Coronavirus Disease 2019-Associated Coagulopathy

Abstract

Patients with the severe form of coronavirus disease 2019 (COVID-19) have been frequently found to suffer from both arterial and venous thrombotic events due to the perpetuation of a hypercoagulable state. This phenomenon, termed COVID-19-associated coagulopathy, is now considered a major component of the pathophysiology of this novel infectious disease, leading to widespread thrombosis. While at first, the vascular insults may be limited to the pulmonary microvasculature, as the disease progresses, systemic involvement occurs, culminating in distant organ thrombosis and multiorgan dysfunction syndrome. In this review article, we discuss recent insights into the pathophysiologic mechanisms of COVID-19-associated coagulopathy and review the clinical, histopathologic, and laboratory evidence, which leads us to conclude that COVID-19 is both a pulmonary and vascular disorder.

Figure

Pathogenesis of thrombosis in coronavirus disease 2019. FVIII, factor VIII; NET, neutrophil extracellular trap; NO, nitric oxide; PAI-1, plasminogen activator inhibitor 1; PGE2, prostaglandin E2; PGI2, prostaglandin I2; SARS-CoV-2, severe acute respiratory syndrome coronavirus; TF, tissue factor; ULVWF, ultra-large von Willebrand factor; VWF, von Willebrand factor.