Cardionerds: A Cardiology Podcast

CardioNerds
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12 snips
Dec 17, 2023 • 50min

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

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.
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Dec 8, 2023 • 32min

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

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. “To study the phenomena of disease without books is to sail an uncharted sea, while to study books without patients is not to go to sea at all.” – Sir William Osler. CardioNerds thank the patients and their loved ones whose stories teach us the Art of Medicine and support our Mission to Democratize Cardiovascular Medicine. Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. 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.
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Nov 30, 2023 • 1h 9min

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

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.
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Nov 26, 2023 • 34min

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

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.  Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. US Cardiology Review is now the official journal of CardioNerds! Submit your manuscript here. 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. Meet Our Collaborators International Cardio-Oncology Society ( IC-OS). IC-OS exits to advance cardiovascular care of cancer patients and survivors by promoting collaboration among researchers, educators and clinicians around the world. Learn more at https://ic-os.org/.
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Nov 22, 2023 • 1h

345. Case Report: A Case of Unrepaired Congenital Heart Disease – University of Chicago – Northshore University

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. “To study the phenomena of disease without books is to sail an uncharted sea, while to study books without patients is not to go to sea at all.” – Sir William Osler. CardioNerds thank the patients and their loved ones whose stories teach us the Art of Medicine and support our Mission to Democratize Cardiovascular Medicine. Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. 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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Nov 17, 2023 • 42min

