COVID-19 and Hypercoagulability: A Review

Asim Kichloo1,2, Kirk Dettloff2, Michael Aljadah3

  • 1St. Mary's of Saginaw Hospital, Saginaw, MI, USA.

Insights

Thrombotic complications in COVID-19 are linked to a hypercoagulable state. Understanding the pathophysiology and targeting specific pathways may improve outcomes for patients with coronavirus disease 2019.

Area of Science:

  • Cardiovascular Medicine
  • Infectious Diseases
  • Pathophysiology

Background:

  • Thrombotic complications are a significant concern in coronavirus disease (COVID-19), particularly in critically ill patients.
  • COVID-19 is associated with a hypercoagulable state, but the underlying pathophysiology remains incompletely understood.

Purpose of the Study:

  • To review the proposed pathophysiologic mechanisms contributing to thrombotic complications in COVID-19.
  • To discuss current and potential treatment strategies for these thrombotic complications.

Main Methods:

  • Literature review of existing studies on COVID-19 and thrombosis.
  • Analysis of proposed mechanisms including immune response, endothelial injury, coagulation activation, and fibrinolysis shutdown.

Main Results:

  • COVID-19 pathogenesis involves immune response, endothelial cell injury, and activation of coagulation via tissue factor.
  • Impaired fibrinolysis also contributes to the hypercoagulable state observed in COVID-19 patients.

Conclusions:

  • Effective treatments targeting the identified pathophysiologic pathways are crucial for improving clinical outcomes.
  • Addressing thrombotic complications may decrease overall mortality in patients with COVID-19.

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