Cardionerds: A Cardiology Podcast

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,

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?

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.

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.

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 popula...

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.

CardioNerds (Drs. Amit Goyal, Jason Feinman, and Tiffany Dong) discuss Beyond the Boards: Diseases of the Peripheral Arteries with Dr. Amy Pollak. We review common presentations of peripheral vascular disease, ranging from aortic disease to the more distal vessels in an engaging case-based discussion. Dr. Pollack talks us through these cases, including the diagnosis and management of peripheral vascular diseases. Show notes were drafted by Dr. Matt Delfiner and episode audio was edited by student doctor Tina Reddy. The CardioNerds Beyond the Boards Series was inspired by the Mayo Clinic Cardiovascular Board Review Course and designed in collaboration with the course directors Dr. Amy Pollak, Dr. Jeffrey Geske, and Dr. Michael Cullen. CardioNerds Beyond the Boards SeriesCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls and Quotes - Disease of the Peripheral Arteries Risk factors for abdominal aortic aneurysm include traditional atherosclerotic risk factors such as age, hypertension, hyperlipidemia, and tobacco use. Screening for AAA should be for men over the age of 65 years with a history of tobacco use. If present, medical management includes blood pressure and lipid lowering therapies to decrease the risk of expansion. Decision for surgical intervention relies on size and rate of growth of AAA, with clear indications if it grows> 10 mm in a year or diameter of 5.5 cm in men and 5.0 cm in women. When diagnosis of PAD is not straightforward (presence of symptoms but ABI is normal), an exercise ankle-brachial index (ABI) test can be useful. An exercise-induced decrease in ABI by 20% or in ankle pressure by 30 mmHg is consistent with PAD. For PAD, treatment with low dose rivaroxaban and aspirin yields lower event rates than with antiplatelet therapy alone. This in combination with lifestyle therapies (diet + exercise) and risk factor management (hypertension and hyperlipidemia) are the cornerstones of therapy. Revascularization is indicated for continued PAD symptoms despite conservative therapy. Acute limb ischemia is an “acute leg attack” and is a life-threatening emergency. Common symptoms include pain, pallor, pulselesess, parasthesias, cold temperature (poikilothermia), and paralysis. Restoration of blood flow is paramount, and emergent or urgent revascularization is the first line therapy for those with symptoms < 2 weeks. Notes - Disease of the Peripheral Arteries Learning Objectives: Describe screening and therapeutic strategy for AAA management. Understand the risk factors and diagnosis of peripheral arterial disease. Compare different management approaches for PAD. Be able to recognize acute limb ischemia. Describe the overall treatment strategy for acute limb ischemia. Abdominal Aortic Aneurysms Abdominal aortic aneurysms are a source of high morbidity and mortality. The US Preventative Services Task Force recommends one time screening ultrasound for AAA in men older than 65 years of age with a tobacco use history. Risk factors include age, hypertension, hyperlipidemia, and tobacco use. Patients with AAA between 3-3.9 mm should be monitored every 2-3 years. Sizes 4-5 cm should be re-imaged every 6-12 months.  Additional screening can be done for individuals < 65 years who have a first degree relative with AAA. Women are more likely to have aortic dissection at smaller diameters than men, which is why intervention (open vs endovascular repair) is recommended at 5 cm diameter for women versus at 5.5 cm for men. Additionally, repair is also warranted if a AAA grows more than 5 mm in 6 months or 10 mm in one year. Risk factor management is key with AAA, including blood pressure, glucose, and lipid targeting.  The presence of an AAA should be treated as secondary ASCVD prevention like coronary a...

CardioNerds (Dr. Daniel Ambinder, Dr. Giselle Suero Abreu, Dr. Kahtan Fadah, and Dr. Colin Blumenthal) discuss arrhythmias in CardioOncology with Dr. Michael Fradley. In this episode, Dr. Michael Fradley joins us in the CardioNerds CardioOncology clinic where he uses his unique dual training in cardio-oncology and electrophysiology to walk us through the complex interplay and management of these disorders. We discuss the incidence and pathophysiology of these arrhythmias, including the link with various cancer treatments, screening and detection, and complex management including rate vs rhythm control in atrial fibrillation, need for anticoagulation, effects on the QTc and so much more. Given the unique challenges with this population we also delve into how this affects their oncology care and how to approach changes to their cancer treatment. Show notes were drafted by Dr. Kahtan Fadah and episode audio was edited by student Dr. Tina Reddy. 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 - Arrhythmias in CardioOncology Arrhythmias are common in cancer patients due to shared risk factors and bi-directional risk between cardiac and oncologic disorders. Many cancer therapeutics can be directly arrhythmogenic or lead to cardiotoxicities that pre-dispose to arrhythmias. Though incidence of arrhythmia can be significant increased with some cancer therapeutics (e.g. ibrutinib), there is not specific data to support proactive ambulatory monitoring for arrhythmia without evidence of clear symptoms. Atrial fibrillation is the most common arrhythmia in cancer patients and management of atrial fibrillation, as well as other tachyarrhythmias, is unchanged from management in non-cancer patients. General principles of when to start anticoagulation or rate vs rhythm control are not significantly different (e.g. still use CHA2DS2-VAsC, monitor for symptoms etc), but providers should be more mindful of drug-drug interactions with cancer therapeutics. Cancer therapeutics as well as common medications used to treat side effects or complications (e.g. antiemetics, antibiotics, etc) can prolong the QT interval and increase risk of Torsades de pointes (TdP). The QTc should be monitored with an ECG for patients on these medications. If a patient does develop a serious arrhythmia like TdP, management is similar to that in non-cancer patients. The goal of arrhythmia management in cardio-oncology is to prevent cardiovascular disease from becoming a barrier to appropriate cancer therapy. Though cancer therapeutics should be temporarily or permanently discontinued in potentially fatal events (e.g TdP from QTc prolonging meds), the overall goal is to manage the arrhythmias appropriately to allow cancer therapeutics to be continued or restarted. Show notes - Arrhythmias in CardioOncology What is the prevalence of arrhythmias in patients with cancer? Arrhythmias are common in patients with cancer due to a multitude of factors. Atrial fibrillation is the most common arrhythmia in this population and occurs in approximately 5% of patients with cancer. The driving forces are multifactorial and include the direct arrhythmogenic effects of cancer therapeutics and cardiotoxicities of cancer therapeutics that make arrhythmogenesis more likely. Additionally, there is a bi-directional link between cancer and cardiac disorders. For example, not only is atrial fibrillation more common in patien...