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Author Notes:

Correspondence: Roman M. Sniecinski, rsnieci@emory.edu

Author contributions: CLM and RMS both designed the study, analyzed data, and wrote/edited the manuscript. FS and TS gathered/analyzed data and contributed toward writing/editing the manuscript.

Disclosures: RMS has received research support from Cerus, Grifols, and is part of a scientific advisory board for OctaPharma. TS, FS, and CLM have no relevant disclosures.

Subjects:

Research Funding:

Research reported in this publication was supported in part by COVID Catalyst-I-3 Funds from the Woodruff Health Sciences Center and Emory School of Medicine and made possible through a grant from the O. Wayne Rollins Foundation, and through the Georgia CTSA NIH award (Grant No. UL1-TR002378).

CLM is also supported by NIH/NHLBI K99 HL150626-01.

Keywords:

  • Science & Technology
  • Life Sciences & Biomedicine
  • Cardiac & Cardiovascular Systems
  • Hematology
  • Peripheral Vascular Disease
  • Cardiovascular System & Cardiology
  • Thromboelastography
  • Fibrinolysis
  • COVID-19
  • Severe acute respiratory syndrome coronavirus 2
  • Tissue plasminogen activator
  • Pulmonary embolism
  • Injury

COVID-19 patient plasma demonstrates resistance to tPA-induced fibrinolysis as measured by thromboelastography

Tools:

Journal Title:

Journal of Thrombosis and Thrombolysis

Volume:

Volume 52, Number 3

Publisher:

, Pages 766-771

Type of Work:

Article | Final Publisher PDF

Abstract:

Patients critically ill with COVID-19 are at risk for thrombotic events despite prophylactic anticoagulation. Impaired fibrinolysis has been proposed as an underlying mechanism. Our objective was to determine if fibrinolysis stimulated by tissue plasminogen activator (tPA) differed between COVID patients and controls. Plasma from 14 COVID patients on prophylactic heparin therapy was obtained and compared with heparinized plasma from 14 different healthy donors to act as controls. Kaolin activated thromboelastography with heparinase was utilized to obtain baseline measurements and then repeated with the addition of 4 nM tPA. Baseline fibrinogen levels were higher in COVID plasma as measured by maximum clot amplitude (43.6 ± 6.9 mm vs. 23.2 ± 5.5 mm, p < 0.0001) and Clauss assay (595 ± 135 mg/dL vs. 278 ± 44 mg/dL, p < 0.0001). With the addition of tPA, fibrinolysis at 30 min after MA (LY30%) was lower (37.9 ± 16.5% vs. 58.9 ± 18.3%, p = 0.0035) and time to 50% lysis was longer (48.8 ± 16.3 vs. 30.5 ± 15.4 min, p = 0.0053) in the COVID-19 samples. Clotting times and rate of fibrin polymerization (‘R’ or ‘α’ parameters) were largely the same in both groups. Clot from COVID patients contains a higher fibrin content compared to standard controls and shows resistance to fibrinolysis induced by tPA. These findings suggest the clinical efficacy of thrombolytics may be reduced in COVID-19 patients.

Copyright information:

© The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2021.

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