The Etiopathogenesis of Thrombotic Events in COVID-19

Deep vein thrombosis, pulmonary embolism and peripheral artery thrombosis are among the most important complications of COVID-19. SARS-CoV-2 has been identified as a single-stranded RNA virus that enters cells by binding to angiotensin-converting enzyme 2, found in lung alveoli, cardiac myocytes, and vascular endothelial cells. The virus can survive on contaminated surfaces for up to 24-72 hours. In addition, transmission occurs after inhalation of viral particles from contaminated surfaces and their entry into the respiratory tract. SARS-CoV-2 is often associated with a cytokine storm, a hypercoagulable state, and the induction of marked autoimmune reactions. ACE receptors are also found in the human nasal epithelium, alveolar and gastrointestinal systems (small intestinal cells), as well as in the heart and kidneys; therefore, the pathological effects of infection are commonly observed in these areas. This multitrophic virus can cause multiple organ failure, particularly in the lungs, heart, and kidneys in severe cases. In this review we aim to investigate the pathophysiological mechanisms of thrombosis observed in COVID-19. In this context, studies on identifying prognostic markers as well as predictors of bleeding and thrombosis and selecting agents that will improve coagulation management will be beneficial in disease course and treatment.