Discussion
COVID-19 is a global pandemic evolving in real time. Our knowledge of the novel coronavirus and its cardiovascular manifestations is limited and evolving daily. Cardiovascular complications, thus far, have been commonly found in patients with COVID-19 and such patients are at a higher risk of morbidity and mortality. Acute myocardial injury is present in more than 12% of critically ill COVID-19 patients and acute heart failure can develop as the illness severity intensifies. Herein, we describe a patient without a history of cardiovascular disease admitted to the hospital with 3rd degree heart block who was tested positive for COVID-19. Although the exact pathophysiological mechanism underlying cardiac electrical conduction system is not fully understood, a previous study showed that SARS-CoV genome was detected in the heart of 35% the patients with SARS-CoV infection. This raises the possibility of direct damage of cardiac conduction system and cardiomyocytes by the coronavirus (11). One potential mechanism is angiotensin-converting enzyme 2 (ACE2). Coronavirus appears to be affecting cells that express the ACE2 protein, including myocardial and vascular cells. Other suggested mechanisms include a cytokine storm, mediated by abnormal T helper cells and hypoxia-induced high intracellular calcium resulting in cardiac myocyte apoptosis. This case report highlights the first 3rddegree heart block case in a patient with COVID-19. Novel coronavirus is an important differential to consider in a patient presenting with symptomatic bradycardia and diagnosed with AV conduction abnormalities.
Disclosures: None