344. Beyond the Boards: Disease of the Peripheral Arteries with Dr. Amy Pollak

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. Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. US Cardiology Review is now the official journal of CardioNerds! Submit your manuscript here. 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 arterial disease, since AAA is an atherosclerotic disease equivalent. Tobacco cessation is of the utmost importance here. Regarding strategy for repair: if the patient is not a surgical candidate, then endovascular repair is a reasonable option. If they are a surgical candidate, then the location of the aneurysm comes into play. Infrarenal or juxtarenal disease are more likely to require open repair. Peripheral Arterial Disease When a patient presents with claudication, in addition to thorough history and physical exam, checking for ABIs is important. Risk factors include known coronary disease, hypertension, hyperlipidemia, and diabetes. Women often report cramping in their calves/legs rather than outright pain. ABI < 0.9 are consistent with PAD, with > 1.3 consistent with calcified and non-compressible vessels. Toe brachial index (TBI) cutoff is 0.7. If there is strong clinical suspicion but normal ABI, then performing the test after a period of exercise (calf raises, treadmill) can be clinically useful. An exercise induced decrease in ankle pressure by 30 mm or change in ABI by 20% is consistent with PAD. Therapy for PAD includes supervised exercise training, lifestyle changes (e.g., tobacco cessation) and risk factor modification (blood pressure/lipids/glucose). Additionally, low dose rivaroxaban (2.5 mg twice daily) plus aspirin has been shown to decrease events compared to aspirin alone. If there are continued symptoms despite the above therapy, then invasive management can be considered. This includes percutaneous or surgical revascularization.  This would be proceeded with CTA imaging for further guidance. Invasive angiography is reasonable for someone with a higher likelihood of a single lesion amenable to percutaneous repair.  Discrete and singular lesions are usually repaired percutaneously while more diffuse or multivessel disease, then surgical management may be indicated. Acute Limb Ischemia ALI can present with the 6 Ps: pain, pallor, pulselessness, parasthesias,  poikilothermia, and paralysis. Limbs may (rarely) remain viable, with signs being a clear Doppler-able pulse without sensory or muscle loss. Otherwise, a limb is salvageable if there is a faint arterial Doppler signal. If there is muscle weakness, then the limb is considered threatened. If an arterial Doppler signal is completely lost, then the limb is considered non-viable. ALI is an “acute leg attack.” The initial therapy is systemic anticoagulation with unfractionated heparin. If symptoms have been present for less than two weeks, then endovascular therapy with either thrombectomy or catheter-directed lysis are indicated. Major contraindications to lytic therapy include recent surgery, any history of intracranial bleeding or neoplasm, or if they are otherwise at a high bleeding risk. Non-viable limbs may better be served with amputation rather than revascularization. References – Disease of the Peripheral Arteries 1. Eikelboom JW, Connolly SJ, Bosch J, et al. Rivaroxaban with or without Aspirin in Stable Cardiovascular Disease. N Engl J Med. 2017;377(14):1319-1330. doi:10.1056/NEJMoa1709118 https://www.nejm.org/doi/full/10.1056/NEJMoa1709118 2. Criqui MH, Matsushita K, Aboyans V, et al. Lower Extremity Peripheral Artery Disease: Contemporary Epidemiology, Management Gaps, and Future Directions: A Scientific Statement From the American Heart Association  Circulation. 2021;144(9):e171-e191. doi:10.1161/CIR.0000000000001005 https://www.ahajournals.org/doi/full/10.1161/CIR.0000000000001005?rfr_dat=cr_pub++0pubmed&url_ver=Z39.88-2003&rfr_id=ori%3Arid%3Acrossref.org 3. Lanzi S, Belch J, Brodmann M, et al. Supervised exercise training in patients with lower extremity peripheral artery disease. Vasa. 2022;51(5):267-274. doi:10.1024/0301-1526/a001024 https://econtent.hogrefe.com/doi/full/10.1024/0301-1526/a001024 4. Sabouret P, Cacoub P, Dallongeville J, et al. REACH: international prospective observational registry in patients at risk of atherothrombotic events. Results for the French arm at baseline and one year. Arch Cardiovasc Dis. 2008;101(2):81-88. doi:10.1016/s1875-2136(08)70263-8 https://www.sciencedirect.com/science/article/pii/S1875213608702638?via%3Dihub 5. Zucker EJ, Misono AS, Prabhakar AM. Abdominal Aortic Aneurysm Screening Practices: Impact of the 2014 U.S. Preventive Services Task Force Recommendations. J Am Coll Radiol. 2017;14(7):868-874. doi:10.1016/j.jacr.2017.02.020 https://www.jacr.org/article/S1546-1440(17)30200-4/fulltext 5. Hensley SE, Upchurch GR Jr. Repair of Abdominal Aortic Aneurysms: JACC Focus Seminar, Part 1. J Am Coll Cardiol. 2022;80(8):821-831. doi:10.1016/j.jacc.2022.04.066 https://www.jacc.org/doi/abs/10.1016/j.jacc.2022.04.066 6. Shishehbor MH, White CJ, Gray BH, et al. Critical Limb Ischemia: An Expert Statement. J Am Coll Cardiol. 2016;68(18):2002-2015. doi:10.1016/j.jacc.2016.04.071 https://www.jacc.org/doi/full/10.1016/j.jacc.2016.04.071 7. Kinlay S. Management of Critical Limb Ischemia. Circ Cardiovasc Interv. 2016;9(2):e001946. doi:10.1161/CIRCINTERVENTIONS.115.001946 https://www.ahajournals.org/doi/full/10.1161/CIRCINTERVENTIONS.115.001946 8. Gerhard-Herman MD, Gornik HL, Barrett C, et al. 2016 AHA/ACC Guideline on the Management of Patients With Lower Extremity Peripheral Artery Disease: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines [published correction appears in Circulation. 2017 Mar 21;135(12 ):e791-e792]. Circulation. 2017;135(12):e726-e779. doi:10.1161/CIR.0000000000000471 https://www.ahajournals.org/doi/10.1161/CIR.0000000000000471?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub%20%200pubmed
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Nov 1, 2023 • 40min

