Is it hyperfibrinolysis or fibrinolytic shutdown in severe COVID-19?. Issue 210 (February 2022)

• Record Type: Journal Article
• Authors: Nielsen, Nathan D.; Rollins-Raval, Marian A.; Raval, Jay S.; Thachil, Jecko
• Is Part Of: Thrombosis research. Issue 210(2022)
• Page Start: 1
• Page End: 3
• Publication Date: 2022-02
• Subjects: COVID-19 -- Fibrinolysis -- Hyperfibrinolysis -- Fibrinolytic shutdown -- D-dimer -- Viscoelastic testing; ARDS acute respiratory distress syndrome -- ICU intensive care unit -- LT clot lysis time -- PAI-1 plasminogen activator inhibitor-1 -- PAI-2 plasminogen activator inhibitor-2 -- PAP plasmin-alpha 2-antiplasmin complexes -- ROTEM rotational thromboelastometry -- SARS-CoV-2 Severe acute respiratory syndrome coronavirus 2 -- TAFI thrombin activatable fibrinolysis inhibitor -- TAT thrombin-antithrombin complex -- TEG thromboelastography assay -- tPA tissue plasminogen activator -- uPA urokinase plasminogen activator -- VET viscoelastic testing -- VTE venous thromboembolism; Thrombosis -- Periodicals; 616.135
• DOI: 10.1016/j.thromres.2021.12.012
• Languages: English
• ISSNs: 0049-3848

Abstract

Highlights: Understanding of the disorders of coagulation/fibrinolysis associated with COVID-19 is lacking. D-dimer levels have been demonstrated to be consistently elevated in the setting of COVID-19. These D-dimer elevations are found even in the absence of VTE or systemic hyperfibrinolysis. COVID-19 patients have depressed systemic fibrinolysis and resistance to exogenous fibrinolytics. This paradox may be due to tissue level hyperfibrinolysis but insufficient systemic fibrinolysis.