Cardionerds: A Cardiology Podcast

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 3 Dr. Packer reflects on the value of neutral trials and recounts the journey that led to the PARADIGM Trial 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 2 Dr. Packer shares his journey as the trailing spouse and tells the story of how the neurohormonal hypothesis was developed. 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 1 Dr. Packer discusses taking risks, upsetting people and the ridiculousness of humanity and how stand-up comedy helped contribute and shape his career in cardiovascular medicine. Dr. Packer also discusses how the study of afterload agents in heart failure and the discovery of tachyphylaxis with prazosin helped inspire a long and prosperous career in academic cardiology by changing the status quo. 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 and Daniel Ambinder), ACHD series co-chair Dr. Agnes Koczo (UPMC), and ACHD FIT lead Dr. Katia Bravo (UCLA) join ACHD expert Dr. Carole Warnes (Professor of Medicine and founder of the Adult Congenital Heart Disease Clinic at Mayo Clinic), to discuss adult congenial heart disease and pregnancy. They cover preconception counseling in women with congenital heart disease, appropriate risk stratification to estimate maternal and neonatal morbidity using existing tools and an individualized care approach and preparation for a multidisciplinary delivery plan. Audio editing by CardioNerds Academy Intern, Dr. Leticia Helms. 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 Women with congenital heart disease can safely carry a pregnancy if appropriate risk stratification and management is performed by an expert multidisciplinary cardio-obstetrics team. There are a myriad of hemodynamic and vascular changes which impact congenital cardiac physiology and evolve throughout the different stages of pregnancy. Therefore, planning is key. An evaluation of heart rate response to exercise and optimization of potential factors that could worsen during pregnancy, such as arrhythmias, are recommended. Maternal morbidity & mortality risk-stratification systems such as the modified WHO, CARPREG or ZAHARA criteria are helpful starting points. Ultimately, each patient requires individualization given the heterogeneity that exists among congenital heart defects. Vaginal delivery is generally preferred over C-section from a cardiac standpoint. An assisted second stage of labor during the period of greatest hemodynamics changes should also be considered if vaginal delivery is pursued. Show notes Pregnancy and Adult Congential Heart Disease: Created by Dr. Katia Bravo and Dr. Teodora Donisan and reviewed by Dr. Candice Silversides 1. Why is preconception counseling important in women with congenital heart disease and what does it entail? Ensuring women with congenital heart disease are optimized prior to conception decreases maternal and neonatal complications. For this reason, preconception counseling is paramount for these patients. In addition, counseling leads to patients making more informed decisions about family planning. The integral parts of preconception counseling include: (1) discussing the current anatomical and physiological status, (2) discussing possible complications during pregnancy specific to the patient’s congenital heart defect (with genetic counseling referral if appropriate), (3) evaluating cardiac medications, taking into account benefits vs teratogenic potential, (4) discussing and planning for necessary pre-pregnancy tests or interventions (exercise stress testing is an important tool in evaluating how the patient will tolerate the stressors of pregnancy), (5) organizing antepartum care with high-risk obstetrics teams, (6) discussing location, timing and mode of delivery, (7) discussing alternative options to carrying a pregnancy in women who are at extreme risk (ie Fontan physiology, Eisenmenger syndrome) and (8) discussing postpartum contraception.  2. How do we risk stratify women with congenital heart disease who are contemplating pregnancy? An expert evaluation by an ACHD specialist is recommended using a thorough clinical and hemodynamic assessment centered around the individual patient and her values. Several risk prediction tools are available and should be used as a starting point. These include the modified World Health Organization (mWHO) classification, risk factors derived from CARPREG II (CARdiac disease in PREGnancy II), and ZAHARA (acronym based on Dutch translation for Pregnancy in congenital heart defects – Zwangerschap bij Aangeboren HARtAfwijkingen I) studies.  The mWHO classification groups congenital hearts conditions into class I to IV, with higher classes indicating higher predicted risk of cardiovascular matern

CardioNerds (Amit Goyal and Daniel Ambinder) join Dr. Kushani Gajjar and Dr. Mitha Naik from the Allegheny Health Network for a walk along the Three Rivers Trail in Pittsburgh. They discuss a case of young woman in her third trimester of pregnancy with a known history of pulmonary arterial hypertension. The management of pulmonary hypertension in pregnancy and RV failure in the context of pregnancy is described. The E-CPR segment is provided by Dr. Nandita Scott, Co-Director Corrigan Women’s Heart Health Program and Cardiovascular Disease and Pregnancy Service at Massachusetts General Hospital. Special cameo appearance by Dr. Dani Crousillat. If you’re a current internal medicine resident, interested in the intersection between medical education, cardiovascular disease and digital media, consider applying to the CardioNerds Academy using this link. The deadline for this application is October 15th 2021. Learn more by visiting the CardioNerds Academy page. Claim free CME just for enjoying this episode! Disclosures: None 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 – Pulmonary Hypertension in Pregnancy A 33-year-old woman in the third trimester of pregnancy, with a known history of untreated PAH in the setting of TKI therapy, presents with shortness of breath. She is found to have PA pressure greater than systemic pressure with PASP >130. We describe the management of PH and RV failure in the context of a pregnancy. The patient was admitted to the ICU where a multidisciplinary team was mobilized, involving high risk ob-gyn, maternal fetal medicine, critical care, anesthesiology, and advanced heart failure. They began pulmonary vasodilators including treprostinil, tadalafil and inhaled nitric oxide. They also added inotropic and vasopressor support for right ventricular dysfunction with her severe PAH. Fetal heart monitoring was performed. PAH also led to worsening of known chronic thrombocytopenia in the setting of CML. HELLP syndrome was ruled out. The patient had preterm rupture of membranes at 32 weeks of gestation and the team pursued assisted vaginal delivery to prevent vagal response. Following successful delivery, the patient elected to undergo intra-uterine device placement. Post-delivery, vasopressors and inotropes were weaned, and she was discharged on treprostinil, ambrisentan and tadalafil. Thankfully both the mother and baby returned healthy and well at 1 month follow up. Case Media – Pulmonary Hypertension in Pregnancy CMR CXR TTE TTE Click to Enlarge Episode Teaching – Pulmonary Hypertension in Pregnancy Pearls – Pulmonary Hypertension in Pregnancy Pulmonary Hypertension is defined as a mean pulmonary arterial pressure (mPAP) of >20mmHg. There are 5 major types of pulmonary hypertension. Risk modifiers include symptom burden, exercise capacity, presence of pericardial effusion, RV function and hemodynamics. Multidisciplinary care teams are the key to achieving optimal pregnancy outcomes in patients with PH. It is critical to create a team of experts with experience in pulmonary hypertension and plan for constant communication before, during, and after pregnancy. Pregnant women who are already on PAH therapy outpatient should continue them during pregnancy (under the direction of PH experts) except for endothelin receptor blockers which fall in pregnancy category X. PH during pregnancy is associated with up to 38% maternal mortality rate as the right ventricle (RV) is often unable to handle the volume shifts and hemodynamic changes that occur during pregnancy, labor, and delivery. Patients with RV failure leading to low cardiac output and hypotension, like in this case, may benefit from vasopressors with the goal to maintain systemic blood pressure above pulmonary arterial pressures, preserving right coronary blood flow and preventing intracardiac shunting. Swan-guided management may be useful – to titrate inotropes and vasopressors, optimize pulmonary vasodilators and ensure that the patient is being adequately fluid-optimized to maintain a CVP of around 8-10. Notes – Pulmonary Hypertension in Pregnancy 1. What are the different types of pulmonary hypertension (PH)?The WHO separates PH into 5 groups: Group 1 Pulmonary arterial hypertension (e.g., idiopathic, heritable [BMPR2], anorexigen associated, drug or toxin-associated, HIV, connective tissue disease associated, schistosomiasis, portal hypertension, congenital heart disease, etc)   Group 2 Pulmonary hypertension due to left sided heart disease (e.g., HFrEF, HFpEF, left-side valvular heart disease)   Group 3 Pulmonary hypertension due to lung disease or hypoxia: (e.g., COPD, ILD, OSA, hypoxia with

CardioNerds Dr. Rick Ferraro, Director of the #CardsJC Journal Club and cardiology fellow at Johns Hopkins, and Dr. Tommy Das, Program Director of the CardioNerds Academy and cardiology fellow at Cleveland Clinic, learn all about the clinical application of the ASCVD primary and secondary prevention guidelines in terms of lifestyle modifications and lipid lowering strategies from Dr. Allison Bailey, Editor-in-Chief of the ACCEL Audio Journal and Advanced Heart Failure and Transplant Cardiologist at Centennial Heart. Dr. Baily was a co-author on the 2018 ACC/AHA Guideline on the Management of Blood Cholesterol. In this episode we will learn about the current guidelines for primary prevention of ASCVD, the evidence for specific dietary changes in improving cardiovascular outcomes, the current guidelines for secondary prevention of ASCVD, how successful are clinicians and patients in meeting LDL-C recommendations, and what the recent SAMSON trial teaches us about statin intolerance. If you’re a current internal medicine resident, interested in the intersection between medical education, cardiovascular disease and digital media, consider applying to the CardioNerds Academy using this link. The deadline for this application is October 15th 2021. Learn more by visiting the CardioNerds Academy page. Relevant disclosure: 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! Qoatables – Lipid Lowering with Dr. Alison Bailey “Lifestyle should be the first step and the last step of everything we do.” Pearls – Lipid Lowering with Dr. Alison Bailey In patients without established clinical ASCVD, the percent reduction in LDL-C is the strongest predictor of cardiovascular benefit. In patients with high LDL-C levels, a 50% reduction in LDL-C levels should be targeted. In high-risk patients with established clinical ASCVD, we should target a 50% reduction in LDL-C levels and an LDL-C level less of than <70mg/dL. Lower LDL-C levels are associated with better ASCVD outcomes, and European guidelines recommend targeting an LDL-C level of <55mg/dL. LDL-C lowering starts with promoting a health-lifestyle with emphasis on regular exercise and heart-healthy diet. Randomized trials support the efficacy of the Mediterranean diet in reducing cardiovascular events. Show notes – Lipid Lowering with Dr. Alison Bailey 1. What are the current guidelines for primary prevention of ASCVD? The 2019 ACC/AHA Guidelines on the primary prevention of Cardiovascular Disease provides the following guidance for clinicians (applicable to those without established clinical ASCVD): For all patients, a heart-healthy lifestyle focused on diet and exercise is the most important way to prevent atherosclerotic disease. For any patient with an LDL-C ≥ 190 mg/dL, a high intensity statin is recommended. Patients aged 40-75 years old who have diabetes mellitus warrant at least a moderate intensity statin, and may benefit from a high-intensity statin based on additional risk factors For patients aged 40-75 years old and with an LDL-C between 70-189 mg/dL without diabetes, the pooled cohort equation can determine 10-year ASCVD risk and guide a patient-centric risk discussion. Percent reduction in LDL-C is the strongest predictor of cardiovascular benefit; a 50% reduction in LDL-C should be targeted for most patients. 2. What evidence exists for specific dietary changes in improving cardiovascular outcomes? A diet emphasizing intake of vegetables, fruits, legumes, nuts, whole grains, and fish is recommended to decrease ASCVD risk factors. Additionally, minimizing intake of processed meats, refined carbohydrates, and sweetened beverages can reduce ASCVD risk. The PREDIMED trial showed that among patients with high cardiovascular risk, a Mediterranean diet supplemented with extra-virgin olive oil or nuts reduced the incidence of major cardiovascular events when compared to a control diet (with advice to reduce dietary fat). In a sub-study analysis of PREDIMED, a Mediterranean diet supplemented with nuts was associated with delayed progression of internal carotid intima-media thickness and plaque height by ultrasound, suggesting a mechanistic cause of the Mediterranean diet’s cardio-protective effect. The Adventist Health Study-2 cohort demonstrated a significant association between vegetarian diets and decreased all-cause mortality and cardiovascular mortality.  3. What are the current guidelines for secondary prevention of ASCVD? Secondary prevention of ASCVD is important for all patients with history of clinical ASCVD (e.g. prior history of ACS, MI, stable or unstable angina, stroke, TIA, or PAD including aortic aneurysm of atherosclerotic origin)

CardioNerds Amit Goal, Daniel Ambinder, & Dr. Alex Pipilas (FIT, Boston University) discuss the clinical examination in patients with heart failure with Dr. Mark Drazner, professor of medicine, clinical chief of cardiology, and medical director of the LVAD and Cardiac Transplantation Program at UT Southwestern. In this pearl laden episode, they discuss how the exam can be used to non-invasively assess a patient’s hemodynamic status, risk stratify and inform prognosis, and guide management. They also discuss ways to master the evaluation of the JVP and categorize patients based on their RA:PCWP ratio. Check out the CardioNerds Failure Heart Success Series Page for more heart success episodes and content! Relevant disclosures: None 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. 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 Heart Success Series PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls – Clinical Examination in Heart Failure Begin hemodynamic assessment with the evaluation of congestion (“wet” vs “dry”) and perfusion (“cold” vs “warm”). In a 2×2 table, this breaks patients into 4 broad hemodynamic profiles The most sensitive markers of congestion (PCWP > 30) are JVP >12 with an OR of 4.6 and the presence of orthopnea with an OR of 3.6 “If you are cold, you are cold, if you are warm, you can still be cold”. Sensitivity for clinical markers of low cardiac index is very poor. Consider a low output state in patients with poor response to what are thought to be appropriate therapies Most patients with acute on chronic heart failure have an RA:PCWP ratio of 1:2. These patients are the so called “concordant” phenotype. There are two other sub-phenotypes: The “RV equalizer group” have an elevated RA:PCWP ratio The “RV compensated” group have a lower RA:PCWP ratio Clinical congestion at the time of hospital admission as well as discharge portends a poor prognosis for patients with heart failure Show notes – Clinical Examination in Heart Failure Figure 1 1. What is the physical exam important in patients with heart failure? Important to view the physical exam as a diagnostic test with strengths and limitations It is a noninvasive way to assess hemodynamics and risk stratify patients Can provide information on prognosis May enhance the provider-patient relationship 2. How might we classify hemodynamics noninvasively? Framework begins with the “Stevenson” Classification, developed by Dr. Lynne Stevenson Classifies patients along two axes: congestion and perfusion Congestion is the assessment of overall volume status and estimation of right and left sided filling pressures, broadly broken up into “wet” or “dry”: “Wet”, PCWP >15mmHg “Dry”, PCWP <15mmHg Perfusion is the assessment of the adequacy of cardiac output to provide oxygen to peripheral tissues, broken up into “warm” (i.e adequate perfusion) or “cold” (i.e poor perfusion): “Warm”, Cardiac index >2.2 “Cold”, Cardiac index <2.2 You then develop a 2×2 table to begin hemodynamic assessment (Figure 1 – above) 3. What is the role of the clinical exam in the assessment of congestion: “Wet” or “Dry” Signs: Elevated jugular venous pressure. The JVP is one of the two most sensitive markers for congestion such that a JVP > 12 predicts PCWP > 30 with an OR of 4.6 (Drazner, 2008). Rapidly developing ascites or edema Square wave test. The square wave test takes advantage of an abnormal response to Valsalva in patients with low systolic function and elevated filling pressures. In those with congestion, the MAP fails to fall with decrease in RV and LV preload from the Valsalva maneuver due to preexisting high filling pressures. This is likely the best evidence that the patient has elevated filling pressures and may help to identify patients with the discordant hemodynamic phenotypes. Symptoms: Orthopnea: one of the two most sensitive markers for congestion such that the presence of orthopnea predicts PCWP > 30 with an OR of 3.6 (Drazner, 2008). Bendopnea: the sensation of feeling breathless within 30 seconds of bending

