Cardionerds: A Cardiology Podcast

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

CardioNerds (Carine Hamo, Amit Goyal and Daniel Ambinder) discuss personalized risk assessment for cardiovascular prevention with Dr. Amit Khera, the immediate past president for the American Society for Preventive Cardiology and Director of the Preventive Cardiology and Professor of Medicine at the University of Texas, Southwestern Medical School in Dallas, Texas. They dive into an illuminating discussion about traditional and next generation personalization of risk assessment which covers the need for personalization, traditional risk stratification, applying risk enhancing factors for decision making, biomarkers, familial hypercholesterolemia, and the use of -Omics. This episode is the 13th and final part of our in-depth prevention series produced in collaboration with the American Society for Preventive Cardiology! Stay tuned for a bonus segment at the end of the episodeas we talk to Dr. Ankur Kalra, interventionist at the Cleveland Clinic, Podcast host of Parallax by Ankur Kalra, and founder of the non-profit startup, makeadent.org for a discussion about the CHAI (Cardiovascular Health in Asian Indians) Collaborative, an initiative that aims to identify genetic markers of heightened atherosclerosis in South Asians. Episode graphic by Dr. Carine Hamo 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 Coming soon! Cardionerds Cardiovascular Prevention Series 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! We are truly honored to be producing the Cardionerds CVD Prevention Series 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! This series is kicked off by a message from Dr. Amit Khera, President of the American Society for Preventive Cardiology and President of the SouthWest Affiliate of the American Heart Association. Guest Profiles Amit Khera, MD, MSc, FACC, FAHA, FASPC Dr. Amit Khera is Professor of Medicine at the University of Texas, Southwestern Medical School in Dallas, Texas where he serves as Director of the Preventive Cardiology, and holder of the Dallas Heart Ball Chair in Hypertension and Heart Disease.  He is also currently President of the American Society for Preventive Cardiology and President of the SouthWest Affiliate of the American Heart Association. His clinical and research interests include the primary and secondary prevention of coronary artery disease, focusing on risk assessment and risk factor modification in those with premature and familial disease. Dr. Khera received his undergraduate degree in American History from the University of Pennsylvania, with magna cum laude honors. He obtained his medical degree from Baylor College of Medicine where he served as class president and was inducted into the Alpha Omega Alpha honor medical society. He completed an Internal Medicine Residency at Brigham and Women’s Hospital, Harvard Medical School, followed by a Cardiology Fellowship at the University of Texas, Southwestern Medical Center. He also completed his Masters degree in Epidemiology at the Harvard School of Public Health. He has published over 150 publications in the field of preventive cardiology and has served on numerous local and national committee and leadership roles for the American Heart Association, American College of Cardiology, and American Society for Preventive Cardiology.  He is currently Digital Strategies Editor and an Associate Editor for the journal Circulation.  Dr. Khera has been named Best Doctor in Dallas and Texas SuperDoctor every year since 2014 and was previously the Program Director for the Cardiology Fellowship at UT Southwestern from 2011-2019.  References and Links Coming soon! Amit Khera, M.D. Carine Hamo, MD Amit Goyal, MD Daniel Ambinder, MD

CardioNerds (Amit Goyal and Daniel Ambinder) are joined by Cleveland Clinic cardiology fellow Dr. Gregory Ogunnowo to discuss hypertension with Dr. Luke Laffin, cardiology faculty in the division of Preventive Cardiology and Rehabilitation and Medical Director of Cardiac Rehabilitation at the Cleveland Clinic. Part 2 of this discussion covers the evaluation for secondary causes of HTN, approach to resistant HTN, interventional anti-hypertensive procedures, and a note on cardiac rehabilitation. Part 1 covered the definition of hypertension, correct measurement of blood pressure, nonpharmacologic HTN management, initial choice of BP agents, and hypertensive disorders of pregnancy. Episode graphic by Dr. Carine Hamo 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 Coming soon! Cardionerds Cardiovascular Prevention Series 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! We are truly honored to be producing the Cardionerds CVD Prevention Series 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! This series is kicked off by a message from Dr. Amit Khera, President of the American Society for Preventive Cardiology and President of the SouthWest Affiliate of the American Heart Association. Guest Profiles Dr. Luke Laffin, serves as cardiology faculty in the division of Preventive Cardiology and Medical Director of Cardiac Rehabilitation at the Cleveland Clinic. Dr. Laffin attended medical school at Vanderbilt University School of Medicine. He trained in internal medicine and cardiology at the University of Chicago where he completed a dedicated fellowship in hypertensive diseases. He is a clinical specialist in hypertension designated by the American Society of Hypertension – which has now merged with the AHA. Dr. Gregory Ogunnowo is a cardiology fellow at the Cleveland Clinic. He completed medical school at the University of South Carolina School of Medicine in Columbia, South Carolina. He went on to complete internal medicine residency at Washington University School of Medicine in St. Louis where he stayed on as faculty in the Department of Hospital Medicine for a year prior to pursing fellowship. His interests include outcomes research in interventional cardiology and medical education In his spare time, Greg enjoys traveling, exercising, and experiencing new cultures through their food. When he’s not in the hospital, you can find Greg planning a trip with close friends and family. References and Links Coming soon! Luke Laffin MD Greg Ogunnowo, MD Amit Goyal, MD Daniel Ambinder, MD

CardioNerds (Amit Goyal and Daniel Ambinder) are joined by Cleveland Clinic cardiology fellow Dr. Gregory Ogunnowo to discuss hypertension with Dr. Luke Laffin, cardiology faculty in the division of Preventive Cardiology and Rehabilitation and Medical Director of Cardiac Rehabilitation at the Cleveland Clinic. Part 1 of this discussion covers the definition of hypertension, correct measurement of blood pressure, nonpharmacologic HTN management, initial choice of BP agents, and hypertensive disorders of pregnancy. Be sure to follow-up with Part 2 to learn about evaluation for secondary causes of HTN, approach to resistant HTN, interventional anti-hypertensive procedures, and a note on cardiac rehabilitation. Episode Graphic by Dr. Carine Hamo 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 Coming soon! Cardionerds Cardiovascular Prevention Series 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! We are truly honored to be producing the Cardionerds CVD Prevention Series 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! This series is kicked off by a message from Dr. Amit Khera, President of the American Society for Preventive Cardiology and President of the SouthWest Affiliate of the American Heart Association. Guest Profiles Dr. Luke Laffin, serves as cardiology faculty in the division of Preventive Cardiology and Medical Director of Cardiac Rehabilitation at the Cleveland Clinic. Dr. Laffin attended medical school at Vanderbilt University School of Medicine. He trained in internal medicine and cardiology at the University of Chicago where he completed a dedicated fellowship in hypertensive diseases. He is a clinical specialist in hypertension designated by the American Society of Hypertension – which has now merged with the AHA. Dr. Gregory Ogunnowo is a cardiology fellow at the Cleveland Clinic. He completed medical school at the University of South Carolina School of Medicine in Columbia, South Carolina. He went on to complete internal medicine residency at Washington University School of Medicine in St. Louis where he stayed on as faculty in the Department of Hospital Medicine for a year prior to pursing fellowship. His interests include outcomes research in interventional cardiology and medical education In his spare time, Greg enjoys traveling, exercising, and experiencing new cultures through their food. When he’s not in the hospital, you can find Greg planning a trip with close friends and family. References and Links Coming soon! Luke Laffin MD Greg Ogunnowo, MD Amit Goyal, MD Daniel Ambinder, MD

CardioNerds (Amit Goyal and Daniel Ambinder) introduce the CardioNerds Narratives in Cardiology Series which will feature the stories of amazing cardiovascular faculty and trainees representing diverse backgrounds, subspecialties, career stages, and career paths. To kick this series off, Dr. Pamela Douglas, who heads the Diversity and Inclusion task force for the American College of Cardiology, provides valuable insights in the field and shares her personal story. We are joined by the CardioNerds Narratives #FIT Advisors, Dr. Zarina Sharalaya, Dr. Norrisa Haynes and Dr. Pablo Sanchez for this very important discussion. Special messages by: Dr. Vanessa Blumer, Dr. Robert Harrington, Dr. Richard Chazal, Dr. Nosheen Reza, Dr. Neha Pagidipati, Dr. Mary Norine (Minnow) Walsh, Dr. Melissa Daubert, Dr. Gerald Bloomfield, Dr. Angela Lowenstern, Dr. Ralph Brindis, Dr. Michael Valentine, Dr. Anna Lisa Crowley, Dr. Malissa Wood and Dr. Geoffrey Ginsberg. 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 What is “Diversity” & “Inclusion”? Facets of diversity are all aspects of human differences.  These include gender, race, ethnicity, age, physical ability, gender identity, national origin, language, religion, sexual orientation, socioeconomic status, and more. Inclusion is making everyone feel welcomed and included. Inclusion requires having a culture & environment where everyone can thrive regardless of background differences.  This inclusive culture fosters respect & belonging in which we hear, appreciate, & value everyone and their perspectives. Inclusive organizations work with individuals to recognize and eliminate both explicit and implicit biases. They may do this with intentional efforts like professional & skills development as well as addressing awareness, education, and policy.  Diversity measures representation by counting the presence of varying identities and characteristics. But Diversity itself is not the final goal. Diversity is the metric while Inclusion is the goal. For now, while representation is so disparate among certain groups, diversity is an important metric. It’s hard to be truly inclusive with such professional inequities.  “Ultimately what we want is for people to belong. So not just be asked to the dance and sitting around and staring at everybody else but really feeling like you can go out on that dance floor and dance, like nobody’s watching and it’s fine because this is your  community.” – Pamela Douglas Why is achieving diversity important? Diversity is a virtue in and of itself.  But more than that, diverse groups make better decisions, are more innovative, are better at problem solving, and have an expanded talent pool. Cardiovascular medicine benefits from having a diverse workforce. Science performed by diverse groups has greater scientific novelty and produces higher impact papers in higher impact journals. Is there a link between professional diversity and healthcare inequities? YES! Physician diversity reduces healthcare disparities and improves healthcare quality. Physicians who train in diverse environments are more culturally competent when treating underrepresented groups. Underrepresented physicians are more likely to serve underrepresented populations. Underrepresented patients are more likely to follow the recommendations of physicians who look like them. This enhanced trust is critical to an effective patient-physician relationship.  In the context of clinical trials and guidelines, underrepresented physician scientists help diversify our clinical trial participants, resulting in a more robust and representative evidence base.  How are we doing in cardiology with respect to diversity? There have been improvements but we have a long way to go. Women comprise 43% of internal medicine resident physicians by only 22% of general cardiology fellows and even lower proportions within procedural fields. Underrepresented minorities–specifically Blacks, Hispanics, and Native Americans–make up about 32% of the US population but only 13% of general cardiology fellows. Benchmarks for other racial and ethnic groups and for other facets of diversity like socioeconomic status, sexual orientation, gender identity, IMG status, and others are even less clear. Inequities amplify in advanced career and leadership positions.  Only 11%, 9%, 11%, and 24% of Asian, black, Hispanic, and white women, respectively, are full professors compared with 21%, 18%, 19%, and 36% of Asian, black, Hispanic, and white men, respectively (Albert 2018). In the top 40 ranked cardiology programs, there are no female cardiology chiefs (Albert 2018). There were no women editors-in-chief for US general cardiology journals between 1998

CardioNerds (Amit Goyal & Karan Desai) join University of Illinois at Chicago cardiology fellows (Brody Slostad, Kavin Arasar, and Mary Rodriguez-Ziccardi) for a cup of tea from atop Hancock Tower! They discuss an illuminating case of altered mental status & electrical instability due to digitalis poisoning. Program director Dr. Alex Auseon and APD Dr. Mayank Kansal provide the E-CPR and a message for applicants. Episode notes were developed by Johns Hopkins internal medicine resident Tommy Das with mentorship from University of Maryland cardiology fellow Karan Desai.   Jump to: Patient summary – Case media – Case teaching – References Episode graphic by Dr. Carine Hamo CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor RollSubscribe to our newsletter- The HeartbeatSupport our educational mission by becoming a Patron!Check out CardioNerds SWAG! Cardiology Programs Twitter Group created by Dr. Nosheen Reza Patient Summary A woman in her late 80s with history of systemic arterial hypertension and dementia presented with 2 weeks of nausea, vomiting, confusion, and yellow-tinted vision. When she presented to the hospital, initial history was limited as her caregiver was unaware of her medications and medical history. An initial ECG showed isorhythmic A-V dissociation and scooping ST segments laterally. Given her clinical history, this raised the suspicion for Digoxin toxicity, and a serum digoxin level was significantly elevated. However, this was not a home medication for the patient, nor did she have access to it! Listen to the episode now as the UIC Cardionerds masterfully take us through this case that would surely stump Dr. House!   Case Media through the Differential A B C D E F Click to Enlarge A. Initial ECGB. CXR- Patchy opacities of the left lower lobe consistent with pulmonary edema and/or aspiration​ pneumonia.C. Repeat ECG: AF with AV block, persistent scooped T waves​D. Post arrest ECG: Flutter/fib with AV block, VERY LONG PAUSES up to 6 secondsE. ECG post TVP: A flutter, slow V response (pacing picking up), intrinsic ventricular rate 20-40, PM set to 50 bpmF. Most recent ECG: Normal sinus rhythm TTE Episode Schematics & Teaching The CardioNerds 5! – 5 major takeaways from the #CNCR case 1) This episode featured a challenging case of digitalis toxicity. Cardionerds, what is the mechanism of action of cardiac glycosides?   Cardiac Glycosides (such as digoxin, digitalis, and oubain), inhibit the myocardial Na/K ATPase pump. This leads to an increased concentration of intracellular sodium, which then drives the influx of calcium into cardiac myocytes via the Na/Ca exchanger. This increase in intracellular calcium leads to further calcium release from the sarcoplasmic reticulum making even more calcium available to bind to troponin, increasing contractility.  In addition to their effect on inotropy, cardiac glycosides increase vagal tone, reducing SA node activity and slowing conduction through the AV node by increasing the refractory period  2) The first published account of digitalis to treat heart failure dates back to the 18th century, when botanist and physician William Withering published “An account of the Foxglove and some of its medical uses with practical remarks on dropsy, and other diseases”. A lot has changed over the years; what are some of the uses of digoxin in the modern day?   The DIG trial (1997) demonstrated a reduction in hospitalizations in patients with HFrEF treated with digoxin. However, no impact on mortality was shown. A major limitation from randomized trials of digoxin is the lack of contemporary background HF treatment (e.g., ARNI, SGLT2i, MRA, Device Therapy). Thus, its role in modern HFrEF management is typically limited to reducing hospitalizations in patients with persistent NYHA Class III or IV symptoms despite maximally tolerated guideline-directed medical therapy  Digoxin can also be used for acute or chronic rate control in atrial fibrillation, and may be particularly useful in patients with RVR refractory to beta blockers/calcium channel blockers or in those patients who cannot tolerate these agents due to hypotension. Notably, data from the ARISTOTLE trial (2018) showed a significant mortality increase was seen in patients with a digoxin level ≥1.2 ng/ml, while no increase in mortality was seen with levels <0.9 ng/ml.   Recent data from the small, randomized RATE-AF trial showed no difference in quality of life and similar heart rate control in older patients with permanent atrial fibrillation and heart failure symptoms. Thus, while the therapeutic window may be limited, there remains a role for digoxin in the treatment of HFrEF, Afib, or both.  3) While digoxin can

CardioNerds (Carine Hamo, Amit Goyal, and Daniel Ambinder) discuss the obesity epidemic and how it relates to the cardiovascular system with Dr. Chiadi Ndumele, cardiologist and epidemiologist at The Johns Hopkins Hospital and chairs the obesity subcommittee of the American Heart Association (AHA). They cover obesity definitions, epidemiology, strengths and limitations of different biometrics, including BMI, impact on myocardial structure and function, and current pharmacologic & surgical options for weight loss. They also discuss the practical approach to addressing obesity with patients. This episode was produced by Dr. Carine Hamo. Show notes & references by Dr. Daniel Ambinder. Episode graphic by Dr. Carine Hamo Cardionerds Cardiovascular Prevention PageCardioNerds Episode PageSubscribe to our newsletter- The HeartbeatSupport our educational mission by becoming a Patron! Show notes 1. What is obesity and how do we define it at the personal and population level? Obesity is when there is an excess and often dysfunctional adipose tissue that contributes to morbidity and to premature mortality The metric used to define obesity is Body Mass Index (BMI), defined as a person’s weight in kilograms divided by the square of the person’s height in meters (kg/m2) See WHO BMI classification below 2. What is the current epidemiology of obesity and are there certain populations that are affected more than others? Rates of obesity are climbing. Currently, around 70% of the population meets criteria for being either overweight or obese and ~40% are at the level of obesity. Minorities such as African Americans, Native Americans, and Latinos have higher rates of obesity. Higher rates of obesity are also seen in groups with lower socioeconomic status. Certain populations, such as Southeast Asians, tend to develop severe metabolic consequences of obesity such as insulin resistance and cardiovascular consequences with less excess weight than other populations. Adult weight is very important but weight history (long standing obesity) plays a role as well when it comes to cardiovascular risk associated with obesity. 3. Currently the WHO classifies obesity based on BMI. What are the limitations to using BMI as a measure of obesity? Are their benefits to measuring waist circumference instead? BMI is a far from a perfect measure but it correlates nicely at the population level with cardiovascular events and premature mortality BMI is more accessible than a direct quantitative or functional measure of adipose tissue A major limitation of BMI is that it does not reflect body composition. Body composition is very important in understanding risk associated with obesity. For example, football players may fall into the category of grade 1 obesity if just using BMI to classify their weight status. Waist circumference (WC) is a good way of getting a sense of body composition. Abdominal obesity is most closely linked to insulin resistance and various metabolic consequences such as diabetes, hypertension, and inflammation. This is why WC is incorporated into the metabolic syndrome construct. Adding WC measurements to the BMI measurements, particularly for individuals in the overweight and grade 1 obesity group (BMI 25-29.9, and 30-34.9) provides significant prognostic information about the development of cardiovascular disease. 4. How do obesity and metabolic syndrome impact myocardial structure and function? How does obesity and increased adiposity fit into the larger scheme of metabolic risk and metabolic syndrome? Obesity is independently associated with myocardial remodeling and with increased heart failure risk. This contrasts with coronary heart disease (CAD) and stroke. For CAD and stroke, most associations with obesity are largely mediated by diabetes, hypertension and dyslipidemia. However, in heart failure, there is a strong unexplained association that remains after you consider those associated conditions. The independent association of obesity with heart failure pertains almost exclusively to heart failure with preserved ejection fraction (HFpEF) and not heart failure with reduced ejection fraction (HFrEF). The mechanism for this independent association is not well understood and is an area of active research. In mice that are predisposed to obesity have several inflammatory processes that occur locally in the myocardium and systemically that likely contribute to cardiac risk. At the local level, lipotoxicity occurs within the myocardium as it does in nonalcoholic fatty liver disease. At the systemic level, adipose tissue releases adipokines and cytokines that are linked to myocardial damage, injury, and fibrosis. There is a spectrum of metabolic risk among individuals with excess weight. And when obesity is associated with metabolic syndrome in individuals, the risk for cardiovascular disease markedly rises. 4. What are some core tenants of addressing obesity when working with patients when

