Cardionerds: A Cardiology Podcast

Latest Episodes:

354. Obesity: Obesity & Cardiovascular Disease Risk with Dr. Jaime Almandoz Jan 09, 2024

Show notes

CardioNerds Dr. Rick Ferraro (cardiology fellow at Johns Hopkins Hospital) and Dr. Eunice Dugan (cardiology fellow at the Cleveland Clinic) join episode lead Dr. Tiffany Brazile (cardiology fellow at the University of Texas Southwestern Medical Center and postdoctoral fellow at the Institute for Exercise and Environmental Medicine) to discuss the impact of obesity on cardiovascular disease risk, differential risk in specific populations, and effective strategies for counseling patients. They are joined by expert Dr. Jaime Almandoz, Medical Director of the Weight Wellness Program and an Associate Professor of Medicine at the University of Texas Southwestern Medical Center. 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 - Obesity & Cardiovascular Disease Risk The durability of metabolically healthy obesity (i.e., normal A1c, lipids, LFTs, BMP, normotensive) is limited. Within 5 years, a third of adults with “metabolically healthy” obesity will develop a cardiometabolic complication. The biomechanical and psychosocial complications of obesity are just as important as the cardiometabolic complications. Biomechanical and psychosocial complications, including obstructive sleep apnea, joint pain, and mood disorders also influence cardiovascular disease risk. Weight loss is not always the patient’s goal. Meet patients where they are and understand their challenges, concerns, and long-term goals with respect to their cardiovascular health and obesity. This information provides an opportunity to frame the conversation in a supportive and engaging way that allows for patient education. Body mass index (BMI) is a screening tool for obesity, but is not sufficient for providing individualized care. Obesity management methods that result in rapid weight loss may not be appropriate for all patients. These methods, such as bariatric surgery and GLP1-receptor agonists, require regular monitoring, follow-up, and multidisciplinary care (e.g., nutritionist, exercise physiologist, endocrinologist, cardiologist, psychologist, etc.). Show notes - Obesity & Cardiovascular Disease Risk Is it possible to be healthy at any size? Whether an individual can be healthy at any size depends on the definition of health and its durability.Approximately 10-15% of adults with obesity are metabolically healthy.The risk for developing cardiometabolic disease is higher in obese versus non-obese adults. One in three adults with metabolically healthy obesity will develop cardiometabolic complications (i.e., insulin resistance/diabetes, hyperlipidemia, hypertension) within five years. Thus, metabolically healthy obesity may represent a transient phenotype with adverse long-term consequences. Consider non-metabolic health consequences of obesity that also influence cardiovascular disease risk. Obstructive sleep apnea, joint pain leading to decreased physical activity, and mood disorders are key considerations here and encompass the biomechanical and psychosocial consequences of obesity. Does large, rapid weight loss result in poorer long-term weight loss than slower, gradual weight loss? When approaches to weight loss are not sustainable, such as extremely low-calorie diets or extreme fitness regimens, the results and associated health benefits are less likely to be durable. Rapid, large-magnitude weight loss is appropriate for some adults with obesity and can be achieved through bariatric surgery and/or anti-obesity medications. Safety and sustainability are supported by regular follow-up, monitoring, and multidisciplinary care to incorporate nutritional and physical activity recommendations. Obesity management must be individualized to meet patient needs and goals while accounting for comorbid conditions (e.g., frailty, fall risk, disordered eating, etc.) What are some best practices for incorporating the diagnosis of obesity into a patient’s assessment, including cardiovascular disease risk? Seek to understand what the patient wants to achieve during the office visit. Inquire about the patient’s health journey, goals, concerns, and challenges. In addition to addressing the patient’s expressed goals, frame the conversation in terms of concerns you have about the patient’s health. Incorporate objective measures, such as body composition, waist circumference, cardiorespiratory fitness, and biomarkers that can help support your concerns and management goals. Does obesity impact men and women differently? Prevalence: of adults with obesity, women are more likely than men to have severe obesity. Obesity is also more prevalent in women of certain racial/ethnic minorities as compared to men. Fat distribution: men tend to have more visceral or central adiposity, which is associated with increased cardiometabolic risk. Earlier in adulthood, women tend to have more body fat in the gluteofemoral region. With advancing age and menopause, the distribution of excess adipose tissue in women often shifts to the visceral/central region and may enhance cardiometabolic risk. What are the practical methods for evaluating and measuring obesity during a patient visit? BMI is a screening tool for obesity. It is blind to body composition and fat distribution. Cut points for BMI and the association with cardiovascular disease risk vary by race/ethnicity. Consideration of different BMI cut points for patients of various racial/ethnic backgrounds is important when evaluating candidacy for bariatric surgery or anti-obesity medications. Waist circumference is a useful measure to estimate visceral/central adiposity. Cut points for men and women have been established that are associated with increased cardiovascular disease risk across multiple studies. Measures of body composition provide valuable information about fat and lean body masses. DEXA scans and MRIs also provide data on fat distribution; however, they are impractical and expensive for regular use in the clinical setting. Bioelectrical impedance can provide body composition data efficiently during a clinic visit. What are alternative validated tools beyond the Pooled Cohort Equation that can be used to estimate ASCVD risk in various ethnic/racial groups? The QRISK3 calculator is an alternative assessment tool for 10-year ASCVD risk that has been validated in 9 different ethnic groups. The calculator includes novel variables, such as chronic kidney disease, history of migraines, severe mental illness, erectile dysfunction, and family history of premature ASCVD. https://www.qrisk.org/ What are the mechanisms by which obesity impacts the development of cardiovascular disease? Obesity and lipotoxicity can impact cardiovascular disease development through multiple mechanisms, including inflammation that can lead to a prothrombotic state, insulin resistance, and alterations in lipid metabolism that can promote atherosclerosis. The distribution of body fat is highly heterogeneous and is partially driven by genetics. Brown adipose tissue has a high mitochondrial load and is involved in adaptive thermogenesis. White adipose tissue is considered more of a storage form of adipose tissue that also functions as an endocrine organ and provides insulation/protection for vital organs. Ectopic fat depots, such as hepatic steatosis or epicardial adipose tissue, are metabolically active and can influence adjacent tissues through humoral and neurohormonal signals. These fat depots may also exert mechanical effects on the organs they surround. The ways in which individuals accrue fat in these different locations, the specific mechanisms by which they may increase cardiovascular disease development, and whether targeted therapies to reduce specific fat depots are incompletely understood. References - Obesity & Cardiovascular Disease Risk 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/

