Summary
Project Summary Many studies have highlighted a large incidence of hemostatic derangements in the form of hypercoagulable and hypofibrinolytic states following SARS-CoV-2 infection. These hemostatic disturbances are fueled by and a consequence of the concomitant activation of the endothelium following a severe inflammatory response, with likely contribution from many other pathways and components, such as the complement pathway and neutrophil activation. In COVID-19 patients, the resulting hyperinflammation, vascular dysfunction, and systemic hypercoagulability, collectively referred to as COV