CardioNerds (Amit Goyal and Daniel Ambinder) discuss diabetes mellitus with Dr. Dennis Bruemmer. This is a must-listen for anyone engaged in the case of the cardiovascular patient. Given the alarming obesity epidemic, we anticipate a rising worldwide tide of diabetes mellitus and ensuing cardiovascular disease. Here we discuss the epidemiology and approach to diabetes management, with emphasis on what CardioNerds need to know. Dr. Bruemmer is board-certified in both cardiology and endocrinology, and is the director of the Center for Cardiometabolic Health in the section of Preventive Cardiology and Rehabilitation at the Cleveland Clinic. Episode graphic by Dr. Carine Hamo Cardionerds Cardiovascular Prevention PageCardioNerds Episode PageSubscribe to our newsletter- The HeartbeatSupport our educational mission by becoming a Patron! Show notes Why should CardioNerds pay attention to diabetes mellitus (DM)?  As a cardiovascular risk equivalent, DM is a key CVD risk factor, associated with a 2-4 fold increased risk. 70% of ACS patients have DM.  Cardiologists will see more patient with DM given the rising prevalence of obesity, subsequent diabetes and ensuing CVD.   Only 6% of patients with DM and cardiovascular disease (CVD) get appropriate care for DM and CVD.  Historically, hypoglycemic agents improved microvascular outcomes (retinopathy, nephropathy, neuropathy), but not macrovascular outcomes (MI, CVA, PAD). However, this has changed with the advent of mandatory cardiovascular safety trials with positive data for GLP1 agonists and SGLT2 inhibitors!  There aren’t enough endocrinologists! They only see ~5% of DM patients. In 2012 the US generated 280 endocrinologists versus  100 million patient with DM or pre-DM. Primary care physicians are key allies in the care of these patients.   So as CardioNerds, let’s get over this therapeutic inertia and take ownership of our patients’ DM as we already do for their HTN and HLD; in collaboration with a multidisciplinary team including the PCP, dietician, pharmacist, DM educators, +/- behavioral therapist, +/- endocrinologist, +/- metabolic surgeon.  What is your global approach to the patient with DM?  Optimize the non-DM CVD risk factors with lifestyle intervention and medical management: CVD risk factors are very common in patients with DM (sedentary lifestyle, unhealthy weight, HTN, HLD).  The Steno-2 Study (Gaede et al., NEJM 2008) showed that in patients with T2DM & microalbuminuria, intensive intervention with multiple drug combinations and behavioral modification was better with regards to: vascular complications, death from any cause, and death from CV causes.      Emphasize a healthy lifestyle –  use a patient-centered approach with motivational interviewing and shared decision making, provide education, set realistic goals, identify barriers (socioeconomic, etc), engage family and a multidisciplinary team (nutritionist, exercise physiologist), utilize behavioral interventions.  Pharmacologic intervention – medical weight loss for BMI > 27 and DM (enjoy upcoming Ndumele episode), anti-HTN (enjoy upcoming Laffin episode), and anti-HLD (enjoy the Navar-Shah episode). NOTE that statins have been shown to have a small effect on increasing incident or worsening DM, but the effect size is small and overcome by the benefit in whom statins are indicated.                 Treat the Hyperglycemia itself! Let’s discuss this deeper…  What is your approach to non-insulin DM management?  First-line agents: US guidelines: in addition to lifestyle intervention, start with metformin as the first line agent.  European guidelines: now give preference to GLP1 agonists and SGLT2 inhibitors in patients with or at risk for cardiovascular disease.  Sulfonylureas: increase pancreatic insulin secretion. Dr. Bruemmer feels they obsolete for the preventive cardiologist from the standpoints of safety, efficacy, and cardiovascular disease. There is no efficacy data past 4 years and no cardiovascular benefit. In contrast data suggests increase all-cause mortality and possibly MACE events. Low cost may make these more affordable for some patients.   Thiazolidinediones (aka: “glitazones”): increase insulin sensitivity, the primary defect in T2DM. Rosiglitazone is discouraged due to adverse cardiovascular outcomes. Pioglitazone has better data, especially in those who’ve had a stroke or TIA (IRIS Trial, NEJM 2016). They may have a role in those for whom other classes are contraindicated or cost-prohibitive.   DPP4 Inhibitors: increase incretin levels (GLP-1 and GIP) which inhibit glucagon release, increase insulin secretion, and delay gastric emptying. They do not cause hypoglycemia or weight gain. These have a

The CardioNerds (Carine Hamo and Daniel Ambinder) discuss aspirin as primary prevention, Vitamin D, Calcium, and omega 3 fatty acids supplementation with Dr. Erin Michos, director of women’s cardiovascular health and the associate director of preventive cardiology with Johns Hopkins Ciccarone Center for the Prevention of Cardiovascular Disease. We are also joined by Dr. Michos’ mentees, Dr. Rick Ferraro, Dr. Andi Shahu, and student doctor Sunyoung (Sarah) Jang for a discussion about mentorship and career development. This episode was produced by Dr. Rick Ferraro and Dr. Carine Hamo. Show notes & references by Dr. Amit Goyal. Episode graphic by Dr. Carine Hamo Cardionerds Cardiovascular Prevention PageCardioNerds Episode PageSubscribe to our newsletter- The HeartbeatSupport our educational mission by becoming a Patron! Show notes – Aspirin, Vitamin D, Calcium & Omega 3 Fatty Acids Supplementation What is the role of aspirin for primary ASCVD prevention?  The Conundrum: ASCVD event rates are much lower in the primary prevention than in the secondary prevention population, BUT the bleeding rates are comparable. So in the primary prevention patients, the bleeding risk is just as high, but the propensity for benefit is lower.  The Question: Does low dose aspirin have a place in the primary prevention of ASCVD events.  The Data:  ARRIVE Trial: in moderate risk nondiabetic patients without prior ASCVD events, there was no different in the composite ASCVD end point, but there was an increased risk of bleeding (mostly mild GI bleeding). Thus, in the moderate risk patients –> primary prevention aspirin has an unfavorable risk-benefit profile. The benefit in a higher risk (>10-20% estimated 10-yr risk) remains unclear.   ASCEND Trial: In men and women age ≥ 40yrs with diabetes without prior ASCVD events, there was a modest benefit (NNT = 59 patients for 10 years to prevent 1 major ASCVD event) counterbalanced by a similar magnitude of harm (NNH = 77 patients for 10 years to cause 1 major bleeding event). Thus, in adults with diabetes –> primary prevention aspirin had a neutral risk-benefit profile.  ASPREE Trial: in elderly patients (≥ 70 years; ≥ 65 years for Hispanic or Black patients) without prior ASCVD events, there was no difference in ASCVD events but there was a significant increase in bleeding events (NNH = 42 patients for 10 years to cause 1 major bleeding event). The trial was stopped early due to futility. Interestingly, there was higher all-cause mortality driven primarily by cancer. Importantly, patients had to have a life expectancy longer than 5 years and those with dementia, substantial physical disability, or high estimated bleeding risk were excluded. Thus, in elderly patients –> primary prevention aspirin led to overall harm.   The Recommendations:  There was insufficient evidence to recommend a specific risk threshold for starting primary prevention aspirin. This may be due to more widespread contemporary prevention strategies like lifestyle management, tobacco cessation, statin use, better blood pressure control, etc.   Individualize the decision based on the totality of evidence for an individual’s risk of ASCVD events versus bleeding events. Notably, those with higher ASCVD risk generally also have a higher bleeding risk.            Class IIB: Low-dose aspirin (75-100 mg orally daily) might be considered for the primary prevention of ASCVD among select adults 40 to 70 years of age who are at higher ASCVD risk but not at increased bleeding risk.  There may be a role for primary prevention aspirin in select adults with a high estimated ASCVD risk and low bleeding risk.  CAC score ≥ 100 may help identify those might benefit from primary prevention aspirin.            As always, shared decision making remains           crucial.  Class III: Low-dose aspirin (75-100 mg orally daily) should not be administered on a routine basis for the primary prevention of ASCVD among adults >70 years of age.  Class III: Low-dose aspirin (75-100 mg orally daily) should not be administered for the primary prevention of ASCVD among adults of any age who are at increased risk of bleeding.  What is the role of Vitamin D supplementation in preventing cardiovascular disease?             The Conundrum: Low levels of Vit D is associated with increased risk of CV outcomes including myocardial infarction, stroke, heart failure, atrial fibrillation, and more. But while low Vit D seems to be a marker for bad outcomes, correlation ≠ causation. Notably, this correlation was not confirmed by Mendelian randomi

CardioNerds (Amit Goyal) joins Thomas Jefferson cardiology fellows (Jay Kloo, Preya Simlote and Sean Dikdan – host of the Med Lit Review podcast) for some amazing craft beer from Independence Beer Garden in Philadelphia! They discuss a fascinating case of atrioesophageal fistula (AEF) formation after pulmonary vein isolation (PVI). Dr. Daniel Frisch provides the E-CPR and program director Dr. Gregary Marhefka provides a message for applicants. Johns Hopkins internal medicine resident Colin Blumenthal with mentorship from University of Maryland cardiology fellow Karan Desai.   Jump to: Patient summary – Case media – Case teaching – References Episode graphic by Dr. Carine Hamo The CardioNerds Cardiology Case Reports series shines light on the hidden curriculum of medical storytelling. We learn together while discussing fascinating cases in this fun, engaging, and educational format. Each episode ends with an “Expert CardioNerd Perspectives & Review” (E-CPR) for a nuanced teaching from a content expert. We truly believe that hearing about a patient is the singular theme that unifies everyone at every level, from the student to the professor emeritus. We are teaming up with the ACC FIT Section to use the #CNCR episodes to showcase CV education across the country in the era of virtual recruitment. As part of the recruitment series, each episode features fellows from a given program discussing and teaching about an interesting case as well as sharing what makes their hearts flutter about their fellowship training. The case discussion is followed by both an E-CPR segment and a message from the program director. CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademySubscribe to our newsletter- The HeartbeatSupport our educational mission by becoming a Patron!Cardiology Programs Twitter Group created by Dr. Nosheen Reza Patient Summary A man in his mid-60s with a history of paroxysmal Afib presented to the ED after one week of chest pain and altered mental status. His afib had been difficult to rate and rhythm control, and thus he had undergone catheter ablation with pulmonary vein isolation 3 weeks prior to presentation. In the ED he was found to be febrile and had a witnessed seizure. Blood cultures returned positive for Strep agalactiae and his CT head showed multiple areas of intravascular air. Join the Thomas Jefferson University Cardionerds as they take us through an expert discussion on the differential of post-catheter complications, the diagnosis of atrial-esophageal fistula and ultimately management of this potentially fatal complication! Case Media A B C D E F Click to Enlarge A. ECG: Normal sinus rhythm HR 105 bpmB. CXRC. CT head: Multiple tiny foci of air throughout bilateral cerebral hemispheres. Appearance is most suggestive of intravascular air, although it is unclear if it is venous, arterial or both.D. MRI: 1. Restricted diffusion in bilateral cortical watershed zones, as well as in the posterior medial left cerebellar hemisphere, most consistent with recent infarctions.E. CT Chest: A small focus of air tracking along the left mainstem bronchus anterior to the esophagus, may represent a small amount of pneumomediastinum versus air in an outpouching of the esophagus. No air tracking more cranially along the mediastinal soft tissues. No definite soft tissue defect in the esophagus.F. Surgical repair of LA & Esophagus Episode Teaching The CardioNerds 5! – 5 major takeaways from the #CNCR case What is a pulmonary vein isolation? What are the most common complications? When is catheter ablation indicated? The majority of Afib triggers come from areas where the pulmonary veins attach to the left atrium. Approximately 15-20% of patients undergoing ablation will have non-pulmonary vein triggers. Guided by this anatomic and pathophysiologic underpinning, electrical isolation and ablation of these areas helps prevent propagation of the Afib impulses. The most effective method for pulmonary vein isolation (PVI) is ablation of the PV antrum, areas located near the PV ostia, using an oval mapping catheter to confirm ablation of electrical activity from the PV ostia. Vascular access complications (e.g. hematoma, pseudoaneurysm) are the most common complications following PVI and occur in approximately 1-4% (KD: I think complication rate is lower in studies I’ve reviewed) cases. Most other complications occur in less than 1% of cases and include cardiac tamponade/perforation, TIA/stroke, PV stenosis, pneumonia, phrenic nerve palsy, gastric motility disorders, atrial-esophageal fistula, and death. There is some growing evidence that catheter ablation may be superior to medical management alone in certain symptomatic populations (e.g., HFrEF). However, in the recent CABANA trial, catheter ablation did not significantly reduce death, disabling stroke, or serious bleeding compa

CardioNerds (Amit Goyal & Daniel Ambinder) join Oregon Health & Science University cardiology fellows (Miranda Merrill, Timothy Simpson, Kris Kumar, and Stacey Howell) for a riverside chat at the Portland waterfront! They discuss a case of cardiac arrest associated with mitral valve prolapse (MVP) with mitral annular disjunction (MAD). Dr. Punag Divanji provides the E-CPR and program director Dr. Hind Rahmouni provides a message for applicants. Episode notes were developed by Johns Hopkins internal medicine resident, Eunice Dugan, with mentorship from University of Maryland cardiology fellow Karan Desai. Jump to: Patient summary – Case media – Case teaching – References Episode graphic by Dr. Carine Hamo The CardioNerds Cardiology Case Reports series shines light on the hidden curriculum of medical storytelling. We learn together while discussing fascinating cases in this fun, engaging, and educational format. Each episode ends with an “Expert CardioNerd Perspectives & Review” (E-CPR) for a nuanced teaching from a content expert. We truly believe that hearing about a patient is the singular theme that unifies everyone at every level, from the student to the professor emeritus. We are teaming up with the ACC FIT Section to use the #CNCR episodes to showcase CV education across the country in the era of virtual recruitment. As part of the recruitment series, each episode features fellows from a given program discussing and teaching about an interesting case as well as sharing what makes their hearts flutter about their fellowship training. The case discussion is followed by both an E-CPR segment and a message from the program director. CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademySubscribe to our newsletter- The HeartbeatSupport our educational mission by becoming a Patron!Cardiology Programs Twitter Group created by Dr. Nosheen Reza Patient Summary Coming soon! Case Media A B C D E F G Click to Enlarge A. CXRB. Rhythm Strips – ventricular fibrillationC. ECG: 1st degree AVB (PR ~ 215), borderline RAD, Qtc ~460 msec, slight ant. convexity with inferior terminal T waveD: TTE E: TTE with Pickelhaube Spike seen in mitral valve prolapse F-G: Cardiac MRI TTE 1 TTE 2 TTE 3 Cardiac MRI Episode Schematics & Teaching Coming soon! The CardioNerds 5! – 5 major takeaways from the #CNCR case Coming soon! References Coming soon! CardioNerds Case Reports: Recruitment Edition Series Production Team Bibin Varghese, MD Rick Ferraro, MD Tommy Das, MD Eunice Dugan, MD Evelyn Song, MD Colin Blumenthal, MD Karan Desai, MD Amit Goyal, MD Daniel Ambinder, MD

CardioNerd (Amit Goyal) join Emory University School of Medicine cardiology fellows (Sonali Kumar, John Lisko, and John Ricketts) for a lovely stroll on the BeltLine in Atalanta, GA. They discuss an interesting case of severe mitral stenosis treated with Valve-in-MAC transcatheter mitral valve replacement (TMVR) with LAMPOON. Drs. Vasilis Babaliaros and Adam Greenbaum provide the E-CPR and program director Dr. B. Robinson Williams III provides a message for applicants. Episode notes were developed by Johns Hopkins internal medicine resident Bibin Varghese with mentorship from University of Maryland cardiology fellow Karan Desai.    Jump to: Patient summary – Case media – Case teaching – References Episode graphic by Dr. Carine Hamo The CardioNerds Cardiology Case Reports series shines light on the hidden curriculum of medical storytelling. We learn together while discussing fascinating cases in this fun, engaging, and educational format. Each episode ends with an “Expert CardioNerd Perspectives & Review” (E-CPR) for a nuanced teaching from a content expert. We truly believe that hearing about a patient is the singular theme that unifies everyone at every level, from the student to the professor emeritus. We are teaming up with the ACC FIT Section to use the #CNCR episodes to showcase CV education across the country in the era of virtual recruitment. As part of the recruitment series, each episode features fellows from a given program discussing and teaching about an interesting case as well as sharing what makes their hearts flutter about their fellowship training. The case discussion is followed by both an E-CPR segment and a message from the program director. CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademySubscribe to our newsletter- The HeartbeatSupport our educational mission by becoming a Patron!Cardiology Programs Twitter Group created by Dr. Nosheen Reza Patient Summary Coming soon! Case Media A B C D E F G H I J K Click to Enlarge A. CXRB. ECGC. TTE: Trasns-mitral PW Doppler D. Laceration in swineE-F: CT planningG. Transeptal catheters H. Trans-mitral PW Doppler (post procedure) I. LVOT gradients J-K. Post procedure CT TTE 1 TTE 2 TTE 3 TEE 1 TEE 2 Fluoroscopy 1 Fluoroscopy 2 Fluoroscopy 3 TEE 3 Fluoroscopy 4 TEE 4 TEE 5 Fluoroscopy 5 Fluoroscopy 6 Fluoroscopy 7 TEE 6 TEE 7 https://youtu.be/1gUyat6pg30 LAMPOON Procedure Episode Schematics & Teaching Coming soon! Click to enlarge! The CardioNerds 5! – 5 major takeaways from the #CNCR case Coming soon! References Coming soon! CardioNerds Case Reports: Recruitment Edition Series Production Team Bibin Varghese, MD Rick Ferraro, MD Tommy Das, MD Eunice Dugan, MD Evelyn Song, MD Colin Blumenthal, MD Karan Desai, MD Amit Goyal, MD Daniel Ambinder, MD

Aloha! CardioNerds (Amit Goyal & Karan Desai)  join University of Hawaii cardiology fellows (Isaac Mizrahi, Nath Limpruttidham, Nishant Trivedi, and Shana Greif) for some shaved iced on the Big Island’s north shore! They discuss a fascinating case of a patient presenting with decompensated heart failure found to have a giant coronary aneurysm. Program director Dr. Dipanjan Banerjee provides the E-CPR as well as a message for applicants. Episode notes were developed by Johns Hopkins internal medicine resident Tommy Das with mentorship from University of Maryland cardiology fellow Karan Desai.   Jump to: Patient summary – Case media – Case teaching – References Episode graphic by Dr. Carine Hamo CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademySubscribe to our newsletter- The HeartbeatSupport our educational mission by becoming a Patron!Cardiology Programs Twitter Group created by Dr. Nosheen Reza Patient Summary A man in his early 60s with history of hypertension, peripheral arterial disease, atrial fibrillation, and AAA s/p repair presented with subacute fatigue, palpitations, shortness of breath, and lower extremity edema. On exam he was warm and well perfused, though hypotensive, tachycardic with an irregular rhythm, and had an elevated JVP. ECG showed AF with RVR without evidence of acute MI, and troponin was negative. TTE revealed a reduced LVEF and WMA in the inferolateral walls with akinesis of the basal mid septum; additionally, two large extracardiac structures were noted, one with heterogenous echotexture in the AV groove, and a second with an echolucent interior adjacent to the RA. The patient underwent coronary angiography, showing a dilated and calcified proximal LAD with high grade stenosis adjacent to the first septal perforator, a ectatic LCX that supplied left to right collaterals, and a giant RCA aneurysm with TIMI 0 flow distally. CCTA confirmed these findings, showing thrombosed aneurysms of the LAD, LCX, and RCA. Interventional cardiology and cardiac surgery both evaluated the patient’s case, and determined that he was not a candidate for intervention. He was ultimately diuresed to euvolemia with significant improvement in symptoms, and plans to follow-up as an outpatient for heart transplant evaluation. Case Media A B C D Click to Enlarge A. CXRB. ECG: atrial fibrillation with RVR, left axis deviation, poor r wave progressionC. Wide complex tachycardia D. CT chest demonstrating giant aneurysm TTE Coronary Angiography Episode Schematics & Teaching The CardioNerds 5! – 5 major takeaways from the #CNCR case 1) This case featured a patient with a giant coronary aneurysm – how are coronary artery aneurysms defined and classified?   Coronary artery aneurysms (CAA) are defined as a focal dilation of a coronary segment at least 1.5x the adjacent normal segment. Contrast this with coronary artery ectasia, which refers to a diffuse, as opposed to focal, coronary dilation.   CAA morphology can be classified as either saccular (transverse > longitudinal diameter) or fusiform (transverse < longitudinal diameter).  Giant CAA’s are >20mm in diameter.  Aortocoronary saphenous vein graft aneurysms have distinct characteristics and natural history compared to native coronary aneurysms. These aneurysms tend to present late (e.g., > 10 years following CABG) and tend to be larger than native CAA.  IVUS can help differentiate between a true aneurysm with preserved integrity of all 3 vessel layers (intima, media, and adventitia) and a pseudoaneurysm with loss of wall integrity and damage to the adventitia.  2) Now that we have the language to define and classify coronary artery aneurysms, what are some causes these lesions?   Atherosclerosis: lipid deposition, focal calcification, and fibrosis can weaken the vessel wall and predispose to subsequent coronary artery dilation. Up to 50% of CAAs are linked to arteriosclerosis.   Autoimmune/inflammatory processes: Lupus and systemic vasculitis, such as Kawasaki’s disease and Takayasu arteritis, can all lead to CAAs. Vasculitic CAAs usually affect more than one artery.   Connective Tissue Disease: Marfan’s syndrome and Ehlers-Danlos disease, for instance, are characterized by deficiencies in vessel wall integrity, leading to CAAs.  Dynamic Wall Stress: Episodic hypertension and vasoconstriction, such as that seen in frequent cocaine use, can lead to wall stress, endothelial damage, and coronary artery aneurysms.   Direct Vessel Wall Injury: Intracoronary interventions, such as angioplasty, stent delivery, and brachytherapy, can cause shear wall stress that leads to CAAs.   Infectious Causes: Direct vessel wall invasion or immune co