In the PA.ACC – CardioNerds Narratives in Cardiology episode, CardioNerd Amit Goyal joins Dr. Miranda Merrill (FIT, Oregon Health & Science University), Dr. Stephanie Fuentes Rojas (FIT, Houston Methodist Hospital), and Dr. Natasha Cuk (FIT, Cedars-Sinai Medical Center) for a discussion with Dr. Kamala Tamirisa (Clinical Cardiac Electrophysiologist, Texas Cardiac Arrhythmia, National ACC Women in Cardiology Leadership Council Member and Co-Chair for ACC Women in Cardiology Advocacy Work Group, and current co-chair of the Texas Chapter ACC EP section) about gender equity and women in cardiology and electrophysiology. This episode focuses on the experiences of women in cardiology across the spectrum of training, from medical school, fellowship, through the procedural field of electrophysiology, to local and national leadership and beyond. Listen to the episode to learn about the factors which have led to Dr. Tamirisa’s success as a private practice electrophysiologist incorporating leadership roles in medical education and national organizations. Closing remarks by Texas ACC chapter governor, Dr. Kenneth Shaffer. Episode script was developed by Dr. Miranda Merrill and episode notes were developed by Dr. Natasha Cuk. 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 – Women in EP https://youtu.be/e7Cjv4vPXqg Quotables – Women in EP “The exciting part today is to see three women who are interested in EP… like RBG said, when all EP physicians are women, that’s the day we’re going to celebrate” 07:15 “There’s nothing (more) exciting… than EP, just that technology, the marriage between analytical thinking, tactile, touch, with a deductive logic.” 09:18 “Multiple studies have documented sex disparities in cardiovascular care… (Historically) women and minorities did not receive implantable cardioverter defibrillators or even BiV (biventricular) pacers… a potential driver for these disparities in cardiovascular disease is lack of diversity in the workforce. Very simple.” 19:28 “I still want to wear my lipstick. I still want to wear my heels. I want to do my hair. I still want to be a proceduralist and that’s okay. Make room.” 28:00 Show notes – Women in EP While this episode and the following notes are specific to women in electrophysiology, these same basic principles apply to fostering a more inclusive and welcoming environment in other subspecialties for all persons regardless of sex, gender, race, ethnicity, IMG status, and the other factors which make us different from one another and which enrich our workforce. 1. Why choose electrophysiology? An EP career is unique – it combines the biology, physiology, and procedural skills learned in residency and fellowship training with engineering, mathematic, and imaging principles learned and refined in advanced EP fellowship.1 EPs work in a spectrum of settings and with a spectrum of modalities: inpatient, outpatient clinic, EP lab and with fluoroscopy, echocardiography (including intracardiac echo), 3D mapping systems, intracardiac EGMs, surface EKGs. Bedside medicine is still key to this field. Curative procedures performed in EP have a meaningful impact on patients’ quality and quantity of life1 and life saving devices such as implantable cardioverter defibrillators have profound impacts on mortality with a number needed to treat to save one life between 3-27 for both primary and secondary prevention indications from multiple randomized controlled trials.2 If you LOVE EKGs, find yourself dissecting telemetry strips, and bonding with your mentors over EKG analysis, then EP is the field for you! 40% of the 130 clinical cardiac electrophysiology fellowship positions in the U.S. remain unfilled and there is a decline in the number of fellows choosing EP for advanced training over the last 5 years. Early exposure to internal medicine residents and first year cardiology fellows to the field will allow time

CardioNerds Dr. Rick Ferraro, Director of the #CardsJC Journal Club and cardiology fellow at Johns Hopkins and Dr. Tommy Das, Program Director of the CardioNerds Academy and cardiology fellow at Cleveland Clinic join Academy fellow and episode lead Dr. Julie Power, chief fellow at the University of Minnesota to learn all about the link between LDL-C and cardiovascular events and disparities in care from Dr. Keith Ferdinand, Professor of Medicine and Chair in Preventative Cardiology at Tulane University School of Medicine. As we’ve learned in prior episodes, LDL-C plays a key role in lipid pathophysiology.  But how does it lead to cardiovascular events?  LDL-C directly leads to plaque expansion and deposition in the arterial intima. Increasing levels of LDL-C are directly related to worsening plaque burden, a principle exhibited powerfully by the dose-dependent nature of coronary atherosclerosis in patients with underlying mutations leading to LDL-C elevation, such as familial hypercholesterolemia. Importantly, the treatment of atherosclerosis and implementation of lipid-lowering therapies are not uniform, with significant disparities throughout the community. The message is clear: Reducing LDL-C is of paramount significance in the prevention and treatment of coronary atherosclerosis and ensuring equitable access to care is critical to addressing the societal burden of cardiovascular disease and improving the health of our communities. There is no CME associated with this episode. To get free CME from other CardioNerds episodes, please visit VCU Health here. Relevant disclosure: Dr. Ferdinand reported severing as a consultant for Medtronic, Amgen, and Novartis. Pearls • Quotables • 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 – LDL, Cardiovascular Events, & Disparities in Care LDL-C is a major stimulant for the initiation and progression of atherosclerosis. The lower the LDL-C level, the greater the clinical benefit in both primary and secondary ASCVD prevention. Our healthcare systems continue to have major disparities in access to quality care and it is essential to reduce barriers to cardiovascular wellness for all communities. Lowering LDL-C in individuals at high cardiovascular risk, especially in those with familial hypercholesterolemia, prevents ASCVD events. Quotables – LDL, Cardiovascular Events, & Disparities in Care “Empower patients to be partners in their care” Dr. Keith Ferdinand Show notes – LDL, Cardiovascular Events, & Disparities in Care 1. What is the link between LDL-C and cardiovascular events? LDL-C is a major stimulant for the initiation and progression of atherosclerosis. The key events in the initiation of ASCVD are the retention and accumulation of cholesterol-rich lipoproteins within the arterial intima at sites with a predilection for plaque formation. As serum levels of LDL-C increase, the probability of intimal retention of LDL leading to the development of atherosclerotic plaque increases in a dose-dependent manner [4]. The WOSCOPS trial demonstrated genes associated with lower LDL-C levels are also associated with a three-fold reduction in the risk of cardiovascular disease per unit reduction in LDL-C [4]. The Emerging Risk Factors Collaboration (ERFC) and Prospective Studies Collaboration reported plasma LDL-C was associated with increased risk of non-fatal MI or CHD death [4]. Statins uniformly reduce atherosclerotic risk across varying levels of baseline LDL-C and are first line therapy for primary and secondary prevention of ASCVD. In high-risk individuals and secondary prevention populations, AHA/ACC guidelines recommend 50% reductions in LDL-C, regardless of baseline, to < 70 mg/dL, using a combination of statins, ezetimibe, and PCSK9 inhibition [6]. Intravascular ultrasound studies of coronary atherosclerosis involving statin-treated patients demonstrated that progression of coronary atherosclerotic plaque volume can be arrested once an LDL-C of 70 mg/dL is reached [4, 10, 11]. The effect of LDL-C on the risk of ASCVD is both causal and cumulative over time; therefore, lowering the LDL-C level early will lead to greater reductions in the lifetime risk of ASCVD. Each millimole per liter reduction in LDL-C reduces the relative risk of ASCVD events by ∼10% in the first year of treatment and ∼20–25% after 5 years [4]. 2. What is Familial Hypercholesterolemia? Familial hypercholesterolemia (FH) is an autosomal co-dominant disorder that results from a mutation in an LDL receptor gene, ApoB gene, or PCSK9 gene. FH is characterized by markedly elevated levels of LDL-C and premature atherosclerosis. Siblings who inherit an FH mutation have markedly elevated plasma LDL-C levels and a corresponding markedly

CardioNerds (Amit Goyal and Daniel Ambinder) join fellow lead, Dr. Giselle A. Suero-Abreu (FIT, Massachusets General Hospital), Dr. Isadora Sande Mathias (FIT, Houston Methodist and CardioNerds Academy Fellow), and Dr. Victor Nauffal (FIT, Brigham and Women’s Hospital) for a discussion with Dr. William Zoghbi (Chair, Department of Cardiology, Houston Methodist Hospital, Methodist DeBakey Heart & Vascular Center, Past President, the American College of Cardiology) about international medical graduates in the cardiology workforce. This episode focuses on the narratives of international medical graduates (IMGs) who make important contributions to the US medical workforce and scientific innovation. Listen to the episode to learn the state of IMGs in the US physician workforce and the field of Cardiology, an overview of factors that influence IMG selection when applying to residency and fellowship training programs in the US, the impact of recent changes in licensing exams and immigration restrictions, and how to address challenges and support IMGs throughout their medical careers. Audio editing by CardioNerds Academy Intern, Dr. Leticia Helms. Claim free CME just for enjoying this episode! Disclosures: None 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. What is the definition of an international medical graduate (IMGs)? International medical graduates (IMGs) are physicians who who graduated from a medical school outside the United States, regardless of nationality. This group of foreign-trained physicians include US-IMGs (US citizens) and non-US IMGs (non-US citizens). Nearly 80% of IMGs are born abroad [1]. In a paper senior authored by Dr. Zoghbi, IMGs in the US physician workforce are described as “the multicultural, multiethnic, open-minded, and plural fabric that has defined American medicine and contributed to its success over the years” [2]. 2. Why are IMGs important? IMGs are an integral part of the U.S. healthcare system. They constitute about 25% of the physician workforce and, since 2010, the number of IMGs in practice has grown by nearly 18% [1, 3]. IMGs play a critical role in addressing healthcare inequities across the US, comprising a significant proportion of physicians in high-need rural and underserved urban areas [1, 3, 4]. IMGs contribute to the diversity and cultural competence in the US physician workforce with 98% of them speaking two or more languages fluently. They help patients overcome linguistic and cultural barriers that can interfere with their care [5]. Learn more about Diversity and inclusion (Episode 95) and Latinx representation in cardiology  (Episode 129). Racial and ethnic concordance between physicians and their patients results in improved healthcare outcomes, and IMGs are essential in matching the needs of the increasingly diverse US population [6]. Many IMGs pursue the opportunity to train in the best academic programs in the US and return as leaders to serve their country. This becomes an avenue for international collaboration to help patients and contribute to research, innovation, and education. 3. What is the state of the IMG workforce in Cardiology? IMGs in cardiology serve as an important source of cardiac care in the United States. Data from the 2020 Physician Specialty Data Report from the Association of American Medical Colleges (AAMC) [7] showed that: Among active US physicians, IMGs comprise 31% of general cardiologists, 46% of interventional cardiologists, and 26% of pediatric cardiologists. Among ACGME trainees, IMGs constitute 38% of fellows in cardiovascular disease, 53% in interventional cardiology, and 20% in pediatric cardiology. Many IMGs have non-immigrant visas, including the J-1 Visitor Exchange visa, and pursue visa waivers at the end of their training. This provides an important source of care to patients in rural and underserved urban areas but can also pose restrictions that affect the career choices and post-training employment opportunities of these physicians [4, 8]. For example, only a third of visa waiver positions can go to specialists, creating difficulty for highly trained cardiovascular subspecialists who are IMGs (such as interventionalists and electrophysiologists) who sometimes have limited options to find a job that matches their training when integrating into the US cardiology workforce [4]. 4. What are some challenges IMGs face? IMGs face a series of barriers when entering US residency programs, during their training experiences, and upon the transition into practice [2, 4, 8-11]. There are disparities and biases concerning IMGs during the residency and fellowship match process. For instance, data from the 2020 NRMP Program Director survey showed that 36% of program directors would “seldom” interview a non-US IMG and 18% would “never” do so. Whe

CardioNerds Cardio-OB series co-chairs University of Texas Southwestern Cardiology Fellow, Dr. Sonia Shah (FIT, University of Texas Southwestern) and Dr. Natalie Stokes, (FIT, University of Pittsburgh) join  Dr. Nanette Wenger, Professor of Medicine in the Division of Cardiology at the Emory University School of Medicine and a consultant to the Emory Heart and Vascular Center and Dr. Sharonne Hayes, Professor of Internal Medicine and Cardiovascular Diseases and founder of the Women’s Heart Clinic at Mayo Clinic for an in depth discussion about lifelong advocacy for women’s cardiovascular health. Audio editing by CardioNerds Academy Intern, Dr. Leticia Helms. 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 – Advocacy for Women’s Cardiovascular Health Dr. Nanette Wenger Dr. Nanette Wenger is Professor of Medicine in the Division of Cardiology at the Emory University School of Medicine. Dr. Wenger received her medical degree from Harvard Medical School in 1954 as one of their first female graduates followed by training at Mount Sinai Hospital where she was the first female to be chief resident in the cardiology department. She is among the first physicians to focus on heart disease in women with an expertise in cardiac rehabilitation and geriatric medicine.Dr. Wenger has received numerous awards including the Distinguished Achievement Award from the Scientific Councils of the American Heart Association and its Women in Cardiology Mentoring Award, the James D. Bruce Memorial Award of the American College of Physicians for distinguished contributions in preventive medicine, the Gold Heart Award, the highest award of the American Heart Association, a Lifetime Achievement Award in 2009 and the Inaugural Bernadine Healy Leadership in Women’s CV Disease Distinguished Award, American College of Cardiology. She chaired the U.S. National Heart, Lung, and Blood Institute Conference on Cardiovascular Health and Disease in Women, is a Past President of the Society of Geriatric Cardiology and is past Chair, Board of Directors of the Society for Women’s Health Research. Dr. Wenger serves on the editorial boards of numerous professional journals and is a sought-after lecturer for issues related to heart disease in women, heart disease in the elderly, cardiac rehabilitation, coronary prevention, and contemporary cardiac care. She is listed in Best Doctors in America. Dr. Sharonne N. Hayes Sharonne N. Hayes, M.D., studies cardiovascular disease and prevention, with a focus on sex and gender differences and conditions that uniquely or predominantly affect women. With a clinical base in the Women’s Heart Clinic, Dr. Hayes and her research team utilize novel recruitment methods, social media and online communities, DNA profiling, and sex-specific evaluations to better understand several cardiovascular conditions. A major area of focus is spontaneous coronary artery dissection (SCAD), an uncommon and under-recognized cause of acute coronary syndrome (heart attack) that occurs predominantly in young women. Dr. Hayes also studies the diagnosis and treatment of nonobstructive (microvascular) coronary artery disease and chest pain syndromes and the subsequent risk of arrhythmias and other cardiac conditions in women who have had hypertension, diabetes or preeclampsia during a pregnancy. With the Pericardial Disease Study Group, Dr. Hayes is assessing the optimal management of pericarditis. Additionally, Dr. Hayes is involved in several research initiatives aimed at addressing health equity and reducing health disparities. Through partnerships with national professional women- and minority-serving organizations, Dr. Hayes assesses barriers faced by women and minorities that prevent or deter them from participating in research studies. Through surveys and national databases, Dr. Hayes is also studying the professional development of women and minorities in the health science professions, including the effects of pregnancy and childbearing during training, and evaluating disparities in academic promotion. CardioNerds Cardioobstetrics Production Team Natalie Stokes, MD Sonia Shah, MD Amit Goyal, MD Daniel Ambinder, MD

