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    Health & Fitness

    Cardionerds: A Cardiology Podcast

    Welcome to CardioNerds, where we bring you in-depth discussions with leading experts, case reports, and updates on the latest advancements in the world of cardiology. Tune in to expand your knowledge, sharpen your skills, and become a true CardioNerd!

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    Latest Episodes:
    114. Cardio-Obstetrics: Pregnancy and Coronary Disease with Dr. Malissa Wood Apr 16, 2021
    Show notes

    CardioNerds Amit Goya and Daniel Ambinder, cardioobstetrics series co-chair Dr. Natalie Stokes, and episode lead Dr. Priya Kothapalli (University of Texas at Austin, Dell Medical School) discuss pregnancy and coronary artery disease with Dr. Malissa Wood, co-founder and co-director of the Corrigan Woman’s Heart Health center at Massachusetts General Hospital. They discuss the differential diagnosis of chest pain in the pregnant patient, the diagnostic approach and management of acute coronary syndromes in the patient population, and manifestations and management of SCAD in pregnancy. Episode introduction by Dr. Julie Power. Claim free CME for enjoying this episode! 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! Guest Profiles - Episode 114. Pregnancy Coronary Disease Dr. Malissa Wood Dr. Malissa Wood is a cardiologist at MGH, where she is one of the founders and co-director of the Corrigan Woman’s Heart Health center at MGH. She has authored two books “Smart at Heart” and “Thinfluence” and she’s made substantial contributions globally in promoting awareness of gender disparities in cardiovascular disease. She is the incoming chair elect for the ACC board of governors and current Governor of the Massachusetts ACC chapter, and is one of the leading experts in the world of Spontaneous Coronary Artery Dissection, or SCAD. Dr. Priya Kothapalli Dr. Priya Kothapalli is a second-year cardiology fellow at The University of Texas at Austin, Dell Medical School. Her clinical interests include endothelial dysfunction and vulnerable plaque. She looks forward to advanced training in interventional cardiology. CardioNerds Cardioobstetrics Production Team Natalie Stokes, MDSonia Shah, MDAmit Goyal, MDDaniel Ambinder, MD


    113. Cardio-Obstetrics: Pregnancy, Heart Failure, and Peripartum Cardiomyopathy with Dr. Julie Damp Apr 12, 2021
    Show notes

    CardioNerds (Amit Goyal and Daniel Ambinder), cardioobstetrics series co-chair Dr. Natalie Stokes, Northwestern University CardioNerds Ambassador Dr. Loie Farina, and episode lead fellow, Dr. Agnes Koczo (University of Pittsburgh) join Dr. Julie Damp of Vanderbilt University Associate Director of the VUMC Cardiovascular Disease Fellowship for a discussion about pregnancy, heart failure, and peripartum cardiomyopathy. Episode introduction by Dr. Luis Calderon. Audio editing by Pace Wetstein. Claim free CME for enjoying this episode! Abstract • Pearls • Quotables • 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! Episode Abstract In this episode we discuss the presentation of peripartum cardiomyopathy (PPCM), tips for examining a late antepartum patient, and review management of pregnancy complicated by cardiogenic shock. Weaved throughout the case, we discuss important concepts including the role of prolactin in PPCM which factors into both treatment decisions like prescribing bromocriptine (what!) as well as counseling on breastfeeding. Be sure to tune in to hear Dr. Damp’s review of the latest evidence regarding the diagnosis and management of PPCM, as well as her personal experience counseling patients on heart failure therapies and ICD placement in the context of important factors like breastfeeding status, contraception and future pregnancies. Pearls 1) PPCM most typically presents in the early postpartum period and is defined as an LVEF 50%) by 1 year following diagnosis. However, none of the patients with both LVEF 6 cm at presentation recovered to normal LVEF. For those who do not recover normal cardiac function, studies show nearly 50% will go on to further deterioration with a subsequent pregnancy and are at the highest WHO classification risk for pregnancy.Progesterone-releasing subcutaneous implants are first line for contraception, but likely all contraceptive methods have a benefit which outweighs potential risks of a subsequent pregnancy with abnormal baseline cardiac function. References Davis, M et al. Peripartum Cardiomyopathy. J Am Coll Cardiol. 2020 Jan 21;75(2):207 221. Koczo A, Marino A, Jeyabalan A, Elkayam U, Cooper LT, Fett J, Briller J, Hsich E, Blauwet L, McTiernan C, Morel PA, Hanley-Yanez K, McNamara DM; IPAC Investigators. Breastfeeding, Cellular Immune Activation, and Myocardial Recovery in Peripartum Cardiomyopathy. JACC Basic Transl Sci. 2019 Jun 24;4(3):291-300. Elkayam U, Schäfer A, Chieffo A, Lansky A, Hall S, Arany Z, Grines C. Use of Impella heart pump for management of women with peripartum cardiogenic shock. Clin Cardiol. 2019 Oct;42(10):974-981. Olson TL, O'Neil ER, Ramanathan K, Lorusso R, MacLaren G, Anders MM....


    112. Narratives in Cardiology: Advocacy for Women’s Heart Health and Empowering Women in Cardiology with Dr. Gina Lundberg Apr 05, 2021
    Show notes

