field. After initial stabilization, care of the critically ill post-arrest patient hinges on hemodynamic support, mechanical ventilation, temperature management, attending to adverse sequelae of arrest, and diagnosis and treatment of underlying causes of arrest. Coronary artery disease is common in the setting of VT/VF cardiac arrest, with up to 96% of patients with STEMI on post resuscitation EKG and up to 85% of refractory out-of-hospital VT/VF arrests. In the early post-arrest state, it is also important to diagnose and treat infections and any neurologic injury. Neurologic compromise is a common cause of mortality in patients who achieve ROSC. Over 50%, and in some cohorts around 75%, of patients with death after resuscitated OHCA die of neurologic injury. 2. What is the current evidence for targeted temperature management (TTM)? “[This is] the most hotly debated topic right now in the field of cardiac arrest.” – Dr. Jason Bartos Current AHA guidelines recommend initiation of targeted temperature management between 32°C and 36°C for at least 24 hours for all patients who do not follow commands after ROSC in both OHCA and IHCA. TTM is a relatively safe and effective strategy that can improve neurological outcomes in patients who remain comatose after achieving ROSC from cardiac arrest. Current evidence supports a broad range of TTM from 33°C to 3

CardioNerd (Amit Goyal), Dr. Zarina Sharalaya (Interventional cardiology fellow at the Cleveland Clinic), Dr. Ashley Mohadjer (Interventional cardiology fellow, Vanderbuilt Heart and Vascular Institute), and Dr. Laurie Mbuntum (Cardiology fellow, UTSW) join Dr. Ki Park (Associate professor of medicine and an interventional cardiologist at the University of Florida and Malcom Randall VA Medical Center in Gainesville, FL.) for a a well-rounded discussion on all things ‘Women-in-Cardiology’ #WIC . Dr. Ki Park discusses how she nurtured her interest in interventional cardiology, and further shares her thoughts and passion for cardio-obsetrics. She shares her advice for trainees thinking about interventional or cardioobetrics and anecdotes from her training as a successful woman in the field. We discuss the need for education on pregnancy outcomes and long-term cardiovascular risk, ideas to lower maternal mortality, how to start a women’s cardiovascular clinic, and her thoughts on how the field may look in the future. Special message by Florida ACC State Chapter Governor, Dr. David Perloff. Episode introduction and audio editing by CardioNerds Academy Intern, Shivani Reddy. The PA-ACC & CardioNerds Narratives in Cardiology is a multimedia educational series jointly developed by the Pennsylvania Chapter ACC, the ACC Fellows in Training Section, and the CardioNerds Platform with the goal to promote diversity, equity, and inclusion in cardiology. In this series, we host inspiring faculty and fellows from various ACC chapters to discuss their areas of expertise and their individual narratives. Join us for these captivating conversations as we celebrate our differences and share our joy for practicing cardiovascular medicine. We thank our project mentors Dr. Katie Berlacher and Dr. Nosheen Reza. Video Version • Notes • Production Team Claim free CME just for enjoying this episode! There are no relevant disclosures for this episode. The PA-ACC & CardioNerds Narratives in Cardiology PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Video version – Interventional Cardiology, Cardioobstetrics, & Work Life Integration with Dr. Ki Park https://youtu.be/_oYUc-_sdfU Tweetorial – Interventional Cardiology, Cardioobstetrics, & Work Life Integration with Dr. Ki Park https://twitter.com/gurleen_kaur96/status/1495921275545563136?s=21 Quotables – Interventional Cardiology, Cardioobstetrics, & Work Life Integration with Dr. Ki Park “I like the work life integration as opposed to work life balance. Balance just implies that you always have everything aligned perfectly at all times and that is just not doable.” Dr. Ki Park Show notes – Interventional Cardiology, Cardioobstetrics, & Work Life Integration with Dr. Ki Park Why is screening for OB-GYN history for cardiovascular risk is important, and who should be responsible? Pregnancy is nature’s stress test and in some women can unmask someone’s predisposition to cardiac disease Yearly screening for diabetes, hypertension, dyslipidemia Big interdisciplinary effort in attempt to try to capture all women at risk, as many will not present with manifestation of disease initially How did you nurture your interest in cardioobsetrics? In interventional cardiology? Meetings and societies Connect with those who work in the field, social media Regarding interventional cardiology – having interest in procedures, do as many cases “hands on” as possible, learning from mistakes What advise do you have to achieve work and life balance? It’s important to understand the various occupational hazards of radiation exposure which include but are not limited to brain tumors, cataracts, thyroid disease, cardiovascular diseases, musculosketal problems and reproductive side effects. Have grace, one can’t be 100% at every single thing all the time Its more work life integration as opposed to a balance Prioritize different things on different days, be honest with children and explain why you do what you do in age appropriate terms Maternal mortality is high in this country with cardiovascular disease as a leading cause. What are important factors to improve maternal mortality? Education Improving access to care in the peripartum stage for mothers, particularly since the focus in that period is on baby Legislature to improve insurance coverage         Where do you see cardioobsetrics field going in the next few years? Make the knowledge more mainstream Education of subspecialty fellows within cardiovascular education Collaboration with ACOG and maternal fetal medicine societies More registries of patients to continue to learn more about these women What was involved to create the women’s heart clinic in your institution? St

CardioNerds (Amit Goyal and Daniel Ambinder), ACHD series co-chair Dr. Daniel Clark (Vanderbilt University), and ACHD FIT lead Dr. Danielle Massarella (Toronto University Health Network) join ACHD expert Dr. Yuli Kim (Associated Professor of Medicine & Pediatrics at the University of Pennsylvania), to discuss single ventricular heart disease and Fontan palliation. They cover the varied anatomical conditions that can require 3-step surgical palliation culminating in the Fontan circulation, which is characterized by passive pulmonary blood flow, high venous pressures, and low cardiac output. Audio editing by Dr. Gurleen Kaur (Director of the CardioNerds Internship and CardioNerds Academy Fellow).  The CardioNerds Adult Congenital Heart Disease (ACHD) series provides a comprehensive curriculum to dive deep into the labyrinthine world of congenital heart disease with the aim of empowering every CardioNerd to help improve the lives of people living with congenital heart disease. This series is multi-institutional collaborative project made possible by contributions of stellar fellow leads and expert faculty from several programs, led by series co-chairs, Dr. Josh Saef, Dr. Agnes Koczo, and Dr. Dan Clark. The CardioNerds Adult Congenital Heart Disease Series is developed in collaboration with the Adult Congenital Heart Association, The CHiP Network, and Heart University. See more Claim free CME for enjoying this episode! Disclosures: None Pearls • Notes • References • Guest Profiles • Production Team CardioNerds Adult Congenital Heart Disease PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls There are various forms of unpalliated ‘single ventricle’ congenital heart disease. The three main hemodynamic issues that need to be addressed in any form are unbalanced flow, pulmonary over-circulation, and blood mixing.  The Fontan palliation is a series of operations for congenital heart disease patients in whom biventricular repair is not feasible.  In the completed Fontan circulation, systemic venous blood is surgically routed directly to the lungs, effectively bypassing the heart, and creating passive pulmonary blood flow.  The hallmarks of the Fontan circulation (and Fontan failure) are elevated central venous pressure and low cardiac output.  Patients with Fontan circulation may experience significant morbidity in the long term from both cardiac and non-cardiac sequelae, and require lifelong specialist care.  Show notes 1. Why do some patients require Fontan palliation?  Many different types of anatomies may ultimately require single ventricular palliation via the Fontan procedure due to inadequate biventricular function to support both pulmonary and systemic circulations. Some examples include Tricuspid Atresia (hypoplastic RV), Double Inlet Left Ventricle (DILV; hypoplastic RV), Hypoplastic Left Heart Syndrome (HLHS; hypoplastic LV), and atrioventricular septal defects (AVSD; either RV or LV may be inadequate based on “commitment” of the common AV valve).  The Fontan procedure was first described in 1971; at this time, mortality of single ventricular patients exceeded 90% in the first year of life.  2. What are the stages of Fontan palliation?  Effective pulmonary blood flow/balancing flow to the pulmonary and systemic circulations: for many conditions, this involves retrograde pulmonary blood flow from a systemic -> PA shunt (i.e. Blalock-Taussig-Thomas “BTT” shunt in which the subclavian artery is turned down and anastomosed to the pulmonary artery). In infants, the pulmonary vascular resistance (PVR) is high perinatally and gradually lowers over the first 3 months of life to adult levels with exposure to the atmosphere’s natural pulmonary vasodilator: oxygen. Thus, in the first 3 months of life babies have an intrinsic PVR that is too high to directly connect the venous system to the lung arteries and thereby require staged surgeries.  Protect the pulmonary vasculature from overcirculation: ultimately, the goal of single ventricular palliation is rerouting systemic venous drainage directly to the pulmonary vasculature passively, without a cardiac pumping chamber. This volume unloads the common ventricle and allows it a better chance to function over the lifespan by pumping only to a single circuit: the systemic vascular bed. Thus, steps 2 and 3 of Fontan palliation are passive head/neck venous connection to the pulmonary arteries (now typically accomplished with the modified bidirectional Glenn operation that anastomoses the SVC to the RPA typically) and finally total cavopulmonary connection by the Fontan conduit connecting the lower body’s venous return from the IVC to the Fontan tunnel and up to the RPA.  3. What is the ultimate “plumbing” of Fontan circu

CardioNerds (Amit Goyal), Dr. Natalie Stokes (Cardiology Fellow at UPMC and Co-Chair of the Cardionerds Cardio-Ob series), fellow lead Dr. Victoria Thomas (Cardionerds Ambassador, Vanderbilt University Medical Center), join Dr. Rachel Bond (Women’s Heart Health Systems Director at Dignity Health, Arizona) for a cardio-obstetrics discussion about Black maternal health. Episode introduction by CardioNerds Clinical Trialist Dr. Chistabel Nyange. Audio editing by CardioNerds Academy Intern, Christian Faaborg-Andersen. This episode was developed in collaboration with the Association of Black Cardiologists. ABC is a 501(c)3 nonprofit organization whose mission is to promote the prevention and treatment of cardiovascular disease, including stroke, in Black persons and other minority populations, and to achieve health equity for all through the elimination of disparities. Learn more at https://abcardio.org/. Notes • References • Guest Profiles • Production Team CardioNerds Cardio-Obstetrics Series PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Show notes 1. Why does Black Maternal Health need to be deliberately highlighted episode on CardioNerds? Black women are three-four times more likely to die during their pregnancy. The deaths are primarily tied to cardiomyopathy and cardiovascular conditions such as coronary artery disease, pulmonary hypertension, chronic hypertension, preeclampsia, and eclampsia. 63-68% of this cardiovascular mortality is preventable depending on one’s racial identity.  As CardioNerds, we must educate ourselves on why this occurs and identifying diseases that may place patients at increased risk. Studies have shown the Black maternal mortality crisis exist irrespective of one’s education or socioeconomic status. We must recognize and admit that some patients are being treated differently because of their race and ethnicity alone. 2.     When we consider or acknowledge a patient’s race, what should CardioNerds think about? Race is an important factor to think about, but we must remember that it is an imperfect variable. We should not focus on biology or genetic make-up. We should think about social determinants of health. 60% of the time social and personal aspects dictate one’s health. Unconscious biases and structural racism are likely playing a major role in race-based health inequities. 3.     What are other vulnerable groups that have increased mortality rates related to cardioobstetric care? Native American women have similar maternal mortality rates to Black populations. Women who are veterans, live in rural communities, and/or are currently incarcerated have increased risk of mortality 4.     What are some of the social determinants of health that should be considered for these patients? Food deserts or having poor access to nutrient rich/quality foods make these vulnerable patients have increased risk factors for high cholesterol, high blood pressure, obesity, and diabetes which increase the risk for pregnancy complications and infertility. The above vulnerable populations can have less access to higher levels of care for high-risk pregnancies. 5.     What are some of the preventable causes of maternal mortality? Clinicians should actively listen to their patients’ concerns. There have been several media stories in the news and on CardioNerds episodes where women’s concerns were not acknowledged or taken seriously. Preconception counseling is important to provide to all patients. 50% of women have one risk factor for cardiovascular disease when entering pregnancy. We should have discussions with patients regarding their lifestyles, with an emphasis on exercise and diet. 6.     What are some of the psychosocial or health related differences we see in black mothers when compared to other races? The effect of stress is affecting not just black mothers but black women in general by predisposing them to increased cardiovascular disease and cognitive impairment. The stress effects on black women are being called superwoman schema. Superwoman schema is a combination/phenomenon of gender and racial oppression’s effect on the allostatic load (cumulative biological stress).  Studies have shown that black women’s chronic stress levels affect their sympathetic nervous system with an inability to fight off or perhaps produce too much inflammatory response. This increases the risk of a variety worsening chronic morbidities in particular worsening cardiovascular health. One in eight women will struggle with infertility. Black women are two times more likely to suffer from infertility compared to their White counterparts. This is largely due to increased uterine fibroids. Black women are also less likely to be referred to a reproductiv

