Abstract

Background: Coated-platelets, a subset of procoagulant platelets observed upon dual agonist stimulation with collagen and thrombin, support a robust prothrombinase activity and provide a unique measure of platelet thrombotic potential. Our recently published data show that coated-platelet levels are increased in large artery stroke compared to controls, and higher levels are associated with early stroke recurrence. Because carotid occlusive disease and recurrent strokes are known risk factors for cognitive decline, we investigated the impact of coated-platelets on cognitive function among patients referred for carotid Doppler evaluation. Methods: Sixty consecutive patients without known dementia or stroke referred for carotid Doppler evaluation were screened for evidence of cognitive impairment using the Montreal Cognitive Assessment (MoCA). Coated-platelets were determined at baseline and are reported as percent of cells converted to coated-platelets. Differences in mean coated-platelet levels between groups were assessed using the independent t-test and ANCOVA. Results: Fifty-seven percent (34/60) had evidence of cognitive impairment (MoCA<26, range 17-25). Mean coated-platelets for patients with cognitive impairment were significantly higher compared to patients with normal cognitive function (42.7 ± 11.5% vs. 34.1 ± 12.3%; mean ± SD; p=0.008), which remained significant after adjusting for age, remote history of stroke, carotid stenosis, and statin use (p=0.013). Conclusions: Coated-platelets are elevated in patients at risk for cerebrovascular disease who have cognitive impairment compared to those with normal cognition. The increased prevalence of vascular risk factors and range of abnormal MoCA scores (17-25) suggest that the cognitively impaired individuals are in the early stages of vascular cognitive impairment. The key finding in this study is the existence of a link between coated-platelets, cerebrovascular disease risk, and early vascular cognitive impairment, which is in keeping with the chronic disease model of vascular dementia etiology.

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