Reduced ADP-induced platelet aggregation may predict poor clinical outcomes in patients with COVID-19

COVID-19-associated coagulopathy remained a major contributor to mortality and morbidity even after mutation to the Omicron strain. Pathologic platelet hyperactivation caused by COVID-19 infection is generally recognized as an important mechanism of thrombotic complications; however, evaluating platelet aggregation in the emergency department remains challenging. This study explains the relationship between poor clinical outcomes and platelet aggregation capacity, based on viscoelastic testing.

This single-center retrospective study enrolled adult COVID-19 patients admitted to our hospital who underwent thromboelastography (TEG) with platelet mapping from August 2021 to April 2022. Patients were classified into two groups based on 28-day mortality. Using univariate analysis, multiple logistic regression modeling, and survival analysis, we statistically analyzed whether platelet aggregation abnormalities were related to poor clinical outcomes in COVID-19.

Forty-seven cases were allocated to survival (N = 40) and mortality Groups (N = 7). Compared to the survival group, the mortality group had significantly higher ages and Charlson scores, and was associated with poor consciousness levels upon admission, high APACHE II scores, and high SOFA scores. Time from onset to admission, strain type, and clinical severity of COVID-19 were statistically equivalent in the two groups. TEG analysis revealed that the mortality group showed significantly decreased LY30 and impaired platelet aggregation via the ADP pathway. ADP aggregation impairment was an independent predictor for 28-day mortality and demonstrated significantly poorer outcomes. ADP aggregation inhibition was not associated with clinical severity, time since COVID-19 onset, or platelet count.

Impaired ADP-induced platelet aggregation is an independent predictor of poor clinical outcomes in COVID-19 patients.