CardioNerds (Amit Goyal and Daniel Ambinder) join Dr. Jaya Kanduri, Dr. Dan Lu, and Dr. Joe Wang from Weill Cornell Cardiology for Levain cookies in Central Park. The ECPR is provided by Dr. Harsimran Singh (Cardiology Program Director and Interventional Cardiologist with expertise in ACHD). Episode introduction by CardioNerds Clinical Trialist Dr. Jeremy Brooksbank. We discuss a case of a 24-year-old female with a history of unicuspid aortic valve with associated aortopathy status post mechanical aortic valve replacement and Bentall procedure at age 16 presents with acute onset substernal chest pain and shortness of breath. She was found to have mechanical aortic valve obstruction and severe aortic regurgitation resulting in cardiogenic shock. Unfortunately, the shock quickly progressed to refractory cardiac arrest requiring mechanical support with VA-ECMO before valve debridement was performed in the operating room. The differential for mechanical prosthetic valve stenosis includes pannus, thrombus, or vegetation. She was eventually found to have thrombus obstructing the outflow tract and holding the mechanical leaflets open leading to torrential regurgitation. She underwent successful surgical debridement. We discuss unicuspid aortic valve and associated aortopathy, surgical considerations regarding AVR, diagnosis and management of prosthetic valve dysfunction, approach to cardiogenic shock and considerations around activating and managing VA-ECMO. With this episode, the CardioNerds family warmly welcomes Weill Cornell Cardiology to the CardioNerds Healy Honor Roll. The CardioNerds Healy Honor Roll programs support and foster the the CardioNerds spirit and mission of democratizing cardiovascular education. Healy Honor Roll programs nominate fellows from their program who are highly motivated and are passionate about medical education. The Weill Cornell fellowship program director, Dr. Harsimran Singh has nominated Dr. Jaya Kanduri for this position. Claim free CME just for enjoying this episode!  Disclosures: NoneJump to: Pearls – Notes – 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 ECG CXR Echo RHC PSL AP3 Color LHC – LCA LHC – LCA RCA Aortogram TEE TEE 2 Episode Teaching Pearls – Mechanical Valve Thrombosis (1) Unicuspid aortic valves present with aortic stenosis earlier in life. There can be concurrent aortic regurgitation and, like bicuspid aortic valves, unicuspids can be associated with aortopathy as well as other congenital anomalies. (2) Prosthetic valve stenosis is assessed with different echocardiographic parameters than what we use for native valves. The differential for mechanical valve stenosis includes pannus, thrombus, or vegetation. Patient prosthesis mismatch may also lead to elevated gradients. (3) VA-ECMO provides robust flow in the setting of cardiogenic shock as well as gas exchange. While this flow may improve end-organ perfusion, it also increases left ventricular afterload, thereby potentially worsening LV ischemia and impeding LV recovery. Elevated afterload may also decrease innate contractility and prevent aortic valve leaflets from opening. Therefore, if a patient with a mechanical valve is on VA-ECMO, ensuring valve opening to prevent valve (or ventricular) thrombosis is paramount. (4) Venting is sometimes necessary to decrease the left ventricular end diastolic pressure from the high afterload imposed by VA-ECMO. A microaxial temporary LVAD (example – Impella device) directly unloads the left ventricle, but cannot be used in the setting of a mechanical aortic valve. TandemHeart is also a consideration (inflow cannula placed across the interatrial septum in the left atrium) to unload the LV, but does not improve flow across the aortic valve so can lead to thrombus if a mechanical valve is present. Intra-aortic balloon counterpulsation using an IABP can be used to decrease afterload on the native heart and increase coronary perfusion, but does not directly unload the left ventricle. (5) Acute mechanical valve thrombosis can be managed with emergency surgery or with low dose fibrinolytic therapy. Surgery is preferable when operative risk is low and if there are contraindications to fibrinolytic therapy such as prior intracranial hemorrhage or active bleeding. (6) VA-ECMO can be weaned by slowly decreasing flow rates and assessing native cardiac function, hemodynamic response, and end-organ perfusion with assessments including echocardiography and pulmonary artery catheterization. Notes – Mechanical Valve Thrombosis 1. What is a unicuspid aortic valve? Unicuspid aortic valves (UAVs) are rare with an incidence of only 0.02%. There are two types of UAVs. Acommisural UAVs have a single cusp with a stenotic central orifice and rudimentary commissures

The hemodynamic evaluation of cardiogenic shock obtained via a Swan-Ganz catheter plays an essential role in the characterization of cardiogenic shock patients. Join Dr. Nosheen Reza, (Assistant Professor of Medicine and Advanced Heart Failure and Transplant cardiologist at the Hospital of the University of Pennsylvania), episode fellow lead Dr. Brian McCauley (Interventional and Critical Care Fellow at the Hospital of the University of Pennsylvania), Dr. Mark Belkin (Cardiac Critical Care Series Co-Chair and AHFT fellow at University of Chicago), and CardioNerds Co-Founders, Amit Goyal and Dan Ambinder, for this tour through the heart aboard the Swan-Ganz catheter. In this episode, we evaluate three separate admissions for a single patient to highlight pearls regarding waveform assessment, evaluating cardiac output, phenotyping hemodynamic profiles, targeted therapies based on hemodynamics and so much more. Episode introduction and audio editing by Dr. Gurleen Kaur (Director of the CardioNerds Internship). Claim free CME for enjoying this episode! Disclosures: None Pearls • Notes • References • Guest Profiles • Production Team CardioNerds Cardiac Critical Care PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls and Quotes – Hemodynamic Evaluation of Cardiogenic Shock Swan-Ganz catheters are not dead #ReviveTheSwan!  They remain a useful tool to characterize cardiac patients & to help direct therapy, especially in Cardiogenic Shock. When looking at Swan-Ganz catheter data, it is important to always interpret your own tracings, to know what values are acquired directly, and which values are derived. It is important to understand the strengths and weakness of hemodynamic characterization by Swan-Ganz catheters Advanced metrics such as cardiac power output, pulmonary artery pulsatility index, and aortic pulsatility index are extremely useful in further phenotyping patients as well as guiding mechanical support platforms “The data will be wrong if the preparation is not right” Show notes – Hemodynamic Evaluation of Cardiogenic Shock 1. Swan-Ganz catheters are a useful tool to characterize cardiac patients and to direct therapy.  With the ESCAPE trial in 2004, Swan-Ganz catheter utilization dropped drastically outside transplant centers across the United States (2).  While the ESCAPE trial did demonstrate the possibility of harm when using a Swan-Ganz catheter, many of the truly ill cardiac patients we care for would have been excluded from the trial. For instance, patients on dobutamine at doses above 3 µg/kg/min or any dose of milrinone during the hospitalization were excluded from the trial. This is a classic example of “throwing the baby out with the bath water.” In a recent large, multicenter cardiogenic shock registry, complete hemodynamic assessment using pulmonary artery catheters prior to MCS is associated with lower in-hospital mortality compared with incomplete or no assessment (3). 2. When looking at Swan-Ganz catheter data, it is important to always interpret your own tracings, to know what values are acquired directly, and which values are derived. Incomplete or incorrect data can lead to mischaracterization of our patients.  Therefore, it is essential to review all of the tracings, calculations, and data acquired for each individual patient before any clinical adjustments are made (1).  An incomplete pulmonary capillary wedge tracing is an example from clinical practice (causing the PCWP, and therefore the left-sided filling pressures to be overestimated).  It is equally important to know the limitations of cardiac output equations, and that no one measurement is perfect. Foibles of the Fick equation include assumed rather than measured oxygen consumption and variations in hemoglobin concentration.  Traditionally, thermodilution has been thought to be likely less accurate in presence of tricuspid regurgitation, which could lead to blending of the cold dilutant, but recent data suggests even in these circumstances it remains the preferred method for estimating cardiac output over indirect Fick. 3. What are some tips of measuring a PCWP correctly? To ensure that we get the wedge pressure correctly, we must first make sure we understand the wedge pressure in relation to the respiratory cycle. For the majority of patients, the end expiratory intrathoracic pressure will be close to 0, and it will have the least influence on our readings. Thus, for most patients, that is why we measure the wedge pressure at end expiration. However, in patients with severe lung disease or significant obesity, the intrathoracic pressure may not be close to 0 at end expiration or there may be wide swings in intrathoracic pressure. For these patients, it is a reminder to look at the tracings yourself, and we may need to average

CardioNerds (Amit Goyal and Daniel Ambinder), Dr. Zarina Sharalaya (Interventional Cardiology Fellow at the Cleveland Clinic), and Dr. Simrat Kaur (General Cardiology Fellow at the Cleveland Clinic) join Dr. Samir Kapadia, the Chair of the Robert and Suzanne Tomsich Department of Cardiovascular Medicine, Sydell and Arnold Miller Family Heart, Vascular & Thoracic Institute at Cleveland Clinic. They discuss future advancements in the field of structural interventional cardiology. Dr. Kapadia sheds light on his journey starting as an international medical graduate from India and speaks about his mentors that helped shape his career and his life. We later delve into several advancements in the field of structural and interventional cardiology, along with the amalgamation of different sub-specialities with intervention such as heart failure and critical care cardiology. We also discuss the measures being taken to reduce the occupational hazards associated with interventional cardiology and how to make this field more appealing to women in cardiology. Special message by Ohio ACC State Chapter Governor, Dr. Kanny Grewal. The PA-ACC & CardioNerds Narratives in Cardiology is a multimedia educational series jointly developed by the Pennsylvania Chapter ACC, the ACC Fellows in Training Section, and the CardioNerds Platform with the goal to promote diversity, equity, and inclusion in cardiology. In this series, we host inspiring faculty and fellows from various ACC chapters to discuss their areas of expertise and their individual narratives. Join us for these captivating conversations as we celebrate our differences and share our joy for practicing cardiovascular medicine. We thank our project mentors Dr. Katie Berlacher and Dr. Nosheen Reza. Video Version • Notes • References • Production Team Claim free CME just for enjoying this episode! There are no relevant disclosures for this episode. The PA-ACC & CardioNerds Narratives in Cardiology PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Tweetorial on Innovation, Excellence and Leadership in Interventional Cardiology with by Dr. Gurleen Kaur https://twitter.com/gurleen_kaur96/status/1484205728663576590?s=21 Video version – Innovation, Excellence and Leadership in Interventional Cardiology with Dr. Samir Kapadia https://youtu.be/BfqnRkaVGkk Quotables – Innovation, Excellence and Leadership in Interventional Cardiology with Dr. Samir Kapadia “A very important thing for all international medical graduates and for everybody, for that matter – it is important to recognize that the opportunities are what you perceive and not what others perceive.” Dr. Samir Kapadia Show notes – Innovation, Excellence and Leadership in Interventional Cardiology with Dr. Samir Kapadia How do international medical graduates contribute to the work force in medicine across the United States of America? International medical graduates account for 25% of the physician work force, with over 85% being involved in direct patient care. IMGs are usually accomplished, consummate and highly motivated physicians who often have to overcome challenges such as language proficiency, acculturation and difficulties with obtaining a visa status in the United States. IMGs also help fill gaps in health care by working in geographical areas that are otherwise not desirable by US or Canadian medical graduates. IMGs contribute to diversity of the field which provides a richer training environment, improved access to health care for underrepresented minorities, as well as better patient outcomes. What are key qualities of a good mentor? A good mentor is responsible for enhancing the education of his or her mentees along with motivating them to challenge their limits. Qualities of a good mentor extend beyond mere mentorship to sponsorship, where the mentor opens up his or her network for the mentee allowing them to pursue a path of success. A mentor serves as an advisor and a counselor, helping his or her mentees navigate difficult paths teaching them to become resilient physicians. A mentor also serves as a confidante for the trainee with whom mentees can share their dreams, aspirations and vulnerabilities knowing not only will this be kept in confidence but will also provide a catalyst for their growth. What are the recent advancements in minimizing radiation exposures for structural cardiologists? It’s important to understand the various occupational hazards of radiation exposure which include but are not limited to brain tumors, cataracts, thyroid disease, cardiovascular diseases, musculosketal problems and reproductive side effects. When dealing with possible occupational radiation exposure, we should strive for the ALARA (as low as reasonably achievable) principle of radiopro