353. Atrial Fibrillation: Anticoagulation Pharmacology & Clinical Decision-Making with Dr. Ashley Lochman and Dr. Chris Domenico Dec 29, 2023

Show notes

CardioNerds co-founder Dr. Amit Goyal, series co-chair Dr. Colin Blumenthal, and episode lead Dr. Anushka Tandon to discuss pharmacologic anticoagulation options in atrial fibrillation with Drs. Ashley Lochman and Chris Domenico. The case-based review helps clarify some key concepts, such as when warfarin is preferred for anticoagulation, who may be a good DOAC (direct-acting oral anticoagulant) candidate, how to choose an appropriate DOAC agent, and how to manage anticoagulation therapy in patients already on antiplatelet therapies. Notes were drafted by Dr. Anushka Tandon. The episode audio was edited by student Dr. Shivani Reddy. This CardioNerds Atrial Fibrillation series is a multi-institutional collaboration made possible by contributions of stellar fellow leads and expert faculty from several programs, led by series co-chairs, Dr. Kelly Arps and Dr. Colin Blumenthal. This episode was planned and recorded prior to the release of the 2023 ACC/AHA/ACCP/HRS Guideline for the Diagnosis and Management of Atrial Fibrillation. Please refer to this guideline document for the most updated recommendations. We have collaborated with VCU Health to provide CME. Claim free CME here! CardioNerds Atrial Fibrillation 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 - Anticoagulation Pharmacology Avoid potentially fatal errors with this terminology tip for correctly referencing non-warfarin oral anticoagulant agents: it’s DOAC (like, please DO use AntiCoagulation), not NOAC (imagine someone interpreting that as “NO AntiCoagulation for this patient” at discharge – yikes)! Sometimes, an oldie really is a goodie – warfarin is recommended over DOACs for patients with mechanical heart valves, moderate-to-severe mitral stenosis, anti-phospholipid antibody syndrome (APLS), left ventricular (LV) thrombus, higher INR goals, or DOAC failure. Patient preference and medication costs should also be considered – at the end of the day, “the best drug is the drug that a patient is willing to take!” Standard-dose rivaroxaban or apixaban may be considered for use in patients weighing >120kg or with BMI >40; use of other DOACs should be limited to pts weighing =/120kg or with a BMI >40. However, ISTH updated their guidance in 2021 [6] to support using rivaroxaban and apixaban for VTE treatment or prevention “regardless of body weight and BMI”; these DOACs are often used in patients with obesity for non-VTE indications (e.g., thromboprophylaxis in atrial fibrillation). Data to support this include a post-hoc analysis of the ARISTOTLE trial (apixaban in atrial fibrillation), which showed that patients weighing >120kg (~5% of the study population) had similar results to the overall study population. It’s important to use adjusted body weight when calculating CrCl to estimate renal function and determine DOAC dosing in obese patients. Other DOACs should be avoided in pts >120kg/with BMI >40 due to limited or unconvincing data at this time.Hepatic impairment: DOACs have varying hepatic metabolism (apixaban is the most hepatically cleared and dabigatran the least), but limited data exist for DOAC dose adjustments in patients with hepatic impairment. DOACs should NOT be used in Child-Pugh Class C/severe hepatic disease, while rivaroxaban (and betrixaban)[GU1] should also NOT be used in moderate/CP Class B patients. DOACs should be avoided in patients with decompensated/unstable cirrhosis. Aside from these caveats, DOACs may be considered for use in mild-moderate (Class A/B) hepatic impairment (with exceptions as above).Renal impairment: DOACs may be used in stable CKD with appropriate renal dose adjustments; DOAC therapies should be held in the context of AKI. Dabigatran is the most renally cleared and generally avoided for this reason. Apixaban is the least renally cleared and is generally the preferred agent in patients with renal impairment, including ESRD (in the context of which apixaban use is supported by data, including that from a 2022 cohort study [7] vs. warfarin).Drug Interactions: rivaroxaban, apixaban, edoxaban, and dabigatran are all P-gp substrates that will be affected by P-gp inducers or inhibitors (e.g., dronedarone, amiodarone, digoxin, diltiazem, verapamil, antiepileptics, antifungals, chemotherapy agents, and St. John’s Wort). Rivaroxaban and apixaban are substrates of CYP450 enzymes, prominently 3A4, 3A5, and 2J2. Apixaban is also metabolized by 1A2 and 2C 8/9/19 to a lesser degree. Some DOACs may interact with atorvastatin or ticagrelor, but these interactions are not typically a barrier to concurrent therapy if clinically indicated. Running a drug interaction report or consulting a pharmacist to help evaluate and safely navigate drug interactions is extremely helpful in these scenarios. *In addition to DOAC package inserts, the AHA guide to DOAC use [8] is a great resource that summarizes renal/hepatic dosing considerations, drug interactions, and anticoagulant transition recommendations. What safety profile and bleeding risk considerations exist for warfarin versus DOACs? Warfarin has been studied versus individual DOACs; generally, DOACs are preferred from a safety standpoint due to lower risk of bleeding. The RE-LY trial [9] showed no difference in major bleeding but less intracranial hemorrhage (ICH) with dabigatran when compared to warfarin. The ROCKET-AF [10] trial showed a greater Hgb drop/need for transfusion with rivaroxaban but higher critical/fatal bleeding (including ICH) incidence with warfarin. In the ARISTOTLE [11] trial, apixaban was associated with significantly lower bleeding outcomes than warfarin, except for GI bleeding (for which there was no significant difference between groups). Edoxaban had a lower incidence of overall GI bleed (upper and lower GI bleeding combined), but not individual upper or lower GI bleeding, than warfarin in the ENGAGE [12] trial.There are no direct head-to-head trials comparing DOACs, though some data suggest apixaban is associated with a lower bleeding risk than rivaroxaban (no difference in ICH), and that rivaroxaban may be associated with a higher risk of hemorrhagic stroke. In older adults, DOACs can be used without safety concerns over warfarin, though avoiding dabigatran may be suggested due to a signal for increased bleeding outcomes in older adult patients. The ELDERCARE-AF [13] trial from Japan showed no difference in major bleeding, but higher rates of GI bleeding and all bleeding, with edoxaban vs. placebo in adults >/= 80 years. Overall, apixaban is generally considered safe to use/the preferred DOAC option in patients with a history of GI bleeding. What is the recommended anti-thrombotic approach for patients with indications for both antiplatelet therapy and anticoagulation

