Barnes, Jaime

Introduction: Thrombo-inflammatory syndrome (TIS) characterized by a pathophysiological state of hypercoagulability, heightened platelet function, and inflammation has been observed in patients with acute myocardial infarction, and HIV. Hypothesis: The incidence of TIS is observed at a high rate in COVID-19 patients and worsens with symptom severity Methods: Blood samples from COVID-19 positive hospitalized patients (n=24) was collected for coagulation and platelet function analysis using point-of-care thromboelastography, TEG6s (Haemonetics, Corp) and routine labs were collected to measure markers of inflammation, coagulation, and organ damage (Table). Disease severity was grouped according to oxygen supplementation requirements and comparisons were made using unpaired t-test and chi-squared tests. Thrombo-inflammation was defined as the presence of both hypercoagulability by TEG [Clot initiation (R) < 4.6, fibrin clot strength (FCS) >32mm, and platelet fibrin clot strength (PFCS) >69] and D-dimer >ULN. Results: Ninety- five percent of COVID positive patients had at least one co-morbidity with the incidence of hypertension (71%), diabetes (50%), and obesity (42%) being the most frequent. A total of 63% (16/24) of patients had TIS, the incidence was significantly increased with escalating disease severity (p=0.03). A significant stepwise (p<0.05) increase in FCS, D-Dimer, WBC count, lactate dehydrogenase, and procalcitonin was observed with worsening respiratory function (table). MA-ADP a measure of platelet function was in the high normal range for 81 % of patients. Conclusions: Thrombo-inflammatory is observed with most COVID patients, importantly heightened platelet function is a component of the syndrome and raises the question if antiplatelet therapy is needed in select COVID patients. Selective assessments with TEG6s may facilitate antithrombotic personalization.

Background: Thromboelastography (TEG®) is used across a wide range of clinical settings to identify patients at risk for thrombosis and coagulopathic bleeding and may be a useful diagnostic tool to guide antithrombotic treatment in patients with COVID-19. Hypothesis: TEG® identifies symptom progression in COVID -19 patients, particularly in the high-risk minority population known to have worse clinical outcomes. Methods: Whole blood from African American and Hispanic hospitalized COVID positive (n=22) and negative outpatients (n=24) was analyzed using point-of-care TEG®6s (Haemonetics, Corp). TEG® parameters including clot initiation (R), fibrin clot strength (FCS), platelet-fibrin clot strength (PFCS) and clot lysis (LY30) were compared across disease severity groups (table). Routine labs including D-Dimer, C-reactive protein (CRP), ferritin, and procalcitonin were also collected. Results: Ninety- five percent of COVID positive patients had at least one co-morbidity with the incidence of hypertension (73%), diabetes (55%), and obesity (45%) being the most frequent. R time was more rapid, and FCS and PFCS was significantly higher in COVID positive as compared to negative groups (p<0.03). A stepwise increase in FCS and PFCS was observed with worsening respiratory function (table). Similarly, D-Dimer, CRP, ferritin, and procalcitonin levels were highest in patients receiving ventilator support. No differences were observed in clot lysis between the groups despite elevated D-Dimer levels. Conclusion: We have demonstrated that TEG®6s can identify a prothrombotic phenotype characterized by rapid clot initiation and increased fibrin and platelet-fibrin clot strength in a minority population with COVID-19. Future studies are warranted implementing the TEG6s® in clinical trials to personalize antithrombotic therapy in COVID-19 and improve outcomes.