CardioNerds (Amit Goyal & Daniel Ambinder) join Georgetown University/Washington Hospital Center cardiology fellows (Nitin Malik, AJ Grant, and Tsion Aberra) for some fresh Maryland blue crab cakes at the Georgetown waterfront in Washington, DC. They discuss a rare case of histoplasmosis pericarditis complicated by cardiac tamponade. Dr. Patrick Bering provides the E-CPR and program director Dr. Gaby Weissman provides a message for applicants. Johns Hopkins internal medicine resident Colin Blumenthal with mentorship from University of Maryland cardiology fellow Karan Desai.   Jump to: Patient summary – Case media – Case teaching – References Episode graphic by Dr. Carine Hamo The CardioNerds Cardiology Case Reports series shines light on the hidden curriculum of medical storytelling. We learn together while discussing fascinating cases in this fun, engaging, and educational format. Each episode ends with an “Expert CardioNerd Perspectives & Review” (E-CPR) for a nuanced teaching from a content expert. We truly believe that hearing about a patient is the singular theme that unifies everyone at every level, from the student to the professor emeritus. We are teaming up with the ACC FIT Section to use the #CNCR episodes to showcase CV education across the country in the era of virtual recruitment. As part of the recruitment series, each episode features fellows from a given program discussing and teaching about an interesting case as well as sharing what makes their hearts flutter about their fellowship training. The case discussion is followed by both an E-CPR segment and a message from the program director. CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademySubscribe to our newsletter- The HeartbeatSupport our educational mission by becoming a Patron!Cardiology Programs Twitter Group created by Dr. Nosheen Reza Patient Summary A woman in her early 30s with a history of Crohn’s disease on TNF-inhibitor therapy and chronic prednisone presented to the ED after two months of abdominal pain and fevers. She was found to have a perforated bowel and taken to emergent surgery and eventually found to have disseminated histoplasmosis. Post-surgery, her hypotension worsened. At this point, the Georgetown University Cardionerds were involved. Listen to the podcast now to learn about histoplasmosis, it’s cardiac involvement, and management of acute effusive pericarditis! Case Media A B C D E Click to Enlarge A. Left: Admission chest x-ray (PA film), which was overall unremarkable. Right: Chest x-ray from hospital day 12 – which revealed pulmonary edema with bilateral perihilar haziness, increased prominence of pulmonary vascularity, and small-moderate bilateral pleural effusions. Note increased size of cardiac silhouette. At the corresponding time, pericardial effusion (without tamponade) had been diagnosed.B. EKG: Sinus tachycardia and low-voltage QRS complexes.C. CT abdomen/pelvis on hospital day 14. Free air noted within the abdomen (left). Moderate pericardial effusion also incidentally appreciated (right).D. Pulse-Wave Doppler of mitral inflow. Flow variation is present, but variation is less than <30%.E. (A) Small bowel resection showing focal mucosal ulceration, serositis, and formation of a granuloma. (B) Transmural inflammation seen on small bowel resection. (C) Pathology of ileocecectomy showing focal histoplasmosis characterized by intracytoplasmic yeast-like forms (black circles) Parasternal short axis view on echocardiogram showing a moderate pericardial effusion without diastolic septal flattening. Apical view showing profound tachycardia but without chamber collapse. Ejection fraction was moderately reduced. Parasternal short axis view on echocardiogram showing a moderate pericardial effusion with intermittent septal flattening. Apical view showing early diastolic RV chamber collapse.  Episode Schematics & Teaching The CardioNerds 5! – 5 major takeaways from the #CNCR case How does one diagnose acute pericarditis? What are the most common etiologies? Based on the 2015 ESC guidelines on pericardial disease, acute pericarditis is diagnosed when at least two of the following four criteria are present: Chest pain characteristic of pericarditis Acute onset, improves with leaning forward, pleuritic Pericardial rub EKG changes consistent with pericarditis PR depressions, ST segment elevation though depending on time course these can normalize or become T wave inversions New or worsening pericardial effusion Etiology can vary by geography. In most developed countries, viruses are thought to be the most common cause, though even when a viral cause is suspected, the majority of cases end up being idiopathic. Other etiologies include bacterial (TB is the most common cause of pericarditis in developing countries), autoimmune, hypothyroidism, malignancy, r

CardioNerds (Amit Goyal & Karan Desai) join Medical University of South Carolina cardiology (MUSC) fellows (Carson Keck, Samuel Powell, and Ishan Shah) at MUSC Children’s Hospital cafeteria overlooking the gorgeous Charleston Harbor. They reflect on an informative case of exertional intolerance due to tricuspid regurgitation. Dr. Ryan Tedford provides the E-CPR and program director Dr. Daniel Judge provides a message for applicants. Episode notes were developed by Johns Hopkins internal medicine resident, Eunice Dugan, with mentorship from University of Maryland cardiology fellow Karan Desai. Jump to: Patient summary – Case media – Case teaching – References Episode graphic by Dr. Carine Hamo The CardioNerds Cardiology Case Reports series shines light on the hidden curriculum of medical storytelling. We learn together while discussing fascinating cases in this fun, engaging, and educational format. Each episode ends with an “Expert CardioNerd Perspectives & Review” (E-CPR) for a nuanced teaching from a content expert. We truly believe that hearing about a patient is the singular theme that unifies everyone at every level, from the student to the professor emeritus. We are teaming up with the ACC FIT Section to use the #CNCR episodes to showcase CV education across the country in the era of virtual recruitment. As part of the recruitment series, each episode features fellows from a given program discussing and teaching about an interesting case as well as sharing what makes their hearts flutter about their fellowship training. The case discussion is followed by both an E-CPR segment and a message from the program director. CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademySubscribe to our newsletter- The HeartbeatSupport our educational mission by becoming a Patron!Cardiology Programs Twitter Group created by Dr. Nosheen Reza Patient Summary Coming soon! Case Media A B Click to Enlarge A. Tricuspid valve CW DopplerB. Hepatic vein flow TTE: TV inflow TTE: TV inflow with color Doppler TTE: Apical 4 chamber TTE: RV focused color Cardiac MRI – 4 chamber CINE Cardiac MRI – Short-axis stack CINE Episode Teaching The CardioNerds 5! – 5 major takeaways from the #CNCR case Coming soon! References Coming soon! CardioNerds Case Reports: Recruitment Edition Series Production Team Bibin Varghese, MD Rick Ferraro, MD Tommy Das, MD Eunice Dugan, MD Evelyn Song, MD Colin Blumenthal, MD Karan Desai, MD Amit Goyal, MD Daniel Ambinder, MD

CardioNerds (Amit Goyal & Daniel Ambinder) join Brown University cardiology fellows (Greg Salber, Vrinda Trivedi, and Esseim Sharma) for a gorgeous coastal boat ride in Providence, RI. They discuss an educational case of hypertrophic cardiomyopathy with superimposed stress cardiomyopathy. Dr. Katharine French provides the E-CPR and program director Dr. Raymond Russell provides a message for applicants. Episode notes were developed by Johns Hopkins internal medicine resident Evelyn Song with mentorship from University of Maryland cardiology fellow Karan Desai.   Jump to: Patient summary – Case media – Case teaching – References Episode graphic by Dr. Carine Hamo The CardioNerds Cardiology Case Reports series shines light on the hidden curriculum of medical storytelling. We learn together while discussing fascinating cases in this fun, engaging, and educational format. Each episode ends with an “Expert CardioNerd Perspectives & Review” (E-CPR) for a nuanced teaching from a content expert. We truly believe that hearing about a patient is the singular theme that unifies everyone at every level, from the student to the professor emeritus. We are teaming up with the ACC FIT Section to use the #CNCR episodes to showcase CV education across the country in the era of virtual recruitment. As part of the recruitment series, each episode features fellows from a given program discussing and teaching about an interesting case as well as sharing what makes their hearts flutter about their fellowship training. The case discussion is followed by both an E-CPR segment and a message from the program director. CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademySubscribe to our newsletter- The HeartbeatSupport our educational mission by becoming a Patron!Cardiology Programs Twitter Group created by Dr. Nosheen Reza Patient Summary A man in his mid-70s with history of hypertension and diabetes presented with chest pain and ST elevation in V1-V3. Two weeks prior to his presentation he was diagnosed with HoCM after several months of progressive dyspnea. TTE at that time showed HCM with resting left ventricular outflow gradient of 35 mmHg and 83 mmHg with valsava and systolic anterior motion (SAM) of the mitral valve. Join the Brown University Cardionerds as they take us through the differential of chest pain in HCM, approach to wall motion abnormalities, and the fascinating management questions that arise. Case Media A B C D E Click to Enlarge A. ECG 2 weeks prior to current presentation B. Current ECG C. CXRD. M mode though the mitral valve demonstrating systolic anterior motion of the mitral valveE. LVOT CW Doppler tracings with a peak velocity ~ 5 m/s Coronary angiography – 1 Coronary angiography – 2 TTE – 1 TTE – 2 TTE – 3 TTE – 4 Cardiac MRI Episode Schematics & Teaching Hypertrophic Cardiomyopathy Infographic Click to enlarge! The CardioNerds 5! – 5 major takeaways from the #CNCR case What’s the differential for LVH and what findings are more suggestive of HCM? Causes for LVH can be either pathological or physiological. Pathological causes include infiltrative diseases like hypertrophic cardiomyopathy (HCM), Amyloidosis, or Fabry disease and inflammatory diseases like myocarditis. Physiological causes are due to remodeling from increased cardiac output or workload like in athletic heart or from a high afterload state such as in aortic stenosis and hypertension. In hypertension, AS, and athletic heart, LV hypertrophy is more commonly concentric and rarely exceeds 15mm. In HCM, LV hypertrophy is more commonly asymmetric (basal anteroseptum > posterior wall), often >15mm, and typically involves the basal ventricular septum. Differentiating pathologic versus physiologic causes of LVH can typically be done from a detailed history and exam (e.g., evidence of hypertrophy out of proportion to pressure overload, multisystem involvement). Cardiac MRI can be used to differentiate between HCM and other phenocopies. In HCM, LGE is usually seen at the insertion point of the LV and RV or the most hypertrophied myocardial regions whereas in amyloidosis, endomyocardial LGE is more characteristic. What are some characteristic exam findings seen in HoCM? Systolic murmur at the left sternal border can be heard in patients with obstructive HCM (HoCM). The murmur is a result of LVOT obstruction due to systolic anterior motion (SAM) of the mitral valve and LV basal septal hypertrophy. Maneuvers that decrease preload, such as Valsalva or going from a sitting to upright position, will enhance the obstruction and increase the intensity of murmur. Maneuvers that increase the preload or afterload, such as squatting or handgrip, will decrease the intensity of murmur. Additionally, mitral valve pathology – whether a primary valve process or secondary to SAM/ abnormal

In Episode #82, we met Jeremy Keck as a patient born with L-TGA and DILV treated with Fontan procedure. Now, in this very special episode, we meet Jeremy Keck beyond his heart disease through the eyes of his loving wife Ana Keck. His legacy underscores the importance of seeing our patients as people beyond their illness, in the context of their lives, values, and loved ones. We learn to appreciate the full life one can live with complex adult congenital heart disease but also of the work that remains to be done. This powerful discussion is led by Dr. Evelyn Song (internal medicine resident at Johns Hopkins Hospital), Dr. Pablo Sanchez (cardiology fellow at Stanford University), and Dr. Michael Landzberg (cardiovascular and palliative care faculty and former director of ACHD at Brigham and Women’s Hospital). ​ Jeremy’s gofundme pageJeremy’s case discussion – episode 82Jeremy’s obituary page CardioNerds Case Reports PageCardioNerds Episode PageSubscribe to our newsletter- The HeartbeatSupport our educational mission by becoming a Patron! In Loving Memory of Jeremy Keck Jeremy Keck was a giant within the construction industry and accomplished so much in his 37 years of life. However, his greatest point of pride was his family. He is survived by his wife Ana, two young daughters, Emilee and Kaylee, his parents, Jeff and Terri Keck, brother Kevinn (Deana) Keck, nephews Jeremy and Payne, and nieces Taylore and Payge. Jeremy also had a heart for philanthropy. He was an active supporter of the Heart Center at Phoenix Children’s Hospital. In an interview with The Arizona Republic in 2015, Jeremy said he wouldn’t change his experience even if he had the chance. “I have a perspective on life that you can’t teach anybody,” he said. “You can’t even explain it to people. The small things that happen that might not go your way seem pretty minor.” Jeremy had such a positive impact on those around him, inspiring everyone to live life to the fullest. He will be deeply missed. Visit Jeremy’s gofundme page for more information. Music AcknowledgementsEternal Hope by Kevin MacLeod is licensed under a Creative Commons Attribution 4.0 license. https://creativecommons.org/licenses/by/4.0/ Source: http://incompetech.com/music/royalty-free/index.html?isrc=USUAN1100238. Artist: http://incompetech.com/

CardioNerds (Amit Goyal & Daniel Ambinder) join Stanford cardiology fellows (Pablo Sanchez, Natalie Tapaskar, Jimmy Tooley) for tacos while enjoying the sunshine on the Stanford Oval! They recount the story of a man with adult congenital heart disease (ACHD): L-TGA (levo-transposed great arteries) with double inlet LV post-Fontan complicated by VF arrest. Dr. Christiane Haeffele provides the E-CPR and program director Dr. Joshua Knowles provides a message for applicants. Episode notes were developed by Johns Hopkins internal medicine resident Evelyn Song with mentorship from University of Maryland cardiology fellow Karan Desai and Cleveland clinic cardiology fellow Josh Saef. Jump to: Patient summary – Case media – Case teaching – References The CardioNerds Cardiology Case Reports series shines light on the hidden curriculum of medical storytelling. We learn together while discussing fascinating cases in this fun, engaging, and educational format. Each episode ends with an “Expert CardioNerd Perspectives & Review” (E-CPR) for a nuanced teaching from a content expert. We truly believe that hearing about a patient is the singular theme that unifies everyone at every level, from the student to the professor emeritus. We are teaming up with the ACC FIT Section to use the #CNCR episodes to showcase CV education across the country in the era of virtual recruitment. As part of the recruitment series, each episode features fellows from a given program discussing and teaching about an interesting case as well as sharing what makes their hearts flutter about their fellowship training. The case discussion is followed by both an E-CPR segment and a message from the program director. CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademySubscribe to our newsletter- The HeartbeatSupport our educational mission by becoming a Patron!Cardiology Programs Twitter Group created by Dr. Nosheen Reza Patient Summary A man in his mid-30s with past medical history notable for L-TGA (levo-transposed great arteries) with double inlet LV s/p Fontan palliation was playing golf when he suddenly collapsed. EMS arrived after three minutes of bystander CPR. An AED indicated the patient had suffered a VF arrest. ROSC was achieved after 1 round of Epi and 1 shock delivered. He was intubated and started on targeted temperature management protocol. Home medications were  notable for digoxin 0.25mg daily, sotalol 120mg BID, and warfarin 5mg daily. Initial labs were notable for Na 127, K 5.4, Cr 1.0 (unknown baseline), INR 4.5, Lactate 4.6, Troponin-I 0.532, VBG 7.06/61, and random Digoxin level 2.7. EKG showed AV sequential pacing at a rate of 70 bpm. QTc prolonged at 571ms. No ischemic ST changes. Device interrogation showed sustained VT for 5 minutes prior to external shock. No internal shock was delivered. He was initially stabilized and his acidosis and hyperkalemia were corrected. Course was complicated by hemoptysis due to alveolar hemorrhagic and he was given concentrated prothrombin complex to reverse his coagulopathy. He eventually stabilized, and a formal TTE was obtained which showed a hypoplastic RV, single dilated LV with an akinetic posterior wall and hypokinetic lateral wall, all similar to his prior TTE in 2019. No obstruction noted at the IVC/Fontan anastomotic site. Coronary angiogram performed after his kidney function improved also did not show any significant obstructions or coronary anomalies. After multidisciplinary discussion, his VF arrest was attributed to a combination of prior ventricular fibrosis/scar, suspected digoxin toxicity, sotalol, dehydration, and renal failure. He had a subcutaneous ICD lead placed and was ultimately discharged home.  Case Media A B Click to Enlarge A. CXRB. ECG Episode Schematics & Teaching The CardioNerds 5! – 5 major takeaways from the #CNCR case What’s Transposition of the Great Arteries (TGA)?  TGA is defined by a nontraditional ventricle-arterial relationship so that the aorta arises from the morphological RV and the pulmonary artery (PA) arises from the morphological LV  There are two types of TGA, L or levo and D or dextro.  D (rightward)-TGA: Systemic venous return flows into RA -> RV -> delivered to systemic circulation via Aorta, bypassing the lungs. The pulmonary veins flow into the LA -> LV-> delivered to the pulmonary circulation via the PA. The result is two parallel systems that fail to deliver oxygenated blood to the systemic circulation. This is not compatible with life unless another defect such as ASD, VSD, or PDA is present (or created) to allow mixing of deoxygenated and oxygenated blood. Patients with D-TGA usually require arterial switch procedures within 1 month of life. A simplified way to understand this is to say that the great vessels are malpositioned, leaving patients

CardioNerds (Amit Goyal & Karan Desai) join Massachusetts General Hospital cardiology fellows (Daniel Pipilas, Rachel Frank and Kemar Brown) on a luxurious sailboat for iced coffees and Modern Pastry delicacies! They discuss a rare case of Anomalous Left Coronary Artery from the Pulmonary Artery (ALCAPA). Program director, Dr. Doreen DeFaria Yeh provides the E-CPR and a message for applicants.  Episode notes were developed by Johns Hopkins internal medicine resident Evelyn Song with mentorship from University of Maryland cardiology fellow Karan Desai.  Jump to: Patient summary – Case media – Case teaching – References Episode graphic by Dr. Carine Hamo CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademySubscribe to our newsletter- The HeartbeatSupport our educational mission by becoming a Patron!Cardiology Programs Twitter Group created by Dr. Nosheen Reza Patient Summary A women in her early 30s who’s a Jehovah’s witness presented with three days of intermittent chest pain. Past medical history included anxiety. Initial vitals and physical exam were unremarkable. Labs were notable for an elevated troponin T of 360 ng/L and a low TSH of 0.02 mIU/L with an elevated free T4 of 5.1 ng/dL. EKG demonstrated lateral and inferior ST depressions. TTE demonstrated a normal LVEF of 58% with a subtle anterolateral wall motion abnormality. Given her lack of conventional risk factors for CAD, resolution of her chest pain, and downtrending troponin, coronary CTA was obtained next which did not show any CAD but demonstrated an anomalous left main coronary artery (LMCA) arising from the main pulmonary artery with evidence of left to right shunting from the left main into the PA and extensive coronary and bronchial collateralization. The anterior wall hypokinesis was also seen on CT, consistent with ischemia due to myocardial steal phenomenon. Given the abnormal thyroid function tests, thyroid US was also obtained which showed patchy heterogeneity consistent with thyroiditis. Ultimately, the patient was diagnosed with ALCAPA and her chest pain was attributed to steal phenomenon due to hyperthyroidism and increased cardiac demand. She was treated with long-acting nitrates and beta-blocker with resolution of symptoms and was referred to cardiac surgery on discharge.   After a multidisciplinary discussion involving the cardiac surgery team, patient underwent ligation of LMCA with SVG bypass to LAD. One month after operation, she developed palpitations and chest pain during exertion and was taken to the hospital. Labs showed an elevated hs-troponin T of 711 ng/L and she was treated for type 1 NSTEMI with aspirin, heparin drip, and statin. Repeat TTE demonstrated normal LVEF and lack of WMA. LHC showed occlusion of SVG graft and possible thrombus in LAD near the site of graft anastomosis. RCA was large and patent, providing adequate collaterals to the left coronary system. Ultimately, PCI was deferred and medical management was pursued because she had adequate collaterals from right coronary system. She was treated with DAPT, beta-blocker, and atorvastatin and has been doing well since.   Case Media A B C D E F Click to Enlarge A. CXRB. ECG C. Follow up ECGD-F. Cardiac CT TTE 1 TTE 2 Angiography 1 Angiography 2 Angiography 3 Angiography 4 Angiography 5 Episode Schematics & Teaching The CardioNerds 5! – 5 major takeaways from the #CNCR case How are the coronary arteries formed during embryology and how are anomalous coronary arteries formed?   During embryology, according to one theory, the coronary ostia and artery formation begins with ingrowth of a capillary plexus into the aortic sinuses. This complex process heavily depends on the proliferation and migration of cells that originate outside the heart at the sinus venosus and then differentiate into endothelial cells, vascular smooth muscle cells, and fibroblasts. Proper migration of these cells to aorta, creating the coronary ostia, depend heavily on expression of growth factors like FGF-2, PDGF, and VEGF.   Anomalous origin of a coronary artery from the aorta or from the pulmonary artery have a common defect: the cells of the capillary plexus surrounding the aorta and pulmonary artery fail to reach and/or penetrate the normal sites of developing aorta. This can be caused by different mutations affecting the growth factor signaling pathways.     What is ALCAPA?  ALCAPA stands for anomalous left coronary artery (LCA) origin from the pulmonary artery. There’s also ARCAPA which is anomalous RCA origin from the pulmonary artery.   It occurs at an incidence of 1 in 300,000 live births or 0.25 to 0.5% of all congenital heart disease. It is difficulty to diagnose during infancy as it presents similarly to other more common pediatric

