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Investigating von Willebrand Factor Pathophysiology Using a Flow Chamber Model of von Willebrand Factor-platelet String Formation
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The ADAMTS13-von Willebrand factor axis in COVID-19 patients

Ilaria Mancini1, Luciano Baronciani2, Andrea Artoni2

  • 1Department of Pathophysiology and Transplantation, Università degli Studi di Milano, Milan, Italy.

Journal of Thrombosis and Haemostasis : JTH
|November 24, 2020
PubMed

Insights

Severe COVID-19 is linked to microthrombosis. This study found that an imbalanced VWF-ADAMTS13 axis in COVID-19 patients correlates with disease severity and increases clotting risk.

Area of Science:

  • Hematology
  • Infectious Diseases
  • Critical Care Medicine

Background:

  • Severe COVID-19 is associated with a higher risk of thromboembolic events.
  • Microthrombosis in lung tissue has been observed in patients deceased from COVID-19.

Purpose of the Study:

  • To investigate the underlying mechanisms of microthrombosis in the progression of COVID-19.
  • To analyze the VWF-ADAMTS13 axis in relation to COVID-19 severity.

Main Methods:

  • A cross-sectional study involving 50 COVID-19 patients was conducted.
  • Patients were stratified into three care intensity groups: low, intermediate, and high.
  • Assessed were von Willebrand factor (VWF) antigen (VWF:Ag), VWF ristocetin-cofactor (VWF:RCo), VWF multimers, VWF propeptide (VWFpp), and ADAMTS13 activity.

Main Results:

  • VWF:Ag, VWF:RCo, and VWFpp levels were significantly elevated in COVID-19 patients and increased with care intensity.
  • The ratio of high-to-low molecular-weight VWF multimers and ADAMTS13 activity decreased as care intensity increased.
  • Elevated VWF:Ag to ADAMTS13 activity ratio was strongly associated with COVID-19 severity.

Conclusions:

  • A significant alteration in the VWF-ADAMTS13 axis occurs in COVID-19 patients.
  • This imbalance contributes to the hypercoagulable state and microthrombosis risk in COVID-19.
  • The VWF-ADAMTS13 axis serves as a potential biomarker for COVID-19 severity.
Abstract

Keywords:
ADAMTS13 ProteinCOVID-19MicrovasculatureSevere acute respiratory syndrome coronavirus 2Thrombosisvon Willebrand factor

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