In this episode, CardioNerds (Amit Goyal), ACHD series co-chair,  Dr. Josh Saef (ACHD fellow at University of Pennsylvania) and episode lead fellow, Dr. Brynn Connor (Pediatric Cardiology fellow at Lucile Packard Children’s Hospital at Stanford) are joined by Dr. Maan Jokhadar (Advanced heart failure and adult congenital heart disease specialist at Emory University) to discuss transposition of the great arteries. Audio editing by CardioNerds Academy Intern, Dr. Maryam Barkhordarian. For a brief review of the basic anatomy and physiology of D-TGA, check-out this great video by Dr. Maan Jokhadar! The CardioNerds Adult Congenital Heart Disease (ACHD) series provides a comprehensive curriculum to dive deep into the labyrinthine world of congenital heart disease with the aim of empowering every CardioNerd to help improve the lives of people living with congenital heart disease. This series is multi-institutional collaborative project made possible by contributions of stellar fellow leads and expert faculty from several programs, led by series co-chairs, Dr. Josh Saef, Dr. Agnes Koczo, and Dr. Dan Clark. The CardioNerds Adult Congenital Heart Disease Series is developed in collaboration with the Adult Congenital Heart Association, The CHiP Network, and Heart University. See more Claim free CME for enjoying this episode! Disclosures: None Pearls • Notes • References • Guest Profiles • Production Team CardioNerds Adult Congenital Heart Disease PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! https://www.youtube.com/watch?v=Ifu8nVtXT_c Pearls (1) In D-TGA following an atrial switch operation, the right ventricle IS the systemic ventricle! (2) Evaluation of systemic right ventricular function often requires use of both transthoracic echocardiography and cardiac MRI. (3) Use of medical heart failure therapies should be individualized, without any proven long-term mortality benefit and potential unique complications in this patient population (i.e. SA node dysfunction).  Show notes D-transposition of the great arteries (D-TGA) is one of the most common forms of cyanotic congenital heart disease presenting in the newborn period. Anatomically, d-transposition of the great arteries is characterized by atrioventricular concordance and ventriculoarterial discordance, such that the aorta arises from the morphologic right ventricle and pulmonary artery arises from the morphologic left ventricle. The resultant physiology is that of a parallel circulation, with deoxygenated blood recirculating in the systemic circulation (via the RA-RV) and oxygenated blood recirculating in the pulmonary circulation (via the LA-LV). At birth, this invariably results in cyanosis, with survival dependent upon adequate mixing of the two circulations via an atrial or ventricular level defect. Prior to surgical advances in the late 1950s, this lesion was uniformly fatal, with most infants dying before their first birthday. The subsequent development of the Senning and Mustard atrial-level repairs led to good immediate outcomes and improved long-term survival. However, following these “physiologic” types of repair, patients are far from cured, with several long-term established complications, including (1) dysfunction of the systemic right ventricle, (2) tricuspid regurgitation (the systemic atrioventricular valve), (3) atrial and ventricular arrhythmias, and (4) systemic and pulmonary venous baffles leaks and obstruction. These complications ultimately lead to substantial morbidity and premature mortality, with ACHD providers facing unique challenges in the medical and surgical management of this heterogenous patient population. 1. What are the basic anatomic features of d-transposition of the great arteries (d-TGA)? D-transposition of the great arteries is defined by the origin of the arterial trunks from the morphologically inappropriate ventricle, specifically with the aorta arising from the morphologic right ventricle (now the systemic ventricle) and the pulmonary trunk arising from the morphologic left ventricle. This is termed “ventriculoarterial discordance”, and importantly, does not define the spatial relationship of the great arteries. Rather, the “d” terminology refers to the looping of the ventricles and distinguishes d-TGA from l-TGA (or congenitally corrected transposition), where there is additional atrioventricular discordance.  The resultant physiology is that of a parallel circulation, with deoxygenated blood recirculating in the systemic circulation and oxygenated blood recirculating in the pulmonary circulation. At birth, this invariably results in cyanosis, with survival dependent upon adequate mixing of the two circulations via an atrial or ventricular level defect. There are three major anatomic variations in dTGA, incl

CardioNerds (Amit Goyal and Daniel Ambinder) join Dr. Patrick Azcarate and Dr. Antoinette Birs from the University of California San Diego along with a guest host Dr. Christine Shen from Scripps Health for a hike along Torrey Pines. They discuss a case of a 30-year-old man with a history of malignant thymoma status post two partial lung resections and radiation for pleural/pulmonary metastasis, as well as a history of myasthenia gravis on rituximab, and Ig deficiency on IVIG presents with progressive exertional chest pain. We focus on the differential diagnosis of patients with a history of chest radiation exposure and dive into the complex management and surveillance for patients with radiation associated cardiac disease (RACD). The E-CPR is provided by Dr. Milind Desai (multimodality cardiovascular imaging expert, Director of Clinical Operations, Director of Center for HCM, Medical Director for Center for Aortic Diseases, and Medical Director for Center for Radiation Heart Disease at the Cleveland Clinic). Claim free CME just for enjoying this episode!  Disclosures: NoneJump to: Pearls – Notes – 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 TTE TTE TTE TTE AP Cranial Pre PCI LAO Caudal Pre PCI RAO Caudal Pre PCI RAO Cranial Pre PCI AP cranial Post PCI Episode Teaching Pearls – radiation associated cardiac disease Radiation-associated cardiac disease (RACD) is a heterogeneous disease that can manifest several years, or decades following radiation exposure to the chest and is associated with high morbidity and mortality. Given the non-specific or vague symptoms, one of the greatest challenges for this patient population may be diagnosing RACD which requires high clinical suspicion.  In patients with a history of chest radiation, we should remember to ask three important questions: 1. What was the total dose of radiation given? 2. How long ago was radiation therapy administered? 3. Was the heart exposed? A cumulative dose of >30 Gray (Gy) chest radiation significantly increases the risk of RACD long-term, but cardiac damage can occur at even lower doses.  Effects from chest radiation can take years to become clinically detectable. Screening for radiation induced coronary artery disease with stress testing should start 5 years following XRT and in low-risk patients (without risk factors for typical coronary artery disease) and continue at 5-year intervals, and 2-year intervals in high-risk patients. Valvular heart disease surveillance should begin 10 years post XRT and can be accomplished with echocardiogram.  Regarding revascularization planning, a Heart Team approach is recommended. However, percutaneous intervention is preferred over bypass surgery in most cases. Notes – radiation associated cardiac disease 1. What is Radiation-Associated Cardiac disease (RACD)? A spectrum of disease that can affect any part of the heart and typically develops anywhere from 5 to 20 years after radiation. It may present with non-specific or vague symptoms. Manifestations include myocarditis, pericarditis (typically early in the course) and well as long term sequela such as myocardial fibrosis, valvular heart disease (regurgitation or stenosis), pericardial disease, vasculopathy (CAD), conduction system disease. Radiation may impact any tissue of the heart: Vascular: microvascular, coronary artery disease, macrovascular (ascending aorta) Valvular: has a longer latency ~10-20 years with the left sided valves being more commonly affected; Aorto-mitral curtain thickening/calcification is a hallmark of previous heart radiation and associated with higher mortality  Conduction: Sick sinus syndrome, AV nodal block, atrial fibrillaiton; infra-nodal conduction disease and RBBB are common. Myocardial: fibrosis in the myocardium leading to HFpEF, or HFrEF; XRT + anthracycline is thought to be synergistic. Pericardial: chronic pericardial inflammation, scarring, calcification, restrictive physiology. Constrictive pericarditis from radiation has a particularly poor prognosis given often concurrent myocardial involvement. 2. What is the Pathophysiology of RACD? The severity of disease is related to total radiation dose, fraction size and volume of the heart in the radiotherapy field. The resulting cell damage leads to activation of the acute inflammatory cascade and pro-fibrotic milieu. 3. What are the additional risk factors for RACD? Therapy-related risk factors: Net dosage (dependent on cancer type and tumor site) > 30Gy received by the heart. Proximity to heart to the radiation field. Concomitant chemotherapy – anthracyclines may particularly have a radiation sensitizing effect, thereby increasing the risk of RACD. Patient-related risk factors: Life expectancy – younger ag

Cardiogenic shock is a state of cardiac dysfunction leading to hemodynamic instability and end-organ hypoperfusion. At the bedside, clinicians take various data points – from history to physical exam to labs/imaging and invasive hemodynamics – to make an assessment of the etiology, severity and management of cardiogenic shock. Health systems have developed “Shock Teams” to collectively interpret this data to deliver the optimal care for each patient. In this episode, Dr. Mark Dela Cruz (Advanced Heart Failure and Transplant Fellow at University of Chicago), CardioNerds Critical Care Series Co-Chairs Dr. Mark Belkin (Advanced Heart Failure and Transplant Fellow at University of Chicago) and Dr. Karan Desai (General Cardiology Fellow at University of Maryland), and CardioNerds Co-Founder Dr. Daniel Ambinder (Structural Fellow at Johns Hopkins Hospital) join Dr. Anu Lala (Director of the AHFT Fellowship, Associate Professor of Medicine and Cardiology at Mount Sinai Hospital and Deputy Editor of the Journal of Cardiac Failure) on a Shock Team Call! Dr. Lala leads us in a discussion of the systematic bedside evaluation of cardiogenic shock, from understanding a patient’s physiology and their humanity, to manage their illness and make a rapid but thorough evaluation when on the Shock Call. Audio editing and episode introduction by CardioNerds Academy Intern, Hirsh Elhence. Claim free CME for enjoying this episode! Disclosures: None Pearls • Notes • References • Guest Profiles • Production Team CardioNerds Cardiac Critical Care PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls and Quotes – Shock Team Call The classic definition of cardiogenic shock was derived from studies of left ventricular dysfunction in the setting of acute myocardial infarction. With the advent of early primary percutaneous coronary intervention (PCI) and trends in cardiovascular disease risk factors, the prevalence of non-ischemic etiologies of cardiogenic shock (e.g., progression/exacerbation of chronic heart failure) has increased significantly.  The diagnosis of cardiogenic shock should be made by integrating key clinical features such as physical exam findings and objective laboratory and imaging data in an iterative fashion. Focused transthoracic echocardiography and invasive hemodynamics are helpful in further characterizing the type of shock and the etiology of cardiogenic shock. Early evaluation of right ventricular function is an important aspect of cardiogenic shock evaluation. Significant RV dysfunction portends poor prognosis, can necessitate more aggressive interventions, and defines the types of mechanical circulatory support necessary.  Classification systems for cardiogenic shock help to further characterize a patient’s illness severity. The INTERMACS and SCAI classification systems are particularly designed to allow for early identification of patients who would most benefit from more advanced interventions such as vasoactive medications or mechanical circulatory support.  Shock Team Calls improve mortality for patients in cardiogenic shock. By rapidly bringing together heart failure specialists, interventional cardiologists, cardiothoracic surgeons, and critical care physicians, appropriate interventions and contingencies can be discussed and quickly implemented without adding delays to patient care. Importantly, these calls should attempt to integrate patient goals of care in order to best serve our patients.  Show notes – Shock Team Call 1. What is the classic definition of cardiogenic shock? The classic definition of cardiogenic shock was initially derived from the Shock Trial published in 1999 (1). In this trial, cardiogenic shock was defined as shock due to left ventricular dysfunction occurring in the setting of acute myocardial infarction in the setting of acute MI as confirmed by specific criteria: Clinical criteria: SBP<90mmHg for at least 30 minutes Need for supportive measures to maintain SBP > 90mmHg End-organ hypoperfusion as defined by cool extremities, UOP <30ml/hr, HR > 60bpm Hemodynamic criteria: CI ≤ 2.2 L/min/m2 BSA PCWP ≥ 15mmHg With the advent of primary percutaneous coronary intervention, non-ischemic etiologies have become more prevalent as the etiology of cardiogenic shock such as decompensation of chronic heart failure, valvular heart disease, etc. As discussed on the episode, cardiogenic shock occurs on a spectrum from a “pre-shock” state to “extremis.” To facilitate early recognition of cardiogenic shock, appropriate phenotyping (e.g., LV-predominant, RV-predominant, biventricular, pericardial, valvular, pulmonary vascular, etc), timely interventions, and allocation of advanced therapies (e.g., mechanical circulatory support), a more granular approach to the classification is needed (see below regarding SCAI c

In this episode, CardioNerds (Amit Goyal), Cardio-OB series co-chair and UT Southwestern cardiology fellow, Dr. Sonia Shah, and episode lead fellow, Dr. Laurie Femnou (UT Southwestern) are joined by Dr. Michael Luna (UT Southwestern) to discuss cardiovascular interventions during pregnancy. We discuss practical considerations for performing coronary angiography and valvular interventions in the pregnant patient, the timing and indication of procedures, and ways to minimize radiation exposure to both mom and baby. Audio editing by CardioNerds Academy Intern, Hirsh Elhence. This episode is made possible with support from Panacea Financial. Panacea Financial is a national digital bank built for doctors by doctors. Visit panaceafinancial.com today to open your free account and join the growing community of physicians nationwide who expect more from their bank. Panacea Financial is a division of Primis, member FDIC. Pearls • Notes • References • Guest Profiles • Production Team CardioNerds Cardio-Obstetrics Series PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls- Cardiac Interventions during Pregnancy Attempt should be made to manage pregnant patients with valvular disease with medical therapy, and cardiac interventions during pregnancy should be considered a last resort. Ideally, procedures in the gravid patient should be performed after 20 weeks gestation to minimize fetal risk.  Specific ways to minimize radiation to the pregnant patient and fetus in the catheterization lab include: using an abdominal shield, radial access for coronary procedures, proper positioning of the C-arm to avoid extreme angulation, using collimation, and minimizing fluoroscopic time, frame rate, and use of cine-acquisition. When appropriate, intracoronary imaging modalities (ie. IVUS or OCT) should also be considered. Fetal monitoring should be performed during any cardiac intervention in the pregnant patient Multidisciplinary involvement and contingency planning are critical for the success of any high-risk cardiac intervention in the pregnant patient. Quatables – Cardiac Interventions during Pregnancy “Meetings including all providers— our cardiac surgical colleagues, cardiac anesthesiologists, and our obstetrics team—in the care of [pregnant] patients has to be had well ahead of a cardiac procedure to plan every detail.” Show notes – Cardiac Interventions during Pregnancy 1. What are special considerations for performing a balloon valvuloplasty in a pregnant patient with mitral stenosis?  In pregnant patients with severe mitral stenosis who cannot be adequately managed with medical therapy, percutaneous balloon mitral valvuloplasty (PMBV) is the treatment of choice given the high risk of morbidity and fetal loss with cardiac surgery. Ideally, procedures in the gravid patient should be performed after 20 weeks gestation to minimize risk to the fetus.  Assessment of valve anatomy and consideration of the Wilkin’s score are especially important in pregnant patients to minimize the risk of peri-procedural complications. PBMV should performed at experienced centers with cardiac surgery and MFM available. Complications of PBMV are rare but include atrial perforation, cardiac tamponade, arrhythmias, emboli, mitral regurgitation, hypotension and maternal death. Mechanical support should be readily available and a delivery strategy in place in case there is sudden maternal or fetal deterioration. 2. What are ways to minimize radiation exposure in the catheterization lab to the pregnant patient and fetus? The general principle for imaging during pregnancy is similar to imaging for the general population, with the goal of radiation exposure being as low as reasonably achievable (ALARA). The mean radiation exposure to the unshielded abdomen is 1.5 mGy, and <20% of this reaches the fetus.  Specific ways to minimize radiation to the pregnant patient and fetus in the catheterization lab include the following: using an abdominal shield, radial access for coronary procedures, proper positioning of the C-arm to avoid extreme angulation, using collimation, and minimizing fluoroscopic time, frame rate, and use of cine-acquisition. When appropriate, intracoronary imaging modalities (ie IVUS or OCT) should also be considered. 3. What should we know about coronary angiography and revascularization in the pregnant woman? According to a large US-based study of 859 patients presenting with acute myocardial infarction during pregnancy and the postpartum period, less than half of patients undergo cardiac catheterization. In stable, low-risk NSTEMI, a non-invasive approach should be considered per ESC guidelines. In pregnant patients who present with STEMI, PCI is the preferred revascularization strategy. Radial access should be used if possible, as femoral ar

