Circulating endothelial microparticles in acute ischemic stroke: a link to severity, lesion volume and outcome

Background: Endothelial membrane microparticles (EMP) in plasma are elevated in several vascular diseases. Objectives: To test the hypothesis that EMP would be increased in patients with acute ischemic stroke and would correlate with stroke severity, brain lesion volume and outcome. Patients and methods: Forty-one patients were studied and divided into two groups based on the National Institutes of Health Stroke Scale (NIHSS) score: 20 patients with mild stroke (NIHSS score < 5) and 21 patients with moderate-severe stroke (NIHSS score >= 5). Lesion volume was measured using diffusion-weighted magnetic resonance imaging and discharge outcome was based on the discharge Barthel and Rankin scores. Twenty-three age-matched control subjects were also studied. Using flow cytometry, endoglin-positive EMP: CD105(+) CD41a(-)CD45(-) (E+EMP), specific endothelial EMP expressing VE-cadherin and endoglin: CD105(+)CD144(+) (C+EMP), EMP expressing phosphatidylserine: CD105(+)PS(+) CD41a(-) (PS+EMP) and EMP expressing ICAM-1: CD105(+)CD54(+) CD45(-) (I+EMP) were analyzed. Results: Significantly higher PS+EMP counts were observed in the group of acute ischemic stroke patients [median 59 (25th-75th percentile: 28-86) MP mu L-1] relative to the controls [28 (14-36) MP mu L-1] (P = 0.002). All four EMP phenotypes studied were elevated in the subgroup of moderate-severe stroke patients relative to the controls (all P < 0.05). In the patients with acute ischemic stroke three EMP phenotypes (E+EMP, PS+EMP and I+EMP) correlated significantly with brain lesion volume, with I+EMP (P = 0.002) showing the strongest correlation. Admission counts of C+EMP (P = 0.0003) and E+EMP (P = 0.003) correlated significantly with discharge clinical outcome. Conclusions: Certain circulating EMP phenotypes may be associated with severity, lesion volume and outcome of acute ischemic stroke. EMP analysis shows promising contribution to understanding stroke pathophysiology.