BACKGROUND AND PURPOSE: Spontaneous subarachnoid hemorrhage (SAH) still has a high risk for poor outcome that is frequently attributable to symptomatic cerebral vasospasm (CVS). We hypothesize that cellular microparticles (MP) play a role in the pathogenesis of CVS and may serve as biomarkers for CVS. METHODS: In 20 consecutive SAH patients, endothelial, leukocyte, platelet, and erythrocyte MP were measured during 15 days after ictus. CVS was detected by transcranial Doppler sonography. Twenty matched volunteers served as healthy controls. RESULTS: Endothelial, leukocyte, and erythrocyte MP were elevated in SAH patients compared to healthy controls. CD105(+) and CD62e(+) endothelial MP were significantly higher in SAH patients with Doppler sonographic CVS. CD105(+) endothelial MP were especially increased on the days of Doppler sonographic CVS onset. In patients experiencing cerebral infarction attributable to vasospasm, CD41(+) platelet MP were elevated in addition to endothelial MP. CD41(+) platelet MP were significantly higher in patients with any level of disability (modified Rankin Scale score ≥1) compared to those who made a full recovery (modified Rankin Scale score=0) on discharge from hospital. CONCLUSIONS: Endothelial MP were elevated in patients with SAH. This elevation coincided with the occurrence of Doppler sonographic CVS and therefore could be a novel biomarker for CVS. Platelet MP might be involved in the pathogenesis of cerebral infarction attributable to vasospasm, resulting in neurological morbidity.
BACKGROUND AND PURPOSE: Spontaneous subarachnoid hemorrhage (SAH) still has a high risk for poor outcome that is frequently attributable to symptomatic cerebral vasospasm (CVS). We hypothesize that cellular microparticles (MP) play a role in the pathogenesis of CVS and may serve as biomarkers for CVS. METHODS: In 20 consecutive SAHpatients, endothelial, leukocyte, platelet, and erythrocyte MP were measured during 15 days after ictus. CVS was detected by transcranial Doppler sonography. Twenty matched volunteers served as healthy controls. RESULTS: Endothelial, leukocyte, and erythrocyte MP were elevated in SAHpatients compared to healthy controls. CD105(+) and CD62e(+) endothelial MP were significantly higher in SAHpatients with Doppler sonographic CVS. CD105(+) endothelial MP were especially increased on the days of Doppler sonographic CVS onset. In patients experiencing cerebral infarction attributable to vasospasm, CD41(+) platelet MP were elevated in addition to endothelial MP. CD41(+) platelet MP were significantly higher in patients with any level of disability (modified Rankin Scale score ≥1) compared to those who made a full recovery (modified Rankin Scale score=0) on discharge from hospital. CONCLUSIONS: Endothelial MP were elevated in patients with SAH. This elevation coincided with the occurrence of Doppler sonographic CVS and therefore could be a novel biomarker for CVS. Platelet MP might be involved in the pathogenesis of cerebral infarction attributable to vasospasm, resulting in neurological morbidity.
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