CardioNerds Rounds Co-Chair, Dr. Karan Desai, joins Dr. Michelle Kittleson (Director of Postgraduate Education in Heart Failure and Transplantation, Director of Heart Failure Research, and Professor of Medicine at the Smidt Heart Institute at Cedars-Sinai) to discuss challenging cases of hypertrophic cardiomyopathy. As a guideline author on the 2020 ACC/AHA Hypertrophic Cardiomyopathy Guidelines, Dr. Kittleson shows us how the latest evidence informs our management of HCM patients, while sharing many #Kittlesonrules and pearls on clinical care. Come round with us today by listening to the episodes now and joining future sessions of #CardsRounds! This episode is supported with unrestricted funding from Zoll LifeVest. A special thank you to Mitzy Applegate and Ivan Chevere for their production skills that help make CardioNerds Rounds such an amazing success. All CardioNerds content is planned, produced, and reviewed solely by CardioNerds. Case details are altered to protect patient health information. CardioNerds Rounds is co-chaired by Dr. Karan Desai and Dr. Natalie Stokes.  Speaker disclosures: None Cases discussed and Show Notes • References • Production Team CardioNerds Rounds PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Show notes – Hypertrophic Cardiomyopaty Cases Case #1 Synopsis: Two non-white brothers in their early 20s come to clinic to establish care. They have no cardiopulmonary symptoms, normal EKGs and normal echos, but there was a possible family history of HCM. Their mother had LV hypertrophy and underwent septal myectomy, but she could not afford genetic testing and was no longer in the patients’ lives. The path report suggested “myocyte hypertrophy without disarray or bundles of myocytes.” How would you advise these patients regarding screening and surveillance? Listen to #CardsRounds for the full details!  Quotes from Case #1: “Let’s take a walk down memory lane and let’s get to our evolution of understanding hypertrophic cardiomyopathy… [our understanding] follows the parable of the six blind men and the elephant. Each of the six blind man approached it from different angles, its tusk, its ear, its tail, and they all try to convince each other what an elephant is … because none of them can see the big picture.” Dr. Kittleson on the history of HCM and coming to a unifying diagnosis  “The next time you are sitting there mashing your teeth because you have to memorize what the HCM murmur does squat to stand, Valsalva, or handgrip … remember you are standing on the shoulder of Giants. They [Drs. Braunwald and Morrow] pioneered surgical myectomy based on physical exam and cath lab findings” Dr. Kittleson on the physical exam guiding HCM management Takeaways from Case #1 Before we round, we think it is important to get on the same page regarding the nomenclature around HCM. Since the original characterization of hypertrophic cardiomyopathy (HCM) more than 60 years ago (see the Braunwald Chronicles for the origin stories!), different terms have been used to describe the disease. These include idiopathic hypertrophic subaortic stenosis, hypertrophic obstructive cardiomyopathy (HoCM), and “burnt out HCM” when heart failure develops. The 2020 guideline committee recommended a common language to avoid confusion: since left ventricular (LV) outflow tract obstruction (LVOTO) occurs in >60% of patients over time, but one-third remain non-obstructive, the recommendation is t0 call the disease state HCM with or without outflow tract obstruction. Dr. Kittleson added that when heart failure develops we should characterize the pathology as HCM with heart failure rather than “burnt out HCM.”  Do we use HCM to describe any LV that has thick walls? Some clinicians will use HCM to describe all disease states that can lead to increased LV wall thickness, including those associated with systemic disorders such as RASopathies, mitochondrial myopathies, glycogen/lysosomal storage diseases, Fabry’s disease, hemochromatosis, Danon disease, and amyloidosis (especially in adults). However, the pathophysiologic mechanisms, genetic underpinnings, and treatment of these diseases are different. Secondary causes of left ventricular hypertrophy (LVH) – such as athlete’s heart and hypertensive disorders – can also cause confusion with identifying the correct terminology and diagnosis. As Dr. Kittleson (and the guidelines) made clear, the clinical definition of HCM is a disease state in which (1) the morphologic expression is restricted to the heart, characterized primarily by LVH in the absence of another systemic; (2) a metabolic or cardiac cause; (3) and for which a disease-causing sarcomere (or sarcomere-related) variant is identified or genetic etiology remains undetermined. See some of our original CardioNerds episodes to review the c

CardioNerds (Amit Goyal and Daniel Ambinder) join CardioNerds Ambassadors Dr. Pablo Sanchez (FIT, Stanford University) and Dr. Christine Shen (FIT, Scripps Clinic) for a discussion with Dr. Bob Harrington (Interventional Cardiologist, Professor of Medicine, and Chair of the Department of Medicine at Stanford University) about diversity and inclusion in the field of cardiology. This episode discusses Dr. Harrington’s broader approach to mentorship, sponsorship, and allyship; and particularly how (and why) he used his position as the president of the American Heart Association to advocate against all-male panels, or “manels.” Listen to the episode to learn the background and motivations behind his evidence-based efforts to make Cardiology a more inclusive field. Special message by California ACC State Chapter President, Dr. Jamal Rana. The PA-ACC & CardioNerds Narratives in Cardiology is a multimedia educational series jointly developed by the Pennsylvania Chapter ACC, the ACC Fellows in Training Section, and the CardioNerds Platform with the goal to promote diversity, equity, and inclusion in cardiology. In this series, we host inspiring faculty and fellows from various ACC chapters to discuss their areas of expertise and their individual narratives. Join us for these captivating conversations as we celebrate our differences and share our joy for practicing cardiovascular medicine. We thank our project mentors Dr. Katie Berlacher and Dr. Nosheen Reza. Video Version • Notes • References • Production Team Claim free CME just for enjoying this episode! There are no relevant disclosures for this episode. The PA-ACC & CardioNerds Narratives in Cardiology PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Video version – Diversity and Inclusion https://youtu.be/SnUadVRhH70 Quotables – Diversity and Inclusion “If senior men don’t change the field, it’s not going to change. We have the senior positions. We have to change it.” “You’re missing talent. You’re missing talent of the women who have decided not to go into Cardiology. I say to a lot of my male colleagues…don’t you care about the health of our specialty? Don’t you want the very best people going into it?” “How great is that–to open up an artery in the middle of the night?… What could be better than that?…Why would you not want to be a cardiologist? Frankly, maybe the field is not so friendly to women…And that bothers me greatly because I love the specialty.” “To those who have been given much, much is expected. That’s what people like me should do.” Dr. Bob Harrington Show notes – Diversity and Inclusion What are the gender disparities in the field of Cardiology? 45.8% of residents and fellows in ACGME-accredited programs are women. 14.9% of cardiologists are women. 8% of interventional cardiologists are women [1]. 30.6% of male faculty were full professors, while 15.9% of female faculty are full professors [2]. Men are more likely to be influenced by positive attributes of a field, while women are more likely to be influenced by negative attributes [3]. 3% of percutaneous coronary interventions in the United States are performed by female operators [4]. What is mentorship, sponsorship, and allyship? A mentor provides advice and helps someone develop a skill. A sponsor is an advocate who helps someone secure career advancement opportunities. An ally partners with people, utilizing their power and influence to champion the rights of others [5]. According to some studies, women report less sponsorship experiences than men. Additionally, in women it seems to translate less frequently into experiences that further their career (speaking engagements, serving on editorial boards, etc) [6]. “I’m a mentor to a few people, I’m a sponsor to many, and I’m an ally to all.” – Dr. Bob Harrington Why is a diverse cardiovascular workforce so important? Teams that are diverse pursue innovative and creative solutions. Medicine requires meaningful connections and having a physician with a common background enhances the patient-doctor interaction by a spectrum of constructive effects. Minority groups are less likely to be treated with effective cardiac medications [7]. There continue to be barriers in clinical trials to include diverse and underrepresented patients [8]. A diverse workforce of clinical scientists is crucial to promoting diversity in clinical trials, including understanding the problem, asking the right questions, and proposing solutions [9]. References AAMC 2019. Physician Specialty Data Report. Accessed November 18, 2021. Blumenthal DM, Olenski AR, Yeh RW, et al. Sex Differences in Faculty Rank Among Academic Cardiologists in the United States. Circulation. 2017;135(6):506-517. doi:10.1161/CIRCULATIO

CardioNerds (Amit Goyal and Daniel Ambinder), are joined by guest host Dr. Alex Pipilas (CardioNerds Ambassader, Boston University), and Cleveland Clinic fellows, Dr. Gary Parizher, Dr. Ambreen Ali, and Dr. Tiffany Dong. They discuss a case of an 18-year-old man with Autism Spectrum Disorder presented with advanced nonischemic dilated cardiomyopathy. Due to anxiety, he was unable to tolerate right heart catheterization, and the initial evaluation for advanced heart failure therapies was deferred. With assistance from a multidisciplinary team, catheterization was successful, and he underwent cardiac transplantation. Faculty experts, Dr. Richard Dane Meredith (Cardiovascular Imaging, Mission healthcare), Dr. Julie Niezgoda (Congenital Cardiac Anesthesiologist, CCF), and Dr. Ran Lee (Critical Care Cardiology and Advanced HF/Transplant Cardiologist, CCF) provide the E-CPR for this episode. Audio editing by CardioNerds Academy Intern, Dr. Leticia Helms. Claim free CME just for enjoying this episode!  Disclosures: NoneJump to: Pearls – Notes – 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 Episode Teaching Pearls – Heart Failure with Autism Spectrum Disorder Autism spectrum disorder should not be regarded as a contraindication to organ transplantation. Respect for patient discomfort with procedures, and efforts to mitigate that discomfort, are essential. A multidisciplinary team approach, especially one utilizing allied health support services, is important to provide care to adolescent patients with advanced organ dysfunction, particularly those with developmental disabilities. Notes – Heart Failure with Autism Spectrum Disorder Autism spectrum disorder (ASD) is a developmental disability characterized by impairments in social interaction and the presence of restricted, repetitive patterns of behaviors, interests, or activities (2). In 2016 the CDC estimated one in 54 children age 8 had ASD (3). Despite ASD’s prevalence, studies of organ transplantation in children and adolescents with developmental disabilities are lacking. Guidelines from the International Society for Heart Lung Transplantation indicate that heart transplantation cannot be recommended in patients suffering from severe cognitive-behavioral disabilities (4). However, the definition of “severe” is not clear, so the assessment of severity of a cognitive impairment, as well as whether the impairment constitutes a contraindication to organ transplantation, falls to healthcare providers on a case-by-case basis.             Cardiac transplantation in a patient with ASD has been documented previously (5). Nonetheless our case represents an important example of advocacy for lifesaving care in patients with developmental disability. Without any one component of the team taking care of our patient, including physicians and allied healthcare providers, he would have died of refractory cardiogenic shock. However, with individualized care and a multidisciplinary combined effort, his providers were able to overcome the obstacles posed by his ASD and deliver indicated interventions. References – Heart Failure with Autism Spectrum Disorder 1.  Baran, David A., et al. “SCAI clinical expert consensus statement on the classification of cardiogenic shock” Catheterization and Cardiovascular Interventions 94.1 (2019): 29-37. 2. American Psychiatric Association: Diagnostic and Statistical Manual of Mental Disorders. 5th edition. Arlington, VA: American Psychiatric Association, 2013. 3. Baio J, Wiggins L, Christensen D, et al. Prevalence of Autism Spectrum Disorder among children aged 8 years – Autism and Developmental Disabilities Monitoring Network, 11 Sites, United States, 2014. MMWR Surveillance Summaries 2018; 67:1-23. 4. Mehra M, Canter C, Hannan M, et al. The 2016 International Society for Heart Lung Transplantation listing criteria for heart transplantation: a 10-year update. J Heart Lung Transplant 2016; 35:1-23. 5. Bailey D, Schneider L, Maeda K, et al. Orthotopic heart transplant in a child with nonverbal autism. Austin J Autism & Relat Disabil 2016;2:1017. 6. Chen Y, Shlofmitz E, Khalid N, et al. Right Heart Catheterization-Related Complications: A review of the literature and best practices. Cardiol Rev 2020;28:36-41. CardioNerds Case Report Production Team Karan Desai, MD Amit Goyal, MD Daniel Ambinder, MD