    CardioNerds (Amit Goyal and Daniel Ambinder) join Dr. Gina Lundberg (Associate Professor of Medicine at Emory University School of Medicine, Clinical Director of the Emory Women's Heart Center, and Chair Elect for the ACC WIC Section) and Dr. Zarina Sharalaya (interventional cardiology fellow at CCF, CardioNerds Narratives FIT Council Member) for a Narratives in Cardiology episode. Dr. Lundberg highlights the disparities that exists with representation of women in cardiology and cardiology subspecialties, and how to navigate the challenges that exist for women in cardiology. Dr. Lundberg takes us through her career journey and gives several pearls for fellows-in-training regarding achieving career goals, networking, mentorship, and the use of social media to further your career. Special message from Dr. Annabelle Volgman. Audio editing and episode introduction by Gurleen Kaur. Quotables • Show notes • Guest profiles • About Narratives in Cardiology • Production team Claim free CME just for enjoying this episode! Cardionerds Narratives in Cardiology PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll Subscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Quotables “Improving the work environment for women is going to be really important for job retention and for encouraging more women to go into EP, interventional cardiology, and heart failure...” “One of the words of wisdom I say to a lot of early career women is slow down. You don't have to drink the whole thing in your first 10 years. You can just slowly ease into it- there's a time and a place for everything, a season for everything.” “So start building your network. Build your ‘otter raft’ and by otter, I mean that group of people, men or women who really support you and lift you up, who might recommend you for a position or a lecture that might share opportunities with you” Show notes What are some strategies to improve female representation in cardiology? Practicing cardiologists, both men and women, need to mentor and sponsor trainees to attract more female into the field.Improving the work environment is key to retention of women in cardiology (allowing for more flexibility to meet needs such as child-care etc.).We need to build the pipleline to start recruiting females early on, even in high school. 2. What are some strategies to network as a fellow-in-training? Start building your network early - attend ACC and AHA meetings. The ACC Legislative Conference is great because it’s a bit smaller and allows for more opportunities to meet leaders in the ACC.Share your story with other people (example your old high school or sorority/fraternity) as an opportunity to mentor and inspire others.Build your “otter raft”… that group of people who really support you and lift you up, who might recommend you for a position or a lecture that might share opportunities with you. 3. What is the role or value of social media for professional development? Social medial democratizes the landscape, giving everyone a voice regardless of level of training, background, or beliefs.It is invaluable for connecting and networking, on a global scale.It empowers individuals to share – be it powerful stories, their thoughts, and of course education.We of course need to be responsible with protecting our patient’s privacy, be discerning consumers, and be professional in our interactions. CardioNerds Narratives in Cardiology The CardioNerds Narratives in Cardiology series features cardiovascular faculty representing diverse backgrounds, subspecialties, career stages, and career paths. Discussing why these faculty chose careers in cardiology and their passion for their work are essential components to inspiring interest in the field. Each talk will feature a cardiology faculty from an underrepresented group, within at least one of several domains: gender, race, ethnicity, religion, national origin, international graduate status, disadvantaged backgrounds, etc. Featured faculty will also represent a variety of practice settings, academic ranks, subspecialties (e.g. clinical cardiology, interventional cardiology, electrophysiology, etc), and career paths (e.g. division chief, journal editor, society leadership, industry consultant, etc). Faculty will be interviewed by fellows-in-training for a two-part discussion that will focus on: 1) Faculty's content area of expertise2) Faculty's personal and professional narrative As part of their narrative, faculty will discuss their unique path to cardiology and their current professional role with particular attention to challenges, successes, and advice for junior trainees. Specific topics will be guided by values relevant to trainees, including issues related to mentorship, work-life integration, and family planning. To help guide this important initiative, the CardioNerds Narratives Council was founded to provide mentorship and guidance in producing the Narratives series with regards to guests and content. The CardioNerds Narratives Council members include: Dr. Pamela Douglas, Dr. Nosheen Reza, Dr. Martha Gulati, Dr. Quinn Capers, IV, Dr. Ann Marie Navar, Dr. Ki Park, Dr. Bob Harrington, Dr. Sharonne Hayes, and Dr. Michelle Albert. The Narratives Council includes three FIT advisors who will lead the CardioNerds’ diversity and inclusion efforts, including the current project: Dr. Zarina Sharalaya, Dr. Norrisa Haynes, and Dr. Pablo Sanchez. Guest Profiles Dr. Gina Lundberg Gina Price Lundberg MD FACC FAHA is an Associate Professor of Medicine at Emory University School of Medicine and has served as the Clinical Director of the Emory Women’s Heart Center since it was founded in 2013. She is a Preventive Cardiologist and specializes in heart disease in women, lipid abnormalities and cardiovascular risk reduction. She founded the first women’s heart prevention program in the state of Georgia in 1998. Dr Lundberg’s service at Emory University includes improving outcomes for women with cardiovascular disease but also improving gender equity for women in cardiology and encouraging more women to choose cardiology for their careers. She attended the Medical College of Georgia at Augusta University and trained in Internal Medicine at Atlanta Medical Center. Her cardiology fellowship was at Rush University in Chicago. She is active with the ACC, AHA, and NLA. She is the Chair-elect for the ACC Women in Cardiology Leadership Council and is the co-chair for the WIC Communications and Social Media Committee. She is the Co-chair for the NLA Social Media and Communications committee and the co-Chair for NLA DE&I Committee. She serves on the AHA Clinical Cardiology Communications and Social Media committee and the AHA Familial Hypercholesterolemia and Hyperlipidemia working group. And she serves as the Social Media Supervisor for JACC Case Reports. Dr. Zarina Sharalaya Dr. Zarina Sharalaya is an interventional cardiology fellow at the Cleveland Clinic. She completed medical school at The Ohio State University and then completed her residency at The University of North Carolina Chapel Hill. She moved back to her home state of Ohio to do general cardiology fellowship at The Cleveland Clinic. Zarina has been very involved with the Ohio ACC and this year has served as co-chair of the FIT Council. She is passionate about the Women in Cardiology initiative has been able to help formulate the first WIC chapter for Ohio ACC. She enjoys traveling, music, and spending time with her husband and new puppy Zuma. Narratives in Cardiology Production Team Gurleen KaurAmit Goyal, MDDaniel Ambinder, MD


    111. Cardio-Obstetrics: Normal Pregnancy Physiology with Dr. Garima Sharma Mar 31, 2021
    Show notes

    CardioNerd Amit Goyal, cardioobstetrics series co-chair Dr. Natalie Stokes, and episode lead Dr. Daniela Crousillat discuss normal cardiovascular physiology in pregnancy with Dr. Garima Sharma, Director of the Cardio-Obstetrics Program and the Ciccarone Center ‘s Associate Director of Preventive Cardiology Education in the Division of Cardiology. They discuss physiology from conception to post-partum, including the key hemodynamic, hormonal, and structural changes associated with normal pregnancy in the absence of pre-existing cardiovascular disease. Series introduction by Dr. Sharonne N. Hayes. Claim free CME for enjoying this episode! Abstract • Pearls • Quotables • 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! Episode Abstract Join us for a thrilling ride with our expert as we dive into the normal cardiovascular physiology of women through pregnancy. We discuss physiology from conception to post-partum, including the key hemodynamic, hormonal, and structural changes associated with normal pregnancy in the absence of pre-existing cardiovascular disease. We discuss how these physiologic changes manifest the history, physical exam, and key diagnostic testing (ECG, laboratory markers, and echocardiogram). Armed with these basic principles, we join Dr. Garima Sharma on patient consults to learn about potential signs and symptoms of cardiovascular disease in pregnancy and appropriate ways to risk stratify women with pre-existing or acquired cardiovascular disease in pregnancy. Importantly, we delve deeper into the importance of the growing field of cardio-obstetrics in the context of rising maternal mortality and staggering racial disparities in the care and outcomes of women in pregnancy. Pearls In normal pregnancy, plasma volume increases by up to 50% resulting in an adaptive decrease in systemic vascular resistance (SVR) by 25% and an increase in cardiac output (CO) by ~50% by the 2nd trimester.Brisk carotid upstrokes, an S3 gallop, soft systolic ejection murmurs, pedal edema, and a mildly elevated jugular venous pressure (JVP) can all be normal physiologic findings in pregnancy in the context of no other signs/symptoms to suggest heart failure.A normal NT-proBNP among pregnant patients with pre-existing cardiovascular disease has a high negative predictive value for predicting adverse maternal cardiac outcomes.Pregnancy risk predictor tools (mWHO, CARPREG II, ZAHARA) are a crucial component of pre-conception counseling to help predict which women with existing cardiovascular disease are at highest risk for adverse maternal outcomes.The U.S. ranks 1st in the world for maternal mortality among developed nations and cardiovascular disease is the leading cause of pregnancy-associated mortality in the U.S. Non-Hispanic Black are 3.5 times more likely to die from pregnancy as compared to White women. Quotables “You don’t know where you are going until you know where you have been” - Dr. Garima Sharma on the importance of holding on to hope when encountering difficult situations in our training and career pathways. “Do not fear the pregnant patient! The pregnant patient is going through a normal physiologic process in her life, and the more we are familiar with it, the less we fear it” - Dr. Garima Sharma on taking care of pregnant patients. “If you are going to move the needle on maternal mortality and in making a long-term sustainable change in the lives of these women, you have to focus on prevention” - Dr. Garima Sharma on the importance of prevention in reducing maternal mortality. “Be empathetic. For most women, pregnancy is a normal state. These women need your help!” - Dr. Garima Sharma on the importance of taking care of women in pregnancy. Show notes What are the normal hemodynamic changes that occur in pregnancy? Let’s talk physiology! Pregnancy, nature’s most grueling stress test, is a dynamic process associated with significant hemodynamic and physiological adaptations in the cardiovascular system which have evolved to support the needs of a developing fetus.Predictable and expected hemodynamic changes occur during pregnancy for all women. Healthy women can adapt without significant consequences, whereas in women with underlying cardiac conditions, these changes may unmask a previously unknown condition or exacerbate existing abnormal hemodynamics. Adaptive Physiologic Changes of the Cardiovascular System (1) Source: Me Mehta LS, Warnes CA, Bradley E et al. Cardiovascular Considerations in Caring for Pregnant Patients: A Scientific Statement From the American Heart Association. Circulation 2020;141:e884-e903. Supplemental Table 1: Physiologic Changes Throughout Normal Pregnancy Compared to Pre Pregnancy State (2) Plasma volumeIncreases by about 50-75% by the 2nd trimester of pregnancy to meet greater circulatory needs of placenta and maternal organsErythropoietin causes an increase in red cell mass by 20-30% leading to relative dilution and “physiologic” anemia of pregnancy Systemic vascular resistance (SVR)To accommodate the increase in plasma volume, vasodilatation and vascular remodeling occur with a reduction in SVRSVR decreases starting early in the 1st trimester and falls by 25-30% in the 2nd trimester potentiated by progesterone and estrogen-induced vasodilatationDecreased SVR results in activation of the renal angiotensin-aldosterone system (RAAS) to maintain blood pressure and salt/water balance Cardiac output (CO)Increases by ~ 50% during pregnancy (up to 75% for a twin gestation!), starting at 5 weeks of gestation, and peaks at about 18-24 weeks in the 2nd trimesterCO (stroke volume (SV) x heart rate (HR)) increases predominantly via an increase in SV, but also an increase in HR by about 10-15 bpm by the 3rd trimester due to activation of the sympathetic system There are a multitude of other physiological changes that allow our cardiovascular systems to adapt to the normal hemodynamics of pregnancy. Respiratory: Increase in metabolic rate & O2 consumption, minute ventilation and tidal volume resulting in a mild compensatory respiratory alkalosis.Renal: Systemic vasodilation results in 50% increase in renal plasma flow and glomerular filtration rate (GFR), activation of RAAS to maintain fluid and electrolyte balance.Hematologic: “Physiologic” anemia of pregnancy due to increase in plasma volume > red blood cell mass, increased production of coagulation factors with promotion of a pro-thrombotic state.Endocrine: Increase in total cholesterol, triglycerides, LDL (by 50%) and decrease in HDL; mild insulin resistance. Labor & Delivery and Post-Partum Period: Labor: The maximum CO associated with pregnancy occurs during labor and immediately post-partum.Repeated Valsalva maneuvers with a doubling of CO (up to 10L!) in active laborEach uterine contraction displaces about 300-500 mL of blood back into the maternal systemic circulation Post-partum: Immediate: Caval decompression from evacuation of gravid uterus leads to marked increase in venous return (“auto transfusion”) back into the maternal systemic circulationTwo weeks post-partum: Maternal hemodynamics largely return to the pre-pregnancy state! 2. How are the normal physiological changes of pregnancy reflected in the physical exam and diagnostic cardiac testing? When should we worry? Physical Exam (2)Heart rate: Increases by 10-15 bpm by 3rd trimester, mild sinus tachycardiaBlood pressure: Decrease of 10-15 mm Hg in both SBP and DBP, nadiring in 2nd trimester, improving to pre-pregnancy state in 3rd trimesterWeight: 25-35 lbs considered normal total gestational weight gain in patients who are normal weight pre-partumCardiac exam: Mildly elevated jugular venous pressure with more prominent x and y descents, brisk carotid upstrokes, soft, systolic ejection murmur (flow murmur), S3 gallop, mild pedal edema, varicose veins, mammary flow murmurECG:Mild sinus tachycardiaInfrequent premature atrial and ventricular atrial contractionsLeftward axis deviationQ waves in inferior (II, III, aVF) and/or lateral (V4-V6) leads due to heart’s spatial shift left, anterior, and in the transverse plane to accommodate the gravid uterusCardiac BiomarkersNT-proBNPIncrease up to two-fold in pregnancy but should remain within normal rangeImportant clinical utility in patients with pre-existing cardiac disease to serially assess changes throughout pregnancyBNP


