COVID-19 Coagulopathy: From Pathogenesis to Treatment

Abstract

Coronavirus disease 2019 (COVID-19) has emerged as a pandemic at the end of 2019 and continues to exert an unfavorable worldwide health impact on a large proportion of the population. A remarkable feature of COVID-19 is the precipitation of a hypercoagulable state, mainly in severe cases, leading to micro- and macrothrombosis, respiratory failure, and death. Despite the implementation of various therapeutic regimes, including anticoagulants, a large number of patients suffer from such serious complications. This review aims to describe the current knowledge on the pathophysiology of the coagulation mechanism in COVID-19. We describe the interplay between three important mediators of the disease and how this may lead to a hyperinflammatory and prothrombotic state that affects outcome, namely, the endothelium, the immune system, and the coagulation system. In line with the hypercoagulability state during COVID-19, we further review on the rare but severe vaccine-induced thrombotic thrombocytopenia. We also summarize and comment on available anticoagulant treatment options and include suggestions for some future treatment considerations for COVID-19 anticoagulation therapy.

Keywords: COVID-19; Coagulopathy; Heparin; Hyperinflammation.

Fig. 1

Schematic illustration of the pathophysiology of COVID-19 coagulopathy and the interplay between endothelial, immune, and coagulation systems. VWF, von Willebrand factor; TF, tissue factor; PAI-1, plasminogen activator inhibitor 1; PF-4, platelet factor 4; TFPI, tissue factor pathway inhibitor; AT III, antithrombin III; TNF-α, tumor necrosis factor-α.

Fig. 2

Schematic illustration of the pathophysiology of VITT. PF 4, platelet factor 4; VITT, vaccine-induced thrombotic thrombocytopenia; VWF, von Willebrand factor; TF, tissue factor.