Pregnancy is a hypercoagulable state associated with increased risk of thromboembolism. Managing anticoagulation during pregnancy has implications for both the mother and the fetus. CardioNerd Amit Goyal joins Dr. Akanksha Agrawal (Cardiology Fellow at Emory University), Dr. Natalie Stokes (Cardiology Fellow at UPMC and Co-Chair of the Cardionerds Cardio-Ob series), and Dr. Katie Berlacher (Program Director of the Cardiovascular Disease Fellowship and Director of the Women’s Heart Program at UPMC) as they discuss the common indications for anticoagulation and their management before, during, and after pregnancy. In this episode, we focus on management of pregnant patients with mechanical valves and venous thromboembolism. Audio editing by CardioNerds Academy Intern, Dr. Maryam Barkhordarian. Pearls • Notes • References • Guest Profiles • Production Team CardioNerds Cardio-Obstetrics Series PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls- Pregnancy and Anticoagulation Pregnancy is a hypercoagulable state. Pregnancy-associated VTE is a leading cause of maternal morbidity and mortality. The use of anticoagulation requires a balance between the risks and benefits to the mother and her fetus. The agent of choice for anticoagulation during pregnancy depends on the indication, pre-pregnancy dose of vitamin K antagonist (VKA), and the trimester of pregnancy. For instance, patients with mechanical heart valves, warfarin is generally recommended in the first trimester if the daily dose is less than 5 mg and as the first option for all patients with mechanical valves in the 2nd and 3rd trimester. Use of direct oral anticoagulants (DOACs) has not been systematically studied, they do cross the placenta and their safety remains untested. Warfarin crosses the placenta but is not found in breast milk. LMWH does not cross the placenta and is not found in breast milk. Thus, both these agents can be used by a lactating mother. Quatables – Pregnancy and Anticoagulation “[We] can’t highlight enough that good communication and documentation is vital in such situations” says Dr. Berlacher while discussing the role of a multidisciplinary team including cardiologists, obstetricians and fetal medicine physicians in taking care of a pregnant patient on anticoagulation. “What I love about cardio-obstetrics is that we really can help women in a time that is so important in their life…this is one of the most memorable times in their life..” says Dr. Berlacher when asked what makes your heart flutter about cardio-obstetrics. “Knowledge is power…not just for providers, but also for the patients” says Dr. Berlacher emphasizing the importance of clear communication between physicians and patients. Show notes – Pregnancy and Anticoagulation 1. What makes pregnancy a hypercoagulable state? Pregnancy is a hypercoagulable state associated with higher risk of thromboembolic phenomenon. The three components of Virchow’s triad: hypercoagulability, stasis, and endothelial injury are all present during pregnancy. This leads to a 5-fold increased risk of venous thromboembolism (VTE) during pregnancy that persists for 12 weeks postpartum. The risk for VTE seems to be highest in the first 6 weeks postpartum, with a higher prevalence of clot in the left lower extremity. There are additional risk factors for developing VTE in the postpartum period besides pregnancy itself, and this includes but is not limited to preeclampsia, emergent c-section, hypertension, smoking, and postpartum infection. Choosing anticoagulant therapies during pregnancy involves a fine balance between the risks and benefits to both the mother and fetus. A multidisciplinary team involving the obstetrician, cardiologist, and maternal-fetal medicine team is critical to guide anticoagulation in pregnancy. 2. What are some of the common indications for anticoagulation during pregnancy? One of the most common indications for anticoagulation in pregnancy is valvular disease, and specifically mitral valve stenosis with atrial fibrillation or a prior embolic event. Patients with a mechanical heart valve will require anticoagulation during pregnancy. Patients with a bioprosthetic valve (surgical or transcatheter) are generally continued on low dose Aspirin; in the uncommon scenario of pregnancy in the first 3-6 months following implantation of a bioprosthetic valve, the decision to pursue anticoagulation is individualized. Other indications include acute VTE, atrial fibrillation, antiphospholipid syndrome, and inherited thrombophilias that may predispose a patient to developing VTE during pregnancy. 3. For mechanical heart valves, how do anticoagulation recommendations vary based on trimester? The European Society of Cardiology has divided various valvular heart diseases into 4 classes as per the modifie

The CardioNerds are thrilled to launch The Cardiac Critical Care Series! The series Co-Chairs – Dr. Mark Belkin (Advanced Heart Failure FIT, U Chicago), Dr. Yoav Karpenshif (FIT, U Penn), Dr. Eunice Dugan (CardioNerds Academy Chief Fellow and FIT, Cleveland Clinic), and Dr. Karan Desai (CardioNerds Academy Editor and FIT, U Maryland) – join CardioNerds Co-Founders, Amit Goyal and Daniel Ambinder to delve into high-yield topics in critical care cardiology. We kickstart this series with one of the early pioneers and national leaders in cardiac critical care – Dr. Jason Katz, Director of Cardiovascular Critical Care and Co-Director of Mechanical Circulatory Support and the CICU at Duke University Medical Center. In this episode, we learn about Dr. Katz’s career path and what motivated him to train in Critical Care Cardiology. He shares early struggles, notable changes in this field’s nascent period, and ongoing challenges in training and practice. We discuss collaboration with other cardiac and non-cardiac specialties and their importance in comprehensive care. Furthermore, we discuss how to advance critical care research, including the Critical Care Cardiology Trials Network and future randomized controlled trials to inform our practice and develop standardized protocols. In this small but rapidly growing field, we learn there is much to discover together. Audio editing by CardioNerds Academy Intern, Hirsh Elhence. Claim free CME for enjoying this episode! Disclosures: None Pearls • Notes • References • Guest Profiles • Production Team CardioNerds Cardiac Critical Care PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls and Quotes “I think it’s really important not to be afraid of change in order to potentially succeed […] it’s okay to not entirely know what you want to do.” – Dr. Katz when sharing his non-direct career path in a novel field. “There is no greater team sport in cardiology than Cardiac Critical Care” and “I oftentimes think of the Critical Care Cardiologist as sort of the conductor that helps to orchestrate [the team]…” – Dr. Katz when discussing the importance of multidisciplinary teams and need to collaborate with other cardiac and non-cardiac sub-specialties. Many general surgical or medical residency/fellowship graduates are not comfortable caring for patients in the critical care setting. There is a need to revamp critical care training without significantly prolonging training time in order to complement and enhance our current workforce to care for complex, critically ill cardiac patients. “I don’t think there’s necessarily a one size fits all model, and I think we should be malleable or adaptable to the needs of our trainees and the needs of our patients.” – Dr. Katz when discussing training pathways in Critical Care Cardiology or combining Critical Care with other subspecialties like Interventional Cardiology or Advanced Heart Failure. Dr. Katz suggests that when choosing a Critical Care Cardiology training program: “consider geography, the flexibility of the curriculum, the overall fellowship and social experience, and the clinical setting. Everything that’s really important to choosing a cardiology fellowship is more important in my mind than if they actually have a standardized, cardiac critical care pathway.” Show notes 1. What are some recent changes in the field of Critical Care Cardiology? Compared to even just a decade ago, there is a growing interest from medical students to young faculty in pursuing a career in critical care cardiology. At the same time there is evidence that the patient demographics in our CICUs are changing, including more multi-organ dysfunction and many non-cardiac diagnoses. In a recent paper from the Critical Care Cardiology Trials Network (CCCTN), the proportion of patients with a primary diagnosis of acute coronary syndrome was only approximately 32%. Following overall trends in heart failure, a greater proportion of CICU patients have heart failure and/or heart failure phenotype cardiogenic shock requiring clinicians to be facile with the spectrum of mechanical support devices. These demographic and workforce trends are requiring cardiologists to re-think how to best meet the needs of the modern CICU. 2. What continue to be some challenges in practicing Critical Care Cardiology? CICU patients are a heterogenous group with varying baseline characteristics, comorbidities, illness severity, and treatment responses. Since distinct pathophysiologic targets are lacking, challenges exist when devising strategies to improve outcomes. Similarly, these challenges extend to developing and executing research protocols to inform management. As Dr. Katz discussed on the episode, the lack of standardization, consistent terminology, and even who belongs i

CardioNerds Tommy Das (Program Director of the CardioNerds Academy and cardiology fellow at Cleveland Clinic) and Rick Ferraro (Director of CardioNerds Journal Club and cardiology fellow at the Johns Hopkins Hospital) join Dr. Erin Michos (Associate Professor of Cardiology at the Johns Hopkins Hospital and Editor-In-Chief of the American Journal of Preventative Cardiology) for a discussion about the effect of DHA and EPA on triglycerides and why DHA/EPA combinations may have exhibited limited benefits in trials. This episode is part of the CardioNerds Lipids Series which is a comprehensive series lead by co-chairs Dr. Rick Ferraro and Dr. Tommy Das and is developed in collaboration with the American Society For Preventive Cardiology (ASPC). Relevant disclosures: None Pearls • Notes • References • Guest Profiles • Production Team CardioNerds Lipid Series PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls The best intervention for heart disease is prevention! The InterHeart trial showed that 9 modifiable risk factors (dyslipidemia, smoking, hypertension, diabetes, abdominal obesity, dietary patterns, physical activity, consumption of alcohol, and psychosocial factors) predict 90% of acute myocardial infarction. So many acute events can be prevented1. Atherosclerotic vascular disease events increase across a range of triglyceride levels, even from 50-200mg/dL. So even in a relatively normal range, lower triglycerides seem to be better. Over ¼ of US adults have triglycerides over 150. While 8% of US adults take fish oil supplements, multiple meta-analyses have failed to show any benefit to the use of dietary omega-3 supplementation2. Dietary supplements these are not meant for medical use and are not studied or regulated as such! Show notes 1. What are DHA and EPA? DHA, or docosahexaenoic acid, and EPA, or eicosapentaenoic acid, are n-3 polyunsaturated fatty acids, also known as omega-3 fatty acids. These compounds have been of considerable interest for over two decades given observed association of high dietary omega-3 fatty acid intake with reduced cardiovascular events3. As both are important omega-3 fatty acids, trials on the benefits of DHA and EPA have often focused on the two compounds in combination. 2. What was the GISSI-Prevenzione Trial and why was it Important? GISSI-Prevenzione trial (Lancet 1999), was one of the earliest trials to study DHA and EPA4. In this trial, the authors evaluated the effect of omega-3 supplementation as a combination pill of DHA and EPA on cardiovascular events and death in patients with recent myocardial infarction (the last three months). Over a 3.5-year follow-up period, participants treated with DHA/EPA combination experienced a significant reduction in death, nonfatal MI, and stroke. As this was an early trial, patients were largely not on statins, as these were not supported at the time of study initiation (Only 5% were on cholesterol-lowering medications at baseline, and only 45% were on cholesterol-lowering therapy at study completion). The benefits seen in this trial may not extend to modern practice with patients on contemporary background therapy. The trial participants were also not representative of our modern patients for a variety of other reasons. 85% of participants in the trial were men. 42.2% of patients in EPA/DHA arm were current smokers, and 35.4% were prior smokers. Only 14.2% of patients had diabetes and 14.7% with BMI >30. Notably, the decrease in triglycerides in this trial was only 3%, implying that triglyceride lowering did not entirely explain the benefit in cardiovascular events seen. 3. What about the data after the GISSI-Prevensione Trial? After this positive trial for DHA/EPA in combination, subsequent trial data in support of DHA/EPA has been less robust. The Alpha Omega trial in 2010, ORIGIN in 2012, ASCEND in 2018, and VITAL in 2019 were all trials of DHA/EPA combinations versus placebo, and all exhibited no significant differences in cardiovascular events with DHA/EPA use5–8. The recent STRENGTH trial, published in 2020, also showed no reduction in cardiovascular events when taking DHA/EPA in combination (and as discussed in CardioNerds episode 136!)9. This remained the case upon sub-analysis of patients from the STRENGTH trial with the highest levels of serum EPA, who again exhibited no cardiovascular benefit. 4. Why then don’t DHA and EPA seem to work in combination? In short, we do not know. It seems that the beneficial effects of EPA – which as monotherapy has shown benefit across numerous trials (namely JELIS and REDUCE-IT) – are somehow offset by the combination with DHA, via a mitigation of anti-inflammatory processes or otherwise – this remains theoretical10,11. The EVAPORATE trial of purified EPA showed lower total plaque in participants taking EPA, suggesti

