Cerebral Infarction After Subarachnoid Hemorrhage Contributes to Poor Outcome by Vasospasm-Dependent and -Independent Effects
Cerebral Infarction After Subarachnoid Hemorrhage Contributes to Poor Outcome by Vasospasm-Dependent and -Independent Effects
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DOI：
10.1161/strokeaha.110.597914
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发表时间：
2011-04-01
期刊：
影响因子：
8.3
通讯作者：
Macdonald, R. Loch
中科院分区：
文献类型：
--
作者：
Vergouwen, Mervyn D. I.;Ilodigwe, Don;Macdonald, R. Loch
背景和目的：蛛网膜下腔出血后迟发性脑缺血的发病机制仍不完全清楚。一般认为是由血管造影性血管痉挛引起的。我们的目的是澄清血管造影性血管痉挛，神经恶化，脑梗死和不良结局之间的关系，并探讨脑梗死是否也有助于不良结局的vasospasm-independent effects. Methods，这一探索性分析使用的数据来自413例患者的Clazosentan克服神经缺血和梗死复发后蛛网膜下腔出血（CONSCIOUS-1）试验。我们研究了有和无血管造影性血管痉挛的患者神经功能恶化、脑梗死和预后不良的发生率。实施结构方程模型的路径分析，以确定直接和间接的路径coefficients.Results-of 194例中度至重度血管痉挛，43%的神经系统恶化的任何原因，20%的脑梗死，和46%的不良后果。世界神经外科医师联合会4 ~ 5级、高血压病史、血管造影性血管痉挛、神经功能恶化和新发脑梗死对不良结局的直接影响的通径系数分别为0.20、0.13、0.19、0.16和0.11。脑梗死导致不良结局的vasospasm依赖性和独立的effects. Conclusions，我们的数据显示，大多数中度至重度血管造影性血管痉挛的患者没有任何原因或脑梗死的神经系统恶化。此外，脑梗死对预后也有直接影响，与血管造影性血管痉挛无关。提示迟发性脑缺血的发病机制中可能存在其他因素的共同作用，这也是改善蛛网膜下腔出血后预后的重要研究目标。（中风。2011; 42：924-929）。
Background and Purpose-The pathogenesis of delayed cerebral ischemia after aneurysmal subarachnoid hemorrhage remains incompletely understood. It is generally assumed that it is caused by angiographic vasospasm. Our aim was to clarify the relationship among angiographic vasospasm, neurological worsening, cerebral infarction, and poor outcome and to investigate whether cerebral infarction also contributes to poor outcome by vasospasm-independent effects.Methods-This exploratory analysis used data from 413 patients included in the Clazosentan to Overcome Neurological Ischemia and Infarction Occurring After Subarachnoid Hemorrhage (CONSCIOUS-1) trial. We studied the incidence of neurological worsening, cerebral infarction, and poor outcome in patients with and without angiographic vasospasm. Path analysis implemented by structural equation modeling was performed to determine direct and indirect path coefficients.Results-Of the 194 patients with moderate to severe vasospasm, 43% had neurological worsening of any cause, 20% had cerebral infarction, and 46% poor outcome. Path coefficients for direct effects on poor outcome were 0.20 for World Federation of Neurological Surgeons Grade 4 to 5, 0.13 for history of hypertension, 0.19 for angiographic vasospasm, 0.16 for neurological worsening, and 0.11 for new cerebral infarction. Cerebral infarction contributed to poor outcome by vasospasm-dependent and -independent effects.Conclusions-Our data show that the majority of patients with moderate to severe angiographic vasospasm did not have neurological worsening of any cause or cerebral infarction. Besides, cerebral infarction also has a direct effect on outcome independent of angiographic vasospasm. This suggests that other coexisting factors might be involved in the pathogenesis of delayed cerebral ischemia, which should also be an important research target to improve outcome after subarachnoid hemorrhage. (Stroke. 2011; 42: 924-929.)