352. Case Report: The Culprit in the Pillbox – University of Kansas Dec 27, 2023

Show notes

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. Hydroxychloroquine cardiotoxicity presenting as a rapidly evolving biventricular cardiomyopathy: key diagnostic features and literature revie

351. Case Report: The Tall Tail Heart: Angioleiomyoma – The Christ Hospital Dec 20, 2023

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CardioNerds meet with fellows from The Christ Hospital, Drs. Hanad Bashir, Hyunsoo Chung, and Dalia Aziz to discuss the following case that highlights angioleiomyoma: A 60-year-old woman with a past medical history significant for breast cancer (on tamoxifen) presented as a transfer to our facility for a clot-in-transit. She had initially presented to the outside hospital after progressive dyspnea on exertion and recent syncope. She was found on an echocardiogram to have a right atrial mass spanning into the right ventricle. CTA of the chest and abdomen/pelvis demonstrated extensive thrombus burden spanning from the IVC into the right ventricle. She was transferred to our facility for intervention. Endovascular attempts were unsuccessful, at which point she underwent surgical thrombectomy. Gross examination of the mass revealed a cylindrical shape, homogeneous tan color, rubbery soft tissue, measuring 25.5 cm in length and 2.3 cm in diameter. Histology confirmed the presence of angioleiomyoma. A second, smaller mass (5.2cm long and 4mm in diameter) was removed from under the tricuspid valve, with histology consistent with leiomyoma. Estrogen receptor and progesterone receptor staining were strongly positive, leading to the discontinuation of tamoxifen. Given the presence of uterine fibroids identified on the CT scan, there was concern about a uterine origin. A hysterectomy is planned for her in the near future. Expert commentary is provided by Dr. Wojciech Mazur. Episode audio was edited by student Dr. Adriana Mares. 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 - The Tall Tail Heart: Angioleiomyoma – The Christ Hospital Pearls - The Tall Tail Heart: Angioleiomyoma – The Christ Hospital Although evaluation of cardiac mass by echocardiography can provide information such as size, location, and morphology, adjunctive cross-sectional imaging may be used depending on the need for further temporal resolution (CT) or tissue characterization via cardiac MRI (CMR). If suspicious for elevated metabolic activity, there should be consideration of FDG-PET. Tamoxifen (a selective estrogen receptor modulator) is an agent used for breast cancer therapy. However, its use has been associated with endometrial hyperplasia, uterine fibroids, endometrial and uterine malignancy. Increased risk of malignancy has been seen more often in post-menopausal women and is dose and time-dependent. Clot in transient is a mobile thrombus, typically within the right heart structures. It is estimated to occur in 4-18% of patients with pulmonary embolism and is associated with elevated morbidity and mortality. Treatment includes surgical embolectomy, endovascular embolectomy, systemic thrombolysis, catheter-directed thrombolysis, or systemic anticoagulation. Angioleiomyoma is a rare benign pericystic tumor that most commonly affects the extremities. There are case reports of other affected sites, including the uterus. Invasion into the cardiac structures is exceedingly rare. The only established treatment for angioleiomyoma is surgical resection. Show Notes - The Tall Tail Heart: Angioleiomyoma – The Christ Hospital Syncope Syncope is a transient loss of consciousness secondary to reduced blood flow to the brain. Often, certain presentations are mislabeled as syncope, such as seizure disorders, posttraumatic loss of consciousness, and cataplexy. An organized diagnostic approach should be used to reduce hospital admissions and medical costs and increase diagnostic accuracy. Syncope can be divided into five general subgroups. 1) Neurally mediated reflex syncope (carotid sinus syndrome, vasovagal) 2) Orthostatic syncope 3) Cardiac arrhythmias 4) Structural cardiac and pulmonary causes 5) Cerebrovascular disorders. Initial evaluation should include thorough H&P, including orthostatic vitals and ECG. If diagnosis remains uncertain after initial evaluation, patients’ syncope should be risk stratified into three groups: high, intermediate, and low risk. Additionally, the 2017 ACC/AHA/HRS guidelines stratify patient risk based on short-term (30 days) morbidity and mortality based on initial examination and history. Patients presenting with high-risk and short-term syncope features should be immediately hospitalized for further diagnostic testing and treatment. High-risk features are usually indicative of underlying cardiovascular causes that could lead to sudden death; this includes but is not limited to life-threatening arrhythmias and acute coronary syndrome. Risk stratification also determines the selection of diagnostic tests. When underlying cardiac etiology is suspected, diagnostic tests such as echocardiography, CT angiography, cardiac magnetic resonance, electrophysiology study, exercise stress testing, and coronary angiography may be valuable in establishing timely diagnosis in high-risk patients. Choice of study modality varies greatly based on patient presentation and risk factors. In contrast to patients presenting with high-risk syncope, low-risk patients are discharged home with re-assurance and follow-up. Strategy for Intracardiac Masses First, take into account the patient's age at the time of presentation, as certain medical conditions like rhabdomyomas and fibromas are more commonly observed among pediatric patients. Second, assess the likelihood from an epidemiological perspective and consider the clinical probability. For instance, if a patient has recently experienced an anterior wall myocardial infarction and exhibits an akinetic ventricular apex, the presence of a cardiac mass during echocardiography could indicate the possibility of an intracardiac thrombus. Third, factor in the location of the tumor. If the mass is detected on the valves, potential diagnoses to consider include thrombus or vegetation. While masses within the heart chambers might still indicate thrombus, it's also important to contemplate other possibilities, such as myxomas, lymphomas, and metastases. Fourth, delve into the tissue characteristics of the mass using additional diagnostic imaging methods like cardiac magnetic resonance imaging. Imaging Modalities for Intracardiac Masses Transthoracic echocardiography (TTE) is readily available and non-invasive. Transesophageal echocardiography (TEE) offers insights into size, shape, attachment site, extension, and hemodynamic effects. Ultrasound-enhancing agents in echocardiography help differentiate various masses. Thrombi and benign tumors display a non or low-enhancing pattern. Malignancies and highly vascular tumors display a hyperenhancing pattern. Doppler velocities aid in assessing the hemodynamic impact. Cardiac MRI (CMR) is invaluable in the assessment of cardiac masses. In addition to anatomy, dimensions, and mass consistency, using different signal sequences like T1, T2, early and late gadolinium enhancement differentiate tissue characteristics and unveil fatty presence, necrosis, bleeding, inflammation, and vascularity within a mass. Cardiac CT provides high spatial and temporal resolution, multiplanar image reconstruction, and rapid acquisition. The broad field of view allows for the evaluation of the chest, lung tissue, vascular structures, and potential masses within the chest. Cardiac CT can be used to detect calcifications within the mass, although it has less soft tissue resolution compared with CMR. FDG-PET/CT can help gauge tumors' metabolic activity. When CT alone doesn't decisively determine benign or malignant nature, PET/CT steps in, aiding in malignancy diagnosis and guiding biopsy locations, staging, and cancer therapy planning. Cardiac tumors Cardiac tumors can be categorized into primary and secondary tumors. Secondary tumors, arising from metastasis, are more prevalent and often stem from cancers like melanoma, breast, or lung cancer. Secondary tumors can lead to issues like pericardial effusion with or without cardiac tamponade, myocardial infiltration, obstruction, or embolization. Primary tumors include benign (about 80%) and malignant (about 20%) types. Malignant tumors are mainly sarcomas, such as angiosarcomas and rhabdomyosarcomas. Benign tumors encompass myxomas, gelatinous masses with scattered myxoma cells; papillary fibroelastomas, frond-like masses typically on valves; lipomas, composed of fat cells; fibromas, containing fibroblasts and mostly found in the left ventricle; and rhabdomyomas, made of maldeveloped cardiac myocytes and often seen in ventricles. Other rare tumors include Purkinje cell tumors. However, the latter three mentioned are more common in children. Clot-in-transit Clot-in-transit (CIT) is the presence of mobile echogenic material in the right atrium or ventricle as seen on ultrasound. Right heart clots are classified into three types based on their morphology:Type A (common and carries a high risk of pulmonary embolization)Type B (assumed to originate from the atrium or ventricle) Type C (rare and migratory, resembling cardiac myxomas) Intervention options for CIT include catheter-based thrombolysis, systemic (IV) thrombolysis, surgical/endovascular embolectomy, and anticoagulation therapy. Catheter-based thrombolysis involves high-frequency ultrasound exposure, catheter-directed thrombolysis, mechanical thrombectomy, and endovascular clot suction. It has a high success rate but may not work for bulky thrombi. Surgical embolectomy is recommended for hemodynamically unstable patients with CIT and provides an opportunity to address right-to-left h

