Calcium antagonists in patients with aneurysmal subarachnoid hemorrhage - A systematic review

Calcium antagonists in patients with aneurysmal subarachnoid hemorrhage - A systematic review
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DOI:
10.1212/wnl.50.4.876
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发表时间:
1998-04-01
期刊:
影响因子:
9.9
通讯作者:
van Gijn, J
van Gijn, J
中科院分区:
医学1区
文献类型:
--
作者:
Feigin, VL;Rinkel, GJE;van Gijn, J

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背景和目的:有报道称尼莫地平可降低继发性缺血的频率,改善蛛网膜下腔出血后的预后,但缺乏关于所有可用钙拮抗剂的确切证据。研究方法:对1996年1月之前完成的比较钙拮抗剂与对照药物的随机试验进行系统综述,这些试验在蛛网膜下腔出血(SAH)发作后10天内开始治疗。包括迄今为止研究的所有钙拮抗剂(尼莫地平、尼卡地平和AT 877)。结果:我们分析了10项试验,共计2756例患者。不良结局(死亡或依赖)的相对风险(RR)降低16%(95%CI,6 - 27%),病死率降低10%(95%CI,-6至25%)。为了防止一个不良结局,19名(12至59名)患者需要接受治疗。钙拮抗剂使缺血性神经功能缺损的发生率降低33%(95%,CI 25 - 41),CT扫描记录的脑梗死的发生率降低20%(95% CI,11 - 28)。8例(6 - 11例)患者需要接受治疗,以预防1例缺血性神经功能缺损。在仅尼莫地平的分析中,治疗与不良结局的RR降低24%相关(95%CI,12至38)。为了防止一个不良结果,13例(8至30)患者需要用尼莫地平治疗。AT 877(38%; 95% CI,17 - 54%)和尼卡地平(21%; 95% CI,6 - 34%)的血管造影检测到的脑血管痉挛的RR降低具有统计学显著性,但尼莫地平(9%; 95% CI,-2至19%)无统计学显著性。结论:钙拮抗剂可降低缺血性神经功能缺损的比例,尼莫地平可改善蛛网膜下腔出血3个月内的总体结局;尼卡地平和AT 877可降低所有原因导致的不良结局的证据尚不确定。尼莫地平发挥其有益作用的中间因素仍不确定。
Background and Purpose: 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. Methods: 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. Results: 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%). Conclusion: 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.