    110. Case Report: Feeling Dyspneic & Rejected – University of Maryland Mar 25, 2021
    Show notes

    CardioNerds (Amit Goyal and Karan Desai) enjoy a picnic at Charm City’s Inner Harbor with Dr. Manu Mysore, Dr. Shawn Samanta, and Dr. Rawan Amir from the University of Maryland division of Cardiology as they dive into important case discussion about a patient with of non-ischemic cardiomyopathy s/p orthotopic heart transplantation who presents with dyspnea due to cell mediated rejection. Dr. Gautam Ramani Medical Director of Clinical Advanced Heart Failure at the University of Maryland, provides the e-CPR segment. Claim free CME just for enjoying this episode! Jump to: Patient summary - 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! Patient Summary A 58 year old woman with a history of non-ischemic cardiomyopathy s/p orthotopic heart transplantation in 2015 presented with worsening dyspnea upon exertion. Dyspnea in a post cardiac transplant brings forth a wide differential diagnosis spanning all the typical causes of dyspnea as well as causes more specific or common to the patient with a heart transplant. In this particular case, TTE showed newly reduced ejection fraction and valvular disease. Cell mediated rejection was considered highest on the differential and confirmed on endomyocardial biopsy. Given hemodynamic compromise with multiple foci of myocyte damage on biopsy, she was started on high dose steroids and anti-thymocyte globulin for treatment of rejection. Early identification and management of cell mediated rejection is crucial to the survival of patients like ours. Final diagnosis: orthotopic heart transplantation rejection. Case Media - Orthotopic heart transplant rejection Chest x-ray: Status post sternotomy. Patchy peripheral opacities in the bilateral lower lobes. Blunting of the costophrenic angles consistent with pleural effusion. Sinus tachycardia, HR 111, RBBB, Sub millimeter STE in leads 1, aVL. STD in infero-posterior leads TTE: Short axis TTE: Long axis TTE: Apical 4 Chamber Coronary angiography: RCA Coronary angiography: LAD/LCx Episode Education Pearls New onset heart failure in a post cardiac transplant patient should raise concern for acute cardiac allograft rejection, as well as all the usual culprits in nontransplant patients.Younger African American women and those with elevated HLA mismatches are key risk factors for cell mediated rejection.Treatment for cell-mediated (i.e., T-Cell mediated) rejection includes steroids and antithymocyte immunoglobulin and regimens are based on the severity ofclinical and histologic features.Though infrequent as an initial presentation of acute cellular rejection, new onset arrhythmias in a post cardiac transplant patient should raise concern for rejection as a possible etiology. Reversal of rejection should be verified with endomyocardial biopsy following treatment for rejection. The timing and frequency of biopsy will likely depend upon whether corticosteroids and/or antithymocyte therapy was utilized. Notes - Cell mediated rejection and more! 1) What are some common complications of cardiac transplantation? Common complications following cardiac transplantation can be divided into two major categories: graft-related complications and non-graft-related complications. Graft-related complications include:Early graft dysfunction (EGD) – reversible and irreversible injury related to organ procurement and reperfusion. Remember it is common for transplant patients to require inotropic and vasopressor support coming off cardiopulmonary bypass. Furthermore, LV diastolic dysfunction is also common after transplantation usually reflecting reversible ischemia or reperfusion injury and normally resolves over days to weeks, depending on the severity of reperfusion.Primary graft dysfunction (PGD) is a severe form of EGD that presents as a left, right or biventricular dysfunction occurring within the first 24 hours of transplantation for which there is no identifiable secondary cause (e.g. hyperacute rejection, prolonged ischemic time from massive intra-operative bleeding. The etiology is likely multifactorial including but not limited to reperfusion injury, the effect of donor brain death, and pre-existing donor heart disease.Early RV dysfunction related to pulmonary vascular resistance and fluid shifts early post-transplant may be particularly challenging. The RV is exposed to similar reperfusion injury or ischemic insults as the LV and typically RV dysfunction post-transplant includes RV dilation, subsequent poor coaptation of the tricuspid valve and tricuspid regurgitation. The “untrained” donor RV has to overcome potentially increased afterload (due to increased pulmonary vascular resistance) in the recipient, and as has been covered in previous Cardionerds episodes, the RV systolic function is highly sensitive to changes in afterload.Acute allograft rejection – either cellular-mediated rejection or antibody-mediated rejection, occurring due to the recipient’s immune system reacting against graft antigens (e.g., mainly, but not only, the human leukocyte antigen (HLA) mismatches). Hyperacute rejection is rare and commonly fatal complication of cardiac transplantation. It is mediated by preformed anti-donor antibodies and can lead to diffuse hemorrhage and thrombosis in the allograft. In the current era of panel-reactive antibody screening (PRA) where we screen for preformed anti-HLA recipient antibodies to donor lymphocytes, hyperacute rejection is rare but remains a possibility (especially in highly sensitized patients and/or depending on the technique of obtaining PRAs). See more below on antibody- and cell-mediated rejection.Cardiac Allograft Vasculopathy – an important cause of morbidity and mortality late following heart transplant related to both immune- and nonimmune-mediated coronary injury causing accelerated atherosclerosis and fibroproliferation with diffuse intimal hyperplasia resulting in allograft ischemia. For a detailed discussion on CAV, enjoy Ep #69.Non-Graft-Related ComplicationsInfections – related both to nosocomial exposures and immunosuppression, the typical infectious agents and syndromes predictably vary according to time from transplant. Early following transplant, the recipient is particularly susceptible due to post-operative nosocomial exposures (e.g., surgical wound, vascular access, urinary catheter, etc) and high dose peri-transplant immunosuppression. As such, wound/line/urinary infections and infections involving fungal and multidrug resistant bacterial organisms are common in the early phase (