350. GLP-1 Agonists: Mechanisms to Applications with Dr. Dennis Bruemmer Dec 19, 2023

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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/

349. Case Report: Into the Thick of It – An Unusual Cause of Hypertrophic Cardiomyopathy – Cleveland Clinic Dec 17, 2023

Show notes

CardioNerds cofounder Dr. Amit Goyal and cardiology fellows from the Cleveland Clinic (Drs. Alejandro Duran Crane, Gary Parizher, and Simrat Kaur) discuss the following case: A 61-year-old man presented with symptoms of heart failure and left ventricular hypertrophy. He was given a diagnosis of obstructive hypertrophic cardiomyopathy. He eventually underwent septal myectomy, mitral valve replacement, aortic aneurysm repair, and aortic valve replacement with findings of Fabry’s disease on surgical pathology. The case discussion focuses on the differential diagnosis for LVH and covers Fabry disease as an HCM mimic. Expert commentary was provided by Dr. Angelika Ewrin. The episode audio was edited by student Dr. Diane Masket. 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 - An Unusual Cause of Hypertrophic Cardiomyopathy – Cleveland Clinic Pearls - An Unusual Cause of Hypertrophic Cardiomyopathy – Cleveland Clinic Left ventricular hypertrophy is a cardiac manifestation of several different systemic and cardiac processes, and its etiology should be clarified to avoid missed diagnosis and treatment opportunities. Fabry disease is a rare, X-linked inherited disease that can present cardiac and extra-cardiac manifestations, the former of which include hypertrophic cardiomyopathy, conduction defects, coronary artery disease, conduction abnormalities, arrhythmias, and heart failure. The diagnosis of Fabry disease includes measurement of alpha-galactosidase enzyme activity as well as genetic testing to evaluate for pathogenic variants or variants of unknown significance in the GLA gene. Family members of patients diagnosed with Fabry disease should be screened based on the inheritance pattern. Multimodality imaging can be helpful in the diagnosis of Fabry disease. Echocardiography can show left ventricular hypertrophy (LVH), reduced global strain, aortic and mitral valve thickening, and aortic root dilation with associated mild to moderate aortic regurgitation. Cardiac MRI can show hypertrophy of papillary muscles, mid-wall late gadolinium enhancement and low-native T1 signal. The treatment of Fabry disease involves a multi-disciplinary approach with geneticists, nephrologists, cardiologists, nephrologists, and primary care doctors. Enzyme replacement therapy can delay the progression of cardiac disease. Show Notes - An Unusual Cause of Hypertrophic Cardiomyopathy – Cleveland Clinic What are the causes of left ventricular hypertrophy? LVH is extremely common. It is present in 15-20% of the general population, and is more common in Black individuals, the elderly, obese or hypertensive individuals, with most cases being secondary to hypertension and aortic valve stenosis. In general terms, it is helpful to divide the causes of LVH into three main groups: high afterload states, obstruction to LV ejection, and intrinsic myocardial problems. Increased afterload states include both primary and secondary hypertension and renal artery stenosis. Mechanical obstruction includes aortic stenosis, subaortic stenosis, and coarctation of the aorta. Lastly, several intrinsic problems of the myocardium can cause LV hypertrophy, such as athletic heart with physiological LVH, hypertrophic cardiomyopathy with or without outflow obstruction, and infiltrative or storage diseases such as cardiac amyloidosis, Fabry’s disease, or Danon disease, among others. How does Fabry disease present? Fabry disease is present in all races and is an X-linked lysosomal storage disorder caused by pathogenic variants in the GLA gene that result in reduced alpha-galactosidase enzyme activity, leading to accumulation of lysosomal globotriaosylceramide (Gb3) globotriaosylsphingosine (lyso-Gb3) in affected tissues, including the heart, kidneys, vasculature, and peripheral nervous system. The reported incidence of this disease is said to be between 1 in 40,000 and 1 in 117,000 individuals, but screening in newborns suggests that this incidence may be underestimated, as it is present in up to 1 in 8,800 newborns. Depending on the variant of the mutation or the presence of mosaicism in females, the disease can have variable expression with early-onset presentations in the classical form or late-onset presentations in individuals who have residual a-galactosidase enzyme activity. Fabry disease can have multiple cardiac and extracardiac manifestations. Accumulation of Gb3 occurs in all cell types of the heart, including smooth muscle cells of the endothelium, myocytes, conduction cells, and valvular fibroblasts. Accumulation of glycosphingolipids also leads to biochemical changes in cell function that lead to apoptosis, cellular necrosis, inflammation, and altered membrane ion