SARS-CoV2 at the heart of the vessels: clinical-biological reality to pathophysiological hypotheses!

Abstract

Our knowledge of the pathophysiology of severe acute respiratory syndrome coronavirus 2 infection (SARS-CoV2) is changing very rapidly from day to day. Several clinical and biological arguments reveal the multiple vascular thrombotic facets of this infection. Disseminated intravascular coagulation with multiple organ failure and thromboembolic events have contributed to the poor prognosis. The pathological sequence involves cells (phagocytes, endothelial cells, platelets, leukocytes), cytokines and microparticles. The main mechanisms associated with this prothrombotic state are inflammation, hypoxia and endothelial damage. They probably solicit microparticles, tissue factor, circulating endothelial cells, red blood cells, neutrophil extracellular trap and surely other actors that should be defined and confirmed.