    109. Nuclear and Multimodality Imaging: Cardiac Amyloidosis Mar 22, 2021
    Show notes

    CardioNerd Amit Goyal is joined by Dr. Erika Hutt (Cleveland Clinic general cardiology fellow), Dr. Aldo Schenone (Brigham and Women’s advanced cardiovascular imaging fellow), and Dr. Wael Jaber (Cleveland Clinic cardiovascular imaging staff and co-founder of Cardiac Imaging Agora) to discuss nuclear and complimentary multimodality cardiovascular imaging for the evaluation of multimodality imaging evaluation for cardiac amyloidosis. Show notes were created by Dr. Hussain Khalid (University of Florida general cardiology fellow and CardioNerds Academy fellow in House Thomas). To learn more about multimodality cardiovascular imaging, check out Cardiac Imaging Agora! Collect free CME/MOC credit just for enjoying this episode! CardioNerds Multimodality Cardiovascular Imaging PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll Subscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Show Notes & Take Home Pearls - Nuclear and Multimodality Imaging: Cardiac Amyloidosis Episode Abstract: Previously thought to be a rare, terminal, and incurable condition in which only palliative therapies were available, multimodality imaging has improved our ability to diagnose cardiac amyloidosis earlier in its disease course. Coupled with advances in medical therapies this has greatly improved the prognosis and therapeutic options available to patients with cardiac amyloidosis. Multimodality imaging involving echocardiography with strain imaging, 99mTc-PYP Scan, and cardiac MRI can help diagnose cardiac amyloidosis earlier, monitor disease progression, and even potentially differentiate ATTR from AL cardiac amyloidosis. Five Take Home Pearls Cardiac amyloidosis results from the deposit of amyloid fibrils into the myocardial extracellular space. The precursor protein can either be from immunoglobulin light chain produced by clonal plasma cells (in the setting of plasma cell dyscrasias) or transthyretin (TTR) produced by the liver (which can be “wild type” ATTR caused by the deposition of normal TTR or a mutant ATTR which is hereditary). These represent AL Cardiac Amyloidosis and ATTR Cardiac Amyloidosis respectively.Remember that amyloidosis can affect all aspects of the heart:the coronaries, myocardium, valves, electrical system, and pericardium! Be suspicious in a patient with history of HTN who has unexpected decrease in the need for antihypertensive agents with age or presents with a lower-than-expected blood pressure.Multimodality imaging can assist with the diagnosis of cardiac amyloidosis in patients with a high clinical suspicion, monitor disease progression, and even potentially differentiate ATTR from AL cardiac amyloidosis.Strain imaging assessment of global longitudinal strain (GLS) in patients with amyloid may demonstrate relatively better longitudinal function in the apex compared to the base, termed “apical sparing” or “cherry on top” (though in advanced stages the base to apex strain difference tends to become smaller). This has a 93% sensitivity and 82% specificity in identifying patients with cardiac amyloidosis and is particularly helpful with differentiating true cardiac amyloidosis from “mimics” such as hypertrophic cardiomyopathy, aortic stenosis, or hypertensive heart disease.When the clinical suspicion for cardiac amyloidosis is high, a semiquantitative grade ≥ 2 (myocardial uptake ≥ bone) on 99mTc-PYP Scan combined with negative free light chain and immunofixation assays (to rule out AL cardiac amyloidosis) can diagnose ATTR cardiac amyloidosis and exclude AL cardiac amyloidosis w/ 100% PPV! Furthermore, this can circumvent the need for endomyocardial biopsy. Echocardiography and cardiac MRI (CMR) are helpful for building the clinical suspicion for cardiac amyloidosis.When there is suspicion for AL cardiac amyloidosis, tissue biopsy is mandatory. Quotable: - Nuclear and Multimodality Imaging: Cardiac Amyloidosis “Even if you’re starting fresh, you should not do this test (technetium pyrophosphate scan) without a SPECT CT; you could be sending patients to therapy that costs anywhere between $25,000 to $250,000 per year for a disease that they don’t have.” --13:22 Detailed Show Notes 1. What is amyloidosis? What are the main precursor proteins in cardiac amyloidosis? Amyloidoses are protein-folding disorders in which proteinaceous deposits known as amyloid can infiltrate multiple organs. Cardiac amyloidosis is typically secondary to two main subtypes: 1) immunoglobulin light chain produced by clonal plasma cells (AL cardiac amyloidosis), and 2) transthyretin produced by the liver (ATTR cardiac amyloidosis). AL and ATTR account for >95% of cardiac amyloidosis. Rare precursors include serum amyloid A (AA) and apolipoprotein A-1 (ApoA-1).AL cardiac amyloidosisOverall incidence of AL amyloidosis is estimated to be 8.0-14.4 million persons per year in the USA with cardiac involvement in ~50% of patients. Median survival of patients with cardiac AL amyloidosis is 6 months from the onset of heart failure. Survival has improved with earlier detection and advancements in oncologic treatments.AL may deposit in any tissue outside the CNS and so patients often have multiorgan involvement (kidneys, liver, etc).ATTR cardiac amyloidosisATTR typically results in cardiac amyloidosis, peripheral neuropathy, and MSK sequelae (i.e., bilateral carpal tunnel, lumbar spinal stenosis, biceps tendon rupture) with relative proportions dependent on the mutant variant.Transthyretin amyloidosis can occur secondary to the deposition ofnormal TTR (known as “ATTR wild type” or “ATTRwt”) or a mutant form (hereditary form known as “ATTR mutant” or “ATTRm”).ATTRwtHas a 15:1 male to female prevalence ratio and usually occurs in older patients (>65 y.o.)Almost always involves the heartMay be responsible for as many as 30% of heart failure with preserved ejection fraction (HFpEF) cases in patients >75 years old!ATTRmHas only a slight male predominance and occurs in younger patients (>40 y.o.)Inherited in an autosomal dominant fashion with multiple genotypes with variable degrees of penetrance and cardiac involvementThere are more than 100 genetic variants of ATTR that are associated with amyloidosis. However, only a few of these variants, including Val30Met, Thr60Ala, Ser77Tyr, and Val122Ile, are responsible for the majority of cases of hereditary ATTRAs stated in Podcast Episode #7, the specific mutation is closely linked with the age of onset, natural history, and phenotype of the affected individual!The Val122Ile mutation is the most common variant in the USA and a has prevalence of 3-4% in the US African American population. It is associated with cardiac amyloidosis with minimal neuropathy.Thr60Ala is the 2nd most common variant in the USA and is seen most commonly in those of Irish descent. It is associated with a mixed cardiomyopathy and neuropathy phenotype.Val30Met causes a prototypical hATTR polyneuropathy (heriditary ATTR with polyneuropathy also known as “Familial Amyloid Polyneuropathy”The specific genetic variant affects treatment decision and screening is indicated for individuals with known or suspected familial amyloidosis presenting w/ new symptomatic heart failure. 2. What are some classic cardiac and extracardiac manifestations of amyloidosis? For fantastic case presentations of cardiac amyloidosis including suggestive history and physical exam findings, diagnostic considerations, and recommended management, tune in to CardioNerds Podcast Episodes #7-10 and #54! As described in Podcast Episode #7, amyloidosis is associated with many classic extracardiac findings based on which organ it deposits in, and can also deposit in every layer of the heart—coronary, ventricular, valvular, electrical, and pericardial tissues! Below is a brief outline of some of the classic extracardiac and cardiac manifestations of amyloidosis.Extracardiac:ATTR: peripheral nerves (sensorimotor and autonomic defects) and musculoskeletal sequelae (bilateral carpal tunnel syndrome, lumbar spinal stenosis, biceps tendon rupture). Degree of cardiac vs nerve involvement differs by mutant variant as above. A prior Cleveland Clinic study showed Congo red staining of tenosynovial tissue detected amyloid deposits in 10.2% of patients undergoing carpal tunnel release surgeryAL: any tissue outside the CNS. For instance, typical organs involved include the kidneys (nephrotic syndrome), liver, intestines, and nervous system. On exam one may find macroglossia and periorbital bruising.Cardiovascular:Decreased antihypertensive medication requirements with increasing age or presenting with lower than expected blood pressurePostural hypotensionCoronary microvascular diseaseChronically elevated but flat troponin (infiltration into the coronary microvasculature)Almost all patients with cardiac amyloidosis have significantly reduced peak stress myocardial blood flow (