343. Cardio-Oncology: Arrhythmias in CardioOncology with Dr. Michael Fradley

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.  Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. US Cardiology Review is now the official journal of CardioNerds! Submit your manuscript here. 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 patients with cancer, but there is also a higher incidence of cancer in patients with atrial fibrillation, likely due to shared risk factors. Risk factors in patients with cancer that make arrhythmias more likely include advanced age, metabolic disturbances, electrolyte abnormalities, and elevated levels of inflammation and catecholamines. (How) Do cancer therapeutics increase the risk of arrhythmias? Many cancer therapies are either directly or indirectly arrhythmogenic. Though therapies like the BTK inhibitor ibrutinib have a direct link to an increase incidence of atrial fibrillation, other medications like immune checkpoint inhibitors can cause myocarditis, reduce cardiac function, and predispose to arrhythmias. The following table includes broad categories of cancer therapeutics that are linked to arrhythmia: What is the appropriate arrhythmia monitoring strategy for patients receiving cancer therapy? Though there is a clear increased risk of arrhythmia in many patients with cancer receiving specific therapeutics, there is not specific data to support proactive monitoring in these patients. One meta-analysis showed that when compared to alternative regimens, ibrutinib increased the risk of incident AF compared to alternative therapies (RR 3.9, 95% CI 2.0-7.5, P <0.0001), with overall AF incidence of 3.3 per 100 person-years compared to 0.84 per 100 person-years in the ibrutinib and non-ibrutinib groups, respectively. Though proactive monitoring might lead to more or earlier detection of AF in this population, there is a lack of data to support improved outcomes with monitoring asymptomatic patients. Additionally, the clinical relevance of subclinical and/or short episodes of atrial fibrillation remains uncertain. Because of this, there are no current recommendations for broad proactive monitoring, though monitoring should be considered in patients with signs or symptoms that could be consistent with arrhythmia. What is the management of arrhythmias in patients with cancer? Management of arrhythmias in patients with cancer is similar to general management in non-cancer patients. For AF, a rhythm control strategy is preferred for patients with paroxysmal AF and in patients who are symptomatic. For other patients who are asymptomatic, a rate control strategy is reasonable. One notable exception is when control of the AF becomes a barrier to the oncology team. In these situations, more aggressive rhythm control is preferred to facility oncologic care. Anticoagulation is also approached in a similar way to non-cancer patients. Patients with a CHA2DS2-VAsC score >2 for men and >3 for women warrant anticoagulation. Many patients with cancer are anemic, thrombocytopenic, or prone to bleeding, which should also be taken into account when prescribing anticoagulation. Left atrial appendage closure may be a consideration for select patients. As for medications that cause QT prolongation, malignant arrhythmias are quite rare and mostly occur in patients with QTc > 500 ms. This can be multifactorial as many patients with cancer may have episodic metabolic or electrolyte abnormalities in addition to cancer therapeutics or symptom/complication management medications (e.g. antiemetics, antibiotics, etc) which can prolong the QTc or lower the threshold for arrhythmogenesis. Life threatening arrhythmias like Torsades de pointes (TdP) are treated similar to that in non-cancer patients, which can include magnesium, increasing HR with isoproterenol or transvenous pacing, anti-arrhythmic drugs, or cardioversion in addition to addressing the underlying cause. Balancing arrhythmia risk with cancer therapeutics An important goal in cardio-oncology is to prevent cardiovascular disease from becoming a barrier for a patient to receive appropriate cancer therapy. The goal is to facilitate the treatment plan that the oncologist thinks is optimal for their cancer, not to protect the heart at the expense of appropriate oncologic care. This is a difficult balancing act and, in the case of serious or potentially fatal events (e.g. Torsades from QTc prolonging meds, vasospasm with ischemia from 5FU, severe myocarditis from immune checkpoint inhibitors etc.), it is often necessary to discontinue the cancer therapeutic temporarily or permanently. Ideally, the arrhythmia should be treated and controlled allowing the patient to continue therapy while minimizing the cardiac symptoms and side effects. References – Arrhythmias in CardioOncology Leiva O, AbdelHameid D, Connors JM, Cannon CP, Bhatt DL. Common Pathophysiology in Cancer, Atrial Fibrillation, Atherosclerosis, and Thrombosis: JACC: CardioOncology State-of-the-Art Review. JACC CardioOncol. 2021;3(5):619-634. doi:10.1016/j.jaccao.2021.08.011 Fradley MG, Beckie TM, Brown SA, et al. Recognition, Prevention, and Management of Arrhythmias and Autonomic Disorders in Cardio-Oncology: A Scientific Statement From the American Heart Association. Circulation. 2021;144(3):e41-e55. doi:10.1161/CIR.0000000000000986 Leong DP, Caron F, Hillis C, et al. The risk of atrial fibrillation with ibrutinib use: a systematic review and meta-analysis. Blood. 2016;128(1):138-140. doi:10.1182/blood-2016-05-712828 Meet Our Collaborators International Cardio-Oncology Society ( IC-OS). IC-OS exits to advance cardiovascular care of cancer patients and survivors by promoting collaboration among researchers, educators and clinicians around the world. Learn more at https://ic-os.org/.
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Oct 30, 2023 • 0sec