CardioNerds (Amit Goyal and Daniel Ambinder), join CardioNerds FIT Ambassador, Dr. Natasha Cuk and her co-fellows, Dr. Lily Stern, and Dr. Paul Marano from the Cedars-Sinai Cardiology Fellowship for some late afternoon smoothies on the beach. They discuss the case of a 46-year-old woman who presented with sudden cardiac arrest and was ultimately found to have a mobile intraluminal aortic thrombus adherent to a penetrating ulcer in the ascending aorta. This mobile thrombus was ultimately thought to be the cause of transient ischemia and the patient’s cardiac arrest. We discuss a differential for sudden cardiac arrest, initial management after resuscitated cardiac arrest, a differential for arterial thrombus, and review an illness script for penetrating atherosclerotic ulcers. Dr. Dominick Megna provides the provides the E-CPR for this episode. Audio editing by Dr. Gurleen Kaur (Director of the CardioNerds Internship). This Case Report has been published in JACC Case Reports! Claim free CME just for enjoying this episode!  Disclosures: NoneJump to: Pearls – Notes – 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! Episode Teaching https://twitter.com/LilySternMD/status/1460811173113184263?s=20 Pearls – Cardiac Arrest due to Aortic Thrombus After cardiac arrest, the initial ECG obtained after the return of spontaneous circulation can provide important information on the etiology of the arrest. The ECG can narrow our structured differential, for which one approach would be the following breakdown: acute ischemic events, structural heart disease, arrhythmogenic syndromes with no structural abnormality, and then non-cardiac causes such as drugs, toxins, trauma, metabolic arrangements The risk vs benefit of emergent angiography after sudden cardiac arrest depends on balancing the potential benefit from revascularization in an acute ischemic event vs bleeding risks and potential delays in other aspects of care, particularly given that a large percentage of mortality is related to neurologic injury from the arrest, which would not be impacted by immediate angiography. The available randomized controlled trial evidence has not demonstrated a survival or neurologic outcome benefit to immediate angiography, and the decision depends on weighing the risk/benefit for each patient. Due to high flow, a thrombus in the aorta should prompt an investigation for causes focused on the other two ‘points’ of Virchow’s triad (aside from stasis): endothelial injury and hypercoagulability. A penetrating atherosclerotic ulcer (PAU) is a deep atherosclerotic lesion where there is a focal ulceration of the elastic lamina that extends through the medial layer of the aortic wall. These lesions are most commonly associated with extensive atherosclerosis, but can also occur related to inflammatory, infectious, or traumatic causes. A PAU is a type of acute aortic syndrome and accounts for up to 8% of total acute aortic syndromes. It may present with a spectrum of symptoms, including as an incidental finding on cardiothoracic imaging or a severe chest and back pain, like an aortic dissection. While it is a subtype of aortic syndrome, PAU can also progress to become aortic dissection and rupture. Notes – Cardiac Arrest due to Aortic Thrombus 1. How might a post-ROSC ECG help determine the etiology of a sudden cardiac arrest? During our case, we discussed a systematic approach to the differential diagnosis for sudden cardiac arrest. We broke down the causes into the buckets of: Acute ischemic events Structural heart disease Arrhythmogenic syndromes with no structural heart disease Non-cardiac causes such as drugs, toxins, trauma, and metabolic arrangements The post-ROSC ECG can provide immediate information to help narrow our differential. Evidence of acute ischemia (e.g. STEMI) would provide a likely etiology and would direct immediate next steps. We can look at ECG features such as axis and conduction abnormalities to look for evidence of an underlying structural abnormality. We can also see features of arrhythmogenic syndromes without underlying structural defects, such a short or long QT or a Brugada pattern. 2. Should all patients who present with sudden cardiac arrest and for whom ROSC is achieved undergo immediate coronary angiography? In considering the timing of coronary angiography after sudden cardiac arrest, clinical experience and the available evidence indicate a tension between: The high pre-test probability for acute ischemic events as the etiology for VT/VF arrest, and possible improvement in post-ROSC outcomes from immediate coronary angiography (and revascularization). A large portion of the morbidity and mortality associated with sudden cardiac arrest is driven by neurologic injur

CardioNerds (Amit Goyal and Daniel Ambinder),  ACHD series co-chair Dr. Agnes Koczo (UPMC), and episode FIT lead, Dr. Natasha Wolfe (Washington University) join Dr. Ari Cedars   (Director of the Adult Congenital Heart Disease Program at Johns Hopkins) for a discussion about coarctation of the aorta.   In this episode we discuss the presentation and management of unrepaired and repaired coarctation of the aorta in adults. We discuss the unique underlying congenital anatomy of coarctation and how that impacts physiology, clinical presentation, and diagnostic findings. We discuss the importance of long-term routine follow-up and screening of patients (including those who have been “repaired”) for common complications such as hypertension, re-coarctation, and aneurysm development. We end with a discussion of treatment options for coarctation and its complications. Audio editing by CardioNerds Academy Intern, Dr. Maryam Barkhordarian. The CardioNerds Adult Congenital Heart Disease (ACHD) series provides a comprehensive curriculum to dive deep into the labyrinthine world of congenital heart disease with the aim of empowering every CardioNerd to help improve the lives of people living with congenital heart disease. This series is multi-institutional collaborative project made possible by contributions of stellar fellow leads and expert faculty from several programs, led by series co-chairs, Dr. Josh Saef, Dr. Agnes Koczo, and Dr. Dan Clark. The CardioNerds Adult Congenital Heart Disease Series is developed in collaboration with the Adult Congenital Heart Association, The CHiP Network, and Heart University. See more Claim free CME for enjoying this episode! Disclosures: None Pearls • Notes • References • Guest Profiles • Production Team CardioNerds Adult Congenital Heart Disease PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls Coarctation of the aorta can occur as a discrete stenosis or as a long and hypoplastic hypoplastic aortic arch segment. Most commonly it is a discrete stenosis located at the insertion site of the ductus arteriosus just distal to the left subclavian artery. Three quarters of patients with coarctation of the aorta also have a bicuspid aortic valve. Hypertension is the most common long-term complication of coarctation of the aorta, whether repaired or unrepaired. Unrepaired coarctation is a rare cause of secondary hypertension in young adults with a difference in upper extremity and lower extremity BP by ≥ 20 mmHg. Systemic hypertension may not be consistently identifiable at rest in those with repaired coarctation, thus guidelines recommend ambulatory blood pressure monitoring or stress testing to identify hypertension with exertion. Chest and brain imaging via CT or MRI should be done every 5-10 years to screen for other long-term complications including re-coarctation (rate ~11%), aortic aneurysm development (higher risk in those with concurrent bicuspid aortic valve), pseudoaneurysm, aortic dissection, and cerebral aneurysms. Repair of coarctation or re-coarctation is indicated for patients who are hypertensive with a BP gradient ≥ 20 mmHg (Class I recommendation). Catheter-based stenting is the preferred approach when technically feasible. Show notes 1. What is the proposed embryologic origin of coarctation of the aorta? The aortic arch and its branches develop at 6-8 weeks fetal gestation. We all start with six aortic arches that go on to become the great arteries of the head and neck. The 4th arch forms the thoracic aortic arch and isthmus. The 6th arch persists as the proximal pulmonary arteries and ductus arteriosus. Thoracic aortic coarctation is therefore a manifestation of abnormal embryologic development of the 4th and 6th arches. There are two main theories regarding how aortic coarctation occurs. The first is the “ductus tissue theory”, which proposes that coarctation develops as the result of migration of ductal smooth muscles cells in the periductal aorta, with subsequent constriction and narrowing of the aortic lumen. The “hemodynamic theory” proposes that coarctation develops because of hemodynamic disturbances from other left sided congenital lesions that reduce the volume of blood flow through the fetal aortic arch – recall the “no flow, no grow” tenet. In all likelihood, both are true and play a role in aortic coarctation embryologic development. 2. What are the key features of aortic coarctation anatomy? Coarctation is, strictly speaking, a congenital narrowing of the aorta. Most commonly, this occurs at the insertion of the ductus arteriosus just distal to the left subclavian artery and is more of an isolated ridge or shelf that causes obstruction and narrowing. There are several other variants, however and include discrete thoracic lesions, long-segmen

CardioNerds (Amit Goyal and Daniel Ambinder), Cardio-OB series co-chair and University of Texas Southwestern Cardiology Fellow, Dr. Sonia Shah, and episode FIT lead and UT Southwestern Cardiology Fellow Dr. Laurie Femnou discuss valvular heart disease in pregnancy with cardio-obstetrics expert Dr. Uri Elkayam, Professor of Medicine and OB Gyn at the University of Southern California. In this pearl-packed episode, we discuss the diagnosis, acute management, and long-term considerations of valvular heart disease in pregnancy. Through a series of cases, we review the physiologic changes in pregnancy that make certain valvular lesions well-tolerated, while others are associated with a much higher risk of peripartum complications. We also discuss which patients to consider referring for valvular intervention, the ideal timing, and which valvular interventions are safest in the peripartum period. We promise, you won’t want to miss this clinically high-yield episode with Dr. Elkayam, the father of cardio-obstetrics and an absolute legend in the field! Audio editing by CardioNerds Academy Intern, Adriana Mares. Pearls • Notes • References • Guest Profiles • Production Team CardioNerds Cardio-Obstetrics Series PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls Most women with severe valvular heart disease can be managed medically throughout pregnancy. Right sided valvular lesions are generally better tolerated than left-sides lesions, and regurgitant lesions are generally better tolerated than stenotic lesions. However, the context and etiology of the valve dysfunction must be taken into consideration. Severe tricuspid valve regurgitation, for example, can be associated with a failing right ventricle and undiagnosed pulmonary hypertension.  Changes in BNP, severity of symptoms, and right ventricular systolic pressure (RVSP) assessed by echocardiography can be helpful in differentiating normal pregnancy-related symptoms from symptoms due to hemodynamically significant valvular lesions. Valvular interventions during pregnancy are safe when well-planned and performed by experienced operators, and they can significantly improve morbidity and mortality in women who remain symptomatic despite medical management. A multidisciplinary team-based approach is important when managing patients with valvular heart disease during pregnancy. Quatables “We do not need to perform prophylactic valvular intervention in women prior to pregnancy if they do not meet criteria for intervention otherwise. A patient with regurgitant lesion will tolerate pregnancy well, provided that they are not                candidates for surgery already.” “Valvuloplasty during pregnancy is a great and effective procedure, but restenosis occurs. For women who desire future pregnancies, preconception evaluation is important to determine if valve intervention is indicated prior to conceiving.” Show notes What is the epidemiology of valvular heart disease in pregnancy? Cardiovascular conditions affect up to 4% of pregnancies, with valvular heart disease being the most common cardiac pathology encountered during pregnancy worldwide. In the developing world, rheumatic valve disease is still the most common etiology, with mitral valve most commonly affected, followed by the aortic valve. In the developed world, congenital aortic valve pathology is most common. What are the hemodynamic effects of stenotic vs. regurgitant lesions during pregnancy? In normal pregnancy, there is a significant drop in systemic vascular resistance as early as 5 weeks gestational age. This drop leads to a transient decrease in perfusion to the kidneys, causing an increase in fluid retention and expansion of plasma volume. At the same time, there is an increase in heart rate which becomes more pronounced later in the second trimester. These changes ultimately lead to an increase in cardiac output. Patients with stenotic lesions have a fixed obstruction, and therefore can have a difficult time adjusting to these physiologic changes of pregnancy. In mitral stenosis for example, the increase in heart rate leads to less atrial emptying time in diastole, which leads to an underfilled left ventricle and increase in left atrial preload. In contrast, regurgitation lesions are often better tolerated than stenotic lesions during pregnancy because of the ability of the cardiac chambers to dilate and accommodate the increase in plasma volume. These rules are generally true, provided that the ventricular systolic function is preserved. A patient with functional mitral regurgitation secondary to a failing left ventricle may not tolerate the hemodynamic changes of pregnancy well. What is involved with preconception evaluation and valvular heart disease? Preconception evaluati

CardioNerds (Amit Goyal and Daniel Ambinder), join CardioNerds FIT Ambassador, Dr. Pablo Sanchez, and his co-fellows, Dr. Jimmy Tooley and Dr. Maggie Ning from Stanford University for an important case discussion about an An otherwise healthy young adult presented with fatigue and was found to be in complete heart block due to sarcoidosis. Dr. Ronald Witteles, (Stanford University Program Director for the Stanford Internal Medicine residency program and advanced heart failure specialist who’s particular expertise focuses in the treatment of amyloidosis, sarcoidosis, and cardio-oncology) provides the E-CPR for this episode. Claim free CME just for enjoying this episode!  Disclosures: Dr. Witteles reports that he has served as an advisor for Pfizer, Alnylam, Eidos, Regerenon Pharmaceuticals, Janssen, and IonisJump to: Patient summary – 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! Patient Summary – Notes – Complete Heart Block due to Sarcoidosis An otherwise healthy young adult presented with fatigue and was found to be in complete heart block. Imaging studies were suspicious for cardiac and pulmonary sarcoidosis. Sarcoidosis was confirmed on biopsy. Given the high risk of future cardiac events our patient underwent a dual chamber ICD implantation. He was started on prednisone and methotrexate for immunosuppression. Case Media – Click to enlarge Episode Teaching – Notes – Complete Heart Block due to Sarcoidosis Pearls – Complete Notes – Complete Heart Block due to Sarcoidosis Cardiac sarcoidosis is a disease characterized by noncaseating granulomas involving the heart that can exist alone or together with other organ system involvement Depending on the sites of cardiac involvement it can present as conduction system disease, ventricular arrhythmia, or heart failure Cardiac sarcoidosis should be considered in patients with history of sarcoidosis involving other organ systems who develop left ventricular dysfunction, wall motion abnormalities, or arrhythmias Cardiac sarcoidosis should be considered in patients who present with otherwise unexplained heart block or ventricular tachycardia (VT)  It is generally recommended that patients with cardiac sarcoidosis with an indication for pacemaker receive an ICD at time of implantation regardless of history of VT Notes – Complete Heart Block due to Sarcoidosis 1. What is Sarcoidosis? Sarcoidosis is a rare disorder of inflammation characterized by the formation of noncaseating granulomas in affected tissues. It most commonly involves the pulmonary system, but other organ systems can be involved including the heart. Sarcoidosis typically affects young adults, and its etiology is still uncertain. 2. What is Cardiac Sarcoidosis and how is it diagnosed? Cardiac sarcoidosis (CS) can occur alone or with systemic disease and depending on the cardiac sites of involvement, can present as conduction system disease, ventricular arrhythmia, heart failure, or sudden cardiac death. 3. How is Cardiac Sarcoidosis diagnosed? Diagnosis of CS is challenging as the gold standard is endomyocardial biopsy (EMB), though sensitivity of EMB is low given the often-patchy tissue involvement. Societal guidelines on the diagnosis of CS require either a positive EMB or biopsy-confirmed extracardiac sarcoidosis with evidence of secondary criteria to suggest cardiac involvement – unexplained VT, high grade AV block, third degree AV block, LVEF <40%, or characteristic imaging finding on cardiac MRI and cardiac PET. The diagnosis of CS must be considered in all patients with a diagnosis of extra cardiac sarcoidosis who develop symptoms to suggest cardiac involvement. Additionally, screening for CS should be done in all patients <60 years of age presenting with unexplained Mobitz type II block, 3rd degree AV block, or VT. Our patient was a previously healthy very active gentleman in his 30s with fairly sudden onset of fatigue found to have 100% burden of high-grade AV block and third-degree AV block on ambulatory rhythm monitor. Given his young age and no other explanation for his conduction system disease, he underwent a workup for CS.  Cardiac MRI revealed mesocardial scarring in the mid inferior and anteroseptal walls with prominent mediastinal and hilar lymphadenopathy suggestive of sarcoidosis with pulmonary and cardiac involvement. FDG-PET was also highly suggestive of CS given FDG uptake of the basal septum and lymph nodes. Diagnosis was ultimately confirmed based on FNA of a supraclavicular lymph node, though EMB would have been the appropriate next step if there were no extracardiac sites available for biopsy. 4. What are important considerations of conduction disease associated with cardiac sarcoidosis?