    108. Narratives in Cardiology: Physician Scientists & Women in Electrophysiology with Dr. Christine Albert and Dr. Rachita Navara Mar 16, 2021
    Show notes

    CardioNerds (Amit Goyal and Daniel Ambinder) join Dr. Christine Albert (Professor of Medicine, Founding Chair of the Department of Cardiology at Cedars-Sinai, and President of Heart Rhythm Society) and Dr. Rachita Navara (FIT at Washington University, soon to be EP fellow at UCSF) for a Narratives in Cardiology episode. We learn from their experiences as physician scientists and women in cardiology, and specifically in electrophysiology. Claim free CME just for enjoying this episode! Cardionerds Narratives in Cardiology PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll Subscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Show notes 1. Over the last several decades, what have we learned about the contribution of lifestyle factors to atrial fibrillation? Particularly in women, the development of obesity (BMI > 30 kg/m2) is associated with a 41% increase in the risk of developing atrial fibrillation (AF). Even short-term weight gains are associated with a 18% increased risk of developing AF. Fortunately, losing weight could modify or even reverse this elevated risk [1]Exercise is beneficial for reducing the risk of AF, but higher frequency of vigorous exercise is actually associated with an increased risk of developing AF in young men and joggers. This risk decreases with age, and is offset by the other benefits of vigorous exercise on AF risk factors [2]The link between alcohol consumption and AF was first described in 2008: for healthy middle-aged women, consuming two or more alcoholic drinks is associated with a statistically increased risk of developing AF [3]The recent VITAL trial is the largest and longest randomized trial on primary prevention of AF, following over 25,000 men and women over five years. As recently presented at AHA 2020, Dr. Christine Albert and her study team found that neither vitamin D nor fish oil prevents the development of AF [4] 2. What is some practical advice on giving presentations and preparing research grants from Dr. Albert, renowned physician-scientist, and leader in electrophysiology? Whenever possible, Dr. Albert recommends memorizing your presentation to avoid referencing notes frequently, and to allow for continued eye contact with the audience. Practice delivering your presentation multiple times prior to the scheduled talk.When preparing a grant, start early and seek feedback and edits from those in and out of your field.In many cases, a grant review involves individuals who may not be in your exact scientific field, so the priority is to interest the grant readers regardless of their scientific background. 3. Whether in research or clinical care, what are the common features of a well-oiled clinical team? In an ideal team, every individual adds value and has a clear role. Team members show mutual respect and provide the autonomy for other team members to demonstrate their expertise.Don’t be intimidated by the individuals on your team who are extremely talented or experienced in a given domain – this in turn elevates you by being on the same team!Leaders are most successful when they enable others to succeed. The spirit of collaboration and respect comes from the top, so leaders need to demonstrate respect for every team member and give each person a role, eliminating the need for team members to compete with each other. 4. What is some advice for female trainees navigating a male-dominated field (e.g. electrophysiology)? What makes a good mentor and mentee? It is very important to seek female or otherwise relatable role models in your field. While representation increases, it can also be valuable to seek female mentors outside your specific field.It is just as important for male mentors to continue to support female trainees, especially in fields where females are underrepresented.Often, as a mentee you may change your area of interest or seek a new area of specialization that may no longer be fully aligned with your mentor’s expertise. A good mentor will continue to mentor you and connect you with those who can help you explore your new interests.A good mentee also recognizes that mentors often have very limited time, so it is best to package all of your questions together and prepare for each meeting so that shared time is most high yield. CardioNerds Narratives in Cardiology The CardioNerds Narratives in Cardiology series features cardiovascular faculty representing diverse backgrounds, subspecialties, career stages, and career paths. Discussing why these faculty chose careers in cardiology and their passion for their work are essential components to inspiring interest in the field. Each talk will feature a cardiology faculty from an underrepresented group, within at least one of several domains: gender, race, ethnicity, religion, national origin, international graduate status, disadvantaged backgrounds, etc. Featured faculty will also represent a variety of practice settings, academic ranks, subspecialties (e.g. clinical cardiology, interventional cardiology, electrophysiology, etc), and career paths (e.g. division chief, journal editor, society leadership, industry consultant, etc). Faculty will be interviewed by fellows-in-training for a two-part discussion that will focus on: 1) Faculty's content area of expertise2) Faculty's personal and professional narrative As part of their narrative, faculty will discuss their unique path to cardiology and their current professional role with particular attention to challenges, successes, and advice for junior trainees. Specific topics will be guided by values relevant to trainees, including issues related to mentorship, work-life integration, and family planning. To help guide this important initiative, the CardioNerds Narratives Council was founded to provide mentorship and guidance in producing the Narratives series with regards to guests and content. The CardioNerds Narratives Council members include: Dr. Pamela Douglas, Dr. Nosheen Reza, Dr. Martha Gulati, Dr. Quinn Capers, IV, Dr. Ann Marie Navar, Dr. Ki Park, Dr. Bob Harrington, Dr. Sharonne Hayes, and Dr. Michelle Albert. The Narratives Council includes three FIT advisors who will lead the CardioNerds’ diversity and inclusion efforts, including the current project: Dr. Zarina Sharalaya, Dr. Norrisa Haynes, and Dr. Pablo Sanchez. Guest Profiles - Physician Scientists Women Electrophysiology Dr. Christine M. Albert Dr. Christine Albert is currently President of Heart Rhythm Society. She recently transitioned from Professor of Medicine at Harvard and Director of the Center of Arrhythmia Prevention at the Brigham to now Founding Chair of the Department of Cardiology at Cedars-Sinai. She is an Epidemiologist and R01-grant funded physician scientist with over 200 peer-reviewed publications – with landmark contributions demonstrating the role of lifestyle and genetics on heart rhythm disorders. She has served as PI for numerous large-scale award-winning clinical trials, her latest studying primary prevention of cardiovascular disease and cancer in 25,000 patients across the country. She has served as the associate editor for Circulation, and continues to serve on the editorial board of numerous journals in not only cardiology but also epidemiology, clinical nutrition, and endocrinology and metabolism. Dr. Rachita Navara Dr. Rachita Navara is a bioengineer and senior cardiology fellow at Washington University in St. Louis. She is excited to enter her dream specialty of electrophysiology at UCSF, the birthplace of catheter ablation for arrhythmias. Her interest in EP emerged during bioengineering training at the innovative Olin College of Engineering. She went on to medical school at UT Southwestern, where she was the lead singer of her med school band “The Pacemakers.” Dr. Navara completed her internal medicine training at Stanford University, where she was accepted into the inaugural Biodesign Pathway of Distinction and researched complex atrial fibrillation mechanisms under the mentorship of Dr. Sanjiv Narayan. She joined cardiology fellowship at Wash U, where she researched novel noninvasive cardiac radioablation under the mentorship of Dr. Phillip Cuculich. Dr. Navara’s startup company “SafeBeat Rx LLC” was competitively selected into BioGenerator’s Grants-to-business program, and she recently submitted her first NIH STTR grant. She was appointed as the youngest member of the National ACC EP Leadership Council, and she is currently an HRS representative to the AMA. Dr. Navara aims to lead a research lab conducting trials on EP devices and mapping/ablating technologies she has designed herself. In her free time, she enjoys painting, singing and tandem biking with her husband, and competitive scrabble tournaments (nerd level: ultimate). References - Physician Scientists Women Electrophysiology Tedrow, Usha B., David Conen, Paul M. Ridker, Nancy R. Cook, Bruce A. Koplan, JoAnn E. Manson, Julie E. Buring, and Christine M. Albert. "The long-and short-term impact of elevated body mass index on the risk of new atrial fibrillation: the WHS (Women's Health Study)." Journal of the American College of Cardiology 55, no. 21 (2010): 2319-2327.Aizer, Anthony, J. Michael Gaziano, Nancy R. Cook, Joann E. Manson, Julie E. Buring, and Christine M. Albert. "Relation of vigorous exercise to risk of atrial fibrillation." The American journal of cardiology 103, no. 11 (2009): 1572-1577.Conen, David, Usha B. Tedrow, Nancy R. Cook, M. V. Moorthy, Julie E. Buring, and Christine M. Albert. "Alcohol consumption and risk of incident atrial fibrillation in women." Jama 300, no. 21 (2008): 2489-2496.VITamin D and OmegA-3 TriaL (VITAL) results presented at AHA 2020 ahead of publication: https://www.cedars-sinai.org/newsroom/study-vitamin-d-fish-oil-dont-lower-atrial-fibrillation-risk/ Amit Goyal,...