CardioNerds (Amit Goyal & Daniel Ambinder) join Brigham and Women’s Hospital cardiology fellows (Mounica Yanamandala, Simin Lee and Maria Pabon Porras) for some fun times at the Charles River Esplanade! They discuss a complicated case of prosthetic valve endocarditis with aortic regurgitation. Dr. Dale Adler provides the E-CPR and program director Dr. Donna Polk provides a message for applicants. Episode notes were developed by Johns Hopkins internal medicine resident Bibin Varghese with mentorship from University of Maryland cardiology fellow Karan Desai. Jump to: Patient summary – Case media – Case teaching – References Episode graphic by Dr. Carine Hamo The CardioNerds Cardiology Case Reports series shines light on the hidden curriculum of medical storytelling. We learn together while discussing fascinating cases in this fun, engaging, and educational format. Each episode ends with an “Expert CardioNerd Perspectives & Review” (E-CPR) for a nuanced teaching from a content expert. We truly believe that hearing about a patient is the singular theme that unifies everyone at every level, from the student to the professor emeritus. We are teaming up with the ACC FIT Section to use the #CNCR episodes to showcase CV education across the country in the era of virtual recruitment. As part of the recruitment series, each episode features fellows from a given program discussing and teaching about an interesting case as well as sharing what makes their hearts flutter about their fellowship training. The case discussion is followed by both an E-CPR segment and a message from the program director. CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademySubscribe to our newsletter- The HeartbeatSupport our educational mission by becoming a Patron!Cardiology Programs Twitter Group created by Dr. Nosheen Reza Patient Summary A male in his mid-40s with history of HIV on ART (undetectable VL, CD4 320) and idiopathic thoracic ascending aortic aneurysm (TAAA) with AR s/p bioprosthetic valve replacement 10 years prior presented with acute onset lightheadedness and pre-syncope. He was diagnosed with an idiopathic TAAA at age 30 after he was noted to have an incidental murmur. Over the next few years, his aortic root increased to over 7 cm with severe AR, LV dilation, and reduced LVEF of 45%. He underwent bioprosthetic aortic valve replacement and root repair with a Medtronic freestyle porcine aortic root with subsequent recovery of his  LVEF to 50% and improved LV dilation. Thereafter, he was doing well until he reported a flu like illness 3 weeks prior to presentation with reported fever up to 101.3 F and associated myalgias. He denied any sick contacts or recent travel and was adherent to his HIV regiment. On the day of presentation, he was walking his dogs when he developed acute onset lightheadedness with presyncope. On presentation, he had a low grade fever, tachycardia, tachypnea, and hypoxia. On exam, cardiac exam was notable for loud blowing diastolic murmur, non-distended JVP, decreased breath sounds, warm extremities with bounding pulses and without edema. There were no stigmata of endocarditis. Labs revealed elevated cardiac and inflammatory biomarkers. Blood cultures were initially NGTD. CXR corroborated the exam with bilateral interstitial and airspace opacification with effusions. TTE showed LVEF 35% with global hypokinesis, dilated LV with LVEDD 7.5 cm, mild RV systolic dysfunction, severe AR with holo-diastolic flow reversal in the abdominal aorta, no prosthetic stenosis, and aortic root 31 mm. TEE showed a well-seated AVR with leaflet thickening and several echodensities. CT surgery deemed patient to be high risk for the OR. After a few days, patient required intubation for increased work of breathing and acute decompensation requiring vasoactive infusions. After multidisciplinary discussions, the patient ultimately underwent ViV TAVR with successful placement of a 29 mm Edwards Sapien 3 valve. That day, he was weaned off pressors, and subsequently extubated. Infectious workup remained negative thereby resulting in a final diagnosis of prosthetic aortic valve culture-negative endocarditis vs sterile prosthetic valve deterioration. He was discharged on intravenous empiric antibiotics and was doing well in clinic 2 months later.   Case Media A B C D E F Click to Enlarge A. CXR: Bilateral airspace and interstitial opacification. Small bilateral effusions. No pneumothorax.B. ECG C. CW Doppler across the aortic valve D. PW Doppler showing holodiastolic flow reversal in the descending thoracic aorta E. Pre-TAVR LV and aortic pressure tracings F. Post-TAVR L

CardioNerds (Amit Goyal & Daniel Ambinder) join University of Washington cardiology fellows (Shannon McConnaughey, Betty Ashinne and Andrew Perry – host of the AP Cardiology podcast) for some tacos and beer at the water and discuss a puzzling case of recurrent troponin elevation. Dr. Kelly Branch provides the E-CPR and program director, Dr. Rosario Freeman, provides a message for applicants. Episode notes were developed by Johns Hopkins internal medicine resident Eunice Dugan with mentorship from University of Maryland cardiology fellow Karan Desai.    Jump to: Patient summary – Case media – Case teaching – References Episode graphic by Dr. Carine Hamo CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademySubscribe to our newsletter- The HeartbeatSupport our educational mission by becoming a Patron!Cardiology Programs Twitter Group created by Dr. Nosheen Reza Patient Summary A female is her late 50s with past medical history of alcohol use disorder and intravenous drug use complicated by hepatitis C presented with generalized weakness and was found to have lower extremity fractures. Cardiology was consulted for pre-operative management. When obtaining a cardiac history, she reported rare, intermittent, and non-anginal chest pain. She had no current chest pain or dyspnea. On chart review, she had multiple presentations over the past 3 years for various complaints – some were chest pain – during which she was found to have elevated troponin I values. Most of the elevations were in the 0.5 to 1 ng/mL range, but one time, her peak troponin was 32 ng/mL. At one of those presentations, she had a TTE that showed septal wall motion abnormalities. She underwent coronary angiography on two occasions, which both showed proximal and mid-LAD calcifications, but no significant stenosis and she was managed medically.   At the current presentation, her vitals were within normal limits and her exam did not show any cardiopulmonary abnormalities. Labs were notable for troponin I of 10 ng/mL but CK-MB was normal. Interestingly, alkaline phosphatase was 3 times the upper limit of normal, and rheumatoid factor was 1156 IU/mL compared to 70 previously (normal range 0-20 IU/mL). EKG was without ischemic changes. TTE showed no wall motion abnormalities, normal LVEF, and no significant valvular disease. Cardiac catherization was deferred, and the patient was not interested in cardiac MRI. Due to an incongruent troponin elevation with the clinical presentation, there was concern for interference with the troponin assay due to the elevated rheumatoid factor and alkaline phosphatase levels. Upon further investigation, dilution of the troponin yielded results lower than factor of dilution or undetectable results. Mayo testing of the sample showed troponin-T of 0.024 ng/mL (normal < 0.01 ng/mL), and troponin I of 0.02 ng/mL (normal < 0.04 ng/mL). Although there were still some aspects of her previous presentations including rising troponin pattern and previous wall motion abnormalities that are unexplained at this time, her troponin elevation at this presentation was attributed to assay interference.   Case Media A B C Click to Enlarge A. ECG from MayB. Coronary angiography form MayC. ECG August (same year) TTE 1 (May) TTE 2 (May) TEE 3 (May) TTE 4 (May) TTE 1 (August) TTE 2 (August) TTE 3 (August) TTE 4 (August) Episode Schematics & Teaching Coming soon! The CardioNerds 5! – 5 major takeaways from the #CNCR case What is the universal definition of myocardial infarction?   ·       As per the current 4th universal definition, myocardial infarction is defined as an elevation in cardiac troponin (cTn) above the 99th percentile in high sensitivity assays in the setting of acute myocardial ischemia. It is considered acute if there is a characteristic rise/fall pattern in cTn.   ·       A type 1 event is a spontaneous MI related to ischemia as a result of a primary coronary event (e.g., plaque erosion or rupture, dissection). The definition requires the above biomarker threshold with at least one of the following as evidence of ischemia: symptoms of MI, new ischemic EGG changes including development of pathological Q waves, new imaging evidence of loss of viable myocardium, or identification of thrombosis by intracoronary imaging.  Unstable angina (UA) occurs in patients with symptoms suggestive of acute myocardial infarction but without biomarker elevation.  ·       Criteria for type 2 MI includes the biomarker definition above with evidence of ischemia seconda

CardioNerds (Amit Goyal) join University of Mississippi Medical Center cardiology fellows (Catherine Lowe, Chris Latour and Adi Sabharwal) as they sit at the reservoir enjoying a great view of the water at the Pelican Cove Grill in Jackson, MS. They discuss and educational case of decompensated heart failure and shock in the setting of severe functional mitral regurgitation treated with MitraClip. Dr. Kellan Ashley provides the E-CPR and program director Dr. Trey Clark provides a message for applicants. Episode notes were developed by Johns Hopkins internal medicine resident Richard Ferraro with mentorship from University of Maryland cardiology fellow Karan Desai.   Jump to: Patient summary – Case media – Case teaching – References Episode graphic by Dr. Carine Hamo The CardioNerds Cardiology Case Reports series shines light on the hidden curriculum of medical storytelling. We learn together while discussing fascinating cases in this fun, engaging, and educational format. Each episode ends with an “Expert CardioNerd Perspectives & Review” (E-CPR) for a nuanced teaching from a content expert. We truly believe that hearing about a patient is the singular theme that unifies everyone at every level, from the student to the professor emeritus. We are teaming up with the ACC FIT Section to use the #CNCR episodes to showcase CV education across the country in the era of virtual recruitment. As part of the recruitment series, each episode features fellows from a given program discussing and teaching about an interesting case as well as sharing what makes their hearts flutter about their fellowship training. The case discussion is followed by both an E-CPR segment and a message from the program director. CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademySubscribe to our newsletter- The HeartbeatSupport our educational mission by becoming a Patron!Cardiology Programs Twitter Group created by Dr. Nosheen Reza Patient Summary A man his mid 70s with a history of non-ischemic heart failure status post CRT-D placement, A-Fib, and chronic kidney disease presented with progressive shortness of breath with limited exertion. The patient was found to have severe secondary mitral regurgitation. Listen to the episode now to learn about treatment options for severe mitral regurgitation in heart failure and specifically the evaluation for MitraClip! Case Media A B C D E Click to Enlarge A. Right atrial pressure B. Right ventricular pressureC. Pulmonary artery pressureD. Wedge pressureC. Pre and post MitraClip left atrial pressure Episode Teaching The CardioNerds 5! – 5 major takeaways from the #CNCR case 1. What is Comprehensive Disease Modifying Therapy in HFrEF? Comprehensive disease modifying therapy for heart failure with reduced ejection fraction (HFrEF) has become both more robust and better understood by practitioners inside and outside the cardiology community.  Comprehensive therapy is generally considered to consist of beta-blockade, mineralocorticoid receptor antagonist (MRA), sodium-glucose cotransporter-2 inhibitors (SGLT2i) and angiotensin receptor neprilysin inhibitor (ARNI), with ARNI being the preferred agent over angiotensin converting enzyme inhibitor (ACEi) or angiotensin II receptor blocker (ARB).  Despite a greater understanding of HFrEF therapy by the medical community, significant gaps remain with recent data showing few patients on concomitant beta blockade, MRA, SGLT2i and ACE/ARB/ARNI, and even fewer at target doses. Compared to ACE, BB, and MRA alone, comprehensive therapy with MRA, BB, SGLT2i and ARNI could add an additional 6 years for middle-aged patients. 2. What role does Mitral Valve Disease have in Heart Failure Exacerbations? For patients that remain symptomatic or with repeated hospitalizations for decompensated heart failure despite comprehensive therapy, it is important to look for additional pathology contributing to heart failure exacerbations.  Mitral valve disease is one such etiology, particular secondary mitral valve regurgitation (MR) which can be seen in heart failure due to changes in left ventricular anatomy.  Severe MR is associated with worsening left ventricular function and heart failure. For some time, however, it was an open question if functional MR was secondary to heart failure or an independent cause of heart failure exacerbations. Recent major trials suggest severe MR may act independently to worsen or lead to more frequent heart failure exacerbations. 3. How Do we Assess Mitral Valve Function in Heart Failure? MR is primarily quantified by echocardiography, which allows for close observation of regurgitant flow. Once a diagnosis of secondary MR has been established by evaluating mitral valve morphology and leaflet motion (e.g., Carpentier Classification), there are several parameters including objective quantification of MR hemod

CardioNerds (Amit Goyal & Daniel Ambinder) join Boston University cardiology fellows (Yuliya Mints, Anshul Srivastava, and Michel Ibrahim) for some hotdogs at Fenway Park in Boston, MA. They discuss an educational case of carcinoid heart disease with severe tricuspid regurgitation. Program director, Dr. Omar Siddiqi provides the E-CPR and APD Dr. Katy Bockstall provides a message for applicants. Episode notes were developed by Johns Hopkins internal medicine resident Bibin Varghese with mentorship from University of Maryland cardiology fellow Karan Desai.    Jump to: Patient summary – Case media – Case teaching – References Episode graphic by Dr. Carine Hamo The CardioNerds Cardiology Case Reports series shines light on the hidden curriculum of medical storytelling. We learn together while discussing fascinating cases in this fun, engaging, and educational format. Each episode ends with an “Expert CardioNerd Perspectives & Review” (E-CPR) for a nuanced teaching from a content expert. We truly believe that hearing about a patient is the singular theme that unifies everyone at every level, from the student to the professor emeritus. We are teaming up with the ACC FIT Section to use the #CNCR episodes to showcase CV education across the country in the era of virtual recruitment. As part of the recruitment series, each episode features fellows from a given program discussing and teaching about an interesting case as well as sharing what makes their hearts flutter about their fellowship training. The case discussion is followed by both an E-CPR segment and a message from the program director. CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademySubscribe to our newsletter- The HeartbeatSupport our educational mission by becoming a Patron!Cardiology Programs Twitter Group created by Dr. Nosheen Reza Patient Summary A woman in her mid 60s with history of neuroendocrine tumor (NET) presented to the cardio-oncology clinic with chronic progressive SOB and fatigue. She was diagnosed with NET after presenting with a small bowel obstruction (SBO) several years prior. At the time, she was found to have liver and pulmonary metastasis with MR enterography showing thickening of the terminal ileum. Ileocecetomy and biopsy of the liver lesions confirmed metastatic NET. Despite treatment with octreotide and everolimus, follow up CT showed progression of liver lesions and she was eventually started on telotristat and enrolled in a clinical trial. On presentation, she was not tachycardiac, hypotensive or requiring oxygen supplementation (KD: Correct?). On exam, she demonstrated elevated JVP with a positive hepato-jugular reflex and a 3/6 holosytolic murmur loudest at the LLSB that increased with inspiration. Lab work revealed urinary 5-HIAA was 212 (nl < 6mg/24 hours). TTE showed moderately dilated RV and severely dilated RA. Furthermore, there was a thickened, calcified and retracted TV with severe TR which was consistent with carcinoid heart disease. She was treated with diuretics and was continued on systemic therapies to help achieve control of her NET before surgical intervention for her valvular disease was considered. Case Media A B Click to Enlarge A. ECGB. TTE: CW Doppler through tricuspid valve Carcinoid – TTE 1 Carcinoid – TTE 2 Carcinoid – TTE 3 Carcinoid – TTE 4 Carcinoid – TTE 5 Carcinoid – TTE 6 Carcinoid – TTE 7 Carcinoid – TTE 8 Carcinoid – TTE 9 Episode Schematics & Teaching The CardioNerds 5! – 5 major takeaways from the #CNCR case The patient had an NET history and presented with shortness of breath. Under what circumstances do patients with NETs present with cardiac symptoms?  Amongst patients with neuroendocrine tumors (NETs), carcinoid tumors refer classically to gastrointestinal NETs. Around 30 to 40% of these patients will presents with features of carcinoid syndrome, including vasomotor symptoms (e.g., flushing), diarrhea, and bronchospasm. The majority of patients with carcinoid syndrome have metastases to the liver and the vasoactive substances (e.g., 5-hydroxytryptamine [5-HT]) reach the systemic circulation via the hepatic vein bypassing degradation in the liver.   Similarly, cardiac involvement occurs after metastasis to the liver and exposure of the heart to vasoactive substances. Generally, symptoms are limited to the right heart as the lungs clear carcinoid-related substances. Left-sided involvement may occur, however, in a patient with carcinoid heart disease and an intracardiac right to left shunt is present.   In addition to the symptoms of carcinoid syndrome, patients with carcinoid heart disease including severe dyspnea, fatigue, and signs and symptoms of right heart failure (e.g., ascites, peripheral edema).    The patient was

CardioNerds (Amit Goyal & Daniel Ambinder) join Cleveland Clinic cardiology fellows (Ben Alencherry, Erika Hutt, Zach Il’Giovine, Kara Denby) for some delicious craft beer at Platform Brewery! They discuss a challenging case of Ehlers Danlos Syndrome with Papillary Muscle Rupture. Dr. Vidyasagar Kalahasti provides the E-CPR and program director Dr. Venu Menon provides a message for applicants. Episode notes were developed by Johns Hopkins internal medicine resident, Eunice Dugan, with mentorship from University of Maryland cardiology fellow Karan Desai.   This case has been published in JACC Case Reports: CardioNerds Corner! Jump to: Patient summary – Case media – Case teaching – References Episode graphic by Dr. Carine Hamo CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademySubscribe to our newsletter- The HeartbeatSupport our educational mission by becoming a Patron!Cardiology Programs Twitter Group created by Dr. Nosheen Reza Patient Summary A pregnant woman at 29 weeks gestation presents with postpartum pulmonary edema, found to have papillary muscle rupture, is ultimately diagnosed with vascular Ehlers Danlos Syndrome. For a detailed course, enjoy the JACC case report. Case Media Visit the JACC Case Reports: CardioNerds Corner to review the case media! Episode Schematics & Teaching Coming soon! The CardioNerds 5! – 5 major takeaways from the #CNCR case What is Ehlers-Danlos Syndrome?   Ehlers-Danlos Syndrome (EDS) is a clinically and genetically heterogenous group of heritable connective tissue disorders due to altered collagen metabolism. The inheritance pattern is variable, but is mostly autosomal dominant, with a range of mechanisms including deficiency of collagen-processing enzymes, mutant collagen chains, and haploinsufficiency.    Although the syndrome has varying and overlapping clinical manifestations based on subtype (per the 2017 International ED Consortium there are 17 subtypes) it is largely characterized by hyperextensibility of the skin, hypermobility of joints, atrophic scarring, and tissue fragility. The cardiovascular system is involved in the vascular and cardio-valvular subtypes.  The incidence is estimated to be 1 in 2500 to 5000, however this is likely an underestimation since mild presentations may not be clinically diagnosed nor sent for genetic testing.    The differential diagnosis for suspected EDS includes osteogenesis imperfecta, Marfan syndrome, and Loeys-Dietz syndrome. Those with joint symptoms may be incorrectly diagnosed with fibromyalgia, chronic fatigue syndrome etc.    What is vascular EDS?   There are many subtypes of EDS. Type IV or vascular EDS (vEDS) is an autosomal dominant disorder that affects Type III procollagen protein synthesis. The incidence is rare – 1 in 50,000 to 250,000 people and is ~5% of all EDS cases.    It is commonly caused by a defect in the COL3A1 gene, most of which are single base substitutions, but more than 700 different mutations have been identified. Missense mutations at the C-terminal end of the molecule results in a more severe form of the disease.  Feared vascular manifestations include arterial dissection, rupture, and aneurysm formation. Death is most frequently secondary to complications from arterial dissection or hollow organ rupture. 70% of patients experience a first major event by age 20. Note, surgical repair of a ruptured aneurysm or dissection can be complicated by poor wound healing or hemorrhage because tissue in Ehlers-Danlos is friable.  In this subtype, the usual manifestations of joint hypermobility and skin hyperextensibility may not be as apparent.  The vascular type has the worst prognosis with median expectancy between 40-50 years of age.   How is vEDS diagnosed?   Vascular EDS should be considered in anyone with unexplained arterial or hollow viscus rupture, commonly the sigmoid colon, especially at a young age.  Diagnosis is confirmed by either finding of structurally abnormal type III procollagen in a culture of dermal fibroblasts or COL3A1 gene mutation. Clinical criteria can aid in the decision to pursue testing.    Molecular testing is recommended when meeting one or more major clinical criteria or several minor criteria. Major criteria include family history of vEDS, unexplained arterial rupture at young age, spontaneous intestinal  perforation (in absence of risk factors), uterine rupture during pregnancy and labor, or carotid-cavernous sinus fistula formation.    Some minor criteria include bruising without trauma (especially in unusual locations), spontaneous pneumothorax, tendon/muscle rupture, gingival recession, early onset varicose veins, and characteristic facial appearance amongst other criteria. Characteristic fac

