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Insights into Fibrinogen-Mediated COVID-19 Hypercoagubility in Critically Ill Patients

Andrea Miltiades1, Philipp J Houck1, Matthew Monteleone2

  • 1Departments of Anesthesiology.

Journal of Neurosurgical Anesthesiology
|December 6, 2021
PubMed

Insights

Severe COVID-19 causes hypercoagulability, increasing clot risk. This is linked to reduced fibrinolysis due to elevated plasminogen activator inhibitor-1, impacting anticoagulation strategies for critical patients.

Area of Science:

  • Hematology
  • Infectious Diseases
  • Critical Care Medicine

Background:

  • Coronavirus disease-2019 (COVID-19) is linked to hypercoagulability and thrombotic complications.
  • Severe COVID-19 cases, particularly those requiring mechanical ventilation, exhibit heightened risks.

Purpose of the Study:

  • To investigate the mechanisms of hypercoagulability in patients with severe COVID-19.
  • To identify specific factors contributing to increased clot formation in these patients.

Main Methods:

  • Utilized rotational thromboelastometry to assess coagulation in severe COVID-19 patients versus controls.
  • Measured components of the fibrinolytic pathway, including fibrinogen, tissue plasminogen activator, plasminogen activator inhibitor-1, and plasminogen.

Main Results:

  • Nearly all severe COVID-19 patients showed signs of hypercoagulability, with significantly increased clot firmness.
  • Elevated levels of fibrinogen, tissue plasminogen activator, and plasminogen activator inhibitor-1 were observed in COVID-19 patients.
  • Findings suggest hypercoagulability is driven by decreased fibrinolysis due to high plasminogen activator inhibitor-1 levels.

Conclusions:

  • Hypercoagulability in severe COVID-19 is associated with impaired fibrinolysis.
  • Elevated plasminogen activator inhibitor-1 likely inhibits plasmin, contributing to clot formation.
  • Understanding these mechanisms is crucial for developing effective anticoagulation treatments for critically ill COVID-19 patients.

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