The Role of Platelet Activation and Inflammation in Early Brain Injury Following Subarachnoid Hemorrhage.
The Role of Platelet Activation and Inflammation in Early Brain Injury Following Subarachnoid Hemorrhage.
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DOI：
10.1007/s12028-016-0292-4
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发表时间：
2017-03
影响因子：
3.5
通讯作者：
Aledort L
中科院分区：
文献类型：
--
作者：
Frontera JA;Provencio JJ;Sehba FA;McIntyre TM;Nowacki AS;Gordon E;Weimer JM;Aledort L
蛛网膜下腔出血（SAH）后的早期脑损伤（EBI）是功能预后不良的重要预测因素，但其潜在机制尚不清楚。动物实验表明，血小板活化和炎症反应以及随后的微血栓形成和缺血可能是EBI的一种机制。对自发性SAH患者和对照进行了一项前瞻性、假设驱动的研究。在SAH发作后的第一个72小时内，连续测量血小板活化（血栓弹性描记术最大振幅[MA]）和炎症（C反应肽[CRP]）。比较了对照组和轻度（Hunt-Hess [HH] 1-3）与重度（HH 4 -5）EBI的SAH患者的血小板活化和炎症标志物。评估这些生物标志物与3个月功能结局的相关性。我们招募了127例患者（106例SAH; 21例对照）。随着EBI/HH分级的加重，血小板活化和CRP水平逐渐升高，并在72 h内升高（P均<0.01）。重度EBI组与轻度EBI组相比（MA 68.9与64.8mm，P=0.001; CRP 12.5与1.5mg/L，P=0.003）均高于对照组（均P<0.003）。迟发性脑缺血（DCI）患者在发作后72小时内有更多的血小板活化（66.6 vs 64.9，P=0.02）。3个月时，血小板活化（mRS 4 -6 OR 1.18，95% CI 1.05-1.32，P=0.007）和CRP（mRS 4 -6 OR 1.02，95% CI 1.00 - 1.03，P=0.041）水平较高时，死亡或重度残疾的可能性更大。血小板活化和炎症在SAH后急性发生，并与EBI、DCI和3个月功能结局差相关。这些标志物可能有助于了解SAH后EBI的机制。
Early brain injury (EBI) following aneurysmal subarachnoid hemorrhage (SAH) is an important predictor of poor functional outcome, yet the underlying mechanism is not well understood. Animal studies suggest that platelet activation and inflammation, with subsequent microthrombosis and ischemia may be a mechanism of EBI. A prospective, hypothesis-driven study of spontaneous, SAH patients and controls was conducted. Platelet activation (thromboelastography maximum amplitude [MA]) and inflammation (C-reactive peptide [CRP]) were measured serially over time during the first 72h following SAH onset. Platelet activation and inflammatory markers were compared between controls and SAH patients with mild (Hunt-Hess [HH] 1-3) versus severe (HH4-5) EBI. The association of these biomarkers with 3-month functional outcomes was evaluated. We enrolled 127 patients (106 SAH; 21 controls). Platelet activation and CRP increased incrementally with worse EBI/HH grade and both increased over 72h (all P<0.01). Both were higher in severe versus mild EBI (MA 68.9 versus 64.8mm, P=0.001; CRP 12.5 versus 1.5mg/L, P=0.003) and compared to controls (both P<0.003). Patients with delayed cerebral ischemia (DCI) had more platelet activation (66.6 versus 64.9 in those without DCI, P=0.02) within 72h of ictus. At 3-months, death or severe disability was more likely with higher levels of platelet activation (mRS4-6 OR 1.18, 95% CI 1.05-1.32, P=0.007) and CRP (mRS4-6 OR 1.02, 95% CI 1.00 −1.03, P=0.041). Platelet activation and inflammation occur acutely after SAH and are associated with worse EBI, DCI and poor 3-month functional outcomes. These markers may provide insight into the mechanism of EBI following SAH.
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