In this special CardioOB series patient perspective episode, CardioNerds (Amit Goyal and Daniel Ambinder), join three incredible WomenHeart Champions, Ms. Porothea Dennis, Ms. Brandie Taylor, and Ms. Ellen Robin in the presence of two legendary leaders in cardiovascular medicine, Dr. Nanette Wenger and Dr. Sharonne Hayes. In addition to this episode being featured on our Cardio-Obstetrics topic page, you can also find this episode in our Patient and Family Perspective collection which features several moving and meaningful patient and family stories that remind us of why we do what we do. Special message by Ms. Celina Gorre, CEO of WomenHeart. Audio editing by CardioNerds Academy Intern, Dr. Leticia Helms. The CardioNerds Cardio-Obstetrics series is a comprehensive series led by series co-chairs Dr. Natalie Stokes CardioNerds ambassador from UPMC and Dr. Sonia Shah CardioNerds ambassador from UTSW, and produced in collaboration with WomenHeart. There is no CME for this episode. Relevant disclosures: None. CardioNerds Cardio-Obstetrics Series PageCardionerds Patient and Family Perspective PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Why Cardio-Obstetrics❓ Because it’s important, and relevant to anyone taking care of women who are, may become, or have been pregnant as cardiovascular disease is the #1 cause of pregnancy-related death.  In order to raise awareness we’ve put together an fun, sometimes sobering, but comprehensive curriculum, so get ready, because this CardioNerds Cardio-Obstetrics cruise will dock at several ports along the way: ✔normal pregnancy physiology, ✔hypertensive disorders, ✔arrhythmia, ✔valvular heart disease, ✔anticoagulation, ✔pulmonary hypertension, ✔congestive heart failure, ✔aortopathies, ✔coronary artery disease, ✔critical care, ✔4th trimester, ✔Racial disparities in care, ✔interventional considerations, ✔patient perspectives including from womenheart champions, and more! CardioNerds Cardioobstetrics Production Team Natalie Stokes, MD Sonia Shah, MD Amit Goyal, MD Daniel Ambinder, MD

Join CardioNerds for a great discussion about key ACC 2021 Prevention highlights featuring the ADAPTABLE and STRENGTH trials. This episode is produced in collaboration with the American College of Cardiology Prevention of Cardiovascular Disease Council with mentorship from the Council’s Chair Dr. Eugene Yang (University of Washington Medical Center) who provides a message at the end of the episode.   First, Dr. Amit Goyal and Council Representative Dr. Mahmoud Al Rifai (FIT, Baylor College of Medicine) discuss the implications of the ADAPTABLE Trial with Dr. Gina Lundberg (Emory University School of Medicine).   Then Dr. Tommy Das (FIT, Cleveland Clinic), Dr. Rick Ferraro (FIT, Johns Hopkins) and Council Representative Dr. Anum Saeed (FIT, University of Pittsburgh Medical Center) discuss the results of the STRENGTH trial’s secondary analysis with Dr. Steven Nissen (Cleveland Clinic). Disclosures: Dr Nissen reported grants from AstraZeneca during the conduct of the STRENGTH trial Cardionerds Cardiovascular Prevention PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll Subscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Show notes ADAPTABLE Trial  The ADAPTABLE trial is a randomized open label pragmatic trial comparing two doses of aspirin (325 mg vs. 81 mg) for the secondary prevention of cardiovascular disease. The trial employed a range of innovative and low-cost methods to simplify the identification, recruitment, and follow-up of patients. The primary effectiveness outcome was a composite of death from any cause, hospitalization for myocardial infarction, or hospitalization for stroke. The primary safety outcome was hospitalization for major bleeding.  A total of 15,076 patients were followed for a median of 26.2 months. The primary effectiveness and safety outcomes were not significantly different between the two groups. Together with Dr. Lundberg we discuss design and methodological issues related to the trial and applicability to clinical practice.   ASA 81 mg is as effective as ASA 325 mg for reducing cardiovascular events  ASA 325 mg does not cause more bleeding episodes than ASA 81 mg  ASA dosing should be based on a clinician-patient risk discussion incorporating patients’ risk profile and their values and preferences   Future trials should ensure adequate representation of women and race/ethnic minorities   The results of the present trial suggest that either dose of ASA (81 mg or 325 mg) would be adequate to lower patients’ risk of death or atherosclerotic cardiovascular events with similar risk of bleeding. ASA dosing should be based on patient values and preferences and clinician judgement as the effectiveness and safety profile of these two regiments appears to be equivalent on the basis of the present trial.   STRENGTH Trial, Secondary Analysis  Whether omega-3 fatty acids eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) reduce cardiovascular risk has been long debated. Data have largely remained inconclusive with several previous trials, particularly the VITAL and ASCEND, showing no significant cardiovascular benefit DHA and EPA supplementation. However, the REDUCE-IT and the JELIS trials showed cardiovascular benefit with higher dose of purified EPA compared to placebo.  Meanwhile, the STRENGTH trial did not show any difference in CVD outcomes in treatment groups using a combined EPA/DHA formulation.  In this episode, we discuss a secondary anaylsis from the STRENGTH trial entitled “Association Between Achieved ω-3 Fatty Acid Levels and Major Adverse Cardiovascular Outcomes in Patients With High Cardiovascular Risk” presented at the ACC 2021 addressing the effects of carboxylic acid formulation of EPA/DHA (omega-3 CA) compared with placebo among patients with dyslipidemia and high cardiovascular risk.   This analysis showed that there was no added clinical benefit or harm in those who achieved the highest tertiles of EPA and DHA.  “It is very important to use a neutral comparator as a placebo and this is what we aimed to do in the STRENGTH trial by using corn oil as the placebo against EPA/DHA… you can only optimally interpret a clinical trial in the context of a neutral placebo.”   The STRENGTH trial used carboxylic acid derivative which is better absorbed than other ester formulations used in other studies and its absorption is independent of food.  The EPA concentration in the blood reached adequate levels (even up to 268% in the pooled analysis) in this study however, there was only a ~39% increase in DHA even though a formulation of both EPA and DHA was used. Reasons for this remain to be uncovered.   Three most recent trials including REDUCE-IT, STRENGTH and OMEMI trial have all consistently showed an

CardioNerds (Amit Goyal and Daniel Ambinder), Dr. Victoria Thomas (Cardionerds Ambassador, Vanderbilt University Medical Center), and Dr. Quentin Youmans, cardiology fellow at Northwestern Medicine Bluhm Cardiovascular Institute, join Dr. Clyde Yancy, Vice Dean for Diversity and Inclusion and Chief of Cardiology in the Department of Medicine at Northwestern for an important discussion about underrepresentation in clinical trials and guidelines. This episode was recorded during a live event hosted by the ACC Illinois Chapter. Listen in to hear why diversity matters in clinical trials, how we can recruit more minorities in representation in CV trials and so much more! Stay tuned for a message by chapter Governor, Dr. Annabelle Volgman.   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. Audio editing by CardioNerds Academy Intern, Dr. Gurleen Kaur. 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 https://youtu.be/5gGqWysdCT0 Show notes 1. Why does diversity matter in clinical trials? Having clinical trial enrollment being representative of the general population in which we practice is essential for the generalizability of the trial results. Representative populations matter so we can say to patients, “yes, there were patients that think like you and look like you in the trial.” We can confidently tell them how patients within the trial have done. This is important when we are trying to narrow health disparities to provide confidence and comfort to our patients. Advocacy for health equity is important but not enough. We need data or evidence to support why a change in our behaviors and clinical practice is needed. An evidence base that reflects and includes all our patients is key to bridging health disparities. In medicine, the case for diversity also includes to better serve diverse patients, to promote health equity, to provide diverse mentors at all levels, to bring different points of view to debates and problem solving, to better engage our communities, and to include investigators with a broad range of perspectives in their scholarly activities. (1) 2. How do we recruit more minorities in representation in cardiovascular trials? We need more advocates for diversity in trials in the room when the conversations about trial designs are being made. This is why diversity of leadership is important. There needs to be an intentional approach for every clinical trial to recruit people that are likely to be candidates for enrollment. Stop asking patients to come “downtown” but instead go to their town or their communities. Meet them where they are. Always make sure you are providing some additional advantage or opportunity for the patients you have recruited into your trials. Don’t make it a one-way street. Allow patients to feel that they are getting the best care and generate trust with them. To gain trust, try to get a sense of what is happening in your patient’s life. Find 2-3 minutes to ask them to give a mini biography of their lives. This goes for routine clinical care as well as conducting trials! 3. What advice do you share with people who are underrepresented in medicine, and who may potentially face racism or sexism?   You have two choices when people promote division and hatred. You can choose to be angry, or you can choose to not let others’ poor decisions or thoughts define you. Your best tool as UIM is to control yourself and to be successful. Remember that your uniqueness can make a difference in the lives of so many others. It can help you execute making a large impact for so many more people. 4. How do we recruit more diversity in medicine or cardiology in general? One strategy is to establish new medical school(s) at Historically Black Colleges or Universities (HBCUs). HBCUs recognize broad talent, refine that talent, and propel that talent to success. The current 4 medical schools in part aligned with HBCUs and serving Black medical students represent 2.6% of total medical schoo

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 cardiac sarcoidosis. Show notes 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! Cardiac sarcoidosis is a leading cause of morbidity and mortality for patients with sarcoidosis. A high index of suspicion is needed for the diagnosis as it is often recognized late or unrecognized. It is difficult to diagnose given the focal nature of the cardiac involvement limiting the utility of biopsy and the available clinical criteria have limited diagnostic accuracy. Multimodality imaging plays a large role in the diagnosis and management of patients with cardiac sarcoidosis with the different imaging modalities offering complimentary information and functions. Collect free CME/MOC credit just for enjoying this episode!  CardioNerds Multimodality Cardiovascular Imaging PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Quoatables “It’s not important for you to love the Soviet Union. It’s important for the Soviet Union to love you back [Stalin regarding the famous dissonant Russian poet Anna Akhmatova]. When we talk about PET, you love PET, but the PET has to love you back, and it has to love you back in a way where you have to know how to approach this test. With, first, some humility about its limitations: 1) inflammation is universal…and 2) the prep is extremely important.” — 11:25 “A test without a good preparation is a preparation to fail.” –15:30 “Sarcoidosis is kind of the tuberculosis that we have in medicine—it can present as anything.” –36:40 Pearls Cardiac Magnetic Resonance Imaging (Cardiac MRI) and/or 18-Fluorodeoxyglucose Positron Emission Tomography (FDG-PET) are complimentary tests in the evaluation of cardiac sarcoidosis. Both tests look for scarring and inflammation. Cardiac MRI is a good initial test due to its high negative predictive value (i.e. absence of LGE makes cardiac sarcoidosis less likely) but not great for following a cardiac sarcoidosis patient’s response to therapy. Cardiac FDG-PET is great to follow a patient’s response to therapy especially in patients with intracardiac devices such as a pacemaker. 18-fluorodeoxyglucose (FDG) is a glucose analog and just like glucose, is transported into the cell by transporters. Once in the cell, it is phosphorylated, like glucose is, by hexokinase in preparation for use in glycolysis. Unlike glucose, however, it does not proceed to be metabolized any further in the glycolysis pathway and remains trapped in the cell. In the inflammatory cells within sarcoid granulomas, glycolysis is significantly increased to fuel the large energy requirement. Thus, these inflammatory cells (i.e. macrophages) can take up large amounts of FDG. When planning to obtain a cardiac FDG-PET for evaluation of cardiac sarcoidosis, patient preparation is key! There are several available dietary protocols to accomplish the goal of switching the patient’s metabolism to be reliant on fatty acids instead of glucose as an energy source. One such protocol used by the discussants in the episode is prolonged fasting (10-12 hours) prior to the study preceded by two meals that are high in fat and proteins and low in carbohydrates—a ketogenic diet. By having the patient eat this diet, we are trying to switch the metabolism because there is no ability or no offer of glucose for the body to use as an energy source! After we have switched the body’s metabolism to purely fat, when we inject the patient with FDG, hopefully most of the myocardium not affected by inflammatory cells within a granuloma will not have any uptake! Why do we start with resting perfusion images in the imaging portion of the cardiac FDG-PET protocol for cardiac sarcoidosis? Resting perfusion images allow us to identify any perfusion defects at baseline. These images can be compared to the FDG images to see if there is match or mismatch in areas of abnormalities. Resting perfusion images also allow us to assess LV and RV function. Resting perfusion images in conjunction with FDG images can also allow us to monitor the patient’s response to treatment by demonstrating return to normal myocardium from active sarcoid granuloma after treatment or by showing the progression to development of scar. The hallmark for detecting cardiac sarcoidosis with cardiac MRI is late gadolinium enhancement (LGE) in the mid-wall an

CardioNerds (Amit Goyal and Daniel Ambinder), join cardiology fellows from the University of Chicago, (Dr. Mark Belkin, Dr. Ian Hackett, and Dr. Shirlene Obuobi) for an important discussion about case of a woman presenting with implantable cardioverter-defibrillator (ICD) discharges found to be in ventricular tachycardia (VT) storm and work through the differential of ventricular arrhythmias, etiologies of heart failure, and indications for permanent pacemaker and ICD placement. Advanced imaging modalities that aid in the diagnosis of cardiac sarcoidosis, manifestations and management of cardiac sarcoidosis are also discussed. Dr. Nitasha Sarswat and Dr. Amit Patel provide the E-CPR for this episode. Audio editing by CardioNerds Academy Intern, Leticia Helms. Claim free CME just for enjoying this episode! Disclosures: Dr. Amit Patel disclosed ownership of small stocks in GE Healthcare Bio-Sciences. Jump to: Case media – Case schematic & 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 Click to Enlarge Episode Teaching Pearls The etiology of wide-complex tachycardias (WCT) of ventricular origin can be broken down by structurally normal versus structurally abnormal hearts. WCT in structurally normal hearts can be further broken down into idiopathic or primary arrhythmia syndromes. WCT in structurally abnormal hearts can be broken down into ischemic and non-ischemic etiologies. In patients with an unexplained non-ischemic cardiomyopathy, conduction abnormalities and/or ventricular arrhythmias should raise suspicion for cardiac sarcoidosis. Additional manifestations include atrial arrhythmias and  pulmonary hypertension. Accurate diagnosis and treatment of cardiac sarcoidosis often requires multimodality cardiovascular imaging. Check out these terrific videos from Cardiac Imaging Agora: 1) PET for inflammation/sarcoidosis and 2) Echo and CMR for sarcoidosis. While a pathological tissue diagnosis is the gold-standard, endomyocardial biopsy has a low sensitivity, weven when paired with image guidance. Remember to consider extra-cardiac sites for biopsy. Decisions regarding ablation of ventricular arrhythmia or ICD placement should be done individually with careful assessment of active inflammation secondary to cardiac sarcoidosis and possible response to immunosuppressive medications. Management of cardiac sarcoidosis has two basic principles: 1) Treat the underlying process with immunosuppression and 2) Treat the cardiac sequelae: heart failure, conduction abnormalities, ventricular arrhythmias, atrial arrhythmias, and pulmonary hypertension. Notes 1. The patient in this case was found to be in VT storm. Taking a step back, when we suspect a wide complex tachycardia (WCT) is VT, what are some etiologies we should keep in mind? Differentiating between a supraventricular vs. ventricular origin of a WCT will be a topic for a future episode! But after you have determined that the origin of WCT is ventricular, considerations for the underlying etiology should include ischemia-related, non-ischemic cardiomyopathy-associated, primary arrhythmia syndromes and idiopathic (in addition to common considerations such as medications and electrolyte abnormalities) Chronic ischemia-related WCT is typically scar-mediated, a result of re-entrant mechanism and more commonly presenting as monomorphic VT. WCT in the setting of acute ischemia is likely a result of combination increased automaticity and re-entry, typically manifesting as polymorphic VT.  In fact, acute ischemia is the most common cause of polymorphic VT, not Torsades de Pointes, and should be our first consideration. Torsades de Pointes specifically occurs due to an early afterdepolarization in a patient with an acquired or congenital prolonged QT interval. Non-ischemic related WCT etiologies in structurally abnormal hearts include (but not limited to) cardiac sarcoidosis, myocarditis (specifically giant-cell myocarditis), hypertrophic cardiomyopathy, arrhythmogenic right ventricular cardiomyopathy, left dominant arrhythmogenic cardiomyopathy and Chagas disease. Especially in patients with dilated CM, if your initial evaluation does not reveal an etiology, then genetic testing should be considered to identify genetic sources of arrhythmogenic cardiomyopathies, such as laminin and desmoplakin mutations (See Episode 56: CNCR with Northwestern University!) Primary arrhythmia syndromes include, but are not limited to, Brugada, Long QT, Short QT, and catecholaminergic polymorphic VT (CPVT).  Idiopathic WCT includes outflow tract, fascicular, or papillary muscle ventricular tachycardias (VT). 2. What is the underlying pathophysiology for the cardiac manifestations of sarcoidosis? Typically, the clinical manifestations of cardiac sarcoidosis dep

