Abstract

Introduction: Coated-platelets are a subset of highly procoagulant platelets observed upon dual-agonist stimulation with collagen and thrombin. Coated-platelet levels are elevated in patients with ischemic stroke and associated with stroke recurrence. Lower levels of coated-platelets are present in ischemic stroke patients with early hemorrhagic transformation or in those with microbleeds. We now investigate if the number and location of microbleeds are associated with coated-platelet levels following non-lacunar stroke. Methods: Coated-platelet levels, reported as percent of cells converted to coated-platelets, were assayed in consecutive stroke patients. The number and location of microbleeds (deep vs lobar/mixed) on 1.5 T MRI was recorded by two independent reviewers. Correlations between number of microbleeds and demographics, vascular risk factors, stroke subtype, medications and laboratory values (platelet count, MPV, Hgb, WBC, CRP) were calculated using the Spearman correlation coefficient. Logistic regression was used to identify factors independently associated with location. Results: There were 249 stroke patients analyzed, with a mean age of 65.7 years (range 42 to 91). Microbleeds were present in 72/249 patients (29%), ranged from 1 to 14 lesions and were classified as deep (47) or lobar/mixed (25) distribution. Inter-rater agreement was excellent (91%). The number of microbleeds correlated negatively with coated-platelet levels (adjusted r = -0.41, p < 0.001) after adjusting for age (r = 0.11, p = 0.09). Variables independently associated with lobar/mixed as opposed to deep location of microbleeds included coated-platelet levels (47.0±35.0% vs 26.7±10.2%, p = 0.005) and prior stroke (10/25 vs 9/47, p = 0.028). Conclusions: Lower levels of coated-platelets are associated with increased number of microbleeds. In addition, coated-platelet levels are higher in patients with lobar/mixed as compared to those with deep distribution of microbleeds, a finding possibly linked to amyloid metabolism abnormalities described in this subset of procoagulant platelets. These data support a role for differential involvement of platelet procoagulant potential in mechanisms leading to development of cerebral microbleeds.

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