CardioNerds (Amit Goyal & Daniel Ambinder) join UCSF cardiology fellows (Emily Cedarbaum, Matt Durstenfeld, and Ben Kelemen) for some fun in San Francisco! They discuss a informative case of ST-segment elevation (STEMI) due to coronary vasospasm. Dr. Binh An Phan provides the E-CPR and program director Dr. Atif Qasim provides a message for applicants. Episode notes were developed by Johns Hopkins internal medicine resident Evelyn Song with mentorship from University of Maryland cardiology fellow Karan Desai. Jump to: Patient summary – Case media – Case teaching – References Episode graphic by Dr. Carine Hamo The CardioNerds Cardiology Case Reports series shines light on the hidden curriculum of medical storytelling. We learn together while discussing fascinating cases in this fun, engaging, and educational format. Each episode ends with an “Expert CardioNerd Perspectives & Review” (E-CPR) for a nuanced teaching from a content expert. We truly believe that hearing about a patient is the singular theme that unifies everyone at every level, from the student to the professor emeritus. We are teaming up with the ACC FIT Section to use the #CNCR episodes to showcase CV education across the country in the era of virtual recruitment. As part of the recruitment series, each episode features fellows from a given program discussing and teaching about an interesting case as well as sharing what makes their hearts flutter about their fellowship training. The case discussion is followed by both an E-CPR segment and a message from the program director. CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademySubscribe to our newsletter- The HeartbeatSupport our educational mission by becoming a Patron!Cardiology Programs Twitter Group created by Dr. Nosheen Reza Patient Summary A man in his mid-50s with alcohol use disorder, cirrhosis, atrial fibrillation, and alpha thalassemia complicated by iron overload presented with hematemesis. He was tachycardic and hypotensive. Labs were notable for Hgb 8.1 (baseline of 10.2), INR 1.3, lactate 4.2, and ferritin 4660. He was started on IV PPI and octreotide. Course was complicated initially by Afib with RVR with hypotension. Subsequently, the patient developed unstable VT requiring CPR. Post-code EKG showed inferolateral ST elevations. Troponin-I rose from 19 to 225 and his pressor requirement continued to increase despite resolution of his GIB. TTE showed LVEF 42% with new inferolateral wall motion abnormalities, normal RV systolic function, severe mitral regurgitation, and small pericardial effusion. After treatment of his GIB by IR and GI, he underwent an urgent LHC which showed 30% stenosis in proximal LAD, 70% in LADD2, and 95% in distal RCA. Coronary spasm was noted in all vessels. Intracoronary nitroglycerin and nicardipine were administered with significant improvement in spasm and resolution of STE on EKG. Vasopressors were quickly weaned off after. He was eventually stabilized, extubated, and started on an oral nitrate and calcium channel blocker. Repeat TTE showed normalized systolic function without any wall motion abnormalities.   Case Media A B Click to Enlarge A. Baseline ECG – atrial fibrillationB. ECG with inferior STEMI CORS – left system CORS- RCA pre-vasodilator CORS- RCA post-vasodilator Episode Schematics & Teaching The CardioNerds 5! – 5 major takeaways from the #CNCR case What are the cardiac manifestations of hemochromatosis?  Cardiac hemochromatosis encompasses cardiac dysfunction from either primary or secondary hemochromatosis. Initially, hemochromatosis leads to diastolic dysfunction and arrhythmias. In later stages, it can lead to dilated cardiomyopathy.   Diagnosis of iron overload is established by elevated transferrin saturation (>55%) and elevated serum ferritin (>300 ng/mL). Genetic testing for mutations in the HFE gene should be pursued.  Cardiac MRI with measurement of T2* relaxation times is the diagnostic test of choice as it can both detect and quantify myocardial iron overload. The iron content in the myocardial tissue is inversely proportional to the time constant of decay for relaxation time. Thus the higher the iron content, the shorter T2* relaxation time.   What are the causes of ST-segment elevation on EKG besides acute plaque rupture or vasospasm?  Pericarditis: in acute pericarditis, ST elevation can be seen diffusely in all leads, with PR segment depression (except lead aVR +/- V1). The diffuse ST elevations are due to involvement of subepicardial layer of the ventricular wall. The PR depressions are due to involvement of the subepicardial layer of the atrial wall.   Stress CM: The ECG findings of stress cardiomyopathy may be indistinguishable from STEMI secondary to acute plaque rupture.&#16

CardioNerds (Amit Goyal & Daniel Ambinder) join Summa Health cardiology fellows (Jack Hornick, Phoo Pwint Nandar, and Sideris Facaros) for a hike on the Towpath Trail at Cuyahoga Valley National Park in Akron, Ohio! They discuss an informative case of Arrhythmogenic Right Ventricular Cardiomyopathy (ARVC) complicated by ventricular tachycardia & cardiogenic shock. Dr. Kenneth Varian provides the E-CPR and program director, Dr. Marc Penn provides a message for applicants. Episode notes were developed by Johns Hopkins internal medicine resident, Eunice Dugan, with mentorship from University of Maryland cardiology fellow Karan Desai.   Jump to: Patient summary – Case media – Case teaching – References Episode graphic by Dr. Carine Hamo CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademySubscribe to our newsletter- The HeartbeatSupport our educational mission by becoming a Patron!Cardiology Programs Twitter Group created by Dr. Nosheen Reza Patient Summary A female in her 40s with no past medical history presented 6 years prior with acute onset dizziness, palpitations and fatigue without chest pain. She had no family history of arrythmias, SCD, or prior syncope. Her heart rate was 170 bpm and EKG showed wide complex, regular tachycardia felt to be VT. She underwent synchronized cardioversion to sinus rhythm. Her baseline EKG showed sinus bradycardia with low voltage, incomplete RBBB, and ventricular ectopy. Labs were unrevealing, and social history was negative for toxic insults or illicit substance abuse. TTE showed preserved LVEF and normal valves, but RV was dilated with decreased systolic function. LHC was without obstructive coronary disease. She was diagnosed with ARVC and received an ICD for secondary prevention. She was discharged on sotalol for arrythmia management. Her genetic testing later returned positive for uncertain significance in the DSP gene and JUP gene, both commonly implicated in ARVC. She was followed in the outpatient setting for 5 years with no apparent shocks. Six years later, she presented with acute onset dizziness and palpitations similar to her initial presentation. EKG showed a wide complex tachycardia at 170 bpm treated with amiodarone and cardioversion. On ICD interrogation, she was found to have had several episodes of VT, but at a rates below the VT detection zone programmed in the ICD. Subsequent RHC showed significantly depressed cardiac index and RV dysfunction. She underwent successful inpatient VT ablation. She was then discharged home with plans for close follow up; however, 2 days later, she started feeling nauseous with fatigue and abdominal pain. She was sent straight to the nearest transplant-capable hospital where she was found to be in cardiogenic shock. She was admitted to ICU and started on inotropes. Due to refractory shock, she was cannulated for VA ECMO and successfully underwent cardiac transplantation two days later.   Case Media 1 2 3 Click to Enlarge A. Post cardioversion ECG: NSR, low voltage, incomplete RBBB, PVCB. TTE: RV enlargement C. TTE: Tissue Doppler velocity (S’) low TEE Episode Schematics & Teaching The CardioNerds 5! – 5 major takeaways from the #CNCR case What is ARVC?  Arrhythmogenic Right Ventricular Cardiomyopathy/Dysplasia (ARVC/D) is a heritable cardiac muscle disorder that classically involves the RV (though LV involvement is increasingly being recognized) marked by loss of healthy myocardium and replacement with fibrofatty tissue predominantly due to genetic defects in both desmosomal and non-desmosomal proteins. Clinical manifestations include RV dysfunction, ventricular arrhythmias, and sudden cardiac death (SCD).  This is a progressive disease that can affect the epicardium and/or mid-myocardium first and then move towards the sub-endocardium.   It affects approximately 1 in 5000 individuals and is an important cause of (SCD) in young patients. 50% of patients have a positive family history and it is thought to be inherit in an autosomal dominant fashion, however prevalence is underestimated due to incomplete penetrance. Interestingly, males are more affected than females possibly due to interaction of sex hormones with pathophysiology or historically different levels of participation in competitive sports among men and women.  The differential for ARVC should include Uhl’s anomaly, myocarditis, sarcoidosis, and Brugada syndrome among other considerations.  What genes are implicated and what is the pathophysiology?  While 20-30% of ARVC is due to non-desmosomal gene variants (e.g., desmin, Titin) and non-genetic causes, 40-50% is due to autosomal dominant gene mutations that encode desmosomal proteins. Thes

CardioNerds (Amit Goyal & Daniel Ambinder) join Scripps cardiology fellows (Christine Shen and Andrew Cheng) for some Cardiology and California Burritos in San Diego! They discuss an informative case of Wet Beriberi and Stiff Left Atrial Syndrome. Dr. Thomas Heywood provides the E-CPR and program director Dr. Malhar Patel provides a message for applicants. Episode notes were developed by Johns Hopkins internal medicine resident Tommy Das with mentorship from University of Maryland cardiology fellow Karan Desai. Jump to: Patient summary – Case media – Case teaching – References Episode graphic by Dr. Carine Hamo The CardioNerds Cardiology Case Reports series shines light on the hidden curriculum of medical storytelling. We learn together while discussing fascinating cases in this fun, engaging, and educational format. Each episode ends with an “Expert CardioNerd Perspectives & Review” (E-CPR) for a nuanced teaching from a content expert. We truly believe that hearing about a patient is the singular theme that unifies everyone at every level, from the student to the professor emeritus. We are teaming up with the ACC FIT Section to use the #CNCR episodes to showcase CV education across the country in the era of virtual recruitment. As part of the recruitment series, each episode features fellows from a given program discussing and teaching about an interesting case as well as sharing what makes their hearts flutter about their fellowship training. The case discussion is followed by both an E-CPR segment and a message from the program director. CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademySubscribe to our newsletter- The HeartbeatSupport our educational mission by becoming a Patron!Cardiology Programs Twitter Group created by Dr. Nosheen Reza Patient Summary A woman in her mid-60s with history of rheumatic mitral stenosis s/p mechanical mitral valve replacement, HFpEF, and paroxysmal atrial fibrillation s/p ablation presents with subacute worsening dyspnea despite escalating diuretic doses. TTE shows an EF of 62%, normal gradients across the mitral valve without mitral regurgitation, and a dilated IVC. She is admitted with a presumed diagnosis of decompensated heart failure, and started given IV furosemide. Her symptoms slightly improve though do not resolve, and her creatinine increases from 1.4 to 2.1.   In light of the unclear hemodynamic picture, a RHC is done, showing a RA pressure 9, RV pressure of 80/10, PAP 70/25 with mPAP 40, PCWP 30, SVR 872, CO 11 (by thermodilution), and CI 5.2. Notably, large V waves are noted on the RHC. Given concern for mitral regurgitation in the setting of large V waves, a TEE was pursued, which confirmed the lack of MR seen on TTE. Thus, her large V waves were felt to be due to stiff left atrial syndrome, and a cardiac CT showed a severely calcified “coconut left atrium”. Labwork revealed a profoundly low thiamine level (21, with LLN of 70), raising concern for wet beri beri syndrome.   The patient’s unifying diagnosis was indolent left atrial syndrome that was exacerbated by high outout heart failure due to Wet Beri Beri syndrome. The patient received thiamine supplementation, and was diuresed to euvolemia with dramatic improvement in symptoms. A repeat RHC after thiamine replacement showed a CO of 5.7 and CI of 2.74 by thermodilution, demonstrating resolution of her high output heart failure.   Case Media A B C D E F Click to Enlarge A. CXRB. ECGC. RHC: large V waves are noted on the RHCD. CO 11 and CI 5.2 by thermodilution pre-treatment E. Cardiac CT showed a severely calcified “coconut left atrium”F. Repeat CO of 5.7 and CI of 2.74 by thermodilution after thiamine replacement TTE 1 TTE 2 TEE 1 – Mitral Valve TEE 2 – Mitral Valve Cardiac CT Episode Schematics & Teaching Click to enlarge! The CardioNerds 5! – 5 major takeaways from the #CNCR case 1) This case featured a patient with Stiff Left Atrial Syndrome! Cardionerds, what the heck is that?   Stiff Left Atrial Syndrome (SLAS) is fundamentally a disorder of atrial compliance, wherein a non-compliant left atrium (LA) leads to abnormal atrial diastole. During LV systole (atrial diastole), the LA receives blood from the low-resistance pulmonary veins. Under normal conditions, the LA pressures initially fall (x-descent). Then, as the atrium fills from both RV contraction and passive filling from the pulmonary veins, there is a steady and modest rise in LA pressure (v-wave). In patients with decreased LA compliance, the V-wave may be accentuated.   In SLAS, left atrial compliance is significantly decreased, leading to very large v-waves that reflect the inability to accommodate LA filling and the steepened slope of the pressure-volume c

CardioNerds (Amit Goyal & Karan Desai) join University Hospitals Cleveland Medical Center cardiology fellows (Tarek Chami, Jamal Hajjari, and Haytham Mously) for some amazing pizza and coffee in Cleveland, Ohio! They discuss an important case of effusive constrictive pericarditis. Dr. Brian Hoit provides the E-CPR and assistant program director Dr. Claire Sullivan provides a message for applicants. We are grateful to chief fellow Scott Janus for his leadership in planning this episode! Episode notes were developed by Johns Hopkins internal medicine resident Colin Blumenthal with mentorship from University of Maryland cardiology fellow Karan Desai. Jump to: Patient summary – Case media – Case teaching – References Episode graphic by Dr. Carine Hamo The CardioNerds Cardiology Case Reports series shines light on the hidden curriculum of medical storytelling. We learn together while discussing fascinating cases in this fun, engaging, and educational format. Each episode ends with an “Expert CardioNerd Perspectives & Review” (E-CPR) for a nuanced teaching from a content expert. We truly believe that hearing about a patient is the singular theme that unifies everyone at every level, from the student to the professor emeritus. We are teaming up with the ACC FIT Section to use the #CNCR episodes to showcase CV education across the country in the era of virtual recruitment. As part of the recruitment series, each episode features fellows from a given program discussing and teaching about an interesting case as well as sharing what makes their hearts flutter about their fellowship training. The case discussion is followed by both an E-CPR segment and a message from the program director. CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademySubscribe to our newsletter- The HeartbeatSupport our educational mission by becoming a Patron!Cardiology Programs Twitter Group created by Dr. Nosheen Reza Patient Summary A woman in her mid-70s presented to clinic with subacute onset shortness of breath. Her past medical history includes metastatic breast cancer s/p mastectomy, chemo/radiation, and hormonal therapy. Exam notable for tachycardia without hypoxia, muffled heart sounds, JVD with Kussmaul’s sign, and 1+ LE edema. The patient was sent to the ED for evaluation of possible pericardial effusion. CTA chest in ED did not demonstrate a PE, but did show bilateral pleural effusions, and a moderate pericardial effusion with evidence of metastatic disease extending into the mediastinum. TTE obtained showing normal LVEF, moderate pericardial effusion with thickened pericardium, and significant respirophasic tricuspid and mitral inflow variations. Pulsus paradoxus was manually checked and found to be 16 mmHg.  Due to concern for cardiac tamponade, she was taken to the cath lab for a RHC and pericardiocentesis. RHC prior to pericardiocentesis showed elevated left and ride sided filling pressures, blunted y decent in the RA, and equalization of diastolic pressures. Pericardiocentesis yielded 200 cc of bloody fluid with improvement, but continued elevation, in her L and R sided pressures. Blunted y decent did give way to a now rapid y descent concerning for constrictive pericarditis. She then underwent a cardiac MRI showing respirophasic septal motion suggestive of interventricular dependence and >1 cm thick pericardium with LGE c/w inflammation. Unfortunately, cytology of pericardial fluid was c/w a malignant effusion and despite treatment with a few months of anti-inflammatory therapy her symptoms did not improve. She then underwent a pericardial stripping with subsequent resolution of her symptoms. As her symptoms and hemodynamics were related to both the effusion and constriction, she was ultimately diagnosed with effusive constrictive pericarditis.  Case Media A B C D E F G H I J K L M N O Click to Enlarge A. ECGB. CXRC-F. TTE (inflow velocities (mitral and tricuspid), IVC sniff test G-L: Right heart catheterization tracings M-N: Post pericardiocentesis TTE: Tissue Doppler O: Cardiac MRI CT Scan TEE – 1 TTE – 2 TTE – 3 TTE -4 CMR -1 CMR – 2 Episode Schematics & Teaching Click to enlarge! The CardioNerds 5! – 5 major takeaways from the #CNCR case What is cardiac tamponade, what causes it, and how does it lead to hypotension?  The pericardial cavity typically holds 50 cc of fluid, which acts as a lubricant for the beating heart. Accumulation of additional fluid in this space can increase intrapericardial pressure and cause compression of the cardiac chambers. Rapid accumulation of small amounts of fluid can lead to tamponade as the pericardium will not have time to expand. In instances of a slow accumulation, large volumes might accumulate before tamponade occurs as the pericardium will expand to accommodate

