Cardiological aspects of sars-CoV-2 infection

Abstract

Aim. The aim of the study was to analyze the scientific medical literature on the cardiac manifestations of SARS-CoV-2 virus infection. Material and methods. A review and analysis of current scientific data on cardiac complications combined with acute respiratory syndrome caused by this pathogen has been performed. Results and discussion. Infection caused by the SARS-CoV-2 virus is an urgent aspect of modern practical medicine. In a number of cases it manifests as a severe acute respiratory syndrome. Pulmonary lesion, which is primary, is accompanied by cardiovascular complications. Pulmonary and cardiovascular lesions are determined by the tropism of the virus to the protein, which is the enzyme angiotensin-convertase-2 that is widely expressed on cells of the respiratory and vascular systems, as well as in the myocardium. Thrombotic complications, including deep vein thrombosis of the lower extremities, thromboembolism and pulmonary artery thrombosis are very common. High mortality rate is noted among ICU patients on artificial ventilation with multiple organ failure. Lungs are the main organ affected, but systemic lesions of other organs, such as vessels, heart, kidneys, are also possible. Cardiac damage affects the myocardium, resulting in increased levels of markers of myocardial damage, such as troponin I. Myocardial dysfunction in the background of infection worsens the patient’s condition and is associated with a poor prognosis. The data indicate the possibility of viral infection of the myocardium and direct cyto-pathogenic damage. In the absence of signs of coronary insufficiency, elevated marker levels are considered as myocardial damage of nonischemic nature. Conclusion. An important factor in the pathogenesis of cardiac lesions is the aggravation of existing disorders due to additional activation of the reninangiotensin system. Systemic inflammatory changes can aggravate the severity of the course of infection in patients with metabolic syndrome.