ATHEROSCLEROSIS AND AUTOIMMUNE PHENOMENA IN COVID-19

Abstract

Soon after the outbreak of COVID-19 in Wuhan, China, it became clear that patients with cardiovascular diseases (CVD) had a higher risk of acute complications [1]. The cardiovascular system is one of the main targets of the SARS-CoV-2 virus, resulting in the increased incidence of severe disorders including myocarditis, pericarditis, arrhythmias, heart failure and thromboembolism in COVID-19 cases. The mortality rate of such patients ranges from 11% to 19% [1]. Mortality from COVID-19 among people with CVD is much higher than average. In the presence of CVD accompanied by hypertroponinemia (for example, against the background of severe coronary heart disease), it exceeds 70% in some samples. Up to 25% of COVID-19 cases are accompanied with the development of cardiovascular complications, mainly among older people with pre-existing atherosclerosis and its clinical manifestation. In the very beginning of the COVID-19 pandemic, autopsy studies described fulminant myocarditis with features of direct viral and immunopathologically mediated heart damage [4]. It was assumed that myocarditis is common in COVID-19, but further studies on larger samples with magnetic resonance imaging (MRI) reported a more modest prevalence of severe myocarditis (accompanied by systolic dysfunction, electrocardiogram (ECG) changes and an increase in myocardial cell injury biomarkers in the blood) [5]. Thus, out of more than 168,000 patients hospitalized with COVID-19 in Florida, myocarditis was diagnosed only in 0.4% of cases [6]. Apparently, vascular lesions in COVID-19 are more significant than the cytotoxicity of the virus in cardiomyocytes. Of course, cardiovascular implications of COVID-19 are most dangerous for those who, on the basis of preexisting atherosclerosis, already have chronic lesions of the coronary/cerebral arteries and marginally reduced perfusion reserves of the myocardium and other vital organs [1].