channel properties that may lead to increased conduction velocities. In the myocardium, cell damage produces LVH and diastolic dysfunction. Damage to endothelial cells leads to coronary artery disease and myocardial ischemia. Together, these changes may eventually lead to myocardial fibrosis and systolic dysfunction. Involvement of the conduction cells can manifest as conduction abnormalities and ventricular arrhythmias. Other electrocardiographic findings are a short PQ interval or chronotropic incompetence. Aortic remodeling in FD has been well described and often presents as sinus of Valsalva dilatation or ascending aortic aneurysm, which in turn may lead to secondary aortic regurgitation. Extracardiac manifestations of Fabry disease include neuropathy, gastrointestinal symptoms, angiokeratomas, cornea verticillata (golden-brown or gray discoloration of the corneal epithelium), hypohidrosis and exercise intolerance, proteinuria and renal failure, juvenile or cryptogenic stroke, hearing loss, chronic white matter hyperintensities in brain MRI, and lymphedema. How is Fabry disease diagnosed? Diagnosis of Fabry disease should be suspected in patients with unexplained LVH, especially when there are any extracardiac red flags. LVH presents in more than half of men and more than a third of women after the third decade of life. Other electrocardiographic findings besides high QRS voltages may include inferolateral negative T-waves, short PQ intervals, and a reduced P wave duration. The diagnosis is confirmed through genetic testing that may identify pathogenic variants as well as variants of unknown significance. Enzymatic level activities should be measured as well for confirmation. Absent or reduced alpha-galactosidase activity levels coupled with pathogenic variants in genetic testing confirm a diagnosis of FD. Variants of uncertain significance might require confirmation by endomyocardial biopsy and by lyso-Gb3 level assessment. What is the role of cardiovascular imaging in the diagnosis of Fabry disease? Multimodality imaging may be helpful in the diagnosis and staging of FD. Echocardiography typically reveals LVH with disproportionate hypertrophy of the papillary muscles, loss of base-to-apex circumferential strain gradient, and right-ventricular hypertrophy with normal systolic function. There may also be abnormal thickening of the aortic and mitral valves. Global longitudinal strain and speckle tracking may allow for early detection of cardiac involvement in patients with pathogenic variants. Cardiac MRI (CMR) may help with tissue characterization. Typical CMR findings of FD include late gadolinium enhancement (LGE), initially in the basal inferolateral wall, and low native T1 signal intensity, likely reflecting glycosphingolipid myocardial storage and occurring before the development of significant LVH. Tissue characterization by CMR also allows for staging of FD cardiomyopathy in different and progressive stages of accumulation, with progressive lowering of T1 signal intensity; inflammation and hypertrophy, with low T1, initial LVH, and T2 mapping showing inflammation in the basal inferolateral segment associated with LGE; and fibrosis, with increasing T1 values or pseudo-normalization and LGE with wall thinning in the basal inferolateral segment. What is the management for Fabry disease? The main objective in the treatment of FD is prevention of disease progression and end-organ damage. The mainstay of therapy is enzyme replacement therapy (ERT) with agalsidase-alfa or beta intravenous injections every other week. Agalsidase-alfa is produced in human cell lines, while the beta form of the enzyme is produced by recombinant DNA technology using mammalian cells. ERT is indicated in patients with late-onset FD who have the presence of laboratory, histological, or imaging evidence of injury to the heart, kidney, or central nervous system. It can delay the progression of cardiac disease and reduce the cardiovascular event rate in patients with FD. Another available pharmacological agent is the chaperone agent migalastat, which can be helpful for specific genetic variants of FD by stabilizing the translated form of alpha-galactosidase. This chaperone agent is given in oral tablets every other day. There is ongoing development of novel therapies for FD with second-generation ERTs, substrate reduction therapies, and gene and mRNA therapies. References - An Unusual Cause of Hypertrophic Cardiomyopathy – Cleveland Clinic Weidemann F, Strotmann JM, Niemann M, et al. Heart Valve Involvement in Fabry Cardiomyopathy. Ultrasound in Medicine and Biology. 2009;35(5):730-735. doi:10.1016/j.ultrasmedbio.2008.10.010 Pieroni M, Moon JC, Arbustini E, et al. Cardiac Involvement in Fabry Disease: JACC Review Topic of the Week. Journal of the American College of Cardiology....

348. Case Report: An Interesting Intersection of Cardiology and Hematology/Oncology – Guthrie Robert Packer Hospital Dec 08, 2023

Show notes

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.

