Cardionerds: A Cardiology Podcast

Dr. José Joglar and Dr. Mina Chung discuss the key takeaways from the 2023 ACC/AHA/ACCP/HRS Atrial Fibrillation Guidelines, including the updated staging scheme, the effects of alcohol and caffeine on AF, improving stroke prevention, the evolving importance of rhythm control, shared decision-making, and the process of developing clinical guideline documents.

CardioNerds podcast features Drs. Karishma Rahman, Shu Min Lao, and Constantine Troupes discussing a fascinating case of a 20-year-old woman with hypertension and possible mid-aortic syndrome. They explore the differential diagnosis of early-onset hypertension, imaging for diagnosis and surveillance, and treatment options. They also delve into large vessel vasculitis and the challenges in obtaining tissue diagnosis. Managing hypertension and IgG4-related disease, imaging results, and the importance of considering underlying causes of wall thickening are discussed.

Dr. Jamie Almandoz, an expert in obesity and cardiovascular disease risk, joins the hosts to discuss the impact of obesity on cardiovascular health. They explore the question of whether it is possible to be healthy at any size and highlight the biomechanical and psychosocial challenges of obesity. They also delve into the effects of different types of adipose tissue on metabolic health and organ systems. The speakers analyze the results of a semaglutide trial for obesity and cardiovascular disease, discussing the significant risk reduction in major adverse cardiovascular events. Lastly, they discuss the percentage of body weight reduction needed for cardiovascular disease benefits.

Dr. Ashley Lochman and Dr. Chris Domenico discuss anticoagulation pharmacology and clinical decision-making for atrial fibrillation. They explore topics such as when to use warfarin, choosing appropriate DOAC agents, managing therapy in patients on antiplatelets, and the challenges of clinical pharmacology in cardiology.

CardioNerds (Dr. Amit Goyal) join Dr. Anureet Malhotra, Dr. John Fritzlen, and Dr. Tarun Dalia from the University of Kansas School of Medicine for some of Kansas City’s famous barbeque. They discuss a case of Hydroxychloroquine induced cardiomyopathy. Notes were drafted by Dr. Anureet Malhotra, Dr. John Fritzlen, and Dr. Tarun Dalia. Expert commentary was provided by Dr. Pradeep Mammen. The episode audio was edited by Dr. Akiva Rosenzveig. Drug-induced cardiomyopathy remains an important and under-recognized etiology of cardiomyopathy and heart failure. Hydroxychloroquine is a disease-modifying antirheumatic drug used for various rheumatological conditions, and its long-term use is well-known to have toxic effects on cardiac muscle cells. Multiple cardiac manifestations of these drugs have been identified, the most prominent being electrophysiological disturbances. In this episode, we discuss a biopsy-proven case of hydroxychloroquine-induced cardiotoxicity with detailed histopathological and imaging findings. We develop a roadmap for the diagnosis of hydroxychloroquine-induced cardiomyopathy and discuss the various differentials of drug-induced cardiomyopathy. We highlight the importance of clinical monitoring and early consideration of drug-induced toxicities as a culprit for heart failure. US Cardiology Review is now the official journal of CardioNerds! Submit your manuscript here. CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Case Media - Hydroxychloroquine induced cardiomyopathy Pearls - Hydroxychloroquine induced cardiomyopathy Continued decline in left ventricular systolic function despite appropriate guideline directed medical therapy should prompt a thorough evaluation for unrecognized etiologies and warrants an early referral to advanced heart failure specialists. Transthoracic echocardiogram is a valuable non-invasive screening tool for suspected pulmonary hypertension, but right heart catheterization is required for definitive diagnosis. Cardiac MRI can be used for better characterization of myocardial tissue and can aid in the evaluation of patients with non-ischemic cardiomyopathy. Hydroxychloroquine (HCQ) is a commonly used DMARD that remains an underrecognized etiology of cardiomyopathy and heart failure. In addition to ophthalmological screening, annual ECG, as well as echocardiography screening for patients on long-term HCQ therapy, should be considered in patients at risk for cardiovascular toxicity, including those with pre-existing cardiovascular disease, older age, female sex, longer duration of therapy, and renal impairment. Management of hydroxychloroquine-associated cardiomyopathy consists of discontinuing hydroxychloroquine and standard guideline-directed medical therapy for heart failure.  