    107. Case Report: A Rare Cause of Cardiogenic Shock – More than Meets the Eye – Thomas Jefferson University Hospital Mar 15, 2021
    Show notes

    Join Thomas Jefferson University FITs, Drs. Sean Dikdan, Rachel Debenham and Harsh Doshi, as well as Cardionerds, Dan Ambinder and Karan Desai, on this incredible story of a young man who presented with ventricular arrhythmias and cardiogenic shock. The TJU Cardionerds expertly walk us through a rare diagnosis, his course over several years and his ultimate treatment with heart transplantation. From the evaluation of cardiogenic shock to the role of endomyocardial biopsy to facing inequities in organ allocation, there are learning pearls for every listener! CME is unavailable for this episode. Jump to: Patient summary - Case media - Case teaching - References Episode Graphic by Dr. Carine Hamo 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 A 35 year old healthy male presents with cardiogenic shock and new heart failure with reduced ejection fraction. He has ventricular instability and is diagnosed with giant cell myocarditis by endomyocardial biopsy. His course over several years includes LVAD bridge to heart transplantation. He then has a recurrence of giant cell myocarditis in the transplanted heart which is successfully treated with high dose immunosuppression. Case Media ABClick to Enlarge A. ECG, B. CXR Episode Schematics & Teaching CardioNerds Myocarditis, updated 1.20.21 Giant Cell Myocarditis Pearls Giant cell myocarditis (GCM is a rare – and often fatal - cause of acute myocarditis. A hallmark of GCM is the presence of multinucleated giant cells; however, these may take 1-2 weeks to appear and can also be seen in sarcoidosis.Most etiologies of fulminant myocarditis do not have bradyarrhythmias as a prominent feature, and their presence should increase the suspicion for sarcoidosis, Chagas disease, or GCM.While non-specific, a clue to the diagnosis of GCM amongst other causes of myocarditis could be rapid clinical deterioration with minimal response to guideline directed therapy, including a lack of spontaneous recovery on mechanical support which more commonly occurs in fulminant lymphocytic myocarditis.Mechanical support is typically needed in the management of GCM, either as a bridge to transplantation or recovery.GCM can recur in the transplanted heart. This happens in up to 25% of transplant patients and warrants aggressive immunosuppression which usually is sufficient to ensure disease remission. Notes - Giant Cell Myocarditis What is Giant Cell myocarditis (GCM)?Giant cell myocarditis (GCM) is an extremely rare – and often fatal – cause of acute non-infectious myocarditis. The pathophysiology of GCM is poorly understood, but thought to be a T-cell mediated autoimmune process leading to diffuse or multifocal inflammatory infiltrate, including lymphocytes with multinucleated giant cells (note multinucleated giant cells are not exclusive to GCM and can be seen in sarcoidosis as well). It has been estimated to occur at a rate of 0.13 cases per 100,000 people (one in a million).It typically affects the myocardium in isolation and may not have any extracardiac manifestations, presenting with rapid hemodynamic deterioration, ventricular arrhythmias, and at times bradyarrhythmias. The rate of death or cardiac transplantation has been estimated at 89%, with a median survival of 5.5 months from the onset of symptoms to the time of death or transplantation.When should you be suspicious of GCM?The classic presentation is in a middle-aged Caucasian male who develops acute or subacute nonischemic cardiomyopathy (NICM) with clinical heart failure that progressively worsens. These patients often develop cardiogenic shock or arrhythmic instability – including both ventricular arrhythmia and conduction delays/heart block. See our prior episodes on the basics of building a clinical suspicion for myocarditis and the differential diagnosis (Episodes 29-33).While non-specific, a clue to the diagnosis of GCM amongst other causes of myocarditis should be rapid clinical deterioration with minimal response to guideline directed therapy, including a lack of spontaneous recovery on mechanical support which more commonly occurs in fulminant lymphocytic myocarditis. Furthermore, bradyarrhythmias are less common in myocarditis and should raise the suspicion for GCM, sarcoidosis or Chagas disease.How is GCM diagnosed?Definitive diagnosis of GCM requires endomyocardial biopsy (EMB). Similar to other rare forms of myocarditis like sarcoidosis or eosinophilic myocarditis, GCM requires pathology for diagnosis. Typically, a Class I indication (based on a joint statement 2007 statement from the AHA/ACC/ESC) for performing an EMB are (1) unexplained acute cardiomyopathywith


    106. Case Report: A Hole in the HFpEF Diagnosis – Boston University, Massachusetts General Hospital, and Brigham and Women’s Hospital Mar 08, 2021
    Show notes

