Kim Young Woo, Zipfel Gregory J, Ogilvy Christopher S, Pricola Katie L, Welch Babu G, Shakir Nabeel, Patel Bhuvic, Reavey-Cantwell John F, Kelman Craig R, Albuquerque Felipe C, Kalani M Yashar S, Hoh Brian L
*Department of Neurosurgery, Bucheon St. Mary's Hospital, Catholic University of Korea, Bucheon, Republic of Korea; ‡Department of Neurosurgery, Washington University School of Medicine, St. Louis, Missouri; §Neurovascular Service, Massachusetts General Hospital, Boston, Massachusetts; ¶Department of Radiology, UT Southwestern Medical Center, Dallas, Texas; ‖Department of Neurosurgery, Virginia Commonwealth University, Richmond, Virginia; #Division of Neurological Surgery, Barrow Neurological Institute, St. Joseph's Hospital and Medical Center, Phoenix, Arizona; **Department of Neurosurgery, University of Florida, Gainesville, Florida.
Neurosurgery. 2014 Apr;74(4):351-8; discussion 358-9. doi: 10.1227/NEU.0000000000000282.
Recent experimental evidence indicates that endogenous mechanisms against cerebral vasospasm can be induced via preconditioning.
To determine whether these vascular protective mechanisms are also present in vivo in humans with aneurysmal subarachnoid hemorrhage.
A multicenter retrospective cohort of patients with aneurysmal subarachnoid hemorrhage was examined for ischemic preconditioning stimulus: preexisting steno-occlusive cerebrovascular disease (CVD) and/or previous cerebral infarct. Generalized estimating equation models were performed to determine the effect of the preconditioning stimulus on the primary end points of radiographic vasospasm, symptomatic vasospasm, and vasospasm-related delayed cerebral infarction and the secondary end point of discharge modified Rankin Scale score.
Of 1043 patients, 321 (31%) had preexisting CVD and 437 (42%) had radiographic vasospasm. Patients with preexisting CVD were less likely to develop radiographic vasospasm (odds ratio = 0.67; 95% confidence interval = 0.489-0.930; P = .02) but had no differences in other end points. In terms of the secondary end point, patients with preexisting CVD did not differ significantly from patients without preexisting CVD in mortality or unfavorable outcome in multivariate analyses, although patients with preexisting CVD were marginally more likely to die (P = .06).
This retrospective case-control study suggests that endogenous protective mechanisms against cerebral vasospasm-a preconditioning effect-may exist in humans, although these results could be the effect of atherosclerosis or some combination of preconditioning and atherosclerosis. Additional studies investigating the potential of preconditioning in aneurysmal subarachnoid hemorrhage are warranted.
最近的实验证据表明，可通过预处理诱导抗脑血管痉挛的内源性机制。
确定这些血管保护机制在患有动脉瘤性蛛网膜下腔出血的人类体内是否也存在。
对一个多中心回顾性队列的动脉瘤性蛛网膜下腔出血患者进行检查，以寻找缺血预处理刺激因素：既往存在的狭窄闭塞性脑血管疾病（CVD）和/或既往脑梗死。采用广义估计方程模型来确定预处理刺激因素对影像学血管痉挛、症状性血管痉挛、血管痉挛相关迟发性脑梗死等主要终点以及出院时改良Rankin量表评分这一次要终点的影响。
在1043例患者中，321例（31%）既往存在CVD，437例（42%）发生影像学血管痉挛。既往存在CVD的患者发生影像学血管痉挛的可能性较小（比值比 = 0.67；95%置信区间 = 0.489 - 0.930；P = 0.02），但在其他终点方面无差异。就次要终点而言，在多变量分析中，既往存在CVD的患者与无既往CVD的患者在死亡率或不良结局方面无显著差异，尽管既往存在CVD的患者死亡可能性略高（P = 0.06）。
这项回顾性病例对照研究表明，人类可能存在抗脑血管痉挛的内源性保护机制——一种预处理效应，尽管这些结果可能是动脉粥样硬化的影响，或者是预处理与动脉粥样硬化某种组合的影响。有必要开展更多研究来探究预处理在动脉瘤性蛛网膜下腔出血中的潜力。