HCQ cardiomyopathy may persist despite medical therapy, and advanced therapy options may have to be considered in those with refractory heart failure. Show Notes - Hydroxychloroquine induced cardiomyopathy What are the various cardiotoxic effects of hydroxychloroquine (HCQ) and the mechanism of HCQ-mediated cardiomyopathy? One of the most frequently prescribed disease-modifying antirheumatic drugs (DMARDs), HCQ is an immunomodulatory and anti-inflammatory agent that remains an integral part of treatment for a myriad of rheumatological conditions. Its efficacy is linked to inhibiting lysosomal antigen processing, MHC-II antigen presentation, and TLR functions.8 The known cardiac manifestations of HCQ-induced toxicity include conduction abnormalities, ventricular hypertrophy, hypokinesia, and lastly, cardiomyopathy. Conduction Abnormalities - by binding to and inhibiting the human ether-à-go-go-related gene (hERG) voltage-gated potassium channel, also known as Ikr channel, HCQ can lead to prolongation of corrected QT (QTc) interval. This can lead to an increased risk of drug-induced Torsades de pointes and other lethal ventricular arrhythmias. Cardiomyopathy - HCQ is a lipophilic drug that easily permeates myocytes and binds to lysosomal phospholipids, leading to lysosomal accumulation of phospholipids. Furthermore, by increasing the pH of the lysosome, HCQ inhibits lysosomal enzymes, which interferes with lysosomal function and exocytosis, leading to an acquired lysosomal storage disorder. This results in myofibrillar disorganization, atrophy, and fibrosis, which may lead to cardiomyopathy. Risk factors for the development of cardiotoxicity are thought to be pre-existing cardiovascular disease, older age, female sex, longer duration of therapy, and renal impairment. 8 Extracardiac side effects – With long term use, HCQ can also lead to ocular toxicity, neuropathy, and myopathy with similar pathogenesis as cardiotoxicity, i.e., acquired lysosomal storage disorder. What are the histopathological findings of HCQ induced Cardiomyopathy? HCQ causes an acquired lysosomal storage disorder due to the inhibition of constitutive autophagy present in normal cardiac myocytes. On histopathology, this presents itself as cytoplasmic vacuoles, lamellar bodies and curvilinear inclusion bodies in cytoplasm that can be visualized with electron microscopy. Of these findings, curvilinear bodies are thought to be pathognomonic for HCQ induced cardiotoxicity. On histopathology, these findings can resemble inherited lysosomal storage disorders including Anderson- Fabry disease except for the presence of curvilinear bodies. 9 What is the differential diagnosis for HCQ induced cardiomyopathy? Differentials of HCQ mediated cardiomyopathy include storage disorders like Fabry disease, adult-onset Pompe disease (acid maltase deficiency), and Danon disease. Many drug-induced myopathies such as amiodarone, rituximab, prednisone, cocaine, cobalt, and several chemotherapeutic agents can also resemble HCQ mediated cardiotoxicity. Furthermore, amyloidosis, sarcoidosis and myocarditis also merit consideration as they can lead to restrictive physiology and present similar echocardiographic findings. They can be differentiated using advanced cardiac imaging such as cardiac MRI and histopathological findings on endomyocardial biopsy. How can Cardiac MRI (CMR) assist in the work up of non-ischemic cardiomyopathy? CMR can enhance visualization of cardiac structures that may be poorly seen on echocardiogram due to location or poor acoustic windows. CMR also uniquely provides detailed tissue characterization. CMR can be used for assessing many pathologies, including aortic disease, coronary artery disease, cardiomyopathies, pericardial disease, and congenital heart disease. 