Abstract

COVID-19 disease (Corona Virus Disease 19), especially its severe forms, is frequently accompanied by thrombotic or thromboembolic events with various organ localizations. These life-threatening complications are due to enhanced prothrombotic milieu of multifactorial aetiology. Main pathogenetic factors are: 1. dysregulation of the renin-angiotensin aldosterone system (RAAS) with decreased protective activity of ACE2 (angiotensin-converting enzyme), and 2. complex immune response of the infected organism. The incidence of venous thrombosis in studies on severe COVID-19 cases can be as high as 30% and is frequently refractory to prophylactic anticoagulation. Results of both basic and clinical research of the SARS-CoV2 (Severe acute respiratory syndrome coronavirus 2) infection have demonstrated that severe COVID-19 disease is associated with generalized endothelial dysfunction with resulting thrombophilia. This concise review article focuses on current pathophysiological and clinical aspects of both venous and arterial thrombosis in COVID-19 disease. Fig. 1, Schema 1, Tab. 4, Ref. 33, on-line full text (Free, PDF) www.cardiologyletters.sk.

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