CardioNerds Dan Ambinder, Dr. Tommy Das (Program Director of the CardioNerds Academy and cardiology fellow at Cleveland Clinic), and episode lead, Dr. Teodora Donisan (CardioNerds Academy fellow and incoming Chief fellow and Beaumont Health Internal Medicine resident) join Dr. Matthew Budoff (professor of medicine at David Geffen School of Medicine at UCLA and the Endowed Chair of Preventive Cardiology at Harbor-UCLA Medical Center) for a discussion about triglycerides from pathophysiology to clinical outcomes. This episode is part of the CardioNerds Lipids Series which is a comprehensive series lead by co-chairs Dr. Rick Ferraro and Dr. Tommy Das and is developed in collaboration with the American Society For Preventive Cardiology (ASPC). Triglyceride (TG) metabolism can produce a by-product called remnant lipoproteins, which can be atherogenic. Most guidelines consider hypertriglyceridemia to start at values ≥ 150 mg/dl. It is the most common dyslipidemia, as it can occur in 30% of the general population. Although fasting levels are usually obtained per the current US protocol, there is evidence that non-fasting TG levels might be a better indicator of cardiovascular (CV) risk as these levels may better reflect the usual levels that the body is exposed to. There are multiple primary (genetic) causes of elevated TG, but these are rarer than lifestyle factors, medical conditions, or medications. Genetic association studies are helping better define the level of CV risk stemming from elevated TG-levels, which will impact how we target lifestyle and treatment interventions in the future. #CardsJC STRENGTH Trial Journal Club Relevant disclosures: Dr. Matthew Budoff has funding from General Electric. Pearls • Notes • References • Guest Profiles • Production Team CardioNerds Lipid Series PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls – Triglycerides – Pathophysiology to Clinical Outcomes In the process of metabolizing TG, remnant lipoproteins are formed, which have been shown to promote atherogenesis. TG themselves have not been directly linked to this process and have not been studied in large population studies, and so are considered risk enhancing factors, and not risk factors per se. Elevated triglyceride levels measured on our traditional lipid panels act as a proxy for the Apo-B rich lipoproteins, such as VLDL, which directly cause atherogenesis. Hypertriglyceridemia is defined as TG values of ≥150 mg/dl, although there is emerging evidence that even high-normal values (100-140 mg/dl) can still be associated with increased CV risk. You can think of TG in a similar fashion to glucose values (patients with prediabetes are still at higher CV risk than those with normal glycemic level). These are continuous and not binary variables! Fasting lipid levels are not necessarily a better predictor of CV events than non-fasting lipid levels. A non-fasting TG level can potentially provide information on the body’s metabolism similarly to how we interpret glucose tolerance tests, although there isn’t such a standardized approach in the lipid world yet. Before testing for genetic causes, make sure you review secondary causes of elevated TG. Don’t forget to evaluate for lifestyle factors and medical causes (diabetes, alcohol abuse, hypothyroidism, pregnancy) and to review the medication list (pay attention to thiazides, non-selective beta blockers, antipsychotics and others). TG values of ≥ 175 mg/dl are considered a risk enhancing factor and can aid in the decision to be more aggressive with lifestyle changes or starting treatment. Although treatment will be reviewed in depth in future episodes, Dr. Budoff suggests we “back away from using fibrates for CV event protection.” Even though they are efficient at lowering TG levels, they haven’t been shown to have a beneficial impact on ASCVD. New trials are exploring the role of pemafibrate for CV outcomes (1). Furthermore, EPA treatment can be considered for TG < 500 mg/dl with the goal of CV risk reduction. We should remember that omega-3 dietary supplements are impure, may be stored in improper conditions, and may be unsafe, even though more affordable to patients. Show notes – Triglycerides – Pathophysiology to Clinical Outcomes 1. What is the basic biochemical structure of triglycerides (TG), and how are they metabolized by the body? TG are hydrophobic substances packed into the core of lipoproteins. Lipoproteins are made up of a lipid rich core bound to proteins called apolipoproteins and can travel freely through the extracellular environments inside the body. The main way to transport dietary and endogenous TG to the tissues is through 2 types of TG-rich lipoproteins secreted by the intestine and the liver: chylomicrons and very low-density lipoproteins (VLDL). In orde

CardioNerds (Amit Goyal and Josh Saef) join ACHD fellow Dr. Prashanth Venkatesh and ACHD program director Dr. Jeannette Lin, both from the University of California, Los Angeles, for a deep dive into the complex disease entity that is Ebstein anomaly. They discuss the anatomic features of the dysplastic tricuspid valve as well as the right ventricle in patients with Ebstein anomaly, and how these structural features affect cardiovascular physiology and clinical presentation. This is followed by an in-depth discussion into associated entities including arrhythmias and atrial-level shunts as well as the appropriate multimodality evaluation. Finally, they tackle the difficult question of when and how to intervene, delving into the various interventional treatments and exploring their outcomes using illustrative case-based examples. Audio editing CardioNerds Academy Intern, Pace Wetstein. The CardioNerds Adult Congenital Heart Disease (ACHD) series provides a comprehensive curriculum to dive deep into the labyrinthine world of congenital heart disease with the aim of empowering every CardioNerd to help improve the lives of people living with congenital heart disease. This series is multi-institutional collaborative project made possible by contributions of stellar fellow leads and expert faculty from several programs, led by series co-chairs, Dr. Josh Saef, Dr. Agnes Koczo, and Dr. Dan Clark. The CardioNerds Adult Congenital Heart Disease Series is developed in collaboration with the Adult Congenital Heart Association, The CHiP Network, and Heart University. See more Claim free CME for enjoying this episode! Disclosures: None Pearls • Notes • References • Guest Profiles • Production Team CardioNerds Adult Congenital Heart Disease PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls Ebstein anomaly is characterized by an inherent myopathy which is often more clinically consequential than the more obvious tricuspid valvulopathy. This can affect not only the right ventricle due to ‘atrialization’ and severe tricuspid regurgitation (TR) but also the left ventricle that is often small due to chronic preload deprivation from reduced RV outflow (no flow, no grow)! Diagnosing severe TR on echocardiography in patients with Ebstein anomaly is challenging, due to the frequent absence of a clearly defined vena contracta and lack of hepatic vein systolic flow reversal. Be on the lookout for severe low gradient TR, which may manifest as a triangular doppler signal rather than the normal parabolic profile. If an electrocardiogram of a patient with Ebstein anomaly suggests prior inferior myocardial infarction, be very suspicious for a right-sided accessory pathway! These are seen in nearly a third of patients with Ebstein anomaly, and manifest as negative delta waves in the inferior leads, leading to a pseudo-infarct pattern. NOTE: infarction, aberrancy, and ventricular hypertrophy should not be coded in the presence of an accessory pathway (i.e., WPW pattern). Patients with Ebstein anomaly who are planned for tricuspid valve replacement should undergo an electrophysiology study preoperatively, since the cavo-tricuspid isthmus responsible for atrial flutter that plagues a large number (>20%) of these patients will be covered by a tricuspid prosthetic valve ring and be inaccessible for future catheter ablation. Certain patients with Ebstein anomaly with significant baseline RV dysfunction who require tricuspid valve surgery may benefit from a concomitant Glenn shunt, which is a surgical anastomosis of the superior vena cava to the right pulmonary artery. This relieves the dysfunctional RV of a third of its baseline preload, potentially enabling it to recover effectively from the stress of cardiopulmonary bypass. Show notes 1. What is Ebstein anomaly and why does it occur? Ebstein anomaly is a rare congenital heart defect of the tricuspid valve (TV) and the myocardium. It occurs in approximately 1 in 200,000 live births. Ebstein anomaly occurs because of defective delamination of the TV. Delamination is the process by which the TV leaflets form from tissue that peels away from the endocardium and myocardium of the right ventricle. Specifically, the septal and posterior leaflets of the TV are inadequately delaminated in Ebstein anomaly. Since they didn’t peel away sufficiently from the myocardium to form the TV at the valve annulus, these leaflets are small, dysplastic and attach significantly more apical to the true tricuspid valve annulus. The anterior TV leaflet is attached to the true TV annulus, but is long, redundant, and floppy, hence often described as ‘sail-like’. It may have fenestrations and can have fibrous attachments to the free wall of the RV. It may also be non-restricted and prolapse into the RV outflow tract, causing outflow obstruction. 2

CardioNerds, Amit Goyal and Daniel Ambinder, join Duke University CardioNerds Ambassador and Correspondent, Dr. Kelly Arps for the diuretic showdown of a lifetime. Join us for this Cardiology vs. Nephrology discussion and respective approach to volume overload and diuretic strategies with Dr. Michael Felker (Professor of Medicine with tenure in the Division of Cardiology at Duke University School of Medicine), and Dr. Matt Sparks (Founding member of the Nephrology Social Medial Collective and #NephJC and Associate Professor of Medicine and Program Director for the Nephrology Fellowship Program at Duke University School of Medicine). Episode introduction, audio editing and Approach to Diuretic Resistance infographic by Dr. Gurleen Kaur (Director of the CardioNerds Internship). Volume overload is a common indication for hospitalization in patients with heart failure. Loop diuretics are first line therapy for volume overload in heart failure, with assessment for adequate response within 3-6 hours after administration. Elevation in creatinine is common with venous congestion as well as during decongestion. While other causes of renal injury should be considered, an elevated creatinine in this context should not automatically trigger avoidance or cessation of diuresis. Diuretic resistance is an exaggerated form of natural safety mechanisms in the face of diuresis. Strategies for addressing diuretic resistance include optimizing dose and frequency of loop diuretic administration, adding adjunctive medication for sequential nephron blockade (i.e., thiazide diuretic, potassium sparing diuretic, acetazolamide, tolvaptan, SGLT2 inhibitor), and, in refractory cases, hemodialysis with ultrafiltration. In the outpatient setting, transition to a more potent loop diuretic (i.e., torsemide or bumetanide from furosemide), addition of a mineralocorticoid antagonist, or intermittent dosing of thiazide diuretic may augment maintenance diuretic therapy for patients with diminished response to loop diuretics. Check out the CardioNerds Failure Heart Success Series Page for more heart success episodes and content! Relevant disclosures: None Pearls • Notes • References • Guest Profiles • Production Team CardioNerds Heart Success Series PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! The CardioNerds Heart Success Series is developed in collaboration with the Heart Failure Society of America. The Heart Failure Society of America is a multidisciplinary organization working to improve and expand heart failure care through collaboration, education, research, innovation, and advocacy. Its members include physicians, scientists, nurses, nurse practitioners, and pharmacists. Learn more at hfsa.org. Pearls – Cardiology vs Nephrology: A Diuretic Showdown Elevation in creatinine is expected in both congested states and during diuresis. Do not avoid or stop diuresis in a patient who is clearly volume overloaded based on an elevated creatinine. There may be a role for right heart catheterization if the fluid and/or hemodynamic status is unclear.  Alkalosis in the setting of loop diuretic administration and diuretic resistance may represent a natural response to loop diuretics and not volume depletion. Ensure adequate potassium repletion and try using a mineralocorticoid antagonist to correct this alkalosis. Acetazolamide is rarely necessary but may be of use. Currently available evidence does not support extreme fluid or salt restriction in hospitalized patients with volume overload. Consider permissive restrictions and focus on choosing appropriate diuretic dosing for each individual patient.  Diuretic resistance is an exaggerated form of diuretic braking, the kidney’s natural response to prevent dangerous degrees of sodium loss from the NKCC2-blocking effects of loop diuretics.  Torsemide has improved bioavailability and duration of action compared to furosemide and may be a good choice for outpatient therapy in patients with limited diuretic response.   Quotable – Cardiology vs Nephrology: A Diuretic Showdown Permissive hypercreatinemia  Eventually the…body recognizes that, Hey, if we’re going to live without this very important, cotransporter in KCC2, we’re going to have to kick on things in the distal nephron to basically have a steady state. – Dr. Sparks I would rather the patient feel good with a creatinine of 2 than terrible with creatinine of 1 and a half. – Dr. Felker I think it’s pretty clear that in the long run, if they’re accompanied by effective decongestion, [minor elevations in creatinine] are actually if anything, a favorable prognostic indicator in terms of heart failure, prognosis, as opposed to an adverse one. – Dr. Felker I think we hit a record for that. The most number of times a cardiologi