CardioNerds (Amit Goyal & Daniel Ambinder) join University of Michigan cardiology fellows (Apu Chakrabarti, Jessica Guidi, and Amrish Deshmukh) for some craft brews in Ann Arbor! They discuss a challenging case of Ventricular Septal Rupture after acute MI. Dr. Kim Eagle, editor of ACC.org & host of Eagle’s Eye View Podcast, and Dr. Devraj Sukul provide the E-CPR and message for applicants. Episode notes were developed by Johns Hopkins internal medicine resident, Eunice Dugan, with mentorship from University of Maryland cardiology fellow Karan Desai.   Jump to: Patient summary – Case media – Case teaching – References Episode graphic by Dr. Carine Hamo The CardioNerds Cardiology Case Reports series shines light on the hidden curriculum of medical storytelling. We learn together while discussing fascinating cases in this fun, engaging, and educational format. Each episode ends with an “Expert CardioNerd Perspectives & Review” (E-CPR) for a nuanced teaching from a content expert. We truly believe that hearing about a patient is the singular theme that unifies everyone at every level, from the student to the professor emeritus. We are teaming up with the ACC FIT Section to use the #CNCR episodes to showcase CV education across the country in the era of virtual recruitment. As part of the recruitment series, each episode features fellows from a given program discussing and teaching about an interesting case as well as sharing what makes their hearts flutter about their fellowship training. The case discussion is followed by both an E-CPR segment and a message from the program director. CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademySubscribe to our newsletter- The HeartbeatSupport our educational mission by becoming a Patron!Cardiology Programs Twitter Group created by Dr. Nosheen Reza Patient Summary A male in his 60s with medical history of obesity and GERD presents with five days of progressive chest pressure radiating to bilateral arms and associated with dyspnea on exertion. Due to worsening chest pain with new lightheadedness, he decided to come to the ED. His presentation to the hospital was delayed due to fear of contracting COVID-19. In the ED, patient was afebrile, blood pressure 96/56, HR 137, RR 22, and oxygen saturation 94% on room air. On exam, he was ill appearing, acutely distressed, and altered. He had a 3/6 mid systolic murmur loudest at L sternal border, JVP to 10 cm H2O and had crackles up to mid-lung fields. His extremities were cool to touch. Labs notable for Cr 1.5, High-Sensitivity Troponin-T up to 5756, and lactate 3.9. EKG showed incomplete RBBB, PVCs, and ST elevations in the inferior leads with depressions in lateral and precordial leads. Coronary Angiography showed mid-RCA occlusion with faint L to right collaterals. He underwent PCI with restoration of TIMI 3 flow. After PCI, he continued to be hypotensive requiring IABP and norepinephrine. PA catheter demonstrated (in mmHg): RA 26, RV 63/29 (31), 55/36 (44), PCWP 29, and CO 5 L/min, CI 2.2, and SVR 467. Shunt run of mixed venous O2 saturation showed: SVC 71%, RA 72%, RV 62%, PA 85% with oxygen step up in the R-sided circuit. Left ventriculogram then confirmed septal rupture with contrast extravasation from LV into RV. Due to worsening shock, he was stabilized on VA ECMO which was complicated by hemolysis and acute renal failure requiring CVVHD. On day 7 after presentation, he underwent surgery which revealed a large 6×6 cm ventricular septal defect on the posterior aspect of the septum and repaired with a large bovine pericardial path. He was eventually discharged after a prolonged stay and repeat TTE on follow up showed biventricular dysfunction and residual 1cm VSD.   Case Media A B C D Click to Enlarge A. ECG: Incomplete RBBB, PVCs, and ST elevations in the inferior leads with depressions in lateral and precordial leads. B. Coronary angiography: mid-RCA occlusion with faint L to right collaterals.C-D. A large (6x6cm) VSD was found at the posterobasal aspect of the septum.  Infarcted tissues were removed and a large bovine pericardial patch was used to repair the defect (due to the size of the defect, there was very little viable septum remaining and the patch had to be sewn directly into the LV and RV walls). LV gram performed showing a left to right shunt. TEE -1 TEE – 2 Episode Schematics & Teaching Click to enlarge! The CardioNerds 5! – 5 major takeaways from the #CNCR case Classification and Management of Post-AMI VSR  Why and in whom should we worry about VSR?  Ventricular Septal Rupture or VSR is rare in the era of early reperfusion strategies. Historical incidence of VSR after AMI was thought to be 1-2% and has decreased to between

CardioNerds (Amit Goyal & Daniel Ambinder) join University of Connecticut (UCONN) cardiology fellows (Mansour Almnajam, Justice Oranefo, Yasir Adeel, and Srinivas Nadadur) as they enjoy the amazing view from the Heublein tower! They discuss a challenging case of left ventricular free wall rupture & pseudoaneurysm as a complication of a STEMI. Dr. Peter Robinson provides the E-CPR and program director Dr. Joyce Meng provides a message for applicants. Episode notes were developed by Johns Hopkins internal medicine resident Bibin Varghese with mentorship from University of Maryland cardiology fellow Karan Desai.    Jump to: Patient summary – Case media – Case teaching – References Episode graphic by Dr. Carine Hamo The CardioNerds Cardiology Case Reports series shines light on the hidden curriculum of medical storytelling. We learn together while discussing fascinating cases in this fun, engaging, and educational format. Each episode ends with an “Expert CardioNerd Perspectives & Review” (E-CPR) for a nuanced teaching from a content expert. We truly believe that hearing about a patient is the singular theme that unifies everyone at every level, from the student to the professor emeritus. We are teaming up with the ACC FIT Section to use the #CNCR episodes to showcase CV education across the country in the era of virtual recruitment. As part of the recruitment series, each episode features fellows from a given program discussing and teaching about an interesting case as well as sharing what makes their hearts flutter about their fellowship training. The case discussion is followed by both an E-CPR segment and a message from the program director. CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademySubscribe to our newsletter- The HeartbeatSupport our educational mission by becoming a Patron!Cardiology Programs Twitter Group created by Dr. Nosheen Reza Patient Summary A man in his mid 50s with no significant PMH presented with a 10-day history of chest pain that progressed to acute pleuritic pain and shortness of breath in the past 24 hours. On arrival, he was hypothermic, in rapid atrial fibrillation with HR in the 130-150s, and an initial BP was not able to be obtained. He was tachypneic with labored breathing, lethargic, and cyanotic. Exam revealed markedly elevated JVP, cool extremities, and diminished breath sounds with bibasilar rales. Labs demonstrated leukocytosis, significantly elevated liver enzymes, troponin-I at 10.91, elevated NT-proBNP, and lactate at 6. ECG demonstrated tall, broad R-waves in V1-V4 with downsloping STD and upright T-waves concerning for a posterior infarct. He was immediately intubated, cardioverted into NSR, and started on vasopressors. Bedside echocardiogram demonstrated diffuse LV hypokinesis with akinesis of the inferolateral wall, LVEF 25-30%, and pericardial fluid with hyperechoic material adherent to the inferior wall as well as tamponade physiology. Chest CTA was negative for aortic dissection and confirmed hemopericardium. He was taken to the OR where he underwent a subxiphoid pericardial window. They found significant clot burden (both old and new), but no frank rupture. Adherent clot was not removed to prevent further hemodynamic compromise. Intraoperative TEE additionally demonstrated severe eccentric MR with partial posteromedial papillary muscle rupture. An IABP was placed and inotropic and vasoactive support was continued to temporize pending definitive therapy and the patient improved hemodynamically. Repeat TTE prior to surgery demonstrated a large apical and inferolateral pseudoaneurysm. Coronary angiogram revealed proximal occlusion of the LCx and diffuse three vessel coronary disease otherwise. He ultimately underwent CABG, mechanical mitral valve replacement, and pericardial patch repair of the ventricular pseudoaneurysm. Final diagnosis: Free Wall Rupture & Pseudoaneurysm. Thankfully, the patient ultimately made a complete recovery!   Case Media A B C D E F Click to Enlarge A. ECG: tall, broad R-waves in V1-V4 with downsloping STD and upright T-wavesB. CXRC. CT angiogram thoracic aorta: Moderate sized hemopericardium with tamponade physiology. Transmural infarction of LV base to mid inferior wall. Circumflex occlusion just beyond the first obtuse marginal. Normal aorta without dissection or aneurysm.D-F. Coronary angiogram: LCx is occluded proximally, distal vessel fills via faint collaterals from the right, OM1: Fills via right to left collaterals. LAD: 70%, mid; 90%, apical, 1st diagonal: 50%, ostial; 60-70%, proximal; 90% of inferior subdivision, bifurcating vessel. RCA: (Dominant); 50%, mid: 40%, distal. PDA: 60%,

CardioNerds (Amit Goyal & Daniel Ambinder) join University of California San Diego (UCSD) cardiology fellows (Harpreet Bhatia, Dan Mangels, and Quan Bui) for a relaxing beach bonfire in the beautiful city of San Diego! They discuss a challenging case of post-transplant cardiac allograft vasculopathy. Dr. Hao (Howie) Tran provides the E-CPR and program director Dr. Daniel Blanchard provides a message for applicants. Episode notes were developed by Johns Hopkins internal medicine resident Richard Ferraro with mentorship from University of Maryland cardiology fellow Karan Desai.   Jump to: Patient summary – Case media – Case teaching – References The CardioNerds Cardiology Case Reports series shines light on the hidden curriculum of medical storytelling. We learn together while discussing fascinating cases in this fun, engaging, and educational format. Each episode ends with an “Expert CardioNerd Perspectives & Review” (E-CPR) for a nuanced teaching from a content expert. We truly believe that hearing about a patient is the singular theme that unifies everyone at every level, from the student to the professor emeritus. We are teaming up with the ACC FIT Section to use the #CNCR episodes to showcase CV education across the country in the era of virtual recruitment. As part of the recruitment series, each episode features fellows from a given program discussing and teaching about an interesting case as well as sharing what makes their hearts flutter about their fellowship training. The case discussion is followed by both an E-CPR segment and a message from the program director. CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademySubscribe to our newsletter- The HeartbeatSupport our educational mission by becoming a Patron!Cardiology Programs Twitter Group created by Dr. Nosheen Reza Patient Summary A man in his late 20s with a past medical history of orthotopic heart transplant, presents with one-week of progressive lower extremity edema and dyspnea with NYHA class IV symptoms. 5 years prior, he underwent orthotopic heart transplant for arrhythmogenic right ventricular cardiomyopathy. Subsequently, he has had multiple episodes of rejection or recurrent graft dysfunction. On presentation, he was normotensive and borderline tachycardic. Exam revealed elevated JVP, decreased breath sounds, and pitting edema.  Labs demonstrated leukocytosis, acute kidney injury, and elevated pro-BNP. TTE demonstrated LVEF 35%, apical akinesis, and grade III diastolic dysfunction (all similar to prior). He was initially diuresed and RHC/EMB was performed to evaluate for rejection. Early in his course, the patient unfortunately suffered a PEA arrest with ROSC was quickly achieved after 1 minute of CPR. He was intubated and cannulated for VA ECMO. EMB demonstrated ISHLT Grade 1R cellular rejection and he was ultimately listed for re-transplant. Shortly thereafter, the patient received an OHT. His pathology demonstrated intimal thickening of all his coronaries, consistent with coronary artery vasculopathy, felt to be the major contributor to his presentation.   Case Media ECG Episode Schematics & Teaching Click to enlarge! The CardioNerds 5! – 5 major takeaways from the #CNCR case 1. What is CAV?   CAV stands for cardiac allograft vasculopathy. Within the transplanted heart, CAV is the proliferation of vascular smooth muscle and intimal thickening in the epicardial coronary arteries and microvasculature leading to diffuse narrowing. CAV is common, present in greater than 30% of patients at 5 years post-transplant. It is a significant contributor to post-transplant mortality after the first year.   CAV, in contrast to typical atherosclerotic lesions, is diffuse and concentric while atherosclerosis tends to be focal with eccentric luminal narrowing and heterogenous plaque composition. Patients s/p OHT can still develop typical coronary artery disease, likely developed from pre-existing disease in the donor heart. CAV should be high on the differential for the cause of graft dysfunction, especially after the first year post-transplant.   2. How and Why Does CAV Occur?  CAV has multiple contributing factors. There are immunologic and non-immunologic factors, but it appears the immunologic components play the larger role given that the pan-vasculopathy develops in the donor heart and not in the recipient’s vasculature. In CAV, there is chronic immune-mediated injury creating a persistent inflammatory state in the donor coronary endothelium leading to a neointimal proliferative process in the coronaries. Amongst immunologic factors, it appears the number of episodes of cellular rejection correlates with the development of CAV.   CAV occurs when foreign anti

CardioNerds (Amit Goyal & Daniel Ambinder) join Virginia Commonwealth University (VCU) cardiology fellows (Ajay Pillai, Amar Doshi, and Anna Tomdio) for a delicious skillet breakfast and amazing day in Richmond, VA! They discuss a fascinating case of a patient with Wolff-Parkinson-White (WPW) and hypertrophic cardiomyopathy (HCM). Dr. Keyur Shah provides the E-CPR and program director Dr. Gautham Kalahasty provides a message for applicants. Episode notes were developed by Johns Hopkins internal medicine resident Colin Blumenthal with mentorship from University of Maryland cardiology fellow Karan Desai. Jump to: Patient summary – Case media – Case teaching – References Episode graphic by Dr. Carine Hamo The CardioNerds Cardiology Case Reports series shines light on the hidden curriculum of medical storytelling. We learn together while discussing fascinating cases in this fun, engaging, and educational format. Each episode ends with an “Expert CardioNerd Perspectives & Review” (E-CPR) for a nuanced teaching from a content expert. We truly believe that hearing about a patient is the singular theme that unifies everyone at every level, from the student to the professor emeritus. We are teaming up with the ACC FIT Section to use the #CNCR episodes to showcase CV education across the country in the era of virtual recruitment. As part of the recruitment series, each episode features fellows from a given program discussing and teaching about an interesting case as well as sharing what makes their hearts flutter about their fellowship training. The case discussion is followed by both an E-CPR segment and a message from the program director. CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademySubscribe to our newsletter- The HeartbeatSupport our educational mission by becoming a Patron!Cardiology Programs Twitter Group created by Dr. Nosheen Reza Patient Summary A man in his mid-60s presented to the ED after an episode of unwitnessed syncope while drinking. Patient had suddenly passed out from a seated position with no prodrome or post-ictal state. He had episodes like this in the past, which were thought to be seizures, but otherwise PMHx only notable for alcohol use disorder. He denied any FH of SCD or syncope. In the ED, exam was unremarkable. Labs notable for mild thrombocytopenia, mild hyponatremia with AKI, 2:1 AST/ALT ratio, elevated NT-proBNP, and a very high lactate that rapidly corrected with fluids. EKG was notable for sinus tachycardia, short PR interval, wide QRS, and delta waves consistent with Wolff-Parkinson-White (WPW) pattern. Echo showed preserved LVEF, thickened LV septum (1.6 cm) and posterior wall (1.3 cm) concerning for hypertrophic cardiomyopathy (HCM). No outflow tract gradient was noted at rest or with stress, and the strain pattern demonstrated apical sparing. Evaluation for cardiac amyloid, including plasma cell dyscrasia and PYP scan, was negative. Cardiac MRI confirmed severely thickened LV inferior and inferolateral walls at 1.7 cm with no LVOT obstruction. 25% of the myocardium demonstrated patchy LGE.   Due to concern for WPW syndrome, the patient underwent an EP study. This revealed a malignant septal accessory pathway that was successfully ablated with resolution of the WPW EKG features. Given large LGE burden in setting of HCM, patient underwent placement of primary prevention ICD. Genetic testing for PRKAG2 mutation is pending given comorbid WPW and HCM.  Case Media A E C D B F Click to Enlarge A. CXR: Slightly increased interstitial markings in the lung bases, an elevated right hemidiaphragm. No acute airspace disease or pulmonary edemaB. ECG: Sinus tachycardia rate 120bpm, PR interval 80ms, QRS 130ms, WPW pattern.  Arruda algorithm localizes to posterior septum.C. CMR:  Myocardium nulls before blood pool.D. CMR:  Delayed gadolinium enhancementE. Follow up ECG: NSR 78, repolarization abnormalities.  T wave memory inferior leads.F. CXR status post dual chamber ICD implantation TTE: Apical 4 chamber TTE: Apical 2 chamber TTE: Apical 3 chamber TTE: Strain imaging CMR: 4 chamber cine CMR: 2 chamber cine CMR: 3 chamber cine CMR: Short axis cine at base level CMR: Short axis cine at mid-papillary level CMR: Short axis cine at apical level Episode Schematics & Teaching Hypertrophic Cardiomyopathy Infographic Click to enlarge! The CardioNerds 5! – 5 major takeaways from the #CNCR case Our patient was found to have Wolff-Parkinson-White (WPW) pattern. What are the diagnostic criteria for WPW pattern and how does it differ from WPW syndrome? How can you localize the accessory pathway using the EKG?  WPW pattern refers to the presence of the below criteria on a patient’s surface EKG in the absence of symptomatic arrhythmias. If symptomatic arrhythmias related

CardioNerds (Amit Goyal & Daniel Ambinder) join Baylor College of Medicine cardiology fellows (Khurrum Khan, John Suffredini, and Aliza Hussain) during restaurant week in Houston! They discuss an interesting case of STEMI in a patient with a recent diagnosis of e-cigarette or vaping product use-associated lung injury (EVALI). Dr. Vijay Nambi provides the E-CPR and APD Dr. Arunima Misra provides a message for applicants. Episode notes were developed by Johns Hopkins internal medicine resident Bibin Varghese with mentorship from University of Maryland cardiology fellow Karan Desai.    Jump to: Patient summary – Case media – Case teaching – References Episode graphic by Dr. Carine Hamo The CardioNerds Cardiology Case Reports series shines light on the hidden curriculum of medical storytelling. We learn together while discussing fascinating cases in this fun, engaging, and educational format. Each episode ends with an “Expert CardioNerd Perspectives & Review” (E-CPR) for a nuanced teaching from a content expert. We truly believe that hearing about a patient is the singular theme that unifies everyone at every level, from the student to the professor emeritus. We are teaming up with the ACC FIT Section to use the #CNCR episodes to showcase CV education across the country in the era of virtual recruitment. As part of the recruitment series, each episode features fellows from a given program discussing and teaching about an interesting case as well as sharing what makes their hearts flutter about their fellowship training. The case discussion is followed by both an E-CPR segment and a message from the program director. CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademySubscribe to our newsletter- The HeartbeatSupport our educational mission by becoming a Patron!Cardiology Programs Twitter Group created by Dr. Nosheen Reza Patient Summary A male in his mid 40s with a 30 pack year smoking history, EVALI (e-cigarette and vaping associated lung injury), and asthma presented with dyspnea and persistent chest pain. He had been vaping for the past year. One month prior , CT chest showed bilateral patchy infiltrates and he was diagnosed with EVALI and started on a steroid taper with resolution of his CT abnormalities. A nuclear stress test at that time was negative for ischemia. On arrival, he was in sinus tachycardia, normotensive, and not on oxygen supplementation. Physical exam was negative for volume overload or heart murmurs. EKG showed new Q waves with STE in V2-V4, with associated Q waves and TWI in the lateral leads and troponin returned moderately elevated. He was emergently taken to the cath lab which showed an abrupt cutoff of flow to the LAD. He received a single DES with resolution of coronary flow. A post-cath TTE showed an LVEF of 40-45% with apical anterior and anteroseptal WMA. He was monitored in the CCU the next day and he was treated with aspirin, ticagrelor, ACEi, metoprolol succinate and high intensity statin and subsequently discharged in stable condition with cardiac rehab follow-up. Case Media A B Click to Enlarge A. Presentation ECG (Anterior STEMI) B. Baseline ECG LAD occlusion Post PCI RCA TTE 1 TTE 2 TTE 3 Episode Schematics & Teaching Click to enlarge! The CardioNerds 5! – 5 major takeaways from the #CNCR case 1. The patient presented with a STEMI following a diagnosis of EVALI. What is known about the cardiovascular risks of vaping and e-cigarette use?  The overall cardiovascular risks of e-cigarette use remains to be elucidated  In preclinical studies, e-cigarettes use have been linked to increased sympathetic activity, oxidative stress, endothelial dysfunction, vascular injury, and altered platelet activity  One observational study has suggested that daily e-cigarette users were 1.79 times more likely to experience MI than individuals who had never used e-cigarettes.  Additional high-quality randomized controlled trials are needed to conclusively establish the safety and efficacy of e-cigarettes.  2. So the data is still emerging regarding the overall cardiovascular risks of e-cigarette use. Of note, the patient had a negative stress test a month prior. Should that not translate into low likelihood of cardiovascular events?  Remember that stress testing for the diagnosis of obstructive coronary disease is most helpful in patients with an intermediate pretest probability for coronary artery disease. Further myocardial ischemia can occur not only secondary to obstructive epicardial disease (which may be new and acute from plaque rupture/erosion), but also from microvascular disease, vasospastic disease, and so forth. Stress testing with radionuclide myocardial perfusion imaging (e.g., SPECT