347. Case Report: Heartmate 3 with a Side of Mustard – Medical University of South Carolina Nov 30, 2023

Show notes

CardioNerds (Dr. Josh Saef and Dr. Sumeet Vaikunth) join Dr. Sheng Fu, Dr. Payton Kendsersky, and Dr. Aniqa Shahrier from the Medical University of South Carolina for some off-shore fishing. They discuss the following featuring a patient with D-TGA and Eisenmenger’s syndrome treated with a Heartmate 3. Expert commentary was provided by Dr. Brian Houston. The episode audio was edited by student Dr. Adriana Mares. A 39-year-old woman with a history of D-transposition of the great arteries (D-TGA) with prior atrial switch repair (Mustard) was admitted from the clinic with cardiogenic shock. She underwent right heart catheterization which demonstrated elevated biventricular filling pressures and low cardiac index. An intra-aortic balloon pump was placed, and the patient was evaluated for advanced therapies. A liver biopsy showed grade 3 fibrosis, which, in combination with her shock state, made her a high-risk candidate for isolated heart or combined heart-liver transplantation. After a multi-disciplinary discussion, the patient underwent a Heartmate III left ventricular assist device (LVAD) implant in her systemic right ventricle. Although she did well post-operatively, she was admitted after a month with recurrent cardiogenic shock, with imaging showing her inflow cannula had become perpendicular to the septum. The patient and family eventually decided to pursue comfort measures, and the patient passed. 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 - D-TGA and Eisenmenger’s syndrome treated with a Heartmate 3 Pearls - D-TGA and Eisenmenger’s syndrome treated with a Heartmate 3 Early diagnosis of cyanotic congenital heart disease is paramount for treatment and prevention of future complications. Adult congenital heart disease requires a multi-disciplinary team for management in consultation with an adult congenital cardiology specialist. Eisenmenger syndrome is related to multiple systemic complications and has a high rate of mortality. Advancement in PAH medical management can offer noninvasive treatment options for some patients. Transthoracic echocardiography is the cornerstone for diagnosis. Other modalities (e.g. cardiac CT, cardiac MRI, invasive catheterization) can aid in diagnosis and management. Pearls - D-TGA and Eisenmenger’s syndrome treated with a Heartmate 3 While advances in pediatric surgery have allowed many patients born with congenital heart disease to survive into adulthood, adult congenital heart disease (ACHD) patients are complex and prone to numerous adverse sequalae including arrhythmias, heart failure, valvular disease, and non-cardiac organ dysfunction. Heart failure can be a challenging presentation in ACHD patients due to a longstanding history of clinical compensation. Their unique and complex anatomy, as well as highly variable clinical presentation, present unique challenges when it comes to advanced heart failure options such as durable left ventricular assist devices (LVAD) or transplantation. While durable LVAD implantation is possible in patients with systemic right ventricles, anatomic compatibility is paramount and poses ongoing challenges in their management. Goals of care discussions should be had early, as options for treatment may be limited. Show Notes - D-TGA and Eisenmenger’s syndrome treated with a Heartmate 3 What are some common sequelae in ACHD patients? ACHD patients are a heterogeneous population, but atrial tachycardias are extremely frequent in this patient population, often due to re-entrant pathways around surgical suture lines. These can often be treated with radiofrequency ablation while paying close attention to their challenging anatomy. Heart failure is also extremely common (up to 40% incidence) but has variable incidence dependent on the specific anatomy. Valvular heart disease, including infective endocarditis as well as non-cardiac organ dysfunction, are also important contributors to the overall prognosis of ACHD patients. How does heart failure present in ACHD patients? Heart failure presentations in ACHD patients tend to be subacute and insidious, as patients often have become accustomed to their symptoms. They are often unable to identify clear exercise limitations due to the slow, subacute nature of symptoms. However, acute presentations and shock can also be seen. Heart failure is the leading cause of death in ACHD patients. What are the challenges for advanced therapies in the ACHD population? First and foremost, risk stratification for these patients is often difficult due to often unreliable self-reporting of symptoms. Thus, early recognition becomes key, but even then, may not be enough. Several anatomic and physiological challenges remain. ACHD patients have often undergone multiple cardiac surgeries, increasing the surgical risk of redo sternotomies with severe adhesions. Due to the longstanding nature of their disease, ACHD patients often develop irreversible pulmonary hypertension (making transplant prohibitive) or end-organ dysfunction secondary to right heart failure (necessitating dual organ transplant). Is durable LVAD a feasible option for patients with systemic right ventricles? Isolated case reports demonstrate the feasibility of the off-label use of durable LVADs in systemic right ventricles. The complex anatomy of these patients has led to reports of alternative implant sites for the inflow cannula to minimize obstruction. Alternative surgical approaches, such as lateral thoracotomy, have also been described to try to avoid the adhesions that are often seen in these patients as a result of multiple prior cardiac surgeries. While the surgery is technically feasible, long-term data is not available, and this remains a “bail-out” therapy with current-generation LVAD designs. What is the role of goals of care discussions in ACHD patients? Advanced care planning is rarely discussed in routine clinic visits, and most providers wait until the condition has deteriorated significantly. Most ACHD patients want to discuss advanced care early before the disease progresses, but some do not, so it is important to ask about patient preferences. The majority of ACHD patients prefer to have advanced care discussions with their ACHD provider due to an already established and trusting relationship. References Gatzoulis MA, Webb GD, F. DPE, Hornung T, O'Donnell C. Transposition of the Great Arteries. In: Diagnosis and Management of Adult Congenital Heart Disease: Expert Consult - Online and Print. 3rd ed. Elsevier; 2018:513-527. Stout KK, Daniels CJ, Aboulhosn JA, et al. 2018 AHA/ACC guideline for the management of adults with congenital heart disease: A report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines. Circulation. 2019;139(14). Schwerzmann M, Goossens E, Gallego P, et al. Recommendations for advance care planning in adults with congenital heart disease: A position paper from the ESC Working Group of adult congenital heart disease, the Association of Cardiovascular Nursing and Allied Professions (ACNAP), the European Association for Palliative Care (EAPC), and the International Society for Adult Congenital Heart Disease (ISACHD). European Heart Journal. 2020;41(43):4200-4210. doi:10.1093/eurheartj/ehaa614 Khairy P, Clair M, Fernandes SM, et al. Cardiovascular outcomes after the arterial switch operation for D-transposition of the great arteries. Circulation. Jan 22 2013;127(3):331-9. doi:10.1161/CIRCULATIONAHA.112.135046 Piran S, Veldtman G, Siu S, Webb GD, Liu PP. Heart failure and ventricular dysfunction in patients with single or systemic right ventricles. Circulation. Mar 12 2002;105(10):1189-94. doi:10.1161/hc1002.105182 Zandstra TE, Palmen M, Hazekamp MG, Meyns B, Beeres SLMA, Holman ER, Kiès P, Jongbloed MRM, Vliegen HW, Egorova AD, Schalij MJ, Tops LF. Ventricular assist device implantation in patients with a failing systemic right ventricle: a call to expand current practice. Neth Heart J. 2019 Dec;27(12):590-593. Burchill LJ. Heart transplantation in adult congenital heart disease. Heart. 2016;102:1871–1877. doi: 10.1136/heartjnl-2015-309074.

