Figure 1.

Schematic representation of (A) the normal coagulation cascade triggered by an injury to the endothelial cells and (B) the hypercoagulability state related to SARS-CoV-2 infection. Generally, with an injury to the endothelial cell, the first response is platelet aggregation, followed by the activation of both the extrinsic and intrinsic pathways that lead to the generation of factor Xa and common pathway initiation. The product of the secondary coagulation cascade is a fibrin clot which will enhance platelet aggregates. ADPase and tissue factor (TF) pathway inhibitors (TFPI), as well as plasminogen, act as regulatory anticoagulants. The extrinsic and common pathways are initiated due to the increased TF and von Willebrand factor (VWF) in response to inflammatory cytokines such as interleukin (IL)-6 and the expression of TF by mononuclear cells in response to IL-6, which is elevated in SARS-CoV-2 infection. TFPI and ADPase are inhibited by the cytokines as well.