CardioNerds (Amit Goyal & Daniel Ambinder) join University of Pittsburgh Medical Center cardiology fellows (Agnes Koczo, Natalie Stokes, and Kayle Shapero) for a boat cruise down the Allegheny river as we tour all over beautiful Pittsburgh! They discuss an important case of severe pre-eclampsia, and explore some of the exciting dimensions of cardio-obstetrics. Dr. Malamo Eleni Countouris provides the E-CPR and program director Dr. Katie Berlacher provides a message for applicants. Episode notes were developed by Johns Hopkins internal medicine resident Tommy Das with mentorship from University of Maryland cardiology fellow Karan Desai.   Jump to: Patient summary – Case media – Case teaching – References Episode graphic by Dr. Carine Hamo The CardioNerds Cardiology Case Reports series shines light on the hidden curriculum of medical storytelling. We learn together while discussing fascinating cases in this fun, engaging, and educational format. Each episode ends with an “Expert CardioNerd Perspectives & Review” (E-CPR) for a nuanced teaching from a content expert. We truly believe that hearing about a patient is the singular theme that unifies everyone at every level, from the student to the professor emeritus. We are teaming up with the ACC FIT Section to use the #CNCR episodes to showcase CV education across the country in the era of virtual recruitment. As part of the recruitment series, each episode features fellows from a given program discussing and teaching about an interesting case as well as sharing what makes their hearts flutter about their fellowship training. The case discussion is followed by both an E-CPR segment and a message from the program director. CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademySubscribe to our newsletter- The HeartbeatSupport our educational mission by becoming a Patron!Cardiology Programs Twitter Group created by Dr. Nosheen Reza Patient Summary A G12P7 woman in her mid 30s in the third trimester of pregnancy presented with two months of progressive shortness of breath, orthopnea, and abdominal distension. She has a history of chronic HTN, untreated OSA, and obesity. Evaluation revealed a BP of 147/76 and spot urine protein:creatinine ratio elevated to 0.6, which in the context of her presentation was concerning for preeclampsia superimposed on chronic hypertension. TTE showed preserved ejection fraction, flattened interventricular septum during systole consistent with RV pressure overload, and moderate pulmonary HTN.  She was diuresed with IV furosemide with improvement in symptoms and kept on ASA 81mg. The etiology of her elevated PA pressures was thought to be multifactorial, including untreated OSA for which she was started on CPAP. She was ultimately discharged on oral diuretics, and underwent an uncomplicated spontaneous vaginal delivery at 37 weeks. After delivery, follow-up in a clinic specializing in improving cardiovascular health in women with history of hypertensive disorders of pregnancy was arranged.   Case Media A B C Click to Enlarge A. ECG: Sinus tachycardia otherwise unremarkableB. CXR: Within limitations of respiratory motion, no focal airspace consolidation; no pleural effusionsC. TTE: EF 55-60%, flattened IVS c/w RV pressure overload; normal RV size and function; mod TR; moderate pulmonary HTN (PASP 52mmHG); normal diastolic function Episode Schematics & Teaching Click to enlarge! The CardioNerds 5! – 5 major takeaways from the #CNCR case 1. Cardionerds, we all should be familiar with #CardioObstetrics. What are the hypertensive disorders of pregnancy?  There are four major categories for hypertensive disorders in pregnancy: (1) chronic hypertension (2) gestational hypertension; (3) preeclampsia (along with eclampsia and HELLP syndrome); (4) chronic hypertension with superimposed preeclampsia.   Chronic Hypertension: Note, the definition of chronic hypertension was updated in the 2017 ACC/AHA guidelines as SBP ≥ 130 or DBP ≥ 90, but the diagnostic criteria for gestational hypertension, pre-eclampsia and chronic hypertension with super-imposed pre-eclampsia have not changed at this time.   Gestational Hypertension (per ACOG guidelines): defined as SBP ≥  140 mmHg or DBP ≥  90 mmHg at least 4 hours apart diagnosed after 20 weeks of gestation without proteinuria or severe features of pre-eclampsia (e.g., renal insufficiency, elevated liver enzymes, thrombocytopenia, hemolysis, pulmonary edema, or CNS symptoms)  Preeclampsia: diagnosis requires  (1) SBP ≥ 140 mmHg or DBP ≥  90 mmHg at least 4 hours apart after 20 weeks gestation or SBP ≥ 160 mmHg or DBP ≥ 110 mmHg once and (2) end organ damage. This includes proteinuria

CardioNerds (Amit Goyal & Daniel Ambinder) join  join UCLA cardiology fellows (Jay Patel, Hillary Shapiro, and Ruth Hsiao) for some beach bonfire in Santa Monica! They discuss a challenging case of Spontaneous Coronary Artery Dissection (SCAD) requiring heart transplantation. Dr. Jonathan Tobis provides the E-CPR and program director Dr. Karol Watson provides a message for applicants. Episode notes were developed by Johns Hopkins internal medicine resident Evelyn Song with mentorship from University of Maryland cardiology fellow Karan Desai.   Jump to: Patient summary – Case media – Case teaching – References Episode graphic by Dr. Carine Hamo The CardioNerds Cardiology Case Reports series shines light on the hidden curriculum of medical storytelling. We learn together while discussing fascinating cases in this fun, engaging, and educational format. Each episode ends with an “Expert CardioNerd Perspectives & Review” (E-CPR) for a nuanced teaching from a content expert. We truly believe that hearing about a patient is the singular theme that unifies everyone at every level, from the student to the professor emeritus. We are teaming up with the ACC FIT Section to use the #CNCR episodes to showcase CV education across the country in the era of virtual recruitment. As part of the recruitment series, each episode features fellows from a given program discussing and teaching about an interesting case as well as sharing what makes their hearts flutter about their fellowship training. The case discussion is followed by both an E-CPR segment and a message from the program director. CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademySubscribe to our newsletter- The HeartbeatSupport our educational mission by becoming a Patron!Cardiology Programs Twitter Group created by Dr. Nosheen Reza Patient Summary A woman in her late 40s presented with a one day history of intermittent chest pain. EKG showed anteroseptal and lateral STE with reciprocal ST depressions in the inferior leads. High-sensitivity troponin was elevated at 333 ng/mL. Emergent LHC showed a long and narrow left main with areas of additional contrast filling into a false lumen with no flow in the LAD. RCA and LCx were normal appearing (make sure you check out the angiogram videos below!). IVUS showed dissection and heavy thrombus burden in the left main artery. Shortly after the diagnostic angiogram, the patient went into V-fib arrest and received one shock with ROSC. Amiodarone was started and an Impella CP was placed for additional left ventricular support. ECMO and emergent CABG were not readily available at this time so the interventional team attempted revascularization with PCI to the left main given patient’s hemodynamic instability from ongoing ischemia. However, even after PCI to left main, flow to LAD remained poor and the LCx now also appeared occluded. The decision was made to cease further attempts at revascularization. Unfortunately, post-procedure TTE showed a reduced EF of 22% with anterior and anterolateral hypokinesis. She was transferred to CCU on maximal Impella support. Patient eventually developed acute renal and liver failure secondary to cardiogenic shock and suffered an additional V-fib arrest with ROSC. Eventually, Ronald Reagan UCLA was contacted for transfer and the mobile ECMO team was dispatched. They placed the patient on VA-ECMO in the outside facility and transferred her to Ronald Reagan UCLA. At Ronald Reagan, revascularization was attempted given persistent cardiogenic shock and 3 stents were successfully deployed in the LAD. She was eventually weaned off of both Impella and ECMO after successful PCIs to LAD. However, TTE showed persistently low EF and patient eventually underwent successful heart-kidney transplantation.  Case Media A B C D Click to Enlarge A. ECG: Anterior STE, STE in I/aVL but depressedions in V4-V6, inferior reciprocal ST depressionB. X-ray of explanted heart shows stents extending from LM -> dLADC. Cross-section of explanted heart from apex to base showing infarct in the anteroseptal areaD. Histological cross section of the explanted LAD.  This film shows slit like LM with no LAD.  High OM/RI and LCx look ok. BMW wire used to cross distal LM into high OM/RIArrested after diagnostic, got ROSC and then Impella CP inserted L femoral Attempting wiring the true lumen, stuck in mLAD after 1st septal comes off IVUS from RI to LM.  Shows dissection plane and lots of thrombusLM IVUS details: 4.57 x 5.0mm proximally, 4.52mm distally Unable to pass a wire into mid LAD PCI of LM: Synergy 4.0 x 16mm DES deployed in LM and post-dilated with Emerge NC 4.5 x 8mm balloon Flow remained poor at mLAD even after PCI to LM LCx system closed after LM PCI, so no further attempts TTE: Apical 4 Chamb

CardioNerds (Amit Goyal & Daniel Ambinder) join Houston Methodist cardiology fellows (Isaac Tea, Stephanie Fuentes, Peter Rothstein) for a trip to Hermann Park! They discuss a challenging case of right ventricular (RV) infarction leading to acute RV failure treated with right ventricular assist device (RVAD) support. Dr. Mahwash Kassi provides the E-CPR and program director Dr. Stephen Little provides a message for applicants. Episode notes were developed by Johns Hopkins internal medicine resident Tommy Das with mentorship from University of Maryland cardiology fellow Karan Desai.  Jump to: Patient summary – Case media – Case teaching – References Episode graphic by Dr. Carine Hamo The CardioNerds Cardiology Case Reports series shines light on the hidden curriculum of medical storytelling. We learn together while discussing fascinating cases in this fun, engaging, and educational format. Each episode ends with an “Expert CardioNerd Perspectives & Review” (E-CPR) for a nuanced teaching from a content expert. We truly believe that hearing about a patient is the singular theme that unifies everyone at every level, from the student to the professor emeritus. We are teaming up with the ACC FIT Section to use the #CNCR episodes to showcase CV education across the country in the era of virtual recruitment. As part of the recruitment series, each episode features fellows from a given program discussing and teaching about an interesting case as well as sharing what makes their hearts flutter about their fellowship training. The case discussion is followed by both an E-CPR segment and a message from the program director. CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademySubscribe to our newsletter- The HeartbeatSupport our educational mission by becoming a Patron!Cardiology Programs Twitter Group created by Dr. Nosheen Reza Patient Summary A man in his early 70s with ASCVD risk factors and known CAD (PCI to proximal LAD 4 years prior) presented with typical angina refractory to maximal medical therapy. A nuclear stress test showed a reversible perfusion defect in the RCA territory, and he was referred for PCI. Coronary angiogram showed severe stenosis of the proximal RCA and a DES was successfully deployed with TIMI 3 flow, though several large acute marginal branches were jailed.   The night following PCI, the patient developed bradycardia, hypotension, and tachypnea. Physical exam showed newly elevated JVP, lower extremity edema, and bibasilar crackles without a new cardiac murmur. ECG showed ST elevation in V1-V4, and bedside echocardiogram showed a severely dilated RV with decreased systolic function. With concern for acute RV failure, the patient was fluid resuscitated, started on dopamine for chronotropy, and was admitted to the CCU. A Swan-Ganz catheter was placed, showing a CVP 12, RV 41/15, PA 36/20 (25), PCWP 18, CI 1.6 (by Fick method). The calculated PAPi was 0.84.   The patient was transitioned to dobutamine to improve RV inotropy, epinephrine in the setting of hypotension, and inhaled nitric oxide in an attempt to decrease RV afterload. Despite these interventions, the patient had worsening shock, anuric renal failure requiring CVVH, and respiratory failure requiring intubation. A centrifugal RA to PA pump was placed (Protek Duo) for right-sided mechanical circulatory support, with improvement in RV hemodynamics and cardiogenic shock. Notably, a repeat angiogram was done, which showed a patent left coronary circulation as well as a right coronary artery without flow in the acute marginal branches. After 6 days of mechanical circulatory support, the patient was ultimately able to be weaned from vasoactive agents, and the Protek Duo was removed. He continued to have junctional bradycardia, and a permanent pacemaker was placed. After a nearly month-long admission, the patient was discharged to rehab; at 4 months follow-up, the patient’s RV function had improved on TTE, and he was not limited from heart failure symptoms.   Case Media A B C D E F G Click to Enlarge A: ECG, initialB: ECG: 8 hours post PCI he was noted to have junctional bradycardia with ST-segment elevations in V1-V4.C: Pre and post RCA PCI D: TTE: EF 50-55%, Severely enlarged RV with severely reduced systolic function, TAPSE 1.4 cm, Myocardial systolic excursion velocity (S’): 5.9E: CXR- shock F: Swan, Protek Duo Cannula, Temporary pacer G: CXR and TTE images demonstrating Protek Duo cannula placement Left Coronary System -1 Left Coronary System – 2 Severe eccentric serial stenoses in the proximal to mid RCA – 1 RCA – 2 RCA PCI – 1 RCA PCI – 2 RCA PCI – 3 RCA PCI – 4 RCA – Final TTE -1 TTE -2 Repeat angiogram: Patent stents, sluggish flow Prote

CardioNerds (Amit Goyal & Daniel Ambinder) join University of Florida cardiology fellows (Ashley Mohadjer, Hussain Khalid, and Morgan Randall) for an authentic Gainesville-style tailgate! They discuss a fascinating case of severe peripheral artery disease (PAD) and cerebral hyperperfusion syndrome. Dr. Khanjan Shah provides the E-CPR and  a message for applicants. Episode notes were developed by Johns Hopkins internal medicine resident Richard Ferraro with mentorship from University of Maryland cardiology fellow Karan Desai.   Jump to: Patient summary – Case media – Case teaching – References Episode graphic by Dr. Carine Hamo The CardioNerds Cardiology Case Reports series shines light on the hidden curriculum of medical storytelling. We learn together while discussing fascinating cases in this fun, engaging, and educational format. Each episode ends with an “Expert CardioNerd Perspectives & Review” (E-CPR) for a nuanced teaching from a content expert. We truly believe that hearing about a patient is the singular theme that unifies everyone at every level, from the student to the professor emeritus. We are teaming up with the ACC FIT Section to use the #CNCR episodes to showcase CV education across the country in the era of virtual recruitment. As part of the recruitment series, each episode features fellows from a given program discussing and teaching about an interesting case as well as sharing what makes their hearts flutter about their fellowship training. The case discussion is followed by both an E-CPR segment and a message from the program director. CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademySubscribe to our newsletter- The HeartbeatSupport our educational mission by becoming a Patron!Cardiology Programs Twitter Group created by Dr. Nosheen Reza Patient Summary A woman in her 60s with a past medical history of type 2 diabetes, hypertension, and hypothyroidism presented to the University of Florida with a chief complaint of “Someone told me my neck artery was blocked.”  Someone call 227-346-6373.  What does that spell? CardioNerd!    She noted exertional pain in both legs with limited exertion. Has a family history of CAD and MI in her father in his 20s. Her only medications were baby aspirin, atorvastatin 80mg, and thyroid replacement. Her blood pressures were noted to be dropping and so her regimen was being titrated off as a result. Physical exam was notable only for poorly palpable pulses in all extremities. To further work this up, a myocardial perfusion scan, CTA head/neck/abdomen, and ABIs were ordered. ABI on the right was 0.86 and on the left was 0.76 with monophasic doppler waveforms throughout. CT abdomen exhibited an occlusion of the abdominal aorta from just below the renal arteries extending to the common iliac arteries with distal reconstitution. CT head/neck showed occlusion of the right carotid artery, complete occlusion of the right innominate artery, near complete occlusion of the right vertebral artery, and delayed flow in the right posterior cerebral artery. On the left side, she had high-grade subclavian stenosis. Myocardial perfusion imaging exhibited no defects.   On subsequent visits her exercise tolerance improved with an exercise regimen, but blood pressures were more and more difficult to obtain. As a result, revascularization was pursued with stenting of the left subclavian artery. She was discharged, but returned a few hours later with severe left sided pulsatile headache and nausea/vomiting. She was admitted for monitoring, but fortunately improved and discharged with close outpatient follow-up.  She continued to improve in the outpatient setting. After MRI brain and extensive work-up, she was deemed to have cerebral hyperperfusion syndrome following revascularization.  She had no further complications and was monitored thereafter.  Final diagnosis: severe peripheral artery disease (PAD) and cerebral hyperperfusion syndrome. Case Media A B C D E F Click to Enlarge A: ECG B: ABIsC: CT Angiogram D: CT Angiogram – head and neck E: Pre and post subclavian stentinng F: CT head and neck – follow up Subclavian via L radial Aortic Root Cine 1 Aortic Root Cine 2 Stent Post Stent Post Stent 2 Post Stent 3 Episode Schematics & Teaching Click to enlarge! The CardioNerds 5! – 5 major takeaways from the #CNCR case What are the risk factors and prevalence of PAD?  PAD refers to atherosclerotic peripheral artery disease, and is the accumulation of plaque in various peripheral arterial beds akin to CAD involving coronary arteries.  6% of adults over the age of 40 have PAD, and 30% o

CardioNerds (Amit Goyal & Daniel Ambinder) join Johns Hopkins Hospital cardiology fellows (Rick Vakil, Pranoti Hiremath, and Vasanth Sathiyakumar) for some gelato by the bay in Baltimore, Maryland! They discuss a challenging case of RV failure & shock after placement of an AV graft. Dr. Monica Mukherjee provides the E-CPR and program director Dr. Steven Schulman provides a message for applicants. Episode notes were developed by Johns Hopkins internal medicine resident Colin Blumenthal with mentorship from University of Maryland cardiology fellow Karan Desai.   Jump to: Patient summary – Case media – Case teaching – References Episode graphic by Dr. Carine Hamo The CardioNerds Cardiology Case Reports series shines light on the hidden curriculum of medical storytelling. We learn together while discussing fascinating cases in this fun, engaging, and educational format. Each episode ends with an “Expert CardioNerd Perspectives & Review” (E-CPR) for a nuanced teaching from a content expert. We truly believe that hearing about a patient is the singular theme that unifies everyone at every level, from the student to the professor emeritus. We are teaming up with the ACC FIT Section to use the #CNCR episodes to showcase CV education across the country in the era of virtual recruitment. As part of the recruitment series, each episode features fellows from a given program discussing and teaching about an interesting case as well as sharing what makes their hearts flutter about their fellowship training. The case discussion is followed by both an E-CPR segment and a message from the program director. CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademySubscribe to our newsletter- The HeartbeatSupport our educational mission by becoming a Patron!Cardiology Programs Twitter Group created by Dr. Nosheen Reza Patient Summary A man in his early 40s, with a history of type 1 diabetes and prior failed renal and pancreatic transplants currently on iHD, was referred to Johns Hopkins Hospital for dialysis access. A left groin AV loop graft was pursued due to multiple access point failures in the past secondary to severe peripheral artery disease. Pre-op evaluation included risk stratification with RHC which was consistent with WHO Group 2 pulmonary HTN and diffuse atherosclerosis in the RCA on LHC. Intra-op, patient had an episode of significant hypotension after administration of protamine that required phenylephrine and ephedrine. In the PACU, his BPs continued to be low (70s/40s mmHg), requiring admission to the SICU where cardiology was consulted.  In the SICU, patient had ongoing hypotension despite pressors and fluids. Exam demonstrated a systolic murmur consistent with TR and elevated JVP. Labs were notable for a mild elevation in liver enzymes, elevated troponin, high NT-proBNP and elevated lactate. TTE demonstrated a moderately dilated and hypokinetic RV, elevated RVSP and evidence of pressure/volume overload. CTA abdomen/pelvis demonstrated extensive mesenteric atherosclerosis and signs of gastric ischemia. Patient was treated for RV failure with norepinephrine, inhaled epoprostenol, and CVVHD for volume removal. He became febrile and was treated empirically with broad spectrum antibiotics. Due to concern for the new loop graft causing high output heart failure vs RV failure, it was temporarily occluded for testing and then permanently ligated by vascular surgery with significant improvement in his BPs and RV function on repeat TTE.  Case Media A B C D E Click to Enlarge A. Plato’s allegory of the cave by Jan Saenredam, according to Cornelis van Haarlem, 1604, Albertina, ViennaB-C. Anesthesia flow sheets D. CXR: Pulmonary vascular congestion, bibasilar atelectasisE. ECG: Sinus tachycardia to 110, RAD, RBBB, similar to prior TTE: LVEF 60-65%, mild to moderate concentric hypertrophy, trace effusion TTE: Flattened septum in systole and diastole c/f RV pressure and volume overload. RV moderately dilated and hypokinetic. RVSP 63 mmHg. CT Abdomen and Pelvis: Negative for PE, gastric pneumatosis, air within the gastroepiploic veins, and portal venous gas, most concerning for gastric ischemia, extensive atherosclerotic calcifications throughout the mesenteric vessels TTE follow up: Mild/moderate concentric hypertrophy, EF 60%,  G2DD TTE follow up: RV mildly dilated and mild global hypokinesis of the RV. TAPSE 1.54. RV S’ was 9.6 cm/s (normal > 9.5) Episode Schematics & Teaching Click to enlarge! The CardioNerds 5! – 5 major takeaways from the #CNCR case 1. In this case the patient became hypotensive shortly after administration of protamine. What are the risk factors for a protamine reaction and the proposed mechanisms?  Protamine is a protein commonly used in cardiovascular procedures 