346. CardioOncology: Disparities in CardioOncology – Towards Health Equity with Dr. Javier Gomez-Valencia Nov 26, 2023

Show notes

CardioNerds co-founder Dr. Dan Ambinder, series chair Dr. Giselle Suero Abreu, and episode FIT Lead Dr. Rachel Ohman discuss disparities in cardiooncology with Dr. Javier Gomez Valencia, the Director of Cardio-Oncology services at John H. Stronger Jr. Hospital of Cook County. Dr. Rachel Ohman drafted show notes. Audio editing by student doctor Shivani Reddy. A disproportionate burden of both cancer and cardiovascular disease affects racial and ethnic minority groups as well as lower-income communities. Similar patterns of vulnerability exist among cancer survivors with cardiovascular disease, although further investigation in these subpopulations is needed. We discuss a comprehensive approach to the cardio-oncology patient, our current understanding of the social and structural determinants of disparities in cardio-oncology populations, and other contributions to inequity in the field. Given the growing population of cancer survivors and limited accessibility to cardio-oncology specialists, these topics are of critical importance to anyone caring for cancer patients who have or are at risk for cardiovascular disease. This episode is supported by a grant from Pfizer Inc. This CardioNerds Cardio-Oncology series is a multi-institutional collaboration made possible by contributions of stellar fellow leads and expert faculty from several programs, led by series co-chairs, Dr. Giselle Suero Abreu, Dr. Dinu Balanescu, and Dr. Teodora Donisan. CardioNerds Cardio-Oncology 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 - Disparities in CardioOncology Social and structural determinants of health are drivers of cardiovascular and cancer disparities. Existing data on cardiotoxicity outcomes suggests these determinants also contribute to disparities in cardio-oncology. Assessing social and structural determinants of health should be a routine part of evaluating a patient with an active or prior history of cancer. Customs, country of origin, and immigration status matter. Differential risk profiles among Hispanic/Latinx sub-populations require further investigation. Black patients, particularly black women with breast cancer, have elevated morbidity and mortality from cardiotoxicity. Data suggest contributions from social determinants of health. Representation in clinical trials must be diversified for applicability to our diverse patient populations. Concerted efforts should be made to recruit diverse clinical trial participants and help patients from diverse communities effectively participate in the research process, contributing to the advancement of science. Show notes - Disparities in CardioOncology How do you approach the evaluation of a new patient in cardio-oncology? How do social and structural determinants of health impact treatment-associated cardiotoxicity? The evaluation of a new patient should include an assessment of a patient’s intrinsic risk factors, risks associated with cancer treatment, and consideration of cardioprotective therapeutic strategies Social and structural vulnerabilities should also be assessed routinely as a part of risk stratification. Providers should take stock of a patient’s demographic (e.g., race/ethnicity, gender), socioeconomic (e.g., occupation, insurance status, food security, housing security), environmental (e.g., transportation, proximity to health resources, neighborhood safety), and sociocultural (e.g., psychosocial stressors, discrimination, acculturation) determinants that are in turn modulated by larger systemic forces like structural racism. This comprehensive risk assessment can guide the strategies to mitigate cardiovascular risk before, during, and after cancer treatment. What barriers to cardio-oncology care are unique to the Hispanic/Latinx population? The Hispanic/Latinx population now comprises 19% of the US population. A disproportionate fraction of the Hispanic/Latinx population is uninsured (about 20%). In addition to insurance barriers, some members of this population can face difficulties from language barriers and limited access to preventative care. Existing data suggest differential risk profiles for sub-populations of Hispanic/Latinx patients based on country of origin, customs, and immigration status. Further research is needed to investigate disparities among different sub-populations. What disparities are faced by Black patients with cancer? Black patients have an elevated risk of morbidity and mortality from cancer and are more likely to develop cardiotoxicity than their White counterparts. Black patients with breast cancer who receive anthracycline or HER2-directed therapy have a two- to three-fold risk of cardiotoxicity when compared to their White counterparts. Black patients with HER2+ breast cancer treated with trastuzumab are more likely to develop LV dysfunction than White counterparts, even after controlling for age, disease state, and cardiovascular risk factors. This suggests a role for social determinants of health that have yet to be elucidated. How can patients’ sexual orientation and gender identity influence disparities in cardio-oncology, particularly for LGBTQIA+ patients? Some of the barriers this population faces are related to social stigmatization as well as structural discrimination (e.g., lack of providers with appropriate expertise). Difficulties with accessing trusted providers can impair patients’ ability to have longitudinal care and optimal cardiotoxicity surveillance. What other areas of cardio-oncology might contribute to ongoing outcomes disparities, and how should we approach those disparities? Underrepresentation of minority groups in clinical trials is an ongoing issue. It results in our extrapolating data from homogenous populations and applying it to more diverse populations not represented adequately. Clinical trial enrollment requires more diverse and inclusive recruitment and visibility. However, we also should help patients and communities feel included in the research process, particularly given historical examples of medical exploitation. The landscape of cardiology providers also requires diversification. A diverse workforce benefits patients as well as providers. Cardiologists and healthcare providers also need to engage in political advocacy to help advocate for underrepresented vulnerable groups to combat socioeconomic disparities and public health crises that create barriers to optimal care. References - Disparities in CardioOncology Addison D, Branch M, Baik AH, et al. Equity in Cardio-Oncology Care and Research: A Scientific Statement From the American Heart Association. Circulation. 2023;148(3):297-308. doi:10.1161/CIR.0000000000001158. Ahmad J, Muthyala A, Kumar A, Dani SS, Ganatra S. Disparities in Cardio-oncology: Effects On Outcomes and Opportunities for Improvement. Curr Cardiol Rep. 2022 Sep;24(9):1117-1127. doi: 10.1007/s11886-022-01732-2. Epub 2022 Jun 27. PMID: 35759170; PMCID: PMC9244335. Branch B and Cosway D. Health Insurance Coverage by Race and Hispanic Origin: 2021. American Community Survey Briefs. 2022 Nov 22. https://www.census.gov/content/dam/Census/library/publications/2022/acs/acsbr-012.pdf. Ohman RE, Yang EH, Abel ML. Inequity in Cardio-Oncology: Identifying Disparities in Cardiotoxicity and Links to Cardiac and Cancer Outcomes. J Am Heart Assoc. 2021 Dec 21;10(24):e023852. doi: 10.1161/JAHA.121.023852. Epub 2021 Dec 16. PMID: 34913366; PMCID: PMC9075267. Sirufo MM, Magnanimi LM, Ginaldi L, De Martinis M. Overcoming LGBTQI+ Disparities in Cardio-Oncology: A Call to Action. JACC CardioOncol. 2023 Mar 7;5(2):267-270. doi: 10.1016/j.jaccao.2022.11.017. PMID: 37144105; PMCID: PMC10152199. Suero-Abreu GA, Patel S, Duma N. Disparities in Cardio-Oncology Care in the Hispanic/Latinx Population. JCO Oncol Pract. 2022 May;18(5):404-409. doi: 10.1200/OP.22.00045. PMID: 35544659.