4 CMR is also considered the gold standard for assessing cardiac function and can be used to assess valvular pathologies with flow assessment. Late gadolinium enhancement (LGE) refers to the discrimination of regions of scar, necrosis, or inflammation from normal tissue by the prolonged retention of gadolinium-based contrast agents. The pattern of LGE, as well as T1 and T2 mapping, aid in tissue characterization and accurate diagnosis. Key take-home points are as follows: The presence of LGE in a coronary distribution can support the diagnosis of prior myocardial infarction and aid in the assessment of myocardial viability. LGE in the mid-wall and sub-epicardium of the LV is characteristic of viral myocarditis. In addition, T1 mapping helps estimate the extracellular volume, and T2 weighted imaging can show myocardial edema in patients with myocarditis. In amyloidosis, the classic CMR findings include thick LV walls, valves, and interatrial septum and the presence of a pericardial effusion. They may also have the existence of amyloid protein in the myocardial interstitium associated with characteristic patterns of circumferential subendocardial LGE. What is the management of HCQ induced cardiomyopathy? Diagnosis – HCQ cardiomyopathy diagnosis requires a high level of suspicion. A detailed history is an essential first step. CMR can aid in tissue characterization and is a helpful non-invasive tool. Definitive diagnosis can be established by obtaining an endomyocardial biopsy, given its distinctive histopathological findings, and ruling out close mimics of HCQ-induced cardiotoxicity. Treatment – the potentially reversible nature of HCQ cardiomyopathy makes early diagnosis and discontinuation of the offending drug the mainstays of treatment along with guideline directed medical therapy for heart failure. Recovery is variable and may take months or even years for LV function to improve. In some cases, there may be partial or no recovery, requiring advanced therapies evaluations. References - Hydroxychloroquine induced cardiomyopathy Greiner S, Jud A, Aurich M, et al. Reliability of Noninvasive Assessment of Systolic Pulmonary Artery Pressure by Doppler Echocardiography Compared to Right Heart Catheterization: Analysis in a Large Patient Population. Journal of the American Heart Association.2014;3(4).10.1161/JAHA.114.001103 Augustine DX, Coates-Bradshaw LD, Willis J, et al. Echocardiographic assessment of pulmonary hypertension: a guideline protocol from the British Society of Echocardiography. Echo research and practice. 2018;5(3):G11-G24. 10.1530/ERP-17-0071 Page RL, O’Bryant CL, Cheng D, et al. Drugs That May Cause or Exacerbate Heart Failure. Circulation. 2016;134(6).https://doi.org/10.1161/CIR.0000000000000426 Kramer CM. Role of Cardiac MR Imaging in Cardiomyopathies. Journal of Nuclear Medicine. 2015;56(Supplement_4):39S45S.10.2967/jnumed.114.142729. Joyce E, Fabre A, Mahon N.

CardioNerds podcast features Drs. Hanad Bashir, Hyunsoo Chung, and Dalia Aziz discussing a case of angioleiomyoma. They highlight the diagnostic approach to syncope, evaluation of cardiac masses, rare angioleiomyomas, and unique experiences in the Christ Hospital Fellowship Program.

Calling all those with a passion for cardiovascular prevention! In this episode of the CardioNerds Cardiovascular Prevention Series, we take a deep dive into the world of glucagon-like peptide-1 (GLP-1) receptor agonists. Along the way, you’ll hear about the biology of the GLP-1 molecule and its related peptides, learn more about how GLP-1 agonists promote glycemic control, weight loss, and cardiometabolic health, and explore the current body of literature supporting the individualized application of these medications to patients with diabetes, obesity, and/or ASCVD. Join Dr. Christian Faaborg-Andersen (CardioNerds Academy Fellow and Internal Medicine Resident at MGH), Dr. Gurleen Kaur (Director of the CardioNerds Internship, Chief of House Einthoven, and Internal Medicine resident at BWH), and Dr. Rick Ferraro (CardioNerds Academy House Faculty and Cardiology Fellow at JHH) for a wide-ranging discussion on GLP-1 and GIP agonists with Dr. Dennis Bruemmer (Cardiologist and Director of the Center for Cardiometabolic Health in the section of Preventive Cardiology at the Cleveland Clinic). Show notes were drafted by Dr. Christian Faaborg-Andersen. Audio editing was performed by CardioNerds Academy Intern, student Dr. Tina Reddy. This episode was produced in collaboration with the American Society of Preventive Cardiology (ASPC) with independent medical education grant support from Novo Nordisk. See below