Interrelationship between COVID-19 and Coagulopathy: Pathophysiological and Clinical Evidence

Since the first description of COVID-19 infection, among clinical manifestations of the disease, including fever, dyspnea, cough, and fatigue, it was observed a high incidence of thromboembolic events potentially evolving towards acute respiratory distress syndrome (ARDS) and COVID-19-associated-coagulopathy (CAC). The hypercoagulation state is based on an interaction between thrombosis and inflammation. The so-called CAC represents a key aspect in the genesis of organ damage from SARS-CoV-2. The prothrombotic status of COVID-19 can be explained by the increase in coagulation levels of D-dimer, lymphocytes, fibrinogen, interleukin 6 (IL-6), and prothrombin time. Several mechanisms have been hypothesized to explain this hypercoagulable process such as inflammatory cytokine storm, platelet activation, endothelial dysfunction, and stasis for a long time. The purpose of this narrative review is to provide an overview of the current knowledge on the pathogenic mechanisms of coagulopathy that may characterize COVID-19 infection and inform on new areas of research. New vascular therapeutic strategies are also reviewed.

Automated summary

COVID-19 infection leads to a hypercoagulable state, potentially resulting in acute respiratory distress syndrome (ARDS) and COVID-19-associated coagulopathy (CAC). CAC is a key factor in the organ damage caused by SARS-CoV-2. The prothrombotic state of COVID-19 can be explained by increased levels of D-dimer, lymphocytes, fibrinogen, interleukin 6 (IL-6), and prothrombin time. Inflammatory cytokine storm, platelet activation, endothelial dysfunction, and prolonged stasis are potential mechanisms for this hypercoagulable process.