Abstract
The cardiovascular complications of Coronavirus disease 2019 (COVID-19) constitute acute cardiac injury (myopericarditis/myocarditis, myocardial infarction, stress cardiomyopathy, pericardial effusion/tamponade), cardiac arrhythmias and thromboembolic events including stroke, pulmonary embolism, cerebral venous thrombosis and venous thromboembolism (VTE.).1-2Due to its systemic nature, COVID-19 affects vascular endothelium and leads to micro- and macrovascular thrombosis.3 The endothelial damage in COVID-19 may be caused by either direct invasion by the Coronavirus or through inflammatory-induced mechanisms. Inflammatory cytokines, endothelium activation and COVID-19 per se being a procoagulant state with increased platelet reactivity, all may lead to vascular thrombosis. In details, endothelial dysfunction, subintimal inflammation, hemorrhage, edema, dysregulation of vascular tone, as well as disseminated intravascular coagulopathy (DIC), sepsis induced coagulopathy (SIC), increased D-dimer/FDP (fibrin degradation factors) are all possible contributing factors to vascular thrombosis both on arterial and venous side.
Sahrai Saeed, Øyvind Bleie. (2021) Antithrombotic therapy in COVID-19, Pakistan Journal of Medical Sciences, Volume-37, Issue-4.
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