    CardioNerds (Amit Goyal & Karan Desai) join Dr. Alex Pipilas (FIT, Boston University) and Dr. Danny Pipilas (FIT, MGH) for in Boston, MA. Adult congenital heart disease expert Dr. Keri Shafer (Brigham and Women’s Hospital) provides the E-CPR expert segment. They discuss a case of heart failure secondary to sinus venosus defect with partial anomalous pulmonary venous return. Claim free CME just for enjoying this episode! Jump to: Patient summary - 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! Patient Summary A 78-year-old woman with atrial fibrillation and heart failure with preserved ejection fraction presented with recurrent dyspnea and volume overload. A transthoracic echocardiogram demonstrated severe right ventricular enlargement and dysfunction. A CT pulmonary angiogram demonstrated partial anomalous pulmonary venous return and a transesophageal echocardiogram revealed a sinus venosus defect with left to right shunting. A right heart catheterization with oximetry saturation (“shunt run”) demonstrated pulmonary hypertension and a large left to right shunt (Qp/Qs ~ 3). She was referred for cardiac surgery and underwent repair of the sinus venosus defect and baffling of the anomalous pulmonary venous flow to the left atrium. Case Media ABCClick to Enlarge A. CXR, B. ECG, C. TR Velocity TTE: PLAX TTE: RV Outflow TTE: AP4 TEE: Sinus Venosus ASD TEE: Sinus Venosus ASD 2 Episode Schematics & Teaching Figure 1Figure 2 Pearls It is critical to determine whether there is more to a diagnosis of heart failure with a preserved ejection fraction. Utilize all available clinical data and risk calculators to determine if there are more appropriate diagnoses causing the patients symptoms, especially when certain aspects of the presentation does not add up.Right ventricular failure may be related to pressure overload (i.e., pulmonary hypertension, PV stenosis), volume overload (i.e., tricuspid regurgitation, left to right shunt lesions), or primary myocardial process (i.e., ischemia, infiltration, ARVC). In cases of severe right ventricular enlargement and dysfunction without apparent cause, look for a left to right shunt lesion (i.e., VSD, ASD, PAPVR). Sometimes further imaging (TEE, cardiac CT, cardiac MRI) is necessary to detect these lesions if not visualized on TTE.Left to right shunts can be quantified in the cardiac catheterization laboratory by measuring oxygen saturation in each chamber and detecting an O2 “step up” (increase in oxygen saturation from one chamber to the next). Large left to right shunts are quantified using the Fick principle and comparing the ratio of pulmonary blood flow (Qp) to systemic blood flow (Qs).Large left-to-right shunts can cause right ventricular volume overload and pulmonary hypertension. Patients often present with signs and symptoms of right ventricular failure including shortness of breath, exercise intolerance, volume overload, atrial arrhythmias, and recurrent heart failure. Some may develop right-to-left shunting and possible paradoxical embolism.ACC/AHA guidelines recommend closure of a sinus venosus defect if the PA systolic pressure is 2/3 of systemic systolic pressure and/or PVR >2/3 SVR. Quotable: About ACHD - “As we go through this physiology, I just want to remind all of the listeners out there that you have the opportunity to apply the knowledge you have from medical school about physiology to the adult human heart. You can’t make assumptions as we sometimes do in the setting of normal cardiac anatomy. We really need to think about the compliances of the downstream structures and where is the blood flow.” – Keri Shafer, MD Notes What are features and causes of RV failure? The clinical symptoms of right ventricular failure include fatigue, dyspnea, lower extremity edema, elevated JVP, early satiety, and abdominal swelling. Although there is overlap between the symptoms of right ventricular failure and left ventricular failure, in isolated right ventricular failure orthopnea, paroxysmal nocturnal dyspnea, and pulmonary edema are typically absent.It is convenient to break down the etiologies of right heart failure into “buckets”. Specifically, volume overload, pressure overload, and primary cardiomyopathic processes. Causes of right ventricular volume overload include valvular disease (tricuspid regurgitation, pulmonic insufficiency) and left-to-right shunts (ASD, VSD, sinus venosus defect, coronary sinus defect, PAPVR). Causes of right ventricular pressure overload, or excessive afterload, include pulmonary arterial hypertension, pulmonary embolism and chronic thromboembolic pulmonary hypertension, pulmonic stenosis, chronic hypoxemia, and longstanding elevated left atrial pressure causing group 2 PH (mitral regurgitation/stenosis, HFrEF, HFpEF). Cardiomyopathic processes include cardiac amyloidosis, right ventricular myocardial infarction, post-transplant right ventricular dysfunction, and arrhythmogenic right ventricular cardiomyopathy. Also, keep in mind that these disease processes often overlap. 2. What is partial anomalous pulmonary venous return (PAPVR)? Normally, the four pulmonary veins return oxygenated blood to the left atrium.Partial anomalous pulmonary venous return is a spectrum of congenital heart defects when one or more (but not all) of the pulmonary veins return oxygenated blood from the lungs to the systemic venous system (typically the SVC, IVC, or RA).The most common PAPVRs are LUPV (left upper pulmonary vein) à ascending vertical vein à innominate vein or RUPV à SVC. The latter is often associated with a concurrent sinus venosus defect connecting the RA and LA.Scimitar syndrome is a subtype of PAPVR in which part or all of the blood from the right lung is returned into the IVC. On chest X-ray, the outline of the anomalous drainage and associated congestion gives the appearance of a scimitar. 3. What is a sinus venosus defect? What is the sinus venosus? Early in development, the atria are one single chamber. The sinus venosus is the posterior entryway for blood returning to this primitive atrium.Eventually, the sinus venosus closes and moves rightward due to hemodynamic shifts during development.In adults, the sinus venous becomes the smooth posterior wall of the adult right atrium called the sinus venarum and is separated from the anterior wall of the RA by the cristae terminalis.If a persistent channel through the sinus venosus remains into adulthood, it can result in an intra-cardiac shunt. This is termed a sinus venosus defect and accounts for 10-15% of all inter-atrial shunts.Typically, this shunt is left-to-right and may lead to right ventricular volume overload, dysfunction and pulmonary hypertension. Some patients may develop right-to-left shunting or paradoxical embolism. Arrhythmias are an important complication.As above, sinus venosus defects are associated with PAPVR with RUPV à SVC.NOTE: a sinus venosus defect is NOT a defect in the atrial septum and so is not an “ASD”. Rather it is a defect connecting either the SVC-RA junction (more common) or the IVC-RA junction to the LA. The former is associated with a RUPV PAPVR and the latter is associated with a RLPV PAPVR. 4. What are the imaging modalities that are used to identify sinus venosus defects? Sinus venosus defects are poorly visualized on transthoracic echocardiography (TTE).If there is clinical suspicion for an inter-atrial shunt not visualized on TTE, then a transesophageal echocardiogram (TTE) should be performed. Additional imaging modalities include cross-sectional imaging with cardiac CT or cardiac MRI, which may also identify the presence of concomitant PAPVR.In cases of RV dilation and dysfunction without know etiology, evaluation for sinus venosus defect +/- PAPVR should be pursued. 5. What is the role for right heart catheterization in characterizing shunt defects? A right heart catheterization is useful for multiple reasons.Intracardiac pressure measurements serve as a surrogate for volume status.One can also obtain oxygen saturation in each cardiac chamber to identify the presence of a “step up”, or unexpected increase in oxygen saturation, which signifies a left-to-right shunt. To simplify, a left-to-right shunt is when oxygenated blood from the systemic circulation (left) inappropriately mixes with the pulmonary circulation (right), increasing the oxygen concentration. This can occur via anomalous pulmonary veins, defects at the atrial or ventricular level, or sometimes systemic arterio-venous fistulas.To obtain pressure measurements, a balloon-tipped catheter (Swann-Ganz catheter, PA catheter) is inserted through a vein and advanced through the heart and “wedged” in the pulmonary artery to estimate left atrial pressure. Normal pressure measurements are as follows (in mmHg): Right atrium


    105. Narratives in Cardiology: Racial Disparities in Advanced Heart Failure with Dr. Bryan Smith and Dr. Shirlene Obuobi Mar 03, 2021
    Show notes

