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