COVID-19 AND CARDIOVASCULAR DISEASES: FEATURES OF THE COMORBID COURSE

Abstract

The basis of the pathogenesis and progression of almost all life-threatening cardiovascular diseases is atherosclerosis, which leads to coronary heart disease, cerebrovascular disease, venous thromboembolism, and peripheral vascular disease, which subsequently causes myocardial infarction, cardiac arrhythmias or stroke Scientists have discovered a link between the new COVID-19 infection and the severity of cardiovascular disease. The infection in a patient with a history of cardiovascular disease is much more severe and is more often complicated by acute respiratory distress syndrome, which can lead to death. Therefore, the purpose of our review was to study the peculiarities of COVID-19 in patients with cardiovascular disease. In principle, the main cause of death in COVID-19 infection is respiratory failure, but today cardiac manifestations occupy competing positions as causes of death in these patients. Comorbid cardiovascular disease is present in 8–25% of the total population infected with COVID-19 and in a higher proportion of those who died. Similar to an influenza outbreak, myocardial damage due to COVID-19 may be associated with increased viscosity, increased clotting cascade, pro-inflammatory effects, or endothelial cell dysfunction caused by the SARS-CoV-2 virus. It is known that patients with COVID-19 had cardiomyocyte hypertrophy, degeneration and necrosis, mild interstitial hyperemia, and edema, along with infiltration of lymphocytes, monocytes, and neutrophils, but no viral component in myocardial tissue. SARS-CoV-2 can activate the coagulation cascade, leading to thrombocytopenia and sometimes to severe hypercoagulability and its consequences, such as cardiac ischemia. The cardiovascular manifestations of COVID-19 infection range from mild elevations in serum troponin and brain natriuretic peptide levels to fulminant myocarditis, lifethreatening arrhythmias, and refractory shock.