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Pré-Publication, Document De Travail Année : 2021

Altered fibrin clot structure contributes to thrombosis risk in severe COVID-19

Liliana Schaefer
Philipp Markart
  • Fonction : Auteur

Résumé

Abstract The high incidence of thrombotic events suggests a possible role of the contact system pathway in COVID-19 pathology. Here, we demonstrate altered levels of factor XII (FXII) and its activation products in two independent cohorts of critically ill COVID-19 patients in comparison to patients suffering from severe acute respiratory distress syndrome due to influenza virus (ARDS-influenza). Compatible with this data, we report rapid consumption of FXII in COVID-19, but not in ARDS-influenza, plasma. Interestingly, the kaolin clotting time was not prolonged in COVID-19 as compared to ARDS-influenza. Using confocal and electron microscopy, we show that increased FXII activation rate, in conjunction with elevated fibrinogen levels, triggers formation of fibrinolysis-resistant, compact clots with thin fibers and small pores in COVID-19. Accordingly, we observed clot lysis in 30% of COVID-19 patients and 84% of ARDS-influenza subjects. Analysis of lung tissue sections revealed wide-spread extra- and intra-vascular compact fibrin deposits in COVID-19. Together, our results indicate that elevated fibrinogen levels and increased FXII activation rate promote thrombosis and thrombolysis resistance via enhanced thrombus formation and stability in COVID-19.

Dates et versions

hal-03438497 , version 1 (21-11-2021)

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Citer

Malgorzata Wygrecka, Anna Birnhuber, Benjamin Seeliger, Laura Michalick, Oleg Pak, et al.. Altered fibrin clot structure contributes to thrombosis risk in severe COVID-19. 2021. ⟨hal-03438497⟩
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