PB0598 - Demonstration of Prothrombotic Status in patients with COVID-19 using Thromboelastography and a Novel T-TAS assay

Background: COVID-19 is associated with cytokine storm and hypercoagulability, indicating elevated risk for thrombotic events. Thromboelastography (TEG6s) assay has been used to demonstrate hypercoagulability in patients with COVID-19. Total Thrombus formation Analysis System (T-TAS) is a novel microfluidic assay that can be used to assess thrombogenicity in the presence of high shear as present in coronary arteries (PL chip) and 600/s shear stress indicating shear at large arteries (AR chip).

Aims: To demonstrate the prothrombotic state in COVID-19 patients using a novel T-TAS assay and TEG6s.

Methods: Blood samples were collected from 111 patients with COVID-19 during hospitalization for TEG6s and T-TAS analysis, and from 155 healthy volunteers who were not on any antithrombotic agents for TEG6s analysis. Previously published normal ranges for T-TAS assays were used in the analysis.

Results: 57% of COVID-19 patients were male and 65% were African American. All COVID-19 patients were on prophylaxis or full dose heparin during hospitalization. With the T-TAS AR chip, COVID-19 patients exhibited significantly shorter values in initial occlusion time (T10) and occlusion time and higher area under the curve (AUC) (p < 0.001 for all), indicating a prothrombotic state. There were no differences in PL chip parameters. In COVID-19 patients, TEG6s assay demonstrated reaction time within the normal range despite anticoagulant therapy, higher platelet-fibrin clot strength, fibrinogen clot strength and fibrinogen levels compared to healthy subjects (p < 0.001 for all). There were no differences in total platelet function parameters (PL chip) between COVID-19 patients and healthy subjects.

Conclusion(s): Our data indicate that COVID-19 patients exhibit a prothrombotic state that can be assessed by a novel T-TAS assay and TEG6s. This study also indicated that prothrombotic state in COVID-19 patients may be driven by significantly higher fibrinogen levels in the presence of normal platelet function.