for continuing medical education credit. Claim CME for this episode HERE. CardioNerds Prevention PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls and Quotes - GLP-1 Agonists: Mechanisms to Applications The selection and dosing of GLP-1 and GIP agonists (GLP-1s and GIPs) depends on their intended use as an anti-glycemic or anti-obesity agent. The cardiovascular benefits of GLP-1s and GIPs may be independent of improvements in glycemic control, and in part be driven by reduction in inflammation, a key driver of arterial plaque formation. In patients with comorbid coronary artery disease, obesity, and diabetes, GLP-1 agonists and SGLT-2 inhibitors should be used as first-line agents, over metformin. Tirzepatide is a dual agonist that activates GIP and GLP-1 receptors. GIP is highly expressed in the brain, which may mediate satiety, promote energy expenditure, and enhance peripheral glucose metabolism. Caution should be used with GLP-1 agonists in patients with long-standing diabetes complicated by gastroparesis, as well as incompletely treated diabetic retinopathy. GI upset is not uncommon with GLP-1/GIP agonists, and switching to a different agonist is unlikely to help.  Show notes - GLP-1 Agonists: Mechanisms to Applications What are the mechanisms of action by which GLP-1 and GIP controls blood sugar and body weight? Glucagon-like peptide-1 (GLP-1) is an endogenous hormone that is secreted in response to an oral glucose load. It promotes insulin release, inhibits glucagon secretion, and slows gastric emptying via the brain-intestine axis, leading to satiety. GLP-1 agonists are medications that mimic the effect of this hormone and, on average, lower hemoglobin A1C by 0.8% to 1.5%. These medications include semaglutide, liraglutide, and dulaglutide. Glucose-dependent insulinotropic polypeptide (GIP) is also an endogenous hormone, similarly secreted by the body in response to an oral glucose load such as a meal. GIP is highly expressed in the arcuate nucleus and hypothalamus, which may mediate satiety, promote energy expenditure, and enhance peripheral glucose metabolism. Tirzepatide is a dual GLP-1/GIP agonist. What is the role of GLP-1/GIP agonists in patients with overweight/obesity and/or type 2 diabetes? How does the dosing of GLP-1/GIP medications change with their intended disease target? The STEP-1 trial showed that once-weekly semaglutide led to a net 15% weight loss in non-diabetic, obese/overweight patients. The SELECT trial builds on these results, showing that once-weekly semaglutide resulted in a 20% reduction in the primary composite endpoint of cardiovascular death, nonfatal myocardial infarction, or nonfatal stroke in patients with pre-existing cardiovascular disease and BMI ≥ 27kg/m2. Other notable trials in this space include the LEADER trial (liraglutide), the SUSTAIN-6 trial (semaglutide), and the REWIND trial (dulaglutide).  The dosing of GLP-1 agonists depends on their intended use as either an anti-glycemic or anti-obesity agent. For weight management, the current FDA-approved therapies are semaglutide 2.4mg weekly and liraglutide 3mg daily. For diabetes, the approved medications are semaglutide 2mg weekly, dulaglutide 4.5mg weekly, and tirzepadite 15mg weekly. What are the cardiometabolic benefits of GLP-1/GIP agonist therapy, beyond glycemic control and/or weight loss? When are GLP-1/GIP agonists considered first-line therapy? The cardiovascular benefits of GLP-1s may be independent of improvements in glycemic control, and in part be driven by reductions in inflammation and cytokine response driving plaque formation in the arterial wall. In the SELECT trial, once weekly 2.4mg semaglutide led to a 20% reduction in MACE in non-diabetic, obese/overweight patients with established ASCVD. In patients with comorbid coronary artery disease, obesity, and diabetes, national guidelines recommend GLP-1 agonists and SGLT-2 inhibitors as first-line agents, over metformin.  How does tirzepatide differ from GLP-1 agonists? Tirzepetide is a dual GLP-1/GIP agonist. GIP is highly expressed in the arcuate nucleus and hypothalamus, which may mediate satiety, promote energy expenditure, and enhance peripheral glucose metabolism. The SURMOUNT trial showed 20% net weight loss with tirzepatide in patients with overweight/obesity, nearly as effective as metabolic surgery.  