Abstract
TOPIC: Cardiovascular Disease TYPE: Medical Student/Resident Case Reports INTRODUCTION: SARS-CoV-2 has been associated with cardiac complications, especially in patients with pre-existing cardiovascular disease. We present a case of a patient without any history of coronary artery disease (CAD), who contracted COVID-19 and developed severe coronary artery spasms resulting in cardiac arrest. CASE PRESENTATION: A 55-year-old man with past medical history of tobacco use of 30 years was admitted with severe COVID-19 pneumonitis with acute hypercapnic and hypoxemic respiratory failure, requiring invasive mechanical ventilation. On hospital day 9, he had intermittent episodes of polymorphic ventricular tachycardia. An EKG showed acute ST elevations in leads II, III, aVF and V1-V3 with troponin T rise to 0.83 ng/mL. He developed cardiac arrest due to polymorphic ventricular tachycardia. Successful resuscitation was achieved after 5 minutes including defibrillation and 2 cycles of CPR. An emergent left heart catheterization revealed insignificant CAD, normal left ventricular systolic function and no wall motion abnormalities with a presumptive diagnosis of coronary artery spasm (CAS) as the most likely cause for his cardiac arrest. He was started on a nitroglycerin patch, and his vasopressor support was switched from norepinephrine to epinephrine. The previously observed EKG changes resolved within five hours and troponin levels started to decline. A head CT showed diffuse cerebral edema with early uncal herniation and following goals of care discussion, the patient was transitioned to comfort with terminal extubation. DISCUSSION: Rarely does CAS result in polymorphic ventricular tachycardia with cardiac arrest, in patients without CAD. Initial reports showed that patients with COVID-19 and ST segment elevations are found to have myocardial injury with non-obstructive coronary arteries (MINOCA), however there are no reports of COVID-19 patients with CAS resulting in cardiac arrest. The pathophysiology of CAS is not completely understood however, the current literature has described multiple mechanisms including endothelial dysfunction, systemic inflammation, oxidative stress and smooth muscle hyperreactivity, amongst others. CONCLUSIONS: More studies are required to elucidate the mechanism of myocardial injury associated with COVID-19 infection in order to risk stratify those patients at increased risk of CAS and arrthymias and possibly tailor their management;including choice of vasopressor support and use of nitrates to lower the risk of life-threatening complications. REFERENCE #1: Bangalore S, Sharma A, Slotwiner A, et al. ST-Segment Elevation in Patients with Covid-19 — A Case Series. N Engl J Med. 2020;382(25):2478-2480. doi:10.1056/NEJMc2009020 REFERENCE #2: Matta A, Bouisset F, Lhermusier T, et al. Coronary Artery Spasm: New Insights. J Intervent Cardiol. 2020;2020:1-10. doi:10.1155/2020/5894586 REFERENCE #3: Rivero F, Antuna P, Cuesta J, Alfonso F. Severe coronary spasm in a COVID -19 patient. Catheter Cardiovasc Interv. Published online August 2020:ccd.29056. doi:10.1002/ccd.29056 DISCLOSURES: No relevant relationships by Andres Cordova Sanchez, source=Web Response No relevant relationships by Markus Gutsche, source=Web Response No relevant relationships by Matthew Kovach, source=Web Response No relevant relationships by Jasmine Sandhu, source=Web Response
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