Abstract Number: Esoc2026a1267 Hypercoagulability in Carotid Stenosis Assessed by Thrombin Generation Assay: An Exploratory Study

Abstract Background and aims Carotid atherosclerosis is a major cause of acute ischemic stroke (AIS) and is driven by vascular risk factors promoting endothelial dysfunction and plaque progression. While platelet-related mechanisms have been extensively studied, the association between the extent of carotid stenosis and global coagulation activation remains unclear. This study aimed to investigate the relationship between carotid stenosis severity and hypercoagulability using thrombin generation assay. Methods This prospective observational study included asymptomatic patients with moderate carotid atherosclerosis (1-49% stenosis) and advanced carotid atherosclerosis (50-99% stenosis or occlusion), complemented by an additional group of patients with advanced carotid atherosclerosis presenting with AIS. Carotid stenosis was assessed by Doppler ultrasonography. Venous blood samples were collected for laboratory assessment. Thrombin generation was measured in platelet-poor plasma using the calibrated automated thrombogram method, evaluating endogenous thrombin potential (ETP), peak thrombin, time to peak and lag time. Results Ninety patients were analyzed, with 30 patients in each study group across the predefined clinical categories. Patients with advanced stenosis and AIS demonstrated significantly higher thrombin generation, reflected by increased ETP and peak thrombin, compared with both moderate and advanced asymptomatic stenosis groups (p0.01). hsCRP correlated positively with peak thrombin and ETP and in the asymptomatic groups (r=0.2629, p=0.0425; r=0.3016, p=0.019) and the overall cohort (r=0.2973, p=0.0047; r=0.3611, p=0.0005). ETP correlated with cholesterol levels both in the asymptomatic groups (r=0.4134, p=0.0011) and across all patients (r=0.4540, p0.0001). Conclusions Advanced carotid stenosis, particularly when accompanied by acute ischemic stroke, is associated with increased thrombin generation, with parallel associations observed with inflammatory and lipid markers. Conflict of interest István Szegedi: nothing to disclose. Linda Lóczi: nothing to disclose. Dóra Bomberák: nothing to disclose. Renáta Pataki: nothing to disclose. Zsolt Barnabás Éles: nothing to disclose. László Oláh: nothing to disclose. László Csiba: nothing to disclose. Zsuzsa Bagoly: nothing to disclose.