    CardioNerds (Amit Goyal and Daniel Ambinder) join Dr. Bryan Smith (Advanced Heart Failure and Transplant Cardiologist at the University of Chicago) and Dr. Shirlene Obuobi (rising cardiology fellow, CardioNerds ambassador for the University of Chicago, and creator of ShirlyWhirl, M.D.) They discuss the story of a patient with end stage heart failure due to peripartum cardiomyopathy that highlights racial disparities in healthcare and advanced heart failure. They emphasize the importance of providing mentorship for Black and Indigenous People of Color (BIPOC) and share personal stories of their journey to Cardiology. Dr. Andi Shahu joins us to read his AHA blog titled "Let’s Ban the Phrase “Social Issues”: Social Justice and Advanced Heart Failure Therapies". Audio editing by CardioNerds Academy intern, Pace Wetstein. Collect free CME/MOC credit just for enjoying this episode! Cardionerds Narratives in Cardiology PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll Subscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Quotables: “One of the reasons why I went into Heart Failure is because I connected a lot with these young patients, a lot of these young black men and black women who were terrified of the hospital. As a resident and a fellow I would go talk to them and really understand their fears and where they are coming from. I think a lot of times these patients can be labeled as ‘noncompliant,’ or ‘withdrawn,’ or ‘aggressive,’ but a lot of times you just have to understand where they’re coming from. And I really found that just sitting down to talk to them, and to get to know them, I was able to help get them better, or a lot of them went on to get VADs or transplant. And, to be perfectly honest, I’m in touch with a lot of these patients who I met as a fellow who...I feel are part of my life....You have to meet patients where they are. Meaning you need to text them, interact with them on social media, and really connect with them in a way they understand.” Dr. Bryan Smith (12:10) “Being black in America means not getting the benefit of doubt. ...I can’t help but wonder if unconscious bias among providers is imposing...unreasonable scrutiny on patients of color.” Shirlene (21:15) “There are many different ways to combat [racial] disparities. As a Heart Failure physician we have these multidisciplinary meetings where we discuss patients for transplant. And I think it’s...important to highlight to our providers that how we discuss patients really matters. Language definitely matters. Heart failure is art in addition to science. ...Sometimes when discussing these patients...charged words are used, like ‘withdrawn,’ or ‘aggressive,’ or ‘ghetto’ even. And it’s all coded, racist language. ...Part of our responsibility is to educate everyone with implicit bias training....and to make sure we’re able to advocate for patients in the right way.” Dr. Bryan Smith (22:30) “I’ve felt like I’ve been paying the minority tax...which is doing the necessary but unpaid and frequently seldom recognized labor of mentorship, community engagement, etc, and also of being hyper visible and acting as a symbol...” - Shirlene (24:52) “It’s really easy when patients are in the hospital to think of them only as patients and forget that they’re people too, and that people are complex, they have complex emotions, they have reactions to things, sometimes those reactions aren’t necessarily what we would think are appropriate for their medical situation, but they’re what make us human.” - Shirlene (9:50) Notes: 1. What are some of the racial disparities in diagnosis and outcomes of peri-partum cardiomyopathy, and what are some factors that might be contributing to those disparities? CVD disease is the leading cause of pregnancy-associated mortality in the US. Black and American Indian/ Alaskan Native women are 3-4x more likely to die from a pregnancy-related cause than white women. (1,2)The incidence of peripartum cardiomyopathy (PPCM) is 4x higher in black women than in white women. Black women may make up to 40% of the cases. (3,4)Black women with PPCM have lower LVEF at the time of diagnosis, lower rates of recovery of LVEF, higher incidence of mortality and need for LVAD/ transplant. (1,2)Studies looking for genetic reasons for this disparity have come up short.Black women are more likely to have comorbid conditions (i.e., gestational HTN, preeclampsia). 2. What is it like taking care of younger patients with LVEF, especially young black patients? Working in Advanced Heart Failure gives cardiologists the opportunity to work with younger patients due to the prevalence of CMs that present at younger ages.Younger patients tend to feel more invincible, and to have more distrust of the medical system.It is important to get to know these patients, meet them where they are, and communicate with them in ways they understand (text, social media). 3. How can we help to break the black patients’ distrust in the medical system? Understand the history: medicine has historically excluded and abused black patients. (ie. the Tuskegee study withheld treatment from black sharecroppers, gynecological surgery experimentations on black slave women, a legacy of segregation, etc.)Listen to our patients and try to meet them where they are.Understand the social determinants of health (SDOH) that may influence their ability to “adhere” to therapy/ appointments (i.e., difficulty finding childcare, employment restrictions)Partner with community initiatives (i.e., Urban Health Initiative at University of Chicago)Hire and train members of the community to work in the hospital!Invest in Pipeline programs and mentorship. 4. Why is diversity in the medicine important? Concordance of race between providers and patients improves trust, quality of care, and improves patient outcomes! (5)Black patients are less likely to be referred for catheterization, AICDs, etc., despite our best efforts to provide equitable care.Language is important! Consider the use of coded language and racially disparate expectations for patients when discussing issues such as transplant candidacy.Recruit physicians who are interested in disparities research, and make research into disparities a basis for promotion. 5. How do we engage the rest of the cardiology community to be invested in the recruitment and mentorship of underrepresented minorities in medicine (URiMs)? URiMs frequently pay the “minority tax,” or the necessary but unpaid and seldom recognized labor of mentorship, community engagement, etc. That can be a heavy load to carry, especially considering only 5% of cardiology fellows identify as being Black.“You can’t really be what you can’t see” - there’s a responsibility that URMs have in cardiology to be visible to inspire future generations.However, mentorship of URiMs should not be limited to only URiM faculty. Centers should try to recruit and establish a culture that values diversity.Diversity shouldn’t be limited to just attributes like race/ gender, but also in interest. Without diversity of thought, you may not have adequate mentorship and community engagement. Show notes updated as of 3.2.2021 CardioNerds Narratives in Cardiology The CardioNerds Narratives in Cardiology series features cardiovascular faculty representing diverse backgrounds, subspecialties, career stages, and career paths. Discussing why these faculty chose careers in cardiology and their passion for their work are essential components to inspiring interest in the field. Each talk will feature a cardiology faculty from an underrepresented group, within at least one of several domains: gender, race, ethnicity, religion, national origin, international graduate status, disadvantaged backgrounds, etc. Featured faculty will also represent a variety of practice settings, academic ranks, subspecialties (e.g. clinical cardiology, interventional cardiology, electrophysiology, etc), and career paths (e.g. division chief, journal editor, society leadership, industry consultant, etc). Faculty will be interviewed by fellows-in-training for a two-part discussion that will focus on: 1) Faculty's content area of expertise2) Faculty's personal and professional narrative As part of their narrative, faculty will discuss their unique path to cardiology and their current professional role with particular attention to challenges, successes, and advice for junior trainees. Specific topics will be guided by values relevant to trainees, including issues related to mentorship, work-life integration, and family planning. To help guide this important initiative, the CardioNerds Narratives Council was founded to provide mentorship and guidance in producing the Narratives series with regards to guests and content. The CardioNerds Narratives Council members include: Dr. Pamela Douglas, Dr. Nosheen Reza, Dr. Martha Gulati, Dr. Quinn Capers, IV, Dr. Ann Marie Navar, Dr. Ki Park, Dr. Bob Harrington, Dr. Sharonne Hayes, and Dr. Michelle Albert. The Narratives Council includes three FIT advisors who will lead the CardioNerds’ diversity and inclusion efforts, including the current project: Dr. Zarina Sharalaya, Dr. Norrisa Haynes, and Dr. Pablo Sanchez. Guest Profiles Dr. Bryan Smith Dr. Bryan Smith is an Advanced Heart Failure and Transplant Cardiologist at University of Chicago. Dr. Smith completed his medical school training, residency and Cardiology fellowship at University of Chicago, then traversed Lake Shore Drive to complete his advanced HF fellowship at Northwestern. At University of Chicago, he serves as the director of the hemodynamic Cath lab, on the Chicago board for AHA, and as a faculty mentor for SNMA (Student National Medical Association.) Dr. Smith’s interests lie in community-based interventions for heart failure management and racial


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