CardioNerds (Amit Goyal and Daniel Ambinder), join Dr. Anjali Wagle (Internal medicine resident, Johns Hopkins Hospital) and Dr. Nick Smith (Cardiology fellow, Johns Hopkins Hospital) for an important discussion involving a patient with non-ischemic dilated cardiomyopathy and biventricular heart failure who had developed diuretic resistance. They discuss the role for invasive hemodynamic assessment of volume overload, initial strategies in managing a patient with volume overload, the role of guideline directed therapy in the management of patients with recurrent volume overload, and advanced strategies for diuretic resistance. Dr. Nisha Gilotra (Director of the Cardiac Sarcoidosis Program and assistant professor of medicine, Johns Hopkins Hospital) provides the E-CPR for this episode. Audio editing and Approach to Diuretic Resistance infographic by Dr. Gurleen Kaur (Director of the CardioNerds Internship). This episode is made possible with support from Panacea Financial. Panacea Financial is a national digital bank built for doctors by doctors. Visit panaceafinancial.com today to open your free account and join the growing community of physicians nationwide who expect more from their bank. Panacea Financial is a division of Primis, member FDIC. Claim free CME just for enjoying this episode! Disclosures: NoneJump to: Patient summary – 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! Patient Summary – Diuretic Resistance A young woman in her 20s with non-ischemic dilated cardiomyopathy and NYHA class IV ACC stage D biventricular heart failure with an LV ejection fraction of 30-35% on palliative inotropic therapy complicated by cardiogenic cirrhosis and stage IIIb chronic kidney disease presented with acute decompensated heart failure with volume overload. During her hospitalization she exhibited profound signs of diuretic resistance with minimal improvement after increasing inotropes, increasing IV loop diuretics, adding IV thiazides, and trialing continuous IV furosemide. She was given high dose mineralocorticoids, IV acetazolamide, and hypertonic saline paired with IV furosemide and had a durable treatment response. Episode Teaching – Diuretic Resistance Pearls – Diuretic Resistance Diuretic resistance is a complex clinical problem defined as inadequate natriuresis despite an adequate diuretic regimen. However, the practitioner cannot overlook low output heart failure and/or insufficient renal perfusion as the causes for inadequate diuretic response. In cases of inadequate urine output due to low cardiac output, increased inotropic or mechanical support would be the first objective. Confirming adequate cardiac output to support renal perfusion and/or confirming high filling pressures may require invasive hemodynamic assessment. Sodium avidity is most effectively blunted by treating the patient with maximally tolerated guideline directed therapy. This includes but is not limited to a backbone of ARNI (or ACE or ARB), mineralocorticoid receptor antagonists, beta-blockers, and SGLT-2 inhibitors. In cases of advanced diuretic resistance, hypertonic saline paired with high dose IV furosemide can be an effective strategy. In cases of diuretic resistance combined with cirrhosis and heart failure there is a synergistic hyperaldosteronism that can be targeted with higher doses of mineralocorticoid receptors as is seen in the treatment of cirrhosis with ascites. Notes – Diuretic Resistance 1. What is the role for invasive hemodynamic assessment in acute decompensated heart failure? Cases where intracardiac filling pressures are in question: right heart catheterization (RHC) can give insight into the presence and degree of right versus left sided filling pressures. We discussed the concepts of “RV equalizer” vs “RV compensated” groups in Episode 142 with Dr. Mark Drazner. Cases where cardiac output is in question, especially to guide vasoactive infusions during low flow states: RHC can assess cardiac output and cardiac power output. Cases with rising creatinine during diuresis despite a clinical exam suggesting volume overload. Cases where body habitus prevents optimal evaluation. 2. What are the initial strategies in managing a patient with volume overload? Initial furosemide dosing: The patient’s home dose, renal function, and reason for decompensation all help decide the initial IV diuretic dosing. However, in general if a patient has an outpatient furosemide regimen, the initial diuretic dose should 2.5 times the oral dosing for intermittent IV doses. For example, if a patient is taking 40 mg PO daily as an outpatient, a starting dose of 100 mg IV as a starting dose is appropriate. Furosemide escalation IV dosing: constantly assess the appropriatenes

CardioNerds (Amit Goyal and Daniel Ambinder), Cardio-OB series co-chair and University of Texas Southwestern Cardiology Fellow, Dr. Sonia Shah, episode lead fellow, Dr. Kaitlyn Ibrahim (Temple University now practicing with Lankenau Heart Group), join Dr. Afshan Hameed (Maternal-Fetal Medicine, Obstetrics & Gynecology, UC Irvine), Dr. Paul Forfia (Co-Director, Pulmonary Hypertension, Right Heart Failure & CTEPH Program, Temple University Hospital), and Dr. Marie-Louise Meng (Obstetric and Cardiothoracic Anesthesiology, Duke University) to discuss pregnancy and multidisciplinary critical care. Three experts from varied subspecialties including Cardiology, Pulmonary Hypertension, Maternal Fetal Medicine, Cardiac Anesthesia and Obstetrical Anesthesia guide listeners through a case of a patient with a congenital conotruncal ventricular septal defect, Eisenmenger physiology, and pulmonary hypertension who becomes pregnant. The discussion touches on pre-conception risk assessment, pulmonary hypertension medical therapy in pregnancy, maternal monitoring during pregnancy, development of detailed multidisciplinary delivery plans and accessibility of such plans, and peri- and post-partum multidisciplinary management of high-risk patients. Audio editing and episode introduction by CardioNerds Academy Intern, Christian Faaborg-Andersen. Pearls • Notes • References • Guest Profiles • Production Team CardioNerds Cardio-Obstetrics Series PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls Cyanotic congenital heart disease presents multiple risks to the fetus, the most significant being intrauterine growth restriction. In a patient with Eisenmenger physiology, maternal oxygenation should be monitored closely throughout pregnancy, as hypoxia is often a marker of increased right to left shunting in these patients. In patients with pulmonary hypertension, the RV-PA coupling relationship is the best indicator of maternal cardiovascular reserve through the pregnancy and post-partum period. The goal of therapy is to get the pulmonary vascular resistance down to a point where the right heart can adapt to that load and function either at a normal or a near-normal level. When a high-risk patient meets with Anesthesia, it is important to consider the A’s: 1. Airway (anticipating any potential difficulties); 2. Access (whether this may present a challenge at the time of delivery); 3. Anxiety (specifically differentiating true hemodynamic changes in high-risk patients versus physiologic changes from anxiety); 4. Anticoagulation (knowledge of what agent the patient is on to determine safety of neuraxial anesthesia); 5. Availability (determining who else needs to be in the room, i.e. CT surgery, cardiothoracic anesthesia, ECMO team); 6. Arena (where is the safest place for this patient to deliver). In patients with a shunt who undergo a Cesarean section, the uterus should not be exteriorized due to risk of venous micro air emboli. As Dr. Forfia says, “panic is more dangerous sometimes than pulmonary hypertension!” Meaning, it is important to meet as a multidisciplinary team to develop a clear, easily accessible delivery plan for the patient. It is also prudent to have “everyone functioning in the environment they function best” like delivering the baby on the labor and delivery floor where all the necessary equipment and team members are available and bringing in other experts if needed rather than a cardiac operating room. For a deep dive into Pregnancy & Pulmonary Hypertension, enjoy: Episode #124 with Dr. Candice Silversides. Episode #144 – Case Report: A Mother with Shortness of Breath Show notes 1. How does a multidisciplinary team play a role in the care for a high risk cardio-obstetrics patient, particularly one with congenital heart disease and pulmonary hypertension? According to the 2018 ESC guidelines, a multidisciplinary team is required to care for the pregnant patient with PH. This should include a PH expert at an experienced center for pregnancy and cardiac disease. Maternal outcomes in patients with PH have improved with targeted therapies as well as a multidisciplinary, team-based approach. A multidisciplinary team for a high-risk cardio-obstetrics patient should have representation from several subspecialties, typically including Cardiology (and in patients with PH, a PH expert should be included), Maternal Fetal Medicine, and Anesthesiology. Additional subspecialities can be added depending on the underlying diagnosis of the patient and any potential challenges anticipated at the time of delivery. (i.e. CT Surgery if ECMO may be needed). The key is consistent membership within the group for optimal team dynamics, working relationships, and continuity of patient care. Familiarity among group members helps to facilitate improved communication. Team members

CardioNerds (Amit Goyal, Daniel Ambinder) and Dr. Mark Belkin, (CardioNerds Correspondent) and Dr. Shirlene Obuobi (CardioNerds Ambassador) from University of Chicago are honored to bring to you the Dr. Milton Packer perspective on the evolution of the neurohormonal hypothesis as part of The CardioNerds Heart Success Series. In part 6 Dr. Packer reflects on a conversation he had with Dr. Eugene Braunwald about mentorship and its role in immortality. This episode is particularly meaningful to the CardioNerds team as mentorship and sponsorship is such an important part of the CardioNerds mission. Check out the CardioNerds Heart Failure Success Series Page for more heart success episodes and content! This is a non CME episode. Disclosures: Milton Packer reports receiving consulting fees from Abbvie, Actavis, Amgen, Amarin, AstraZeneca, Boehringer Ingelheim, Bristol Myers Squibb, Casana, CSL Behring, Cytokinetics, Johnson & Johnson Health Care Systems Inc., Eli Lilly and Company, Moderna, Novartis, ParatusRx, Pfizer, Relypsa, Salamandra, Synthetic Biologics, Teva Pharmaceuticals USA Inc. and Theravance Biopharma Inc. CardioNerds Heart Failure Success Series PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! This CardioNerds Heart Failure Success Series was created in memory of Dr. David Taylor. We thank our partners at the Heart Failure Society of America which is a multidisciplinary organization working to improve and expand heart failure care through collaboration, education, research, innovation, and advocacy. Its members include physicians, scientists, nurses, nurse practitioners, and pharmacists. Learn more at hfsa.org.

CardioNerds (Amit Goyal, Daniel Ambinder) and Dr. Mark Belkin, (CardioNerds Correspondent) and Dr. Shirlene Obuobi (CardioNerds Ambassador) from University of Chicago are honored to bring to you the Dr. Milton Packer perspective on the evolution of the neurohormonal hypothesis as part of The CardioNerds Heart Success Series. In part 5, Dr. Packer shares his thoughts on the term “guideline directed medical therapy,” guidelines in general, and the challenges of using the ejection fraction to measure systolic function. Check out the CardioNerds Heart Failure Success Series Page for more heart success episodes and content! This is a non CME episode. Disclosures: Milton Packer reports receiving consulting fees from Abbvie, Actavis, Amgen, Amarin, AstraZeneca, Boehringer Ingelheim, Bristol Myers Squibb, Casana, CSL Behring, Cytokinetics, Johnson & Johnson Health Care Systems Inc., Eli Lilly and Company, Moderna, Novartis, ParatusRx, Pfizer, Relypsa, Salamandra, Synthetic Biologics, Teva Pharmaceuticals USA Inc. and Theravance Biopharma Inc. CardioNerds Heart Failure Success Series PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! This CardioNerds Heart Failure Success Series was created in memory of Dr. David Taylor. We thank our partners at the Heart Failure Society of America which is a multidisciplinary organization working to improve and expand heart failure care through collaboration, education, research, innovation, and advocacy. Its members include physicians, scientists, nurses, nurse practitioners, and pharmacists. Learn more at hfsa.org.

CardioNerds (Amit Goyal, Daniel Ambinder) and Dr. Mark Belkin, (CardioNerds Correspondent) and Dr. Shirlene Obuobi (CardioNerds Ambassador) from University of Chicago are honored to bring to you the Dr. Milton Packer perspective on the evolution of the neurohormonal hypothesis as part of The CardioNerds Heart Success Series. In part 4, Dr. Packer shares his perspective on the revolutionary SGLT2 inhibors. We discuss the mechanisms of action and the data regarding their role in the care of heart failure patients. This episode is particularly historic in that Dr. Packer shares his thoughts about the EMPEROR-PRESERVED trial well before the data was available. Also see Dr. Mark Belkin’s DocWire News article EMPEROR’s New Groove? Empagliflozin Provides Long-Awaited Treatment for HFpEF where Dr. Packer is quoted as saying “we are pleased to have the first trial in patients with HFpEF that shows an unequivocally positive and clinically important result. We are looking forward to many secondary papers that will provide detailed information about what we have found, and what it means for patients.” Check out the CardioNerds Heart Failure Success Series Page for more heart success episodes and content! This is a non CME episode. Disclosures: Milton Packer reports receiving consulting fees from Abbvie, Actavis, Amgen, Amarin, AstraZeneca, Boehringer Ingelheim, Bristol Myers Squibb, Casana, CSL Behring, Cytokinetics, Johnson & Johnson Health Care Systems Inc., Eli Lilly and Company, Moderna, Novartis, ParatusRx, Pfizer, Relypsa, Salamandra, Synthetic Biologics, Teva Pharmaceuticals USA Inc. and Theravance Biopharma Inc. CardioNerds Heart Failure Success Series PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! This CardioNerds Heart Failure Success Series was created in memory of Dr. David Taylor. We thank our partners at the Heart Failure Society of America which is a multidisciplinary organization working to improve and expand heart failure care through collaboration, education, research, innovation, and advocacy. Its members include physicians, scientists, nurses, nurse practitioners, and pharmacists. Learn more at hfsa.org.