What are the absolute and relative contraindications to GLP-1/GIP agonist therapy? GLP-1/GIP agonists are contraindicated in patients with a personal or family history of medullary thyroid cancer. Caution should be used in patients with long-standing diabetes with neuropathy and gastroparesis, as well as incompletely treated diabetic retinopathy. Gallstone pancreatitis should not be considered a contraindication to GLP-1/GIP therapy after cholecystectomy, though a history of recent pancreatitis should give one pause in prescribing a GLP-1/GIP agonist. GLP-1 agonists should not be prescribed for type 1 diabetes, during pregnancy, or with breastfeeding.  What are the most common side effects of GLP-1 agonists? GI upset is the most common side effect with GLP-1/GIP agonist therapy, and the incidence of these side effects is similar between tirzepadite and semaglutide in randomized control trials. References - GLP-1 Agonists: Mechanisms to Applications Wilding JPH, Batterham RL, Calanna S, et al. Once-Weekly Semaglutide in Adults with Overweight or Obesity. N Engl J Med. 2021;384(11):989-1002. doi:10.1056/NEJMoa2032183 https://pubmed.ncbi.nlm.nih.gov/33567185/ Marso SP, Daniels GH, Brown-Frandsen K, et al. Liraglutide and Cardiovascular Outcomes in Type 2 Diabetes. N Engl J Med. 2016;375(4):311-322. doi:10.1056/NEJMoa1603827 https://pubmed.ncbi.nlm.nih.gov/27295427/ Marso SP, Bain SC, Consoli A, et al. Semaglutide and Cardiovascular Outcomes in Patients with Type 2 Diabetes. N Engl J Med. 2016;375(19):1834-1844. doi:10.1056/NEJMoa1607141 https://pubmed.ncbi.nlm.nih.gov/27633186/ Gerstein HC, Colhoun HM, Dagenais GR, et al. Dulaglutide and cardiovascular outcomes in type 2 diabetes (REWIND): a double-blind, randomised placebo-controlled trial. Lancet. 2019;394(10193):121-130. doi:10.1016/S0140-6736(19)31149-3 https://pubmed.ncbi.nlm.nih.gov/31189511/

Dr. Amit Goyal and cardiology fellows from the Cleveland Clinic discuss a case of a 61-year-old man with symptoms of heart failure and left ventricular hypertrophy. They explore the differential diagnosis for LVH and focus on Fabry disease as an HCM mimic. They also discuss the importance of genetic testing and various treatment options for fibro disease.

CardioNerds (Daniel Ambinder) joins Dr. Priyanka Ghosh and Dr. Ahmad Lone from the Guthrie Robert Packer Hospital for a day in the Finger Lakes region of New York. They discuss the following case. A 35-year-old man with nonspecific symptoms of headache, fatigue, and chest wall pain was found to have elevated troponin levels, elevated inflammatory markers, EKG with inferior and anterolateral ST depressions, and no obstructive coronary artery disease on cardiac catheterization. His peripheral eosinophilia, cardiac MRI results, and bone marrow biopsy revealed eosinophilic myocarditis from acute leukemia with eosinophilia. This episode discusses this rare type of myocardial inflammation, its potential causes, and the diagnostic workup with the mention of how this patient was ultimately treated for his acute leukemia and myocarditis. Expert commentary is provided by Dr. Saurabh Sharma. Audio editing by CardioNerds academy intern, student doctor Pace Wetstein. US Cardiology Review is now the official journal of CardioNerds! Submit your manuscript here. CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Case Media - Guthrie Robert Packer Hospital Pearls - Guthrie Robert Packer Hospital Myocarditis, especially eosinophilic myocarditis, requires a high level of clinical suspicion. Eosinophilic myocarditis should be considered in a patient presenting with chest pain, normal coronary arteries, and pronounced eosinophilia levels. Causes of eosinophilic myocarditis can vary, and diagnosis requires a thorough, detailed history, which cannot be determined many times. Treatment of eosinophilic myocarditis focuses on the underlying etiology, acute management, and therapy for concomitant heart failure or cardiomyopathy. Consider the whole-patient and cardiac manifestations of non-cardiac illnesses. Show Notes - Guthrie Robert Packer Hospital What is eosinophilic myocarditis? Eosinophilic myocarditis is a type of myocardial inflammation involving eosinophilic cell infiltration and an entity that is likely under-recognized. It requires a high level of suspicion as, many times, patients may not initially present with peripheral eosinophilia, which may develop over the course of their