CardioNerds Academy Chief Fellows Dr. Rick Ferraro (FIT, Johns Hopkins) and Dr. Tommy Das (FIT, Cleveland Clinic) join Academy fellow Dr. Jessie Holtzman (soon, chief resident at UCSF internal medicine residency) to learn all about LDL physiology and function from Dr. Peter Toth! Low-density lipoprotein cholesterol (LDL-C) has been well established as a risk factor for atherosclerotic cardiovascular disease with an ever growing armamentarium of medications to lower LDL-C plasma levels. Yet, LDL-C also plays a number of key physiologic roles across mammalian species, such as cell membrane formation, bile acid synthesis, and steroid hormone production. In this episode, we discuss the definitions of high, normal, low, and ultra-low LDL-C, what functional assays are used to measure LDL-C, and what is considered the safe lower-limit of LDL-C, if there is one at all. Drawing upon experience from rare genetic conditions including abetalipoproteinemia and loss-of-function variants of the PCSK9 gene, we glean pearls that clarify the risks and benefits of low LDL-C. Relevant disclosure: Dr. Toth has served as a consultant to Amarin, Amgen, Kowa, Resverlogix, and Theravance; and has served on the Speakers Bureau for Amarin, Amgen, Esperion, and Novo Nordisk. Pearls • Quotables • 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 1. Lipoproteins are processed via two major pathways in mammals: 1) exogenous fat metabolism that digests ingested lipids and 2) endogenous fat metabolism that synthesizes lipids in the liver and small intestine. High density lipoprotein (HDL)-mediated reverse transport also brings lipids from the periphery back to the liver. 2. LDL-C comprises ~70% of plasma cholesterol due to its long half-life of 2-3 days. It is one of 5 major lipid particles in plasma including chylomicrons, very low-density lipoproteins (VLDL), intermediate-density lipoproteins (IDL), LDL, and HDL. The liver degrades 40-60% of LDL, while no other tissues in the body make up more than 10% of LDL. LDL-C is energy-poor and cholesterol rich, such that peripheral tissues may not utilize these particles as a fuel source. 3. Preserved functions of LDL-C across mammalian species include cell membrane formation, bile acid synthesis, and steroid hormone production. In other mammalian species, LDL-C levels are found in the 35-50 mg/dL range (Way lower than found in the general human population, and likely more representative of baseline human physiology!). 4. Large, randomized control trials do not consistently demonstrate major adverse effects associated with lower serum LDL-C levels, including risks of cognitive decline, hemorrhagic stroke, reduced bone density, or impaired immune function. 5. Initiation of, and education on LDL-lowering therapy remains insufficient, both in terms of long-term adherence to therapy and achieving current guideline directed goals of LDL-C <70mg/dL (And even lower in specific scenarios, such as repeat cardiovascular events). Quotables “It’s pretty clear that this is an area where you can make a profound difference in the lives of people. It’s very clear from the clinical trials that when we initiate therapies, whether it’s lifestyle, through a statin, or an antihypertensive, you impact not only the quality of life, but the quantity of life. You make life better, you make life freer of disability, and you forestall death.” “The bottom line is that LDL is spent garbage liquid and it is tantamount that the body be well-equipped to remove this LDL from the central circulation, because I will argue today that it is the single most important toxin that we produce.” “If you ask what should a normal LDL be? Well, I’ll tell you right now…the best estimate is actually around 38 to 40 mg/dL.” Show notes 1. How does the body metabolize lipoproteins and where does LDL-C fit into these processing pathways? There are two major pathways through which the body metabolizes lipoproteins. The exogenous fat metabolism pathway includes digestion, absorption, and re-packaging of the lipids that we ingest. Dietary fats are disassembled from energy dense lipid macromolecules into chylomicrons. Chylomicrons are the largest, least dense particles followed by VLDL, IDL, LDL, and HDL. Second, there is the endogenous fat metabolism pathway that allows the liver to synthesize and secrete lipids. The structure of LDL-C contains apolipoprotein(B) that serves as a scaffold molecule, with the core compromised of triglyceride and cholesteryl esters, interspersed with phospholipids and cholesterol. VLDL is secreted into the central circulation and is acted upon by lipoprotein lipase primarily – but also hepatic lipase and endothelial lipase – to release fatty acid whi

CardioNerds (Amit Goyal and Daniel Ambinder) are joined by Dr. LaPrincess Brewer and Dr. Norrisa Haynes for a Narratives in Cardiology episode, with a special introduction by Dr. Sharonne Hayes. They discuss health inequities especially in communities of color, impact of projects utilizing community based participatory research (including FAITH! and SHARP founded by Dr. Brewer and Dr. Haynes respectively), and their experiences as underrepresented minority women physician-scientists. This special discussion is brought to you in collaboration with the Association of Black Cardiologists (ABC). The ABC’s mission is to “Promote the Prevention and Treatment of Cardiovascular Disease, including Stroke, in Blacks and other Diverse Populations and to Achieve Health Equity for all through the Elimination of Disparities.” You may join and support the ABC at abcardio.org. 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 for Health Equity, Community Based Participatory Research, & Underrepresented Minority Women Physician-Scientists 1. What healthcare disparities exist in communities of color? The life expectancy of black Americans on average is 3.4 years shorter than that of white Americans. CVD is estimated to explain over 32% of the mortality difference between AA and white men and 43% of the difference between AA and white women. Together these conditions contributed to > 2 million years of life lost in the AA population between 1999-2010. (1) The impact of COVID-19 on minority communities has caused disproportionate morbidity and mortality and devastating health and financial hardship. According to the CDC, black Americans are 1.9x as likely as whites to die from COVID-19. (2) Additionally, at the beginning of the pandemic, a staggering 41% of black owned businesses closed due to COVID-19 as compared to 17% of white owned businesses. (3)  2. Community engagement & Community based participatory research (CBPR) – what is it? CBPR often has a public health bend that focuses on and attempts to address social, structural and environmental inequities through active involvement of community members in all aspects of the research process (from conception to implementation). Community partners provide their unique expertise to enhance understanding of the community and facilitate implementation. (4) 3. What is FAITH!? The Fostering African American Improvement in Total Health (FAITH) program was started by the phenomenal Dr. LaPrincess Brewer. FAITH is a cardiovascular health and wellness program that uses a CBPR approach to promote heart health in the African American faith-based community. Participants in the FAITH program have shown significant improvement in heart health knowledge. Participants have also had improvement in key heart disease risk factors such as blood pressure. The FAITH app was created in collaboration with community members to achieve easy access and easy usability. It provides vital information and a community network that provides support and motivation for participants.  4. Specifics of SHARP? SHARP stands for Safe Haircuts as We Reopen Philadelphia. SHARP was started to assist local barbershops and salons implement proper COVID-19 safety practices to keep their businesses, clients, and staff safe.  In partnership with community members, a safety blueprint was created to meet CDC and Philadelphia Health Department guidelines.  Through donations from UPenn and Accenture, SHARP was able to distribute a significant number of PPE items to 30 businesses in West and Southwest Philadelphia.  Additionally, due to the financial toll that the pandemic has had on small businesses, SHARP organized grant writing sessions through the Netter Center at Penn to help the coalition of businesses in West Philadelphia apply for governmental financial relief. Through collaboration with local mental health professionals, SHARP has also been able to offer free therapy to community members. SHARP is currently working with the coalition of businesses to assist them in becoming positive COVID-19 vaccine ambassadors. 5. What is the concept of #MeWho? #ME_WHO is a brilliant piece authored by Dr. Michelle Albert that was published in Circulation in 2018. In this piece, Dr. Albert eloquently describes how underrepresented minorities and specifically underrepresented minority women physician-scientists (URMWP) are tasked with maintaining an arduous balance. In her words “URMWP are faced with walking a tight rope in academic medicine that requires expertise and excellence in both clinical and scholarly domains, typically with insufficient academic support, social capital, and attainment of senior leadership roles that would turn their zeal and commitment into progress.” D

CardioNerds (Amit Goyal and Daniel Ambinder), join cardiology fellows from Indiana University cardiology fellows (Dr. Asad Torabi, Dr. Michelle Morris, and Dr. Sujoy Phookan) to discuss a case of a patient who developed a nagging cough post PCI and is ultimately diagnosed with Dressler Syndrome. This case describes the work up and management of post infarct pericarditis and briefly reviews the dilemma of utilizing triple anti-thrombotic therapy with high dose aspirin in the post myocardial infarction period. Indiana University faculty and expert, Dr. Julie Clary provides the E-CPR for this episode. Claim free CME just for enjoying this episode! Disclosures: None 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 56-year-old man with recent anterior STEMI and new heart failure with reduced ejection fraction presented with fevers, persistent cough, and pleuritic chest pain following percutaneous coronary intervention for the past two weeks. He was ultimately found to have post cardiac injury syndrome – post infarct pericarditis (formerly known as Dressler syndrome) with elevated inflammatory markers, a small pericardial effusion, and incidentally noted to have an apical left ventricular thrombus. This case describes the work up and management of post infarct pericarditis and briefly reviews the dilemma of utilizing triple anti-thrombotic therapy with high dose aspirin in the post myocardial infarction period.   Case Media CXR EKG Click to Enlarge Episode Teaching Pearls 1. Post cardiac injury syndrome (PCIS) following myocardial infarction can be very debilitating and recurrence is the concern when treatment is not pursued.  2. Acute pericarditis is a clinical diagnosis which does not require imaging and can have a wide spectrum on presentation ranging from fever/cough to the classic positional chest pain. 3. PCIS following myocardial infarction is less common in the post PCI era but we are starting to see more cases in late presenters. 4. We have good level of evidence to suggest the use of colchicine to reduce the recurrence of PCIS. COPPS and COPPS-2, are two such randomized placebo control trials, which show benefit in the cardiac surgical patient. 5. While triple therapy on high dose aspirin is not discussed in the 2013 ACCF/AHA STEMI guidelines, carefully assess your patient’s bleeding risk and invoke patient shared decision making whenever possible. Notes 1. What is Post-Cardiac Injury Syndrome (PCIS) and what are the clinical manifestations? PCIS is an umbrella term for specific clinical scenarios which may result in symptomatic acute pericarditis. PCIS encompasses: Post-myocardial infarction pericarditis which may be early or late (Dressler syndrome – the focus of this case) Post-pericardiotomy syndrome (PPS) Post-traumatic pericarditis including traumatic and iatrogenic (following most percutaneous procedures such as ablations, PCI, lead placement, etc). 2. How is PCIS (or post infarct pericarditis) diagnosed? This is a clinical diagnosis, made when ≥ 2 of the following are present: Fever without alternative cause Pericarditic or pleuritic chest pain Friction rub Pericardial effusion Pleural effusion with elevated CRP Note this is different from the diagnostic criteria for other causes of acute pericarditis which requires 2 of the 4 following features: Pericarditic chest pain Friction rub New widespread ST-elevations or PR depressions on ECG Pericardial effusion (new or worsening) Supporting findings for pericarditis include: Elevation of inflammatory markers (CRP, ESR, WBC) Pericardial inflammation on cross sectional cardiac imaging (CT, CMR) 3. What are the complications of not treating Dressler syndrome? Imazio et al published an excellent case series in 2009 which answers this question. Overall the prevalence of complications for early and late post-infarct pericarditis was low. No cases of constrictive pericarditis were observed but the incidence of recurrent pericarditis was observed at 3.2%. The 2015 ESC pericardial guidelines recommend considering careful follow-up after PCIS to exclude possible evolution towards constrictive pericarditis with echocardiography every 6-12 months according to clinical features and symptoms (Class IIa). 4. What is the evidence for high dose Aspirin in Dressler syndrome? This is a class 1b evidence in the 2013 ACCF/AHA STEMI guidelines. This evidence comes from data from a small case series of 24 patients which compared aspirin to indomethacin head-to-head. Overall aspirin was non-inferior with similar bleeding risk. The guidelines recommend the use of high dose aspirin because of NSAIDS may interfere with DAPT and there is also concern regarding scar thinning and infarct exp

