COVID-19 is known to induce a hypercoagulable state that contributes to increased morbidity and mortality. Platelets are rapid responders to pathogen invasion, stimulating both innate and adaptive immunity. However, in the context of severe infection, dysregulated platelet activation can lead to pathological immunothrombosis. This study aimed to evaluate platelet aggregation in hospitalized COVID-19 patients compared with healthy controls. This prospective comparative study enrolled 50 hospitalized COVID-19 patients and 25 healthy controls. Platelet aggregation was measured using light transmission aggregometry (LTA) with adenosine diphosphate (ADP) as the agonist. Additional laboratory evaluations included inflammatory markers, D-dimer, and liver function tests. Chest computed tomography (CT) was performed to evaluate COVID-19 severity. Associations between platelet aggregation and clinical outcomes, including duration of hospital stay, thrombotic events, mechanical ventilation, and mortality, were analyzed. Compared to healthy controls, COVID-19 patients exhibited lower platelet and lymphocyte counts (p = 0.006 and p = 0.017, respectively). Inflammatory markers such as lactate dehydrogenase (LDH), ferritin, and C-reactive protein (CRP), as well as D-dimer, alanine aminotransferase (ALT), aspartate aminotransferase (AST), and international normalized ratio (INR), were significantly elevated in the COVID-19 group (p < 0.05 for all). The mean maximum platelet aggregation response to ADP was significantly reduced in COVID-19 patients (70.66% ± 29.70) compared to controls (89.80% ± 15.37; p = 0.003). Analysis of the receiver operating characteristic (ROC) curve determined a threshold value of ≤ 65% for maximum platelet aggregation in COVID-19 cases, which yielded a sensitivity of 54.0%, a specificity of 100.0%, and an overall diagnostic accuracy of 71.0% in detecting COVID-19 cases. No statistically significant associations were found between platelet aggregation and COVID-19 severity, thrombotic events, need for mechanical ventilation, or mortality. Platelet aggregation also showed no statistically significant correlation with laboratory parameters, hospital stay, or CT chest severity scores. In vitro platelet aggregation in response to ADP was significantly reduced in patients with COVID-19, despite elevated D-dimer levels, which reflect hypercoagulable state and possible platelet consumption. However, this reduction didn’t correlate with systemic inflammatory markers, D-dimer, or clinical outcomes. These findings raise questions about the predictive utility of platelet aggregation in COVID-19-related thrombotic risk.
El-Badrawy et al. (2026) studied this question.