disease process. The presentation can vary from mild cardiac injury to fulminant cardiogenic shock depending on the degree of infiltration and concurrent other organ involvement. The presentation can include heart failure symptoms as well as electrical conduction abnormalities. How is eosinophilic myocarditis diagnosed? Eosinophilic myocarditis is diagnosed by a thorough history including new medications, exposures, travel, prior allergy history, physical exam, lab work including a complete blood count differential, inflammatory markers, cardiac biomarkers, and cardiac diagnostics which should include a 12-lead ECG and transthoracic echocardiogram as well as potentially cardiac MRI and/or endomyocardial biopsy. What are the causes of eosinophilic myocarditis? The causes of eosinophilic myocarditis include medication-induced, hypersensitivity reactions, infections, malignancy, and immune-mediated disorders such as eosinophilic granulomatosis with polyangiitis and hypereosinophilic syndromes. The hypersensitivity subtype has been reported to be the most common cause. Potential offending medications can include antibiotics, sulfonamides, anticonvulsants, anti-inflammatory medications, and diuretics. What is the treatment for eosinophilic myocarditis? Treatment for eosinophilic myocarditis is multi-faceted, including focusing on the etiology and withdrawal of any potential offending agents, management of the acute clinical presentation, and treatment of any concomitant heart failure or cardiomyopathy. Immunosuppressive therapy has been controversial; however, many case reports have successfully used methylprednisolone, and some patients with cardiogenic shock from eosinophilic myocarditis have received therapy with azathioprine. References Al Ali AM, Straatman LP, Allard MF, Ignaszewski AP. Eosinophilic myocarditis: case series and review of literature. Can J Cardiol. 2006 Dec;22(14):1233-7. doi: 10.1016/s0828-282x(06)70965-5. PMID: 17151774; PMCID: PMC2569073. Takkenberg JJ, Czer LS, Fishbein MC, Luthringer DJ, Quartel AW, Mirocha J, Queral CA, Blanche C, Trento A. Eosinophilic myocarditis in patients awaiting heart transplantation. Crit Care Med. 2004 Mar;32(3):714-21. doi: 10.1097/01.ccm.0000114818.58877.06. PMID: 15090952. Morimoto S, Kubo N, Hiramitsu S, Uemura A, Ohtsuki M, Kato S, Kato Y, Sugiura A, Miyagishima K, Mori N, Yoshida Y, Hishida H. Changes in the peripheral eosinophil count in patients with acute eosinophilic myocarditis. Heart Vessels. 2003 Sep;18(4):193-6. doi: 10.1007/s00380-003-0721-0. PMID: 14520487. Burke AP, Saenger J, Mullick F, Virmani R. Hypersensitivity myocarditis. Arch Pathol Lab Med. 1991 Aug;115(8):764-9. PMID: 1863186. Fozing T, Zouri N, Tost A, Breit R, Seeck G, Koch C, Oezbek C. Management of a patient with eosinophilic myocarditis and normal peripheral eosinophil count: case report and literature review. Circ Heart Fail. 2014 Jul;7(4):692-4. doi: 10.1161/CIRCHEARTFAILURE.114.001130. PMID: 25028351. Brambatti M, Matassini MV, Adler ED, Klingel K, Camici PG, Ammirati E. Eosinophilic Myocarditis: Characteristics, Treatment, and Outcomes. J Am Coll Cardiol. 2017 Nov 7;70(19):2363-2375. doi: 10.1016/j.jacc.2017.09.023. PMID: 29096807. Cheung CC, Constantine M, Ahmadi A, Shiau C, Chen LYC. Eosinophilic Myocarditis. Am J Med Sci. 2017 Nov;354(5):486-492. doi: 10.1016/j.amjms.2017.04.002. Epub 2017 Apr 6. PMID: 29173361. Aggarwal A, Bergin P, Jessup P, Kaye D. Hypersensitivity myocarditis presenting as cardiogenic shock. J Heart Lung Transplant. 2001 Nov;20(11):1241-4. doi: 10.1016/s1053-2498(01)00313-8. PMID: 11704488. Kounis NG, Zavras GM, Soufras GD, Kitrou MP. Hypersensitivity myocarditis. Ann Allergy. 1989 Feb;62(2):71-4. PMID: 2645814. Li H, Dai Z, Wang B, Huang W. A case report of eosinophilic myocarditis and a review of the relevant literature. BMC Cardiovasc Disord. 2015 Feb 26;15:15. doi: 10.1186/s12872-015-0003-7. PMID: 25887327; PMCID: PMC4359588.

Dr. Josh Saef and Dr. Sumeet Vaikunth join Dr. Sheng Fu, Dr. Payton Kendsersky, and Dr. Aniqa Shahrier to discuss a case of a patient with D-TGA and Eisenmenger's syndrome treated with a Heartmate 3. They explore the patient's medical history, evaluation process for heart transplantation, challenges and benefits of ventricular assist device implantation, and the importance of early evaluation and timely support in congenital heart disease.