COVID-19, caused by the SARS-CoV-2 virus, has revealed a complex interplay between inflammation and coagulation, leading to the emergence of the concept of thrombo-inflammation. This concept recognizes that COVID-19 is not solely a respiratory illness, but a systemic disease with significant vascular and hematological components. COVID-19 is associated with an unusual prothrombotic state, with intense endothelial activation leading to vasculopathy, cytokine storm, complement system activation and a hypercoagulability state (the activation of platelets and the coagulation cascade, impaired fibrinolysis). The aim of this review is to discuss the different pathological pathways described in COVID-19 that lead to thromboembolic events. Widespread vaccination and post-COVID-19 immunization allows control over the severity of this pandemic. A better understanding of the pathophysiology of COVID-19 can improve the management of frail patients who are hospitalized in intensive care units.
Keywords: COVID-19; anticoagulation treatment; complement activation; cytokine storm; hypercoagulopathy; platelet activation; vasculopathy.