The causative agent of severe acute respiratory syndrome, corona virus 2 (SARS-CoV-2), the etiological agent of the COVID-19 disease, can infect the heart, vascular tissues and circulating cells via angiotensin-converting enzyme 2 (ACE-2), a cell receptor host for the viral spike protein. The focus of this review article is on the prevalence, risk factors, pathogenesis, clinical course and sequelae of myocardial damage caused by the disease COVID-19. Emphasis is also placed on the interactions of platelets with the vascular endothelium, which includes consideration of the role of the SARS-CoV-2 virus protein in triggering the development of generalized endothelitis, which further in a circle triggers more intense activation of platelets. Acute cardiac lesion is a common extrapulmonary manifestation of COVID-19 with potential chronic consequences. Clinical manifestations include direct cardiac damage and indirect immune response mechanisms that affect the cardiovascular (CV) system and have implications for the treatment of patients after recovery from acute COVID-19 infection. The most common direct cardiovascular lesion is an acute heart lesion, present in more than 12% of all infected patients and defined by a significant increase in cardiac troponins in the serum and echocardiographic signs of damage to the myocardial texture due to inflammation, impairment of segmental mobility or global systolic and diastolic function of the left ventricle and sometimes inflammation of the pericardium. Arrhythmias, venous thromboembolism and cardiomyopathy are predominant KV manifestations described in the patient with COVID-19. An analysis of 72,314 confirmed cases of COVID - 19 (Wuhan) showed total mortality of 1663 patients or 2.3%, with presence of a previous KV disease in 10.5%, diabetes Mellitus in 7.3% and arterial hypertension in 6%. Cardiovascular complications because of COVID-19 associated with comorbidities were: myocardial lesion (20 %), cardiac arrhythmias (16%), myocarditis and fulminant myocarditis with lowered ejection fraction (10%), non-occlusive myocardial infarction and venous thromboembolism and acute' cardiac insufficiency and cardiogenic shock. Hypertension and diabetes are the most frequent_comorbidities in those infected with COVID-19, for whom hospitalization was necessary. A Denmark study based on the national register of over 5000 patients with hospitalized COVID19 revealed that the risk from the acute myocardial infarction and ischemic stroke was 5 and even 10 times higher , respectively , during the first 14 days after COVID-19 infections in comparison with the period which preceded the known infection. Numerous individual cases point to extremely high values and troponin T dynamics typicalfor non-occlusive myocardial infarction with normal coronary arteries. Mechanisms of indirect cardiovascular lesions are: dysregulation of inflammatory or immune responses of hyperinflammation, vascular thrombosis and activation of platelets, autoimmune phenomena and adaptive immunological dysfunction in vascular thrombosis associated with COVID-19. Cardiovascular dysfunction and disease are often fatal complications of a severe COVID-19 virus infection. Cardiac complications can occur even canin patients without basic cardiac insufficiency, as a part of acute infections and they are associated with a more severe form of COVID 19 disease and increased mortality. Of COVID-19 patients treated in the intensive care unit 61% died because they had acute respiratory distress syndrome (ARDS), 44% of them had severe cardiac arrhythmias and 31% percent of them experienced a shock syndrome. Elevated troponin levels were rare in survivors of uncomplicated COVID19 (1%-20%), common in critically ill patients (46%-100%), and almost universally elevated in critically ill (ie, those requiring intensive care or mechanical ventilation) and those who did not survive. Some autopsy findings suggested myocardial infiltration by mononuclear leukocytes and revealed some cases of severe myocarditis with a dilated phenotype. Among patients hospitalized with COVID-19, evidence about acute damage of cardiac functions are frequent _ and include the following: acute cardiac insufficiency (3%-33%), cardiogenic shock ( 9%-17%), ischemia or myocardial infarction (0.9%-11%), left ventricular dysfunction (10%-41%), right ventricular dysfunction (33%-47%), biventricular dysfunction (3%-15%), stress cardiomyopathy (2%-5.6%), arrhythmias (9%-17%), venous thromboembolism (23%-27%) and arterial thrombosis as secondary viral mediated coagulopathy. COVID - 19 is associated with abnormalities of cardiac structures and functions including echocardiographic evidence of left ventricular dysfunction, regional wall movement abnormalities and mild reduction of right ventricular function. Involvement of myocardial lesion because of SARS - CoV -2infection was very much widespread even in patients with mild symptoms.