342. Case Report: A Young Woman With Recurrent ACS – National University Heart Centre Singapore

CardioNerds join Dr. Tony Li Yi Wei, Dr. Rodney Soh Yu Hang, and Dr. Zan Ng Zhe Yan to discuss a case featuring a young woman with recurrent ACS ultimately found to have Takayasu Arteritis. They explore the potential causes of her condition, diagnostic challenges, and treatment options for Takayasu Arthritis.
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Oct 26, 2023 • 7min

341. Guidelines: 2021 ESC Cardiovascular Prevention – Question #35 with Dr. Melissa Tracy

The following question refers to Section 4.9 of the 2021 ESC CV Prevention Guidelines. The question is asked by Dr. Christian Faaborg-Andersen, answered first by UCSD fellow Dr. Patrick Azcarate, and then by expert faculty Dr. Melissa Tracy. Dr. Tracy is a preventive cardiologist, former Director of the Echocardiography Lab, Director of Cardiac Rehabilitation, and solid organ transplant cardiologist at Rush University. The CardioNerds Decipher The Guidelines Series for the 2021 ESC CV Prevention Guidelines represents a collaboration with the ACC Prevention of CVD Section, the National Lipid Association, and Preventive Cardiovascular Nurses Association. Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. Question #35 In patients with a low risk of cardiovascular disease, which of the following is true? A Aspirin does not affect the risk of ischemic stroke B Aspirin increases the risk of fatal bleeding. C Aspirin reduces the risk of non-fatal MI. D Aspirin reduces cardiovascular mortality Answer #35 Explanation In 2019, an updated meta-analysis of aspirin for primary prevention of cardiovascular events found that patients with a low risk of CVD taking aspirin did not have a reduction in all-cause or cardiovascular mortality. There was a lower risk of non-fatal MI (RR 0.82) and ischemic stroke (RR 0.87). However, aspirin was also associated with a  higher risk of major bleeding (RR 1.50), intracranial bleeding (RR 1.32), and major GI bleeding (RR 1.52). There was no difference in the risk of fatal bleeding (RR 1.09). Accordingly, the ESC does not recommend antiplatelet therapy in individuals with low/moderate CV risk due to the increased risk of major bleeding (Class III, LOE A). Although aspirin should not be given routinely to patients without established ASCVD, we cannot exclude that in some patients at high or very high CVD risk, the benefits may outweigh the risks. Main Takeaway In patients with low/moderate risk of CVD, aspirin for primary prevention is not recommended due to the higher risk of bleeding. For those at higher risk of CVD, low-dose aspirin may be considered for prevention in the absence of contraindications. Guideline Loc. Section 4.9.1, Page 3291 CardioNerds Decipher the Guidelines – 2021 ESC Prevention SeriesCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron!
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Oct 25, 2023 • 11min

