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

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.