Pathomechanisms of SARS-CoV-2 infection and development of atherosclerosis in patients with COVID-19: A review

Abstract

The pandemic of coronavirus disease 2019 (COVID-19) has posed a major health challenge for over 2 years. The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) that causes it belongs to single-stranded ribonucleic acid viruses and causes acute respiratory distress syndrome. The initial outbreak was discovered in December 2019 in Wuhan province, where SARS-CoV-2 quickly spread to other countries. In addition to respiratory disorders, it has been shown that during and after COVID-19 infection, cardiovascular diseases are often developed or exacerbated, such as: arterial hypertension, coronary artery disease, arrhythmias, heart failure and thromboembolic complications. In view of the higher prevalence of atherosclerosis in patients with COVID-19, we described the pathomechanisms of the development of this infection and the possible correlations between SARS-CoV-2 infection and thromboembolic complications. We focused on the role of the inflammatory response, renin-angiotensin system and endothelial dysfunction in the development of atherosclerosis in patients with COVID-19. A thorough understanding of the hemodynamic mechanisms and the impact of the infection on the cardiovascular system will allow for the proper selection of appropriate therapy in patients after SARS-CoV-2 infection.