Fibrinolysis Resistance: A Potential Mechanism Underlying COVID-19 Coagulopathy
Emmanuel Weiss, Olivier Roux, Jean-Denis Moyer, Cathérine Paugam‐Burtz, Larbi Boudaoud, Nadine Ajzenberg, Dorothée Faille, Emmanuelle de Raucourt
Abstract
We read with great interest the article by Spiezia et al, published in a recent issue of the journal, showing a severe hypercoagulability on thromboelastometry profiles of 22 critically ill patients with novel coronavirus (SARS-CoV-2).[1] These results are in agreement with a growing body of evidence suggesting that COVID-19 severe infection predisposes to venous thromboembolism and even primary pulmonary thrombosis,[2] and that abnormal coagulation parameters are associated with poor prognosis.[3] The thrombotic risks in COVID-19 are such that consensus guidance has been issued for thromboprophylaxis,[3] [4] [5] leading to a large prescription of high doses of low molecular weight (LMWH) or unfractionated heparin, notwithstanding the need for more evidence. Tang et al reported high rates of overt disseminated intravascular coagulation according to the International Society on Thrombosis and Haemostasis diagnostic criteria.[6] Conversely, in the study from Spiezia et al, standard tests and thromboelastography profiles suggested, rather than a consumptive coagulopathy, a severe hypercoagulability linked to hyperfibrinogenemia.[1]