345. Case Report: A Case of Unrepaired Congenital Heart Disease – University of Chicago – Northshore University Nov 22, 2023

Show notes

CardioNerds (Dr. Josh Saef, Dr. Agnes Koczo) join Dr. Iva Minga, Dr. Kifah Hussain, and Dr. Kevin Lee from the University of Chicago - NorthShore to discuss a case of unrepaired congenital heart disease that involves D-TGA complicated by Eisenmenger syndrome. The ECPR was provided by Dr. Michael Earing. Audio editing by Dr. Akiva Rosenzveig. A 25-year-old woman with an unknown congenital heart disease that was diagnosed in infancy in Pakistan presents to the hospital for abdominal pain and weakness. She is found to be profoundly hypoxemic, and an echocardiogram revealed D-transposition of the great arteries (D-TGA) with a large VSD. As this was not repaired in childhood, she has unfortunately developed Eisenmenger syndrome with elevated pulmonary vascular resistance. She is stabilized and treated medically for her cyanotic heart disease. Unfortunately given the severity and late presentation of her disease, she has limited long-term options for care. CardioNerds discuss the diagnosis of D-TGA and Eisenmenger’s syndrome, as well as long-term management and complications associated with this entity. 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 - Unrepaired Congenital Heart Disease Pearls - Unrepaired Congenital Heart Disease Early diagnosis of cyanotic congenital heart disease is paramount for treatment and prevention of future complications. Adult congenital heart disease requires a multi-disciplinary team for management in consultation with an adult congenital cardiology specialist. Eisenmenger syndrome is related to multiple systemic complications and has a high rate of mortality. Advancement in PAH medical management can offer noninvasive treatment options for some patients. Transthoracic echocardiography is the cornerstone for diagnosis. Other modalities (e.g. cardiac CT, cardiac MRI, invasive catheterization) can aid in diagnosis and management. Show Notes - Unrepaired Congenital Heart Disease Cyanotic congenital heart disease is often diagnosed in infancy and timely treatment is paramount. As these diseases progress over time, pulmonary over-circulation often pulmonary hypertension (PH), elevated pulmonary vascular resistance, and Eisenmenger syndrome will develop, which preclude definitive treatment. For D-TGA, before PH develops, there are surgical options such as the arterial switch procedure that can treat the disease. Unfortunately, once Eisenmenger syndrome develops, there are multiple systemic complications including hyperviscosity, thrombosis, bleeding, kidney disease, iron deficiency, arrhythmias, etc. that can occur. Management requires a multi-disciplinary team including an adult congenital cardiology specialist, but mortality rates remain high, with median survival reduced by 20 years, worse with complex cardiac defects. Bosentan is a first line treatment for patients with Eisenmenger syndrome, with PDE-5 inhibitors as a second line either by themselves or in combination with bosentan. Data are currently limited for latest-generation PH treatments in Eisenmenger syndrome and further study is still underway. References Ferencz C. Transposition of the great vessels. Pathophysiologic considerations based upon a study of the lungs. Circulation. 1966 Feb;33(2):232-41. Arvanitaki A, Gatzoulis MA, Opotowsky AR, Khairy P, Dimopoulos K, Diller GP, Giannakoulas G, Brida M, Griselli M, Grünig E, Montanaro C, Alexander PD, Ameduri R, Mulder BJM, D'Alto M. Eisenmenger Syndrome: JACC State-of-the-Art Review. J Am Coll Cardiol. 2022 Mar 29;79(12):1183-1198. Earing MG, Webb GD. Congenital heart disease and pregnancy: maternal and fetal risks. Clin Perinatol. 2005 Dec;32(4):913-9, viii-ix Østergaard L, Valeur N, Ihlemann N, Bundgaard H, Gislason G, Torp-Pedersen C, Bruun NE, Søndergaard L, Køber L, Fosbøl EL. Incidence of infective endocarditis among patients considered at high risk. Eur Heart J. 2018 Feb 14;39(7):623-629 Opotowsky AR, Moko LE, Ginns J, Rosenbaum M, Greutmann M, Aboulhosn J, Hageman A, Kim Y, Deng LX, Grewal J, Zaidi AN, Almansoori G, Oechslin E, Earing M, Landzberg MJ, Singh MN, Wu F, Vaidya A. Pheochromocytoma and paraganglioma in cyanotic congenital heart disease. J Clin Endocrinol Metab. 2015 Apr;100(4):1325-34. Jaïs X, D'Armini AM, Jansa P, Torbicki A, Delcroix M, Ghofrani HA, Hoeper MM, Lang IM, Mayer E, Pepke-Zaba J, Perchenet L, Morganti A, Simonneau G, Rubin LJ; Bosentan Effects in iNopErable Forms of chronIc Thromboembolic pulmonary hypertension Study Group. Bosentan for treatment of inoperable chronic thromboembolic pulmonary hypertension: BENEFiT (Bosentan Effects in iNopErable Forms of chronIc Thromboembolic pulmonary hypertension), a randomized, placebo-controlled trial. J Am Coll Cardiol. 2008 Dec 16;52(25):2127-34. Gatzoulis MA, Landzberg M, Beghetti M, Berger RM, Efficace M, Gesang S, He J, Papadakis K, Pulido T, Galiè N; MAESTRO Study Investigators. Evaluation of Macitentan in Patients With Eisenmenger Syndrome. Circulation. 2019 Jan 2;139(1):51-63. McLaughlin VV, Gaine SP, Howard LS, Leuchte HH, Mathier MA, Mehta S, Palazzini M, Park MH, Tapson VF, Sitbon O. Treatment goals of pulmonary hypertension. J Am Coll Cardiol. 2013 Dec 24;62(25 Suppl):D73-81. Stoica SC, McNeil KD, Perreas K, Sharples LD, Satchithananda DK, Tsui SS, Large SR, Wallwork J. Heart-lung transplantation for Eisenmenger syndrome: early and long-term results. Ann Thorac Surg. 2001 Dec;72(6):1887-91.

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