Feigin V L, Rinkel G J, Algra A, Vermeulen M, van Gijn J
University Department of Neurology, Utrecht, The Netherlands.
Neurology. 1998 Apr;50(4):876-83. doi: 10.1212/wnl.50.4.876.
It has been reported that nimodipine reduces the frequency of secondary ischemia and improves outcome after aneurysmal SAH, but definitive evidence concerning all available calcium antagonists is lacking.
Systematic overview of randomized trials that were completed by January 1996 compared calcium antagonists with control and started treatment within 10 days after onset of subarachnoid hemorrhage (SAH) was performed. All calcium antagonists studied thus far (nimodipine, nicardipine, and AT877) were included.
We analyzed 10 trials totaling 2756 patients. The relative risk (RR) reduction of poor outcome (death or dependency) was 16% (95% CI, 6 to 27%) and that of case fatality was 10% (95% CI, -6 to 25%). To prevent one poor outcome, 19 (12 to 59) patients need to be treated. Calcium antagonists give a 33% (95%, CI 25 to 41) RR reduction in the frequency of ischemic neurologic deficit and a 20% (95% CI, 11 to 28) RR reduction in the frequency of CT-scan documented cerebral infarction. Eight (6 to 11) patients need to be treated to prevent one ischemic neurologic deficit. In the analyses for nimodipine only, treatment was associated with a 24% RR reduction of poor outcome (95% CI, 12 to 38). To prevent one poor outcome, 13 (8 to 30) patients need to be treated with nimodipine. The RR reduction of angiographically detected cerebral vasospasm was statistically significant for AT877 (38%; 95% CI, 17 to 54%) and nicardipine (21%; 95% CI, 6 to 34%) but not for nimodipine (9%; 95% CI, -2 to 19%).
Calcium antagonists reduce the proportion of ischemic neurologic deficits and nimodipine improves overall outcome within 3 months of aneurysmal SAH; evidence for a reduction of poor outcome from all causes by nicardipine and AT877 is inconclusive. The intermediate factors by which nimodipine exerts its beneficial effect remain uncertain.
据报道,尼莫地平可降低动脉瘤性蛛网膜下腔出血(SAH)后继发性缺血的发生率并改善预后,但缺乏关于所有可用钙拮抗剂的确切证据。
对截至1996年1月完成的随机试验进行系统综述,这些试验将钙拮抗剂与对照组进行比较,并在蛛网膜下腔出血(SAH)发病后10天内开始治疗。纳入了迄今为止研究的所有钙拮抗剂(尼莫地平、尼卡地平及AT877)。
我们分析了10项试验,共2756例患者。不良结局(死亡或依赖)的相对风险(RR)降低了16%(95%CI,6%至27%),病死率降低了10%(95%CI,-6%至25%)。为预防1例不良结局,需要治疗19例(12至59例)患者。钙拮抗剂使缺血性神经功能缺损的发生率相对风险降低33%(95%CI,25%至41%),CT扫描记录的脑梗死发生率相对风险降低20%(95%CI,11%至28%)。为预防1例缺血性神经功能缺损,需要治疗8例(6至11例)患者。仅对尼莫地平进行分析时,治疗使不良结局的相对风险降低24%(95%CI,12%至38%)。为预防1例不良结局,需要13例(8至30例)患者接受尼莫地平治疗。血管造影检测到的脑血管痉挛的相对风险降低在AT877(38%;95%CI,17%至54%)和尼卡地平(21%;95%CI,6%至34%)方面具有统计学意义,但在尼莫地平方面无统计学意义(9%;95%CI,-2%至19%)。
钙拮抗剂可降低缺血性神经功能缺损的比例,尼莫地平可改善动脉瘤性SAH后3个月内的总体预后;尼卡地平和AT877降低所有原因导致的不良结局的证据尚无定论。尼莫地平发挥有益作用的中间因素仍不确定。