CardioNerds (Amit Goyal and Daniel Ambinder), Dr. Pablo Sanchez (CardioNerds Ambassador, Stanford University Medical Center), Dr. Maria Pabon (CardioNerds Ambassador, Brigham and Women’s Hospital), and Karen Malacon (Student doctor and LMSA co-chair at Stanford University Medical Center) join Dean for Students at Harvard Medical School, Dr. Fidencio Saldana, for an important discussion about Latinx representation in cardiology. We established the multifaceted benefits of diversity in healthcare, including improving access, cultural competency, and quality of care delivered. We also talked about the need to increase the number of underrepresented minority students in medicine in addition to the importance of removing barriers to improve education. By providing appropriate resources as well as early mentorship and exposure to the medical field, we can address the “leaky pipeline,” or as Dr. Saldana reframed it, “the clogged pipeline.”  Then, we dove into Dr. Saldana’s experiences in medical school, the barriers he overcame, and how his parents’ hard work and generosity motivated him to become the cardiologist he is now. This event hosted the ACC Massachusetts Chapter. Stay tuned for a message by chapter Governor Dr. Malissa Wood. 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. Audio editing by CardioNerds Academy Intern, Dr. Gurleen Kaur. Video Version • Quotables • Notes • References • Production Team 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 https://www.youtube.com/watch?v=cpq2wVgG8mA Quotable We strive to ensure that we have a diverse set of college students and a diverse set of medical students and residents and fellows. But I think it’s also just as important to ensure that we have the resources to ensure that those individuals that we’ve recruited and have done so hard to recruit, continue to succeed. I’ve realized that you can teach mentoring, you can teach advising. And I think it’s important to be able to create that culture and expectation. Some people may be a little bit better at it than others, but I think it’s important to place an emphasis on that at each level of training, so that you can train to be a better mentor and a better advisor. Show Notes 1. How is the LatinX representation in medicine compared to in the general population? Based on the most recent data from the US census Bureau, as of 2019, the Hispanic proportion of the US population is about 18.5%. A recent report by the AAMC showed that for the academic year 2020-21, of around 22,000 medical school matriculants, only 11% were from LatinX background, although this number was higher compared to 2017 where only 9.8% of the matriculants were of LatinX origin.   2. How does increasing workforce diversity improve quality of care? Cultural competency forms an important cornerstone of high-quality and equitable care for a diverse population, and it is learned not by lecture but by exposure, experience, and atmosphere. Medicine involves not only knowledge but meaningful connection and having a physician with a common background enhances the patient-doctor interaction by a spectrum of constructive effects. Inasmuch as research questions are guided by interests of investigators, the inclusion of underrepresented minorities among the pool of investigators stands to better delineate problems and articulate solutions. Actuating the gears of change at state/local governments and health systems to solve issues of access and quality of care will be only benefited by inclusion of medical-trained underrepresented minorities at the table.  3. How do can we promote diversity in fellowship programs? Participate in and support efforts to promote recruitment of underrepresented minorities for residency and fellowship programs as well as retention at the faculty level. Participate in initiatives focused on mentoring underrepresented minorities early on (high school or college students). Educate ourselves and others about the barriers that underrepresented minorities must overcome such as inadequate housing, food insecurity, and/or financia

CardioNerds (Amit Goyal and Daniel Ambinder), Cardio-OB series co-chair and University of Texas Southwestern Cardiology Fellow, Dr. Sonia Shah, and episode lead and Columbia University Cardiology Fellow Dr. Ersilia DeFilippis discuss hypertensive disorders of pregnancy (HDP) with Dr. Jennifer Lewey from the University of Pennsylvania. In this episode, we cover chronic hypertension, gestational hypertension, and pre-eclampsia—all of which encompass HDP and complicate approximately 5-10% of all pregnancies. We also review risk factors for HDP, diagnostic criteria, peripartum and postpartum management, and much more! Be sure to tune in to hear Dr. Lewey discuss the future impact of HDP on cardiovascular disease for women later in life and strategies that can help improve care. Finally Dr. DeFilippis shares her perspectives from her ACC.org FIT Section article titled “Shattering the Glass” including strategies to shattering the glass and tackling imposter syndrome in improving the representation of women in medicine. Audio editing by CardioNerds Academy Intern, Leticia Helms. Claim free CME for enjoying this episode! 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! Pearls To make a diagnosis of HDP, blood pressure should be measured on at least 2 occasions at least 4 hours apart. Hypertension diagnosed before 20 weeks gestation is considered chronic hypertension whereas hypertension after 20 weeks is categorized as gestational hypertension. Always check for warning signs for pre-eclampsia! One of the key treatments for pre-eclampsia is delivery but pre-eclampsia can occur still in the postpartum period. Aspirin use in pregnancy during second and third trimesters can reduce the risk of pre-eclampsia among women at risk. Quotables “Ideally a lot of these conditions come down to prevention and addressing potential cardio-obstetrics issues before they reach the cardio-obstetrics specialist.” “Blood pressure can continue to be elevated even after delivery.” “Pregnancy complications not only increase cardiovascular risk in the middle age population but also in the postmenopausal population.” “Women feel so relieved when they know that their care team is dedicated to taking care of women with cardiovascular disease when they are pregnant.” Show notes Why should CardionNrds learn and know about hypertensive disorders of pregnancy? Hypertensive disorders of pregnancy (HDP) complicate about 5-10% of all pregnancies. HDP is a term that encompasses chronic hypertension, gestational hypertension, pre-eclampsia, and pre-eclampsia superimposed on chronic hypertension. Women with history of HDP are at increased risk for stroke, ischemic heart disease, and cardiovascular death later in life. It is important to include obstetric history as part of our assessment of cardiovascular risk. This obstetric history should include the number of pregnancies, history of gestational diabetes, gestational hypertension, history of pre-eclampsia as well as history of pre-term birth. Following delivery, these women need close monitoring for development of chronic hypertension as well as primary prevention of cardiovascular disease. 2. How is gestational hypertension distinguished from chronic hypertension? The key factor in distinguishing gestational hypertension from chronic hypertension is the timing of diagnosis. Before 20 weeks gestation, elevated blood pressure (defined as a reading > 140/90 on two occasions at least 4 hours apart) is considered chronic hypertension. After 20 weeks gestation, elevated blood pressures signify a pregnancy-induced process, namely gestational hypertension or pre-eclampsia if blood pressure elevation is severe enough or there is evidence of end-organ damage. Blood pressure is often lower in the 1st and 2nd trimesters due to lower systemic vascular resistance. We think the process of gestational hypertension and pre-eclampsia result from how spiral arteries implant in the uterus. There are a whole host of local factors that lead to an increase in blood pressure later on in pregnancy. 3. What are warning signs of pre-eclampsia? Pre-eclampsia is diagnosed in the setting of high blood pressure, usually after 20 weeks, in the setting of proteinuria or end-organ dysfunction. End-organ dysfunction most commonly includes thrombocytopenia, transaminitis, right upper quadrant pain, headaches, pulmonary edema, and symptoms and signs that are not explained by other causes. Notably, blood pressure readings greater than > 160/110 mm Hg are sufficient for the diagnosis in the absence of other findings. 4. What are risk factors for pre-eclampsia or pre-eclampsia superimposed on chronic hypertension? Risk factors for pre-eclampsia include a personal or family history of

In the last episode, episode 126, we discussed pregnancy and aortic disorders as part of The CardioNerds Cardio-obstetrics Series. This episode brought to mind episode 76, where our colleagues from the Cleveland Clinic taught us about a woman named Lizzie Gasser, who at the young age of 27 tragically presented with postpartum pulmonary edema, found to have papillary muscle rupture, and was ultimately diagnosed with Vascular Ehlers Danlos Syndrome (VEDS) at autopsy. This case has been published in JACC Case Reports: CardioNerds Corner. Now, in this very special episode, we meet Lizzie Gasser, beyond her heart disease through the eyes of her loving husband, Todd Gasser. Her legacy underscores the importance of seeing our patients as people beyond their illness, in the context of their lives, values, and loved ones. This powerful discussion is led by Dr. Erika Hutt (cardiology fellow at the Cleveland Clinic) and Dr. Eunice Dugan,  (internal medicine resident at Johns Hopkins Hospital). Dr. Harry “Hal” Dietz (professor of pediatrics, an associate professor of medicine and an assistant professor of neurological surgery at the Johns Hopkins University School of Medicine and a leading authority on genetic aortopathies (including Loeys-Dietz Syndrome which carries his name). Audio editing by CardioNerds Academy Intern, Dr. Maryam Barkhordarian. This episode is brought to you in collaboration with the VEDS Movement. The VEDS Movement’s mission is to save lives and improve the quality of life of individuals with Vascular Ehlers-Danlos Syndrome (VEDS). By pursuing the most innovative research, educating the medical community, general public and affected individuals, and providing support to patients, families, and caregivers, The VEDS Movement, which is a division of The Marfan Foundation, charges forward and improves the outcomes for those living with VEDS. Individuals affected with VEDS can access medical webinars presented by the experts, join support groups, get involved in events and research, and donate by visiting TheVEDSMovement.org. Providers can also find resources, including CME opportunities, at TheVEDSMovement.org. 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! Photos & Youtube videos featuring Lizzie Gasser and her family https://www.youtube.com/watch?v=W4sVuctrUZs&t=1s Video from the VEDS movement that Lizzie’s family is interviewed in. Their interview is from 7m30s – 17m16s  https://www.youtube.com/watch?v=6CeXYnZHhbg Video of Lizzy’s life life that a friend put together. Episode Guests Dr. Erika Hutt Dr. Eunice Dugan Dr. Harry “Hal” Dietz CardioNerds Case Report Production Team Karan Desai, MD Amit Goyal, MD Daniel Ambinder, MD

CardioNerd Amit Goyal, Cardio-OB series co-chair and University of Texas Southwestern Cardiology Fellow, Dr. Sonia Shah, and episode lead and Johns Hopkins University Cardiology Fellow, Dr. Anum Minhas, discuss pregnancy and aortic disorders with Dr. Nupoor Narula of Weill Cornell Medical College. Special introduction by Sukrit Narula. In this episode we discuss the presentation and management of aortopathies during pregnancy. We begin by examining the pathophysiology of aortic disease during pregnancy, followed by a review of the heritable aortopathies and their risk of dissection. We then discuss preconception evaluation and antepartum care of women with aortopathies. We end with addressing management at the time of labor and delivery. 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 – Pregnancy and Aortic Disorders In this episode we discuss the presentation and management of aortopathies during pregnancy. We begin by examining the pathophysiology of aortic disease during pregnancy, followed by a review of the heritable aortopathies and their risk of dissection. We then discuss preconception evaluation and antepartum care of women with aortopathies. We end with addressing management at the time of labor and delivery. Pearls – Pregnancy and Aortic Disorders 1. Assessment of aortic root and ascending aortic measurements should be performed prior to conception in women with known aortopathies, connective tissue diseases with high risk for aortopathies, bicuspid aortic valve or familial thoracic aortic syndromes. Dimensions should always be verified with multi-modality imaging prior to decision-making. 2. It is important to recognize that the immediate postpartum period is a high risk period for aortic dissection in women with aortopathies. 3. Goal systolic blood pressure is < 120 mmHg and diastolic blood pressure is < 80 mmHg in women with aortopathies. This goal should be discussed with the patient’s obstetric provider during pregnancy, however, to ensure a blood pressure target is chosen that is appropriate for optimal maternal and fetal outcomes. Beta-blockers followed by calcium channel blockers should be used for these targets. Aldosterone receptor antagonists are contraindicated during pregnancy. 4. Per the 2018 ESC guidelines, during pregnancy, women with aortic pathology should have an echocardiogram performed every 12 weeks if low risk, and every month (4 weeks) if high risk. 5. Women with type A dissection during pregnancy should be evaluated for urgent Caesarean section and aortic surgery if the fetus is viable. Women with a stable type B dissection may be managed medically if stable. All decisions should be made in a multidisciplinary fashion with consultation with Maternal Fetal Medicine and Cardiothoracic Surgery. Quotables – Pregnancy and Aortic Disorders 1. “First and foremost, we must verify our dimensions. I’ll say that again. We must verify our dimensions because nothing could have greater impact.” 2. “You know, our most important role is to provide transparency in pre-pregnancy risk counseling. We have to present the data that are available. We need to present the gaps in literature.  We need to present the possibility that in the right individual, we can proceed through pregnancy safely with close clinical and imaging monitoring and follow up in a multidisciplinary construct. Show notes – Pregnancy and Aortic Disorders What is the risk of aortic dissection during pregnancy in Marfan syndrome? Women who undergo pregnancy with prepartum counseling and close clinical and imaging follow-up usually maintain stability of aortic dimensions over time and risk of type A dissection appears low. Type B dissection remains unpredictable. Overall, the risk of aortic complications surrounding pregnancy remains eight-fold higher than in the non-pregnant state. The risk for dissection is higher with greater aortic root size, but there still remains a risk for dissection at diameters less than 40 mm. Note, in the GenTAC registry (which included 184 women with Marfan’s Syndrome in whom pregnancy information was available), lack of knowledge of the underlying diagnosis of Marfan’s was not uncommon. What is the underlying pathophysiology behind increased risk for aortic dissection during pregnancy? Pregnancy is associated with both hemodynamic changes and alterations in tissue architecture which may both increase the risk of exacerbating an underlying aortopathy syndrome. Physiologic changes during pregnancy include increased stroke volume and heart rate, resulting in increased cardiac output, with concomitant decrease in the peripheral r

CardioNerds (Amit Goyal & Karan Desai) join University of Minnesota fellows, Dr. Julie Power, Dr. Sasha Prisco, and Dr. Abdisamad Ibrahim for a riveting discussion in which they were pressured to diagnose a young woman with syncope. The fellows expertly take us through the next steps in the differential diagnosis, and management of pulmonary hypertension in this young patient! University of Minnesota faculty and expert in right ventricular (RV) failure in pulmonary arterial hypertension (PAH) Dr. Kurt Prins provides the E-CPR for this episode. With this episode, the CardioNerds family warmly welcomes The University of Minnesota 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 University of Minnesota fellowship program director, Dr. Jane Chen has nominated Dr. Julie Power for this position. In addition to being a CardioNerds Ambassador, Julie has already done amazing CardioNerds work as part of the CardioNerds Academy fellowship. Claim free CME just for enjoying this episode! Disclosures: None 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- Syncope and Pulmonary Hypertension A Somali woman in her mid-30s with no significant past medical history presented with shortness of breath and exertional syncope. EKG revealed evidence of RV strain. CTA-PE protocol did not show PE. However, there was RV dilation and subsequent echocardiogram demonstrated normal LV, but moderately reduced RV function with evidence of RV pressure and volume overload. RVSP was estimated to be 188 mmHg! Case Media A B C D E F G H Click to Enlarge A. CXR, B. ECG, C. PA measurements: Main PA measures 2.4 cm, right PA measures 2.3 cm, left PA measures 1.9 cm, D. Tricuspid valve Doppler, E. RA tracing, F. RV tracing, G. PA tracing, H. Wedge tracing CTA PE: No PE, markedly dilated pulmonary trunk at 4.7 cm. Right main pulmonary artery measures 3.1 cm. TTE: Parasternal long axis: Moderate right ventricular dilation compressing left ventricle. Global right ventricular function is moderately reduced. TTE: Parasternal long axis- RV view: Right ventricular dilation with mild pulmonary regurgitation TTE: Mild pulmonary regurgitation with dilation of main PA TTE: Paradoxical septal motion consistent with right ventricular pressure and volume overload. TTE: Apical 4 chamberParadoxical septal motion consistent with right ventricular pressure and volume overload. Moderate right ventricular dilation.Global right ventricular function is moderately reduced.Severe right atrial enlargement. Paradoxical septal motion consistent with right ventricular pressure and volume overload.Moderate right ventricular dilation.Global right ventricular function is moderately reduced.Severe right atrial enlargement.Moderate to severe tricuspid regurgitation. TTE: Positive bubble study Episode Teaching Pearls Pulmonary hypertension (PH) can generally be categorized as pre-, post-, or combined pre- and post-capillary PH. Isolated pre-capillary pulmonary hypertension is characterized by: mean pulmonary artery pressure (mPAP) ≥ 20 mmHg, a pulmonary capillary wedge pressure (PCWP) ≤ 15 mmHg, and a pulmonary vascular resistance (PVR) ≥ 3 Woods units (WU). Pulmonary arterial hypertension (PAH) (WHO Group 1) falls under pre-capillary pulmonary hypertension. Schistosomiasis is the most common cause of PAH (WHO Group I) worldwide. Approximately 7% of patient with hepatosplenic schistosomiasis have PAH. Some studies suggest that treatment of with praziquantel reverses vascular remodeling; however, there is point of no return, beyond which, anthelmintic therapies are ineffective to prevent progression. Exertional syncope and pericardial effusion are both risk factors for higher mortality in PAH. Women with severe PAH have extremely high risk of maternal morbidity and mortality. Endothelin receptor antagonists are contraindicated in pregnancy due to teratogenicity. Therefore, a pregnancy test must be obtained monthly while on this therapy. Patients with a lower socioeconomic status, based on median household income, have more advanced PAH at the time of diagnosis. Notes 1. How do you approach syncope? Syncope is a sudden transient loss of consciousness associated with absence of postural tone followed by complete and usually rapid recovery. There should be not be clinical evidence of “non-syncope” conditions including seizures, hypoglycemia, drug or alcohol intoxication, concussion due to head trauma and so forth. One approach to determining the etiology o

