Figure 4.
Dysregulated fibrinolysis in severe COVID-19. (A) Turbidimetric analysis of clot lysis in severe COVID-19, ARDS-influenza, and donor plasma. Representative clot lysis curves are shown. SARS-CoV-2, n = 20; ARDS-influenza; n = 19, donors, n = 20. (B) Turbidity values of the fibrin clots at 60 minutes. SARS-CoV-2, n = 20; ARDS-influenza, n = 19; donors, n = 20. (C-D) Clot lysis time. Clots were generated in a purified system with increasing concentrations of fibrinogen and/or FXII/FXIIa. Clot formation was induced by thrombin and clot lysis by plasmin generated from plasminogen by tPA. In some experiments, FXII was preincubated with CTI. Clot formation and lysis were monitored via turbidimetry (n = 3-5). (E-G) tPA (E), plasminogen activator inhibitor-1 (PAI-1; F), and thrombin-activatable fibrinolysis inhibitor (TAFI; G) levels in plasma of patients with COVID-19 (n = 21) or ARDS-influenza (n = 21) and donors (n = 17), as assessed by enzyme-linked immunosorbent assay. *P < .05; **P < .01.

Dysregulated fibrinolysis in severe COVID-19. (A) Turbidimetric analysis of clot lysis in severe COVID-19, ARDS-influenza, and donor plasma. Representative clot lysis curves are shown. SARS-CoV-2, n = 20; ARDS-influenza; n = 19, donors, n = 20. (B) Turbidity values of the fibrin clots at 60 minutes. SARS-CoV-2, n = 20; ARDS-influenza, n = 19; donors, n = 20. (C-D) Clot lysis time. Clots were generated in a purified system with increasing concentrations of fibrinogen and/or FXII/FXIIa. Clot formation was induced by thrombin and clot lysis by plasmin generated from plasminogen by tPA. In some experiments, FXII was preincubated with CTI. Clot formation and lysis were monitored via turbidimetry (n = 3-5). (E-G) tPA (E), plasminogen activator inhibitor-1 (PAI-1; F), and thrombin-activatable fibrinolysis inhibitor (TAFI; G) levels in plasma of patients with COVID-19 (n = 21) or ARDS-influenza (n = 21) and donors (n = 17), as assessed by enzyme-linked immunosorbent assay. *P < .05; **P < .01.

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