340. Guidelines: 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure – Question #30 with Dr. Shashank Sinha

The following question refers to Section 8.5 of the 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure. The question is asked by Western Michigan University medical student & CardioNerds Intern Shivani Reddy, answered first by University of Southern California cardiology fellow and CardioNerds FIT Trialist Dr. Michael Francke, and then by expert faculty Dr. Shashank Sinha. Dr. Sinha is an Assistant Professor of Medical Education at the University of Virginia School of Medicine and an advanced heart failure, MCS, and transplant cardiologist at Inova Fairfax Medical Campus. He currently serves as both the Director of the Cardiac Intensive Care Unit and Cardiovascular Critical Care Research Program at Inova Fairfax. He is also a Steering Committee member for the multicenter Cardiogenic Shock Working Group and Critical Care Cardiology Trials Network and an Associate Editor for the Journal of Cardiac Failure, the official Journal of the Heart Failure Society of America. The Decipher the Guidelines: 2022 AHA / ACC / HFSA Guideline for The Management of Heart Failure series was developed by the CardioNerds and created in collaboration with the American Heart Association and the Heart Failure Society of America. It was created by 30 trainees spanning college through advanced fellowship under the leadership of CardioNerds Cofounders Dr. Amit Goyal and Dr. Dan Ambinder, with mentorship from Dr. Anu Lala, Dr. Robert Mentz, and Dr. Nancy Sweitzer. We thank Dr. Judy Bezanson and Dr. Elliott Antman for tremendous guidance. Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. Question #30 Ms. V. Tea is a 55-year-old woman with a history of cardiac sarcoidosis, heart failure with mildly reduced ejection fraction (HFmrEF – EF 40%), and ventricular tachycardia with CRT-D who presents with recurrent VT. She has undergone several attempts at catheter ablation of VT in the past and previously had been trialed on amiodarone which was discontinued due to hepatotoxicity. She now continues to have episodic VT requiring anti-tachycardia pacing and ICD shocks despite medical therapy with mexiletine, metoprolol, and sotalol. Her most recent PET scan showed no active areas of inflammation. Currently, her vital signs are stable, and labs are unremarkable. What is the best next step for this patient? A Evaluation for heart transplant B Evaluation for LVAD C Dobutamine D Prednisone E None of the above Answer #30 Explanation The correct answer is A – evaluation for heart transplant. For selected patients with advanced heart failure despite GDMT, cardiac transplantation is indicated to improve survival and quality of life (Class 1, LOE C-LD). Heart transplantation, in this context, provides intermediate economic value. Clinical indicators include refractory or recurrent ventricular arrhythmias with frequent ICD shocks. Patient selection for heart transplant includes assessment of comorbidities, goals of care, and various other factors. The United Network of Organ Sharing Heart Transplant Allocation Policy was revised in 2018 with a 6-tiered system to better prioritize unstable patients and minimize waitlist mortality. VT puts the patient as a Status 2 on the transplant list. There was a contemporary analysis of patients with end-stage cardiomyopathy due to cardiac sarcoidosis, published in Journal of Cardiac Failure, in 2018 that demonstrated similar 1-year and 5-year survival after heart transplant between patients with and without cardiac sarcoidosis. Choice B (evaluation for LVAD) is incorrect. While bridge to transplant with LVAD is definitely a potential next step in patients with cardiac sarcoidosis, it is not recommended in patients presenting primarily with refractory ventricular arrhythmias due to granuloma-induced scarring. In this situation, patients benefit from direct heart transplant rather than bridge to transplant LVAD approach. The same study, described before in the Journal of Cardiac Failure, also showed similar 1-year and 5-year survival after bridge-to-transplant mechanical circulatory support between patients with and without cardiac sarcoidosis. Since cardiac sarcoidosis is not just limited to the left ventricle, patients being considered for LVAD need hemodynamic assessment to determine the risk of post-LVAD RV failure. Choice C (dobutamine) is incorrect. The patient is currently not decompensated in terms of contractility nor is showing signs of cardiogenic shock. Further, dobutamine may worsen arrhythmia burden. Choice D (prednisone) is incorrect as there is no sign of active inflammation on the PET scan. The recurrent ventricular arrhythmias are being driven by granuloma-induced scar. Main Takeaway Cardiac transplantation has a Class 1 (LOE C-LD) recommendation for eligible patients with advanced HF despite GDMT to improve survival and quality of life. Specifically, direct heart transplantation is the best next step in patients with cardiac sarcoidosis and refractory ventricular arrhythmias rather than a bridge-to-transplant approach. Guideline Loc. Section 8.5 Decipher the Guidelines: 2022 Heart Failure Guidelines Page CardioNerds Episode Page CardioNerds Academy Cardionerds Healy Honor Roll CardioNerds Journal Club Subscribe to The Heartbeat Newsletter! Check out CardioNerds SWAG! Become a CardioNerds Patron!

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