CardioNerd (Amit Goyal), cardioobstetrics series co-chair Dr. Sonia Shah (FIT, UT Southwestern) and episode lead Dr. Kayle Shapero (FIT, UPMC) discuss pregnancy in patients with pulmonary hypertension with Dr. Candice Silversides, Associate Professor of Medicine and the Director of the Pregnancy and Heart Disease program and head of the Obstetric Medicine program at the University of Toronto. Disclosures: None 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 important and challenging topic of pulmonary hypertension in pregnancy. We’ll start by discussing the prevalence of pulmonary hypertension in pregnancy, as well as the associated maternal morbidity and mortality associated with each WHO class. We will use a case to help us illustrate the appropriate workup for pulmonary hypertension patients and to help us broach the challenging topic of pregnancy termination. In this case we will further explore advanced management options including pulmonary vasodilators, anti-coagulation, and the use of mechanical support. Don’t miss this opportunity to hear Dr. Silversides’ share her wisdom on the importance of a multidisciplinary care team to plan both the delivery as well as post-partum care to help prevent adverse outcomes for both the mother and baby. Pearls Pregnancy in pulmonary hypertension, regardless of the class, is considered high risk. Even women who appear hemodynamically stable at baseline can easily decompensate in pregnancy, and thus the overall mortality and morbidity are very high. Due to the high risk of maternal morbidity and mortality during pregnancy for women with pulmonary arterial hypertension, the option of termination of pregnancy should be discussed.  Multidisciplinary care teams are the key to achieving optimal pregnancy outcomes in these patients. It is critical to create a team of experts with experience in pulmonary hypertension and plan for constant communication over the course of pregnancy. Pulmonary vasodilators including CCBs, phosphodiesterase inhibitors, and prostacyclin analogues should be initiated early to mitigate adverse outcomes. The majority of the complications in pulmonary hypertension patients occur after delivery, and so having a clear and safe postpartum plan is critical to a positive outcome. Quotables “We will someday identify the women who maternal morbidity and mortality is perhaps lower and we’ll be able to give a better, risk assessment. But we’re not quite there yet. And so currently, any woman who has pulmonary hypertension, true pulmonary hypertension in particular, pulmonary arterial hypertension, should be advised to avoid pregnancy.“ – Dr. Silversides “Women with PH can be falsely reassuring because they can walk in and look pretty good. And they’re young, you know, they’re not like the normal 70-year-old you might see on the ward. And so, you think they’re going to be okay, but they can spiral downward very quickly. So I do think you also have to have a very high, um, uh, level of. Uh, caution in these patients.“- Dr. Silversides on assessing PH patients in pregnancy  “I would tell you that I still think honesty is the best policy. I think you should offer women as much information as we currently know, so they can make informed decisions that are right for them. I think you also do have to really be sensitive to how you’re delivering this information, because remember (for) some women it will have never occurred to them that they can’t have a pregnancy. They may have been planning on having a kids and family and this information can really derail them. So you do have to use sensitivity, but I think you have to do it to accommodate to the patient that you’re seeing. I don’t think there can be a one size fits all approach.”- Dr. Silversides on the challenging topic of how to approach pregnancy termination conversations “… continue to optimize your care, the better shape the woman is going into delivery. The better outcomes you’ll have at the time of labor and delivery.”- Dr. Silversides Show notes 1. How do we define pulmonary hypertension (PH) and why is it such a big deal in pregnancy? According to recent guidelines pulmonary hypertension is a mean pulmonary artery pressure ≥ 20 mmHg. The WHO separates PH into 5 groups: Group 1: Pulmonary arterial hypertension (e.g., idiopathic, heritable [BMPR2], anorexigen associated, drug or toxin-associated, HIV, connective tissue disease associated, schistosomiasis, portal hypertension, congenital heart disease, amongst other causes) Group 2: Pulmonary hypertension due to left sided h

CardioNerd (Amit Goyal), cardioobstetrics series co-chair Dr. Natalie Stokes, Cardionerds Duke University CardioNerds Ambassador and episode lead fellow, Dr. Kelly Arps, join Dr. Andrea Russo, Director of Electrophysiology and Arrhythmia Services at Cooper Medical School of Rowan University and immediate past president Heart Rhythm Society, for a discussion about pregnancy and arrhythmia. Stay tuned for a message from Dr. Sharonne Hayes about WomenHeart. Audio editing by Gurleen Kaur. Claim free CME for enjoying this episode! Dr. Russo’s disclosures: Johnson and Johnson, Medtronic, Inc., Boston Scientific Corporation, Kestra, Medilynx, Up-to-Date, and ABIM. Abstract • 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! Episode Abstract Pregnant patients may have exacerbation of underlying arrhythmic syndromes or unmasking of previously undiagnosed arrhythmic syndromes. Management of atrial and ventricular tachyarrhythmias should proceed with increased urgency in pregnant patients due to risk of adverse hemodynamic events in the mother and fetus. Cardioversion of atrial and ventricular arrhythmias is safe in pregnancy. Preferred antiarrhythmic agents in pregnant patients include metoprolol, propranolol, verapamil, flecainide, propafenone, sotalol, procainamide, and lidocaine. Management of arrhythmias in pregnancy should include collaboration with obstetrics and maternal-fetal medicine teams. Pearls Pre-conception counseling is a shared decision making process; include obstetrics and maternal-fetal medicine colleagues in challenging cases. Have a high sense of urgency for acute arrhythmias in pregnancy due to risk of impaired fetal perfusion. Goals of acute arrhythmic management should include rapid treatment while avoiding hypotension. In scenarios when beta blockers are indicated, metoprolol and propranolol are first choice. Avoid atenolol as this drug has the highest risk of fetal bradycardia and intra-uterine growth retardation in the class. Lidocaine or procainamide should be first line for ventricular arrhythmias in pregnancy. Amiodarone is potentially teratogenic and should not be used in pregnant patients unless all other options have been exhausted. Show notes 1. What are the expected electrophysiologic changes associated with pregnancy? Increase in resting heart rate which peaks in third trimester PR shortening ECG axis shift leftward and upward Non-specific ST and T wave changes These changes, along with increased cardiac output and volume with increased stretch in all chambers, increase the risk of re-entrant arrhythmias in those who are predisposed. ↑ atrial volume -> ↑ stretch -> ↑ ectopy -> ↑ risk for re-entrant arrhythmias 2. What is the approach to pre-conception counseling for patients with known arrhythmias or arrhythmic syndromes? Anticipate frequency and potential severity of adverse arrhythmic outcomes during pregnancy and post-partum period Consider available options for rhythm control and anticoagulation therapy, as appropriate, during the pre-conception, pregnancy, and post-partum periods Consider catheter ablation prior to pregnancy, particularly for curable arrhythmias such as Wolff-Parkinson-White (WPW) and AVNRT Offer genetic counseling about hereditary risk to fetus for inherited arrhythmias such as Brugada syndrome and Long QT syndrome 3. What is the management of SVT in pregnancy? Consider the increased risk of tachyarrhythmias in pregnancy: Typically benign arrhythmias can lead to more rapid decompensation in mother due to increased baseline cardiac output. Typically benign arrhythmias can lead to rapid danger to the fetus due to maternal hypotension and shortened diastolic filling time, both of which contribute to impaired fetal perfusion.  Treatment algorithm is identical to that of non-pregnant patients Attempt vagal maneuvers Adenosine is safe Cardioversion is safe: monitor the fetus during and after cardioversion In stable arrhythmias, choose nodal blocking agents with the best safety profile: metoprolol, propranolol, and verapamil. Evaluation of the pregnant patient with new onset SVT Have a high index of suspicion for underlying structural heart disease such as peripartum cardiomyopathy in a pregnant women with new diagnosis of SVT – presence of structural heart disease significantly increases the risk of maternal morbidity and mortality. Pregnancy can be the first presentation of inherited arrhythmia syndromes that commonly present in young adults such as WPW, Brugada Syndrome, Catecholaminergic Polymorphic VT (CPVT), Long QT Syndrome (LQTS), Arrhythmogenic Right Ventricular Cardiomyopathy / Dysplasia (ARVC/D), and Hypertrophic Cardiomyopathy (HCM). 4. What are some special considerations for acute management of VT in pre

CardioNerd (Amit Goyal), Narratives in Cardiology FIT representative Dr. Zarina Sharalaya and Cleveland Clinic fellow Dr. Gregory Ogunnowo join Dr. Quinn Capers IV, UTSW as Professor of Medicine, Associate Dean of Faculty Diversity, and the inaugural Vice Chair of Diversity, Equity, and Inclusion in the Department of Internal Medicine, for an important and moving discussion about diversity, implicit bias, and #BlackMenInMedicine. Special thanks to Dr. Kimberly Manning for her introductory remarks for Dr. Capers. Audio editing by CardioNerds Academy Intern, Dr. Maryam Barkhordarian. Claim free CME just for enjoying this episode! Click here to see Dr. Caper’s tweet regarding his daughter’s original peice Cardionerds Narratives in Cardiology PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll Subscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! https://twitter.com/DrQuinnCapers4/status/1277715623246733317?s=20 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. Quinn Capers, IV Dr. Quinn Capers, IV grew up in Dayton Ohio and left his hometown to do his undergraduate training at Howard University. He began his journey in medicine at The Ohio State University and went on to do residency, cardiology fellowship, and interventional cardiology training at Emory University. After graduation he worked for 8 years in private practice, and made the switch back to academics and came back to Ohio State to continue his career.  In 2009, he was named associate dean of admissions and in 10 years, the College of Medicine went from 13%  underrepresented minorities to 26% of the 2019 entering class, and in the last 6 years women have outnumbered men in the incoming classes. In 2019 he was promoted to Vice Dean for Faculty Affairs, received the award for professor of the year, and the Diversity Champion Award from the institution. Most recently, the state of Texas gained a gem as Dr. Capers has moved to join the UTSW as Professor of Medicine, Associate Dean of Faculty Diversity, and the inaugural Vice Chair of Diversity, Equity, and Inclusion in the Department of Internal Medicine. He has an expansive list of accolades and awards. Dr. Capers was awarded the AHA Laennec Clinician Educator Award in 2018. He was recognized as the 2020 recipient of the Exemplary Leadership Award of the Group on Diversity and Inclusion from the Association of American Medical Colleges (AAMC). He is an inaugural member of the American College of Cardiology’s Diversity and Inclusion Task Force. In 2021 he received the Pamela S. Douglas Distinguished Award for Leadership in Diversity and Inclusion. He has had an impactful presence on social media where he created the hashtags #BlackMenInMedicine and #TakeAWomanToTheCathLab. Dr. Capers is a passionate advocate for enhancing diversit

CardioNerds (Amit Goyal & Daniel Ambinder) join Dr. Rayan Jo Rachwan, Dr. Anupama Joseph, and Dr. Mohammed Merchant from the University of Wisconsin-Madison for a classic Madison dinner cruise! They discuss the following case: Mixed shock secondary to severe right ventricular outflow tract obstruction with Gemella Haemolysans prosthetic pulmonary valve endocarditis in a young patient with Shone Complex (syndrome). Dr. Ford Ballantyne III provides the E-CPR segment for this episode. Special introductory music composed by Dr. Rayan Jo Rachwan. We are excited to welcome University of Wisconsin- Madison to the CardioNerds Healy Honor Roll and Dr. Rayan Jo Rachwan as the CardioNerds Ambassador. 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 26-year-old male with history of bicuspid aortic valve and Shone Complex (syndrome)—status post coarctation repair, subaortic resection and Ross-Konno operation—presenting with 3 months of constitutional and respiratory symptoms. Initial evaluation demonstrated that patient was in a state of mixed shock due to a large pulmonary Melody valve thrombus with superimposed Gemella Haemolysans prosthetic valve endocarditis. He required treatment with inotropes, pressors, followed by intubation and extracorporeal membrane oxygenation (ECMO). Patient was treated initially via right heart catheterization with balloon dilation and stent placement to his right ventricle-to-pulmonary artery conduit, which lead to significant improvement in his hemodynamics. Patient was then decannulated from ECMO, extubated, weaned off pressor support and later underwent a successful surgical resection of the infected pulmonary homograft and Melody valve/stents and replacement with pulmonary-valved conduit. He was also discharged on a prolonged course of antibiotics. Case Media – Shone Complex A B C DClick to Enlarge A. CXR, B. ECG, C. TV Doppler, D. PV Doppler CTA Chest •Melody pulmonic valve repair with large thrombus arising from the mid-distal valve extending into the main pulmonary artery and proximal left pulmonary artery. Evaluation for distal subsegmental pulmonary emboli is limited. •Tiny focus of air in the thrombus may be related to contrast injection. Infection is less likely. •Enlarged right heart chambers, may be in part chronic right heart enlargement and/or new right heart strain. No pulmonary infarct. CT chest abdomen and pelvis with contrast •Findings suggestive of acute hepatitis and acute pancreatitis. No pancreatic hypoenhancement or peripancreatic fluid collection. •No abscess within the abdomen or pelvis. •Small caliber of the infrarenal abdominal aorta and bilateral iliac arteries, probably congenital.  TTE 1 TTE 2 TTE 3 TTE 4 TTE 5 TTE 6 RHC with balloon dilation of the RV-PA conduit and evidence of multiple levels of stent fracture. Pulmonary angiogram showing no evidence of distal embolization or significant pulmonary embolism and no evidence of perforation. There is evidence of moderate pulmonary insufficiency into a dilated right ventricle. Episode Teaching – Shone Complex Pearls 1. Patients with congenital heart disease are more predisposed to infective endocarditis (IE). Therefore, there should be a low-threshold for infectious workup in the case of unexplained fever or malaise without associated symptoms for >72 hours. Every routine visit should screen for symptoms and signs of IE. 2. Treatment of right ventricular (RV) outflow tract obstruction with balloon dilation +/- stenting can be considered as a bridge to valve replacement in the case of severe hemodynamic compromise; thus, restoring RV and pulmonary artery coupling. As with many complex decisions this should be made in consultation with an experience heart team and shared decision making with the patient or proxy. 3. Patients with RV volume and/or pressure overload from right-sided valve etiology should be assessed serially (i.e., yearly) with transthoracic echocardiography. 4. When precise quantitative data about the RV is required to make important clinical decisions (e.g., when to recommend pulmonary valve replacement), cardiac magnetic resonance imaging (CMR) remains the diagnostic modality of choice. 5. Repairing or replacing the pulmonary valve should be considered when RV end-diastolic volume >160 mL/m2 and/or RV end-systolic volume >80 mL/m2 on CMR. Notes What is Shone syndrome? Shone syndrome (a.k.a. Shone anomaly, Shone complex) is a rare congenital abnormality that accounts for 0.6% of all congenital abnormalities. It is characterized by a series of left-sided obstructive lesions. The diagnosis is made with the presence of at least 3 of 8 described lesions.