CardioNerds (Amit Goyal & Daniel Ambinder) join Medical College of Wisconsin cardiology fellows (Katie Cohen, Div Mohananey, and Dave Lewandowski) for some cold brews by Lake Michigan in Cream City aka Milwaukee, WI! They discuss a case of a pregnant woman presenting cardiac arrest due to peripartum cardiomyopathy. Dr. Sarah Thordsen provides the E-CPR and program director, Dr. Nunzio Gaglianello, provides a message for applicants. Episode notes were developed by Johns Hopkins internal medicine resident, Eunice Dugan, with mentorship from University of Maryland cardiology fellow Karan Desai. Jump to: Patient summary – Case media – Case teaching – References Episode graphic by Dr. Carine Hamo The CardioNerds Cardiology Case Reports series shines light on the hidden curriculum of medical storytelling. We learn together while discussing fascinating cases in this fun, engaging, and educational format. Each episode ends with an “Expert CardioNerd Perspectives & Review” (E-CPR) for a nuanced teaching from a content expert. We truly believe that hearing about a patient is the singular theme that unifies everyone at every level, from the student to the professor emeritus. We are teaming up with the ACC FIT Section to use the #CNCR episodes to showcase CV education across the country in the era of virtual recruitment. As part of the recruitment series, each episode features fellows from a given program discussing and teaching about an interesting case as well as sharing what makes their hearts flutter about their fellowship training. The case discussion is followed by both an E-CPR segment and a message from the program director. CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademySubscribe to our newsletter- The HeartbeatSupport our educational mission by becoming a Patron!Cardiology Programs Twitter Group created by Dr. Nosheen Reza Patient Summary A G2P1 woman in her early 30s with a history palpitations presented after a witnessed out-of-hospital cardiac arrest while at work. She received 6 rounds of CPR and 2 shocks before ROSC was achieved. She was intubated and given fluids but continued to remain hypoxic and hypotensive. Exam demonstrated sinus tachycardia, no murmurs, gravid abdomen and cool extremities. Initial labs demonstrated leukocytosis to 14k, lactic acid at 4.3 mmol/L, troponin-I peak at 0.07 ng/dL and elevated NT-proBNP. CXR demonstrated bilateral effusions and pulmonary congestion, and post-arrest EKG showed a wide complex tachycardia, leading to suspicion of VT arrest. In sinus, there  were no ST segment elevations and TTE showed LVEF 10-20%, global hypokinesis and no valvular disease. Given the severity of her shock, she was placed on central VA-ECMO with Impella support as an LV vent. During ECMO cannulation, she underwent emergent cesarean section due to fetal distress. Coronary angiography showed non-obstructive coronaries, but with sluggish flow in the setting of her cardiogenic shock and possible coronary spasm in setting of multiple vasoactive medications. Endomyocardial biopsy was negative for giant cell myocarditis. Within 4-5 days, she was weaned off all vasoactive agents and ECMO was decannulated; repeat echocardiogram showed LV functional recovery. GDMT was slowly titrated and a subcutaneous ICD was eventually placed before discharge. She and her child have done well over the course of a year!  Case Media A B Click to Enlarge A: ECG: Initially in sustained wide complex irregular tachycardiaB: CXR: Extensive consolidative changes throughout the lungs TTE: Parasternal Long Axis TTE: Apical 4 Chamber Episode Schematics & Teaching Click to enlarge! The CardioNerds 5! – 5 major takeaways from the #CNCR case 1. What is the differential for cardiac arrest in pregnant patients?  When thinking about a cardiac etiology of arrest, the differential should include pregnancy-induced hypertension, peripartum cardiomyopathy, myocardial infarction from acute coronary syndrome or spontaneous coronary artery dissection, pulmonary embolism, amniotic fluid embolism and aortic dissection. Non-cardiac etiologies include hemorrhagic shock, sepsis, stroke, trauma and anesthetic complications. In addition to these unique considerations, pregnant patients are also susceptible to the usual culprits!  As noted in the 2015 AHA Scientific Statement, cardiac arrest in pregnancy is not common, occurring in 1:12,000 admissions for delivery. As of 2016, per the CDC the pregnancy-related mortality rate was ~17 deaths per every 100,000 live births. However, mortality data does not fully capture critical illness in pregnancy, and thus the AHA recommends considering maternal “near-miss” data.   Knowledge gaps, provider unfamiliarity, and lack of medical ward or medi

CardioNerds (Amit Goyal & Daniel Ambinder) join Cedars-Sinai cardiology fellows (Natasha Cuk, Ronit Zadikany, Neal Yuan) for some drinks at the local pub 3rd Stop after a walk down Hollywood boulevard! They discuss a fascinating case of a massive pulmonary embolus presenting as STEMI. Dr. Babak Azarbal provides the E-CPR and program director Dr. Joshua Goldhaber provides a message for applicants. Episode notes were developed by Johns Hopkins internal medicine resident Bibin Varghese with mentorship from University of Maryland cardiology fellow Karan Desai. Jump to: Patient summary – Case figures & media – Case teaching – References – Production team Episode graphic by Dr. Carine Hamo The CardioNerds Cardiology Case Reports series shines light on the hidden curriculum of medical storytelling. We learn together while discussing fascinating cases in this fun, engaging, and educational format. Each episode ends with an “Expert CardioNerd Perspectives & Review” (E-CPR) for a nuanced teaching from a content expert. We truly believe that hearing about a patient is the singular theme that unifies everyone at every level, from the student to the professor emeritus. We are teaming up with the ACC FIT Section to use the #CNCR episodes to showcase CV education across the country in the era of virtual recruitment. As part of the recruitment series, each episode features fellows from a given program discussing and teaching about an interesting case as well as sharing what makes their hearts flutter about their fellowship training. The case discussion is followed by both an E-CPR segment and a message from the program director. CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademySubscribe to our newsletter- The HeartbeatSupport our educational mission by becoming a Patron!Cardiology Programs Twitter Group created by Dr. Nosheen Reza Patient Summary A man in his mid-40s with no known past medical history presented to the ER in PEA arrest with ongoing cardiopulmonary resuscitation (CPR). Prior to his arrest, his coworkers reported that he was complaining of lightheadedness, dizziness and that he was found slumped over at his desk. His EKG in the ambulance showed STE in aVR and V1 – V4 with TWI in III and aVF initially concerning for an anterior STEMI. He was cannulated with VA-ECMO for extracorporeal cardiopulmonary resuscitation (E-CPR) and was taken to the catheterization lab emergently. In the catheterization lab, his coronary angiogram did not show obstructive coronary disease. The interventionalists decided to perform a pulmonary artery (PA) angiogram which revealed a large amount of thrombus bilaterally in the proximal PAs. He underwent surgical embolectomy with removal of almost all his clot burden. The patient was thereafter cooled for neurological protection. Unfortunately, the patient had a very poor neurological exam with lack of brainstem reflexes upon rewarming. There was loss of gray-white differentiation on CT, and EEG and evoked potential testing were consistent with severe anoxic brain injury. After discussions with the patient’s family, the patient was transitioned to comfort care and subsequently passed away peacefully.   Case Media Click to Enlarge Right Coronary Artery Left Coronary System – 1 Left Coronary System – 2 Left Pulmonary Artery Right Pulmonary Artery Episode Schematics & Teaching Click to enlarge! The CardioNerds 5! – 5 major takeaways from the #CNCR case The patient presented initially with STE in aVR as well as the septal and anterior leads. What is the differential for an ST elevation in lead aVR? STE in aVR with diffuse ST depression can be a potential finding of LM or LAD stenosis. However, there have been several studies that have shown that the combination of STE and multi-lead STD was not associated with complete occlusion of a culprit vessel. Thus, the differential for STE in aVR more commonly includes significant LM or LAD stenosis, severe three-vessel disease with diffuse sub-endocardial ischemia (e.g., CAD in the setting of sepsis, anemia, shock), as well as pulmonary embolism with right ventricular injury (see below)! Remember that lead aVR is opposite I, aVL, II and V5-6 and thus elevation in aVR may represent reciprocal changes of diffuse sub-endocardial ischemia. Furthermore, aVR doesn’t directly overlie myocardium but reflects electrical activity from the RV outflow tract and basal septum. Thus, in the context of an anterior STEMI, STE in aVR (> 1mm) strongly predicts LAD occlusion proximal to the first septal perforator, which supplies the basal septum. The patient was found to have non-obstructed coronaries and was ultimately diagnosed with a PE. Could we have suspected that from the initial EKG? What are the EKG changes that have been noted i

CardioNerds (Amit Goyal & Daniel Ambinder) join join Mayo Clinic cardiology fellows (Mays Ali, Charlie Jain, Korosh Sharain) for a scenic walk through gorgeous Rochester, Minnesota! They discuss a fascinating case of constrictive pericarditis and severe mitral regurgitation. Dr. Rick Nishimura provides the E-CPR and program director Dr. Frank Brozovich provides a message for applicants. Episode notes were developed by Johns Hopkins internal medicine resident Bibin Varghese with mentorship from University of Maryland cardiology fellow Karan Desai.   Jump to: Patient summary – Case figures & media – Case teaching – References – Production team Episode graphic by Dr. Carine Hamo The CardioNerds Cardiology Case Reports series shines light on the hidden curriculum of medical storytelling. We learn together while discussing fascinating cases in this fun, engaging, and educational format. Each episode ends with an “Expert CardioNerd Perspectives & Review” (E-CPR) for a nuanced teaching from a content expert. We truly believe that hearing about a patient is the singular theme that unifies everyone at every level, from the student to the professor emeritus. We are teaming up with the ACC FIT Section to use the #CNCR episodes to showcase CV education across the country in the era of virtual recruitment. As part of the recruitment series, each episode features fellows from a given program discussing and teaching about an interesting case as well as sharing what makes their hearts flutter about their fellowship training. The case discussion is followed by both an E-CPR segment and a message from the program director. CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademySubscribe to our newsletter- The HeartbeatSupport our educational mission by becoming a Patron!Cardiology Programs Twitter Group created by Dr. Nosheen Reza Constrictive Pericarditis & Severe Mitral Regurgitation – Patient Summary A woman in her late 40s with a history of lupus and hypertension presented with worsening dyspnea on exertion and orthopnea over a year. She reported intermittent pleuritic chest discomfort that had persisted since an episode of acute pericarditis years prior. A TTE suggested severe mitral regurgitation, and she was referred to the Mayo Clinic for mitral valve intervention.    The official TTE report from the OSH suggested non-dilated LV, EF 55-60%, normal RV function, severe MR with thickened leaflets and sub-valvular apparatus, moderate to severe TR and a dilated IVC. Furthermore, the CXR showed pericardial calcifications. Upon evaluation by the Mayo Clinic fellows, the JVP was elevated to about 10-12 cm with rapid x and y descents, a positive Kussmaul’s sign, and the murmurs of MR and TR. Her lungs were clear to auscultation and extremities did not demonstrate edema. Re-review of the TTE images revealed posterior pericardial thickening, no septal shift on respiration, but suggestion of annulus reversus where medial mitral annulus tissue doppler (9 cm/s) was greater than lateral (8 cm/s). Further, there was evidence of expiratory hepatic vein diastolic flow reversal.  For the team, there was discordance between the apparent severity of her MR reported by echocardiogram and her clinical symptoms. In addition, the echocardiogram was suggestive of specific signs of constrictive pericarditis. Thus, simultaneous RHC/LHC was obtained. There was equalization of RV/LV pressures during diastole, demonstration of a “square root sign” and importantly discordance between LV and RV pressures with respiration. Thus, discordant clinical findings led to a suspicion for constrictive pericarditis and was corroborated by discordance on invasive hemodynamics! Further, the V-waves were not prominent on wedge pressure tracing and to investigate the mitral regurgitation further, an LV ventriculogram was done. This demonstrated 3+ to 4+ MR.  Based on all the findings, the patient was diagnosed with constrictive pericarditis, severe MR and moderate to severe TR. She underwent pericardiectomy, mitral valve replacement (given that repair was not feasible due to the sub-valvular thickening) and given that TR has been shown to worsen after pericardiectomy and is a poor prognostic factor, she additionally underwent tricuspid valve repair. Her symptoms improved markedly following intervention.  Case Media A B C D E F G H Click to Enlarge A. CXR: Heart size was borderline enlarged with biatrial enlargement.  LV does not appear very enlarged. B. Mitral Regurgitation by CW Doppler C. Tricuspid regurgitation by CW Doppler. TR Max 2.43D. Tissue Doppler of the mitral valve annulus: Medial e’ = 9 cm/s, Lateral e’ 8 cm/sE. Hepatic Vein PW Doppler F. Right atrial pressure tracingG. RV and LV simultaneous pressure tracings

CardioNerds (Amit Goyal & Daniel Ambinder) join join University of Tennessee cardiology fellows (Rachel Goodwin, Emmanuel Isang, and William Black) for some chocolate cake and hikes in the Smoky Mountains! They discuss a fascinating case of constrictive pericarditis. Dr. Tjuan Overly provides the E-CPR and a message for applicants. Episode notes were developed by Johns Hopkins internal medicine resident Evelyn Song with mentorship from University of Maryland cardiology fellow Karan Desai.   Jump to: Patient summary – Case figures & media – Case teaching – References – Production team Episode graphic by Dr. Carine Hamo The CardioNerds Cardiology Case Reports series shines light on the hidden curriculum of medical storytelling. We learn together while discussing fascinating cases in this fun, engaging, and educational format. Each episode ends with an “Expert CardioNerd Perspectives & Review” (E-CPR) for a nuanced teaching from a content expert. We truly believe that hearing about a patient is the singular theme that unifies everyone at every level, from the student to the professor emeritus. We are teaming up with the ACC FIT Section to use the #CNCR episodes to showcase CV education across the country in the era of virtual recruitment. As part of the recruitment series, each episode features fellows from a given program discussing and teaching about an interesting case as well as sharing what makes their hearts flutter about their fellowship training. The case discussion is followed by both an E-CPR segment and a message from the program director. CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademySubscribe to our newsletter- The HeartbeatSupport our educational mission by becoming a Patron!Cardiology Programs Twitter Group created by Dr. Nosheen Reza Patient Summary A man in his late 40s with a history of renal failure secondary to IgA nephropathy and now status post a kidney transplant 10-15 years ago was referred by hepatology for evaluation of recurrent ascites and LE edema. He appeared grossly volume overloaded on exam with JVP elevated past the mandible, RV heave, and 2+ pitting edema. TTE demonstrated LVEF of 55-60%, RVSP 40mmHg, abnormal septal motion with respiration, and respirophasic variation in mitral inflow across the mitral valve raising the suspicion for constrictive pericarditis. RHC pressures demonstrated a mean RA pressure of 20mmHg, RV 40/25mmHg, PA 38/30mmHg (mean 32 mmHg) and PCWP mean of 26 with V-waves at 28 mmHg. Simultaneous LV and RV pressure tracings showed ventricular discordance with respirophasic variation, consistent with constrictive physiology. Patient underwent pericardiectomy with markedly improved heart failure symptoms. Repeat TTE showed no evidence of constriction.  Case Media A B C Click to Enlarge! A. ECGB. Pulsed-wave Doppler spectrum of tricuspid inflow velocities demonstrates a marked respiratory variation (In irregular rhythms, such as the atrial fibrillation seen here, respirophasic changes may still be seen but are confounded by the varying R-R interval)C. Simultaneous LV and RV pressure tracings showing discordance with respirophasic variation Apical 4-chamber view demonstrating abnormal septal motion due to interventricular dependence – dissociation of thoracic and cardiac chamber pressures leads to increased RV filling during inspiration Short axis view of the LV demonstrating a D-shaped interventricular septum during inspiration.  Note the presence of a pericardial effusion as well. Episode Schematics & Teaching Click to enlarge! The CardioNerds 5! – 5 major takeaways from the #CNCR case The initial presentation clinically seemed to be right greater than left heart failure. What are the signs and common causes of right heart failure?    The signs and symptoms of RHF are often similar to left-sided CHF, but may describe more severe dyspnea on exertion, significant abdominal distension, and early satiety due to ascites or gut edema. Symptoms of pulmonary edema from elevated left-sided filling pressures (orthopnea, paroxysmal nocturnal dyspnea) may be absent. On examination, there will be elevated JVP with likely prominent v-waves, possibly Kussmaul’s sign (inspiratory rise in JVP rather than fall) depending on the pathology, abdominal ascites, pulsatile hepatomegaly, and lower extremity edema. An RV heave may be discernible along with a loud P2 component and murmur of TR. Broadly, RV failure may be caused by pressure overload (ex: pulmonary hypertension, pulmonic stenosis), volume overload (ex: intracardiac shunt, tricuspid regurgitation), or myocardial disease (ex: cardiomyopathies, ischemia/infarct). The most common cause of chronic right heart failure is LV failure (causing post-capillary pulmonary hypertension). Other causes of RV failure include pre-capilla

CardioNerds (Amit Goyal & Daniel Ambinder) join Penn cardiology fellows (Brian McCauley, Norrisa Haynes, and Mahesh Vidula) for a rooftop picnic in sunny Philadelphia! They discuss an informative case of peripartum cardiomyopathy with cardiogenic shock. Program director Dr. Frank Silvestry provides the E-CPR segment and a message to applicants. Johns Hopkins internal medicine resident Colin Blumenthal with mentorship from University of Maryland cardiology fellow Karan Desai.  Jump to: Patient summary – Case figures & media – Case teaching – References – Production team Episode graphic by Dr. Carine Hamo The CardioNerds Cardiology Case Reports series shines light on the hidden curriculum of medical storytelling. We learn together while discussing fascinating cases in this fun, engaging, and educational format. Each episode ends with an “Expert CardioNerd Perspectives & Review” (E-CPR) for a nuanced teaching from a content expert. We truly believe that hearing about a patient is the singular theme that unifies everyone at every level, from the student to the professor emeritus. We are teaming up with the ACC FIT Section to use the #CNCR episodes to showcase CV education across the country in the era of virtual recruitment. As part of the recruitment series, each episode features fellows from a given program discussing and teaching about an interesting case as well as sharing what makes their hearts flutter about their fellowship training. The case discussion is followed by both an E-CPR segment and a message from the program director. CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademySubscribe to our newsletter- The HeartbeatSupport our educational mission by becoming a Patron!Cardiology Programs Twitter Group created by Dr. Nosheen Reza Patient Summary Two weeks postpartum, a woman in her mid 20s, G1P1, with no past medical history presented following a tonic-clonic seizure. Prior to this, she had been experiencing 1 week of worsening dyspnea and lower extremity edema. Initial work-up revealed a left MCA stroke and she underwent thrombectomy. Limited TTE found LVEF <20% and a LV apical thrombus; she was started on milrinone due to concern for cardiogenic shock and transferred to the University of Pennsylvania.  Upon arrival, she was found to be hypotensive and tachycardic. Exam was notable for elevated JVP, +S3, LE edema and R sided hemiparesis. Labs showed multiorgan injury, elevated NT-proBNP and elevated lactate. EKG demonstrated sinus tachycardia with no ST-T changes. Formal TTE showed severely dilated LV with EF 10%, diffuse LV hypokinesis, and confirmed a large LV apical thrombus. A pulmonary artery catheter was placed for tailored therapy and found elevated L-sided > R-side filling pressures with low cardiac index despite inotropes. Cardiac power output (CPO) was severely decreased with borderline pulmonary artery pulsatility index (PAPI), corroborating left > right heart failure. Patient ultimately required a durable left ventricular assist device (LVAD). Over the course of 9 months her guideline directed medical therapy (GDMT) was titrated and her intrinsic cardiac function and symptoms improved. Her EF improved to 35-40% and she tolerated an LVAD weaning protocol, so her LVAD was ultimately explanted! She is currently doing well on GDMT alone!   Case Media CXR: Mild interstitial edema, +ET tube ST (131), LAD, nonspec T wave flattening, nl intervals Click to Enlarge TTE 1 TTE 2 Episode Schematics & Teaching Click to enlarge! The CardioNerds 5! – 5 major takeaways from the #CNCR case 1. How do we define Peripartum Cardiomyopathy?   Diagnosis is made by the development of heart failure towards the end of pregnancy or in the months following delivery (~5 months postpartum), no other identifiable cause of HF, and demonstration of LV systolic dysfunction with LVEF typically less than 45% with or without dilation.  Risk factors include history of pre-eclampsia, hypertension, cocaine use, multifetal pregnancies, older maternal age, and African descent.     Keep a broad differential diagnosis for new onset heart failure in the peripartum period. The differential includes pre-existing cardiomyopathy, valvular disease or congenital cardiomyopathy unmasked by the hemodynamic changes of pregnancy (see CNCR episode 48 for more on the hemodynamic changes of pregnancy!). Other differentials should include ischemia/spontaneous coronary artery dissection (SCAD), stress-induced cardiomyopathy, CM due to systemic disease (e.g. sepsis, rheumatologic disease), myocarditis and tac