Hemostatic Activation Markers and Early Neurological Deterioration in Branch Atheromatous Disease-Related Stroke

止血激活标志物与分支动脉粥样硬化性疾病相关卒中早期神经功能恶化的关系

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Abstract

AIMS: Branch atheromatous disease (BAD)-related stroke, caused by atherosclerotic occlusion at the origin of a deep penetrating artery, are prone to early neurological deterioration (END). This study aimed to assess the association between hemostatic activation markers and occurrence of END in patients with BAD-related stroke. METHODS: This prospective observational study included 88 patients with BAD-related stroke within 7 days of onset. On admission, plasma beta-thromboglobulin (beta-TG), platelet factor 4 (PF4), and D-dimer levels were measured. END was defined as an increase of ≥ 2 points in the total National Institutes of Health Stroke Scale (NIHSS) score or ≥ 1 point in the motor items of the NIHSS within 7 days of admission. RESULTS: Of the 88 patients, 34 (38.6%) experienced END. Mean beta-TG (158 ng/mL vs. 102 ng/mL; P = 0.021), PF4 (61 ng/mL vs. 35 ng/mL; P = 0.024), and D-dimer (2.0 µg/mL vs. 1.2 µg/mL; P = 0.037) levels were significantly higher in patients with END than in those without END. Multivariate analysis revealed that beta-TG and PF4 levels were independently associated with the occurrence of END, with an adjusted odds ratio per 10 ng/mL increase (95% confidence interval) of 1.09 (1.01-1.20) and 1.21 (1.02-1.49), respectively. In contrast, D-dimer levels were not independent predictors. The optimal cutoff values for predicting END were 130 and 55 ng/mL for beta-TG and PF4, respectively. CONCLUSIONS: Elevated beta-TG and PF4 levels were independent predictors of END in patients with BAD-related stroke. Hence, the measurement of these platelet activation markers helps improve the risk assessment of BAD-related stroke and may provide management implications.

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