CardioNerds (Amit Goyal, Daniel Ambinder, Carine Hamo, and Karan Desai) are honored to bring to you the Braunwald Chronicles. These are stories of discovery, innovation, accidents, perseverance, and more…truly these are the stories of cardiology, directly from a father of modern cardiology himself, Dr. Eugene Braunwald. Dr. Braunwald’s life and stories together are the saga which have brought us to this day in modern cardiology. So please join us for this wonderful series, as we journey through the history of cardiology, across 6 extraordinary chapters. We complete The CardioNerds Braunwald Chronicles with Chapter 6 where Dr. Braunwald discusses triple threats, randomized controlled trials, textbooks & digital education. He reflects on the impact he has had through education through text books and how being an educator has been just as gratifying to him as being a scientist. We thank Dr. Karan Desai, Editorial APD with the CardioNerds Academy, and fellow at University of Maryland, for all the work he put into designing the Braunwald Chronicles. Audio editing by Pace Wetstein. CardioNerds Braunwald Chronicles Series PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron!

CardioNerds (Amit Goyal, Daniel Ambinder, Carine Hamo, and Karan Desai) are honored to bring to you the Braunwald Chronicles. These are stories of discovery, innovation, accidents, perseverance, and more…truly these are the stories of cardiology, directly from a father of modern cardiology himself, Dr. Eugene Braunwald. Dr. Braunwald’s life and stories together are the saga which have brought us to this day in modern cardiology. So please join us for this wonderful series, as we journey through the history of cardiology, across 6 extraordinary chapters. We continue with Chapter 5 where Dr. Braunwald discusses his discoveries related to carotid sinus stimulation, limitation of infarct size & the open artery hypothesis. The open artery hypothesis has revolutionized the way we take care of patients with myocardial infarction. We thank Dr. Karan Desai, Editorial APD with the CardioNerds Academy, and fellow at University of Maryland, for all the work he put into designing the Braunwald Chronicles. Audio editing by Pace Wetstein. Dr. Braunwald’s favorite paper: (Please note the very last paragraph)Kjekshus JK. Factors influencing infarct size following coronary artery occlusion. JOslo City Hosp. 1974;24(11-12):155-175. CardioNerds Braunwald Chronicles Series PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron!

CardioNerds (Amit Goyal, Daniel Ambinder, Carine Hamo, and Karan Desai) are honored to bring to you the Braunwald Chronicles. These are stories of discovery, innovation, accidents, perseverance, and more…truly these are the stories of cardiology, directly from a father of modern cardiology himself, Dr. Eugene Braunwald. Dr. Braunwald’s life and stories together are the saga which have brought us to this day in modern cardiology. So please join us for the Braunwald Chronicles, as we journey through the history of cardiology, across 6 extraordinary chapters. We continue with Chapter 4 where Dr. Braunwald discusses his discoveries related to the A “Royal Screw-up” & The Discovery of Hypertrophic Cardiomyopathy. There are hypertrophic cardiomyopathy centers of excellence sprinkled throughout the world. Comprehensive ACC/AHA guidelines for hypertrophic cardiomyopathy that came out in 2020, there’s incredible drug discovery and randomized controlled trials looking at innovations in the management of HCM. We had a whole series on CardioNerds for hypertrophic cardiomyopathy where we taught about the four “Ps” or four preventions of hypertrophic cardiomyopathy management; prevent symptoms, prevent stroke in atrial fibrillation, prevent sudden cardiac death in the patient and prevent sudden cardiac death in the family. How fortunate are we to now hear all about how hypertrophic cardiomyopathy was discovered. We thank Dr. Karan Desai, Editorial APD with the CardioNerds Academy, and fellow at University of Maryland, for all the work he put into designing the Braunwald Chronicles.Audio editing by Pace Wetstein. CardioNerds Braunwald Chronicles Series PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron!

CardioNerds (Amit Goyal, Daniel Ambinder, Carine Hamo, and Karan Desai) are honored to bring to you the Braunwald Chronicles. These are stories of discovery, innovation, accidents, perseverance, and more…truly these are the stories of cardiology, directly from a father of modern cardiology himself, Dr. Eugene Braunwald. Dr. Braunwald’s life and stories together are the saga which have brought us to this day in modern cardiology. So please join us for the Braunwald Chronicles, as we journey through the history of cardiology, across 6 extraordinary chapters. We continue with Chapter 3 where Dr. Braunwald discusses his discoveries related to the natural history of aortic stenosis, beta-blockers in heart failure and times when seizing the moment led to important contributions to the world of cardiology. Dr. Braunwald also shares insights on mentorship as he speaks fondly of his relationship with the cardiac surgeon, Dr. Andrew “Glenn” Morrow. We thank Dr. Karan Desai, Editorial APD with the CardioNerds Academy, and fellow at University of Maryland, for all the work he put into designing the Braunwald Chronicles. Audio editing by Pace Wetstein. CardioNerds Braunwald Chronicles Series PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron!

CardioNerds (Amit Goyal, Daniel Ambinder, Carine Hamo, and Karan Desai) are honored to bring to you the Braunwald Chronicles. These are stories of discovery, innovation, accidents, perseverance, and more…truly these are the stories of cardiology, directly from a father of modern cardiology himself, Dr. Eugene Braunwald. Dr. Braunwald’s life and stories together are the saga which have brought us to this day in modern cardiology. So please join us for the Braunwald Chronicles, as we journey through the history of cardiology, across 6 extraordinary chapters. We continue with Chapter 2 where Dr. Braunwald discusses his Camelot years, discoveries with regards to myocardial oxygen consumption & how the transseptal approach was developed. We hear about the incredible environment at the NIH during his early days, his delineation of the variables that result in myocardial oxygen demand and the discovery of the transseptal approach, which is so key to so many of our percutaneous interventions today. We thank Dr. Karan Desai, Editorial APD with the CardioNerds Academy, and fellow at University of Maryland, for all the work he put into designing the Braunwald Chronicles. Audio editing by Pace Wetstein. CardioNerds Braunwald Chronicles Series PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron!

CardioNerds (Amit Goyal, Daniel Ambinder, Carine Hamo, and Karan Desai) are honored to bring to you the Braunwald Chronicles. These are stories of discovery, innovation, accidents, perseverance, and more…truly these are the stories of cardiology, directly from a father of modern cardiology himself, Dr. Eugene Braunwald. Dr. Braunwald’s life and stories together are the saga which have brought us to this day in modern cardiology. So please join us for the Braunwald Chronicles, as we journey through the history of cardiology, across 6 extraordinary chapters. We begin with Chapter 1: At The Right Place, At The Right Time & With The Right People.  We learn about how serendipitous events in Dr. Braunwald’s early days, paired with his incredible grit & brilliance got him to the NIH where he quickly became the chief of cardiology at the of age 31, the precipice to an illustrious career ahead. We thank Dr. Karan Desai, Editorial APD with the CardioNerds Academy, and fellow at University of Maryland, for all the work he put into designing the Braunwald Chronicles. A very special thanks Dr. Randall Starling, advanced heart failure faculty at the Cleveland Clinic, former President of HFSA, and a dedicated mentor and support to CardioNerds for introducing us to Dr. Eugene Braunwald and for providing the following introduction. Audio editing by Pace Wetstein. CardioNerds Braunwald Chronicles Series PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron!

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, MD Sonia Shah, MD Amit Goyal, MD Daniel Ambinder, MD

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 <45% (with or without LV dilatation and RV involvement) and no other explanation for the cardiomyopathy. 2) Patients with PPCM  can present with classic heart failure symptoms, which may be challenging to distinguish from the typical symptoms and signs of pregnancy. To help differentiate pathology from normal physiology, consider the constellation of exam findings (e.g., isolated peripheral edema versus peripheral edema, +S3, elevated JVD and rales), the severity of the findings, and comparison of symptoms/findings to prior pregnancies.. There are no specific serum markers for PPCM yet. 3) Prolactin and a vascular etiology have been implicated in the  pathogenesis of PPCM. There are ongoing trials to evaluate treatment with bromocriptine, which blocks prolactin (look out for upcoming the REBIRTH RCT examining this!). Importantly, there is no clear evidence that breastfeeding is prohibitive to myocardial recovery and should not be discouraged given benefits to both mom and baby. 4) Many of these patients recover, but those at highest risk are those with severely depressed LV systolic function, dilated LVs, RV involvement, and of African descent. 5) Goal directed medical therapy with beta-blockers in both ante- and postpartum period is a cornerstone of therapy. ACEi/ARB/MRA/ARNI are contraindicated in pregnancy but may be added postpartum and with breastfeeding. Quotables 1.  “It can be so challenging to distinguish symptoms (in a pregnant patient) from cardiac disease! One thing to keep in mind is severity – the more pronounced a finding or symptoms, the more concerning.” – Dr. Julie Damp 2. ”We often have more options than we think in medical management for heart failure through pregnancy and breastfeeding, but they do need some adjustments from our usual therapies.” -Dr. Julie Damp 3. “Start discussions about prognosis, monitoring, future pregnancies, and contraception early!” -Dr. Julie Damp Show notes 1. How do you distinguish findings of normal pregnancy from signs and symptoms of heart failure? Pregnant patients may normally have basal rales that typically clear with coughing, laterally shifted PMI, bounding PMI and pulse, JVD, S3, systolic murmur, edema/tense soft tissue, and heart rate elevation.  Patients may feel short of breath, exertional fatigue, orthopnea, and palpitations. Think about the combination and severity of signs/symptoms to distinguish normal from abnormal (CHF) in your exam. For instance, isolated mild lower extremity edema in a patient who is otherwise relatively asymptomatic with no other concerning findings on exam will be approached differently than a patient with LE edema along with rales, S3 and significant dyspnea. Asking patients who have had a prior pregnancy to compare their symptoms with the prior pregnancy can be helpful as well. Timing of symptoms is also an important thing to consider.  For patients with underlying cardiac disease, they may start to develop symptoms earlier in pregnancy as hemodynamic changes evolve. 2. Given the prolactin hypothesis, should I use bromocriptine for treatment of PPCM and counsel my patients against breastfeeding? Various etiologies regarding the pathogenesis of PPCM have been proposed including myocarditis-like process, autoimm

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 g

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 (

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 hi

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 amyloidosis Overall 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

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 setting

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 A B Click 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 < 2 weeks duration that is associated with hemodynamic compromise or  (2) u

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 A B C Click 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 1 Figure 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 < 50% systemic pressures AND PVR is <1/3 of SVR. It is a Class III recommendation (potentially harmful) to close a defect if 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

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

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 abnormal coronary anatomy including anomalous coronary arteries and myocardial bridges. 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 Five Take Home Pearls Anomalous coronaries are present in 1-6% of the general population and predominantly involve origins of the right coronary artery (RCA). Anomalous origination of the left coronary artery from the right sinus, although less common, is consistently associated with sudden cardiac death, especially if there is an intramural course. Sudden cardiac death can occur due to several proposed mechanisms: (1) intramural segments pass between the aorta and pulmonary artery making them susceptible to compression as the great vessels dilate during strenuous exercise; (2) an acute angle takeoff of the anomalous coronary can create a “slit-like” ostium making it vulnerable to closure. Anomalous left circumflex arteries are virtually always benign because the path taken behind the great vessels to reach the lateral wall prevents vessel compression. Myocardial bridging (MB) is a congenital anomaly in which a segment of the coronary artery (most commonly, the mid-left anterior descending artery [LAD]) takes an intramuscular course and is “tunneled” under a “bridge” of overlying myocardium. In the vast majority of cases, these are benign. However, a MB >2 mm in depth, >20 mm in length, and a vessel that is totally encased under the myocardium are more likely to be of clinical significance, especially if there is myocardial oxygen supply-demand mismatch such as with tachycardia (reduced diastolic filling time), decreased transmural perfusion gradient (e.g. in myocardial hypertrophy and/or diastolic dysfunction), and endothelial dysfunction resulting in vasospasm. PET offers many benefits over SPECT in functional assessment of MB including the ability to acquire images at peak stress when using dobutamine stress-PET, enhanced spatial resolution, and quantification of absolute myocardial blood flow. For pharmacologic stress in evaluation of MB, we should preferentially use dobutamine over vasodilator stress. Its inotropic and chronotropic effects enhance systolic compression of the vessel, better targeting the pathological mechanisms in pearl 2 above that predispose a MB to being clinically significant. CCTA can help better define the anatomy of MB as well as anomalous origination of the coronary artery from the opposite sinus (ACAOS), help with risk stratification, and assist with surgical planning. Instantaneous wave-free ratio (iFR) measures intracoronary pressure of MB during the diastolic “wave-free” period – the period in the cardiac cycle when microvascular resistance is stable and minimized allowing the highest blood flow. This allows a more accurate assessment of a functionally significant dynamic stenosis than fractional flow reserve (FFR) – which can be falsely normal due to systolic overshooting. Detailed Show Notes What are some examples of abnormal coronary anatomies and how often do they lead to clinical events? Abnormal coronary anatomy can relate to the origin (e.g. anomalous origination of coronary artery from the opposite sinus [ACAOS]), course (e.g. myocardial bridging [MB]), intrinsic properties (e.g. aneurysm or hypoplasia), or termination (e.g. fistula) of the coronary artery. In this episode and in these notes, we examine MB and ACAOS in more detail. For an excellent case discussion of anomalous left coronary artery from the pulmonary artery (ALCAPA) by the team from Massachusetts General Hospital, listen to CardioNerds Podcast Episode 81! MB –Myocardial Bridging MB is a congenital anomaly in which a segment of the coronary artery (most commonly, the mid-left anterior descending artery [LAD]) takes an intramuscular course and is “tunneled” under a “bridge” of overlying myocardium. MB was originally identified at autopsy by Reyman in his dissertation, “Disertatio de vasis cordis propriis “ in 1737. In the largest subsequent autopsy study by Risse et al. involving 1056 patients, MB was demonstrated in 26% of patients. Because it is so prevalent, it is difficult to dete

