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

Int J Mol Sci. 2023 May 18;24(10):8945. doi: 10.3390/ijms24108945.


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.

Keywords: COVID-19 infection; anticoagulant therapy; citokine storm; coagulopathy; endothelial dysfunction; platelet activation.

Publication types

  • Review

MeSH terms

  • Anticoagulants / therapeutic use
  • Blood Coagulation Disorders* / complications
  • Blood Coagulation Disorders* / drug therapy
  • COVID-19* / complications
  • Humans
  • Inflammation / drug therapy
  • SARS-CoV-2
  • Thrombophilia* / complications
  • Thrombosis* / etiology


  • Anticoagulants

Grants and funding

This research received no external funding.