CardioNerds (Amit Goyal & Daniel Ambinder) join University of Maryland cardiology fellows (Manu Mysore, Adam Zviman, and Scott Butler) for some cardiology and an Orioles game in Baltimore! They discuss a rare cause of postpartum angina and cardiac arrest due to coronary vasculitis. Program director Dr. Mukta Srivastava provides the E-CPR expert segment and a message for applicants. Episode notes were developed by Johns Hopkins internal medicine resident Rick Ferraro with mentorship from University of Maryland cardiology fellow Karan Desai. This case has been published in JACC Case Reports! Collect free CME/MOC credit just for enjoying 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 woman in her early 30s with a past medical history of Hashimoto’s thyroiditis and one prior miscarriage at <8 weeks presented with chest pain about 6 weeks postpartum from the birth of her third child. In the ED, she continued to report intermittent sharp chest discomfort and found to have a diastolic decrescendo murmur at the left upper sternal border and labs demonstrating a troponin-I of 0.07 ng/dL. Join the UMD Cardionerds for the incredible course and story of this young patient as we go through the differentia and approach to postpartum chest pain and ultimately arrive in a very rare diagnosis!   For a detailed course, enjoy the JACC case report. Case Media Visit the JACC Case Reports to review the case media! Episode Schematics & Teaching The CardioNerds 5! – 5 major takeaways from the #CNCR case 1. How Do We Evaluate Chest Pain in Younger Patients  Start with the same things as everyone else!  Think broadly about the big three concerning etiologies of chest pain: Cardiac, Gastric, and Pulmonary (The excellent Clinical Problems Solvers 4+2+2 construct here is always a great resource. Find them at: https://clinicalproblemsolving.com/dx-schema-chest-pain/).    Of course it is important to think about non-life threatening etiologies as well – esophageal spasm, gastric ulcer, rib fracture, skin lesion, among many others – given that high-risk chest pain is less likely in younger adults.   While less common, acute coronary syndrome is not uncommon in young patients, as 23% of patients with MI present at age <55 years.   2. What About Chest Pain in Women?   As has been discussed on the Cardionerds podcast (Listen to episodes with Dr. Nanette Wenger, Dr Martha Gulati, and Dr. Leslie Cho), women generally present with acute coronary syndrome at a later age, with a higher burden of risk factors than men, and with greater symptom burden but are less likely to be treated with guideline-directed medical therapies, undergo cardiac catheterization and receive timely reperfusion. In one study of young patients with acute MI, women – 19% of cases overall – were less likely to undergo revascularization or receive guideline-directed therapy  The construct of classifying chest pain as “typical” and “atypical” likely leads to misdiagnosis or delayed diagnosis of acute myocardial infarction in women. Rather, it is important to recognize that while symptoms may not be “typical” for angina, coronary disease can manifest in many different ways.   While many women will presents with chest pain suggestive of angina, women are more likely than men to present with dyspnea, indigestion, weakness, nausea/vomiting and/or fatigue. Note, shoulder pain and arm pain are twice as predictive of an acute myocardial infarction diagnosis in women compared with men.   Furthermore, while obstructive epicardial disease remains the primary cause of acute MI in young women, it is also important to keep other causes of chest pain such as MINOCA, SCAD (see the UCLA episode), peripartum cardiomyopathy (see the Penn and MCW episodes), or coronary vasculitis on the differential. While these etiologies are rare, they are disproportionately represented in young women.   3. How do we think about categorizing vasculitis?  Vasculitis is a broad term encompassing many forms of vessel wall (including arteries, veins or capillaries) inflammation.  This can be secondary to autoimmunity, infection, drug reaction, and malignancy to name a few underlying causes.   Generally vasculitis is divided by large vessel (e.g., Takayasu, Giant Cell), medium vessel (e.g., Polyarteritis Nodosa), and small vessel etiologies (e.g., Granulomatosis with Polyangitis, Eosinophilic Granulomatosis with

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 myocardial viability. Show notes & #Tweetorial 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 CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Show Notes & Take Home Pearls In response to ischemia the myocardium can dynamically change along a spectrum from myocardial stunning to myocardial hibernation to myocardial necrosis. The goals of viability testing are to identify patients who may benefit from revascularization as hibernating or stunned myocardium are potentially reversible causes of LV dysfunction. There are numerous imaging modalities available for the evaluation of myocardial viability. The broad range of ways in which myocardial viability is assessed speaks to the complexity of the disease spectrum and the difficulty in creating a unifying definition of viability to assess in clinical trials.   Five Take Home Pearls 1. In response to an acute episode of ischemia with subsequent reperfusion, the myocardium can be exposed to a large flux of oxygen free radicals or calcium overload that affects the cellular membrane and contractile apparatus. This phenotypically results in decreased contractility of the affected region of myocardium that can persist for weeks, labeled myocardial stunning  2. Repeated episodes of myocardial stunning or chronic low myocardial blood flow can lead to cellular changes such as resorption of the contractile apparatus in order to decrease oxygen demand and allow the myocardial cells to survive. Phenotypically, this might appear as regions of hypokinesis or akinesis at rest with a fixed perfusion defect on myocardial perfusion imaging. This is typically considered hibernating myocardium.   3. The goal of myocardial viability testing is to be able to differentiate between stunned, hibernating and necrosed myocardium. In patients with known epicardial coronary disease, this differentiation allows us to identify who may benefit from revascularization with improved LV systolic function and overall survival.   4. There are several imaging modalities that can be used in the assessment of myocardial viability. The most sensitive modalities are FDG-PET and CMR. The addition of Dobutamine or first pass perfusion with Gadolinium additionally increases the specificity of CMR. These modalities are more expensive and not as widely available.   5. The dynamic nature of the myocardial hibernation and the lack of a unifying definition/phenotypic expression of myocardial hibernation and viability have made it difficult for clinical trials to show that re-establishing myocardial blood flow to hibernating myocardium is beneficial. As Dr. Jaber stated in the episode in his spin on the classic opening phrase from Leo Tolstoy’s masterpiece, Anna Karenina, “All normal hearts are normal in the same way, and all abnormal hearts are abnormal in different ways.”  6. The PARR-2 trial was one of the few randomized, controlled trials of patients with LV systolic dysfunction and coronary artery disease who were randomized to either FDG-PET guided management or standard care with respect to whether to pursue revascularization. Overall, there was not a significant reduction in the primary composite endpoint between the FDG-PET arm and the standard care arm. However, not all patients received the revascularization strategy recommended by imaging. In patients whom the PDG-PET recommendation for revascularization was followed, there was a significant benefit compared to the standard care group.   Quotable:  “All normal hearts are normal in the same way, All abnormal hearts are abnormal in different ways”—0:54  Detailed Show Notes What is myocardial hibernation and myocardial stunning? How do these concepts fit into the discussion of myocardial viability?   A common scenario encountered in clinical practice is the patient who has depressed LV systolic function and known obstructive epicardial coronary disease. For these patients, we may wonder if the myocardium supplied by the epicardial coronary arteries with obstructiv

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 coronary microvascular disease.  To learn more about multimodality cardiovascular imaging, check out Cardiac Imaging Agora!  Collect free CME/MOC credit just for enjoying to the 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! Guest Profiles Wael Jaber, MD Wael Jaber, MD, is a staff cardiologist in the Section of Cardiovascular Imaging, Robert and Suzanne Tomsich Department of Cardiovascular Medicine, at the Sydell and Arnold Miller Family Heart, Vascular & Thoracic Institute at Cleveland Clinic. Dr. Jaber specializes in cardiac imaging (both nuclear cardiology and echocardiography) and valvular heart disease. Dr. Jaber attended college at the American University in Beirut, graduating with a Bachelor of Science in biology. He then went on at the American University to receive his medical degree while making the Dean’s honor list. He completed his residency in internal medicine at the St. Luke’s-Roosevelt Hospital Center at Columbia University College of Physicians and Surgeons, where he also completed fellowships in cardiovascular medicine and nuclear cardiology. Dr. Jaber is currently is the Medical Director of the Nuclear Lab and of the Cardiovascular Imaging Core Laboratory in C5Research. He is fluent in English, French and Arabic. He is the author of Nuclear Cardiology review: A Self-Assessment Tool and cofounder of Cardiac Imaging Agora. Dr. Aldo L Schenone Dr. Aldo L Schenone is one of the current Chief Non-Invasive Cardiovascular Imaging Fellows at the Brigham and Women’s Hospital. He completed medical school at the University of Carabobo in Valencia, Venezuela, and then completed both his Internal Medicine residency and Cardiology fellowship at the Cleveland Clinic where he also served as a Chief Internal Medicine Resident. Dr. Erica Hutt Dr. Erika Hutt @erikahuttce is a cardiology fellow at the Cleveland Clinic. Erika was born and raised in Costa Rica, where she received her MD degree at Universidad de Costa Rica. She then decided to pursue further medical training in the United States, with the goal of becoming a cardiologist. She completed her residency training at Cleveland Clinic and went on to fellowship at the same institution. Her passions include infiltrative heart disease, atrial fibrillation, valvular heart disease and echocardiography among many. She is looking forward to a career in advanced cardiovascular imaging. References and Links Kaski, J.-C., Crea, F., Gersh, B. J., & Camici, P. G. (2018). Reappraisal of Ischemic Heart Disease. Circulation. https://doi.org/10.1161/circulationaha.118.031373 Jaber, W., & Gimelli, A. (n.d.). Cardiac Imaging Agora. https://www.cardiacimagingagora.com/list/ Taqueti, V. R., & Di Carli, M. F. (2018). Coronary Microvascular Disease Pathogenic Mechanisms and Therapeutic Options: JACC State-of-the-Art Review. In Journal of the American College of Cardiology. https://doi.org/10.1016/j.jacc.2018.09.042 Wael Jaber, MD Dr. Aldo L Schenone Dr. Erika Hutt  Dr. Madiha Khan Amit Goyal, MD

CardioNerds (Amit Goyal & Carine Hamo) discuss the past, present, and future of Women’s Heart Health & Women in Cardiology with Dr. Nanette Wenger, Professor of Medicine in the Division of Cardiology at the Emory University School of Medicine. Dr. Wenger is a true leader in the field of women’s heart health and a strong proponent for women in cardiology and medicine. Her passion, dedication, and advocacy have inspired countless trainees to carry this torch and continue to build on her truly impactful work. Special introduction by Dr. Martha Gulati. This is a special encore in recognition of the Go Red campaign and celebration of women’s health. Collect free CME/MOC credit for enjoying this episode! Episode graphic by Dr. Carine Hamo The Cardionerds CV prevention series includes in-depth deep dives on so many prevention topics including the ABCs of prevention, approach to obesity, hypertension, diabetes mellitus and anti-diabetes agents, personalized risk and genetic risk assessments, hyperlipidemia, women’s cardiovascular prevention, coronary calcium scoring and so much more! CardioNerds Prevention PageCardioNerds Women’s Cardiovascular Health PageCardioNerds Episode PageSubscribe to our newsletter- The Heartbeat CardioNerds AcademyCardionerds Healy Honor RollCheck out CardioNerds SWAG!Become a CardioNerds Patron! This episode initially ran as part of the CardioNerds Prevention Series which we produced in collaboration with the American Society for Preventive Cardiology! The ASPC is an incredible resource for learning, networking, and promoting the ideals of cardiovascular prevention! Cardionerds Cardiovascular Prevention Series References and Links 1. Wenger NK (2005) Women in cardiology: The US experience. Heart. 2. Douglas PS, Rzeszut AK, Noel Bairey Merz C, Duvernoy CS, Lewis SJ, Walsh MN, Gillam L (2018) Career preferences and perceptions of cardiology among us internal medicine trainees factors influencing cardiology career choice. JAMA Cardiol. 3. Wenger NK, Speroff L, Packard B (1993) Cardiovascular Health and Disease in Women. N Engl J Med. 4. Burgess S, Shaw E, Zaman S (2019) Women in Cardiology. Circulation. Meet Dr. Wenger! Dr. Nanette Wenger is Professor of Medicine in the Division of Cardiology at the Emory University School of Medicine. Dr. Wenger received her medical degree from Harvard Medical School in 1954 as one of their first female graduates followed by training at Mount Sinai Hospital where she was the first female to be chief resident in the cardiology department. She is among the first physicians to focus on heart disease in women with an expertise in cardiac rehabilitation and geriatric medicine. Dr. Wenger has received numerous awards including the Distinguished Achievement Award from the Scientific Councils of the American Heart Association and its Women in Cardiology Mentoring Award, the James D. Bruce Memorial Award of the American College of Physicians for distinguished contributions in preventive medicine, the Gold Heart Award, the highest award of the American Heart Association, a Lifetime Achievement Award in 2009 and the Inaugural Bernadine Healy Leadership in Women’s CV Disease Distinguished Award, American College of Cardiology. She chaired the U.S. National Heart, Lung, and Blood Institute Conference on Cardiovascular Health and Disease in Women, is a Past President of the Society of Geriatric Cardiology and is past Chair, Board of Directors of the Society for Women’s Health Research. Dr. Wenger serves on the editorial boards of numerous professional journals and is a sought-after lecturer for issues related to heart disease in women, heart disease in the elderly, cardiac rehabilitation, coronary prevention, and contemporary cardiac care. She is listed in Best Doctors in America. Carine Hamo, MD Amit Goyal, MD

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 coronary ischemia. 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 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 Five Take Home Pearls 1. We can broadly differentiate non-invasive testing into two different categories—functional and anatomical. Functional tests allow us to delineate the functional consequence of coronary disease rather than directly characterizing the burden of disease. Anatomical tests such as coronary CTA, on the other hand, allow us to directly visualize obstructive epicardial disease. 2. In general PET imaging provides higher quality images than SPECT imaging for a variety of reasons, including a higher “keV” of energy in PET radiotracers 3. If using a SPECT camera, we should use cameras that have attenuation correction. Without attenuation correction, the specificity of a SPECT camera drops to 50-60%. 4. In evaluating ischemic heart disease, cardiac nuclear imaging can provide a wide range of information including myocardial perfusion (rest and stress), ejection fraction assessment (rest and stress), absolute myocardial blood flow with quantitative flow reserve in all coronary territories (PET), assessment of myocardial viability (PET), and calcium score with CT attenuation correction. 5. To select the best non-invasive test, we should consider a variety of factors such as pretest probability of obstructive epicardial disease, patient-specific factors (e.g., ability to exercise) and whether a functional or an anatomical test will provide the best answer for our clinical question. Detailed Show Notes What are the basic non-invasive testing categories for evaluation of coronary artery disease?   We have a variety of different non-invasive testing modalities that can be broadly separated into functional tests and anatomical tests.   The basic principle underlying functional stress testing is to induce ischemia or coronary vasodilation (discussed below), followed by a functional assessment by different techniques (e.g., EKG, echocardiography, radionuclide imaging) to detect flow-limiting obstructive coronary artery disease. These tests delineate the functional consequence of the coronary disease, rather than directly characterizing the burden of disease itself.   Functional tests can also allow us to assess the nature of a patient’s symptoms. For example, by having a patient exercise on a treadmill we can evaluate whether we can reproduce a patient’s chest pain syndrome.  Anatomical tests allow us to visualize the presence of obstructive epicardial disease. For example, obtaining a Coronary Computed Tomography Angiography (CCTA) for a patient with chest pain would allow you to directly visualize possible obstructive epicardial disease.   How do we induce ischemia for functional stress testing?   To induce ischemia (and/or coronary vasodilation), we have many different stressors that can be broadly separated into exercise stressors and pharmacologic stressors.  Treadmill exercise via standardized protocols is the most common method for inducing ischemia and has the advantage of assessing functional capacity, which has prognostic information. Supine bicycle is another common exercise modality that is utilized.  There are also several pharmacologic stressors that vary in their mechanisms of action. Dobutamine is a synthetic catecholamine that stimulates myocardial beta-1 and beta-2 receptors to increase heart rate, contractility, and consequently myocardial oxygen demand with a small decrease in systemic vascular resistance.    Adenosine and adenosine derivatives (e.g. regadenoson) induce coronary vasodilation and take advantage of differences in coronary flow reserve. With obstructive coronary lesions, the vessels distal to the obstruction are already dilated at baseline and have little flow reserve. Adenosine (and its derivatives) induce vasodilation and increase flow in normal coronary beds, but much less so in areas supplied by an obstructive lesion. Conseque