Postconditioning in ST-elevation myocardial infarction: a systematic review, critical appraisal, and meta-analysis of randomized clinical trials.
Postconditioning in ST-elevation myocardial infarction: a systematic review, critical appraisal, and meta-analysis of randomized clinical trials.
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DOI：
10.2147/vhrm.s67154
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发表时间：
2014
影响因子：
2.9
通讯作者：
Eritsland J
中科院分区：
文献类型：
--
作者：
Abdelnoor M;Sandven I;Limalanathan S;Eritsland J
我们的目的是总结随机临床试验研究的证据，检查缺血后处理（IPost）在ST段抬高心肌梗死的疗效。该研究是一项系统性综述和批判性评价，并对随机临床试验进行了荟萃分析。我们搜索了文献。共确定了21项随机临床试验。固定效应和随机效应模型都被用来综合个别研究的结果。通过亚组和随机效应荟萃回归分析，考虑患者相关变量和研究水平变量，检查研究之间的异质性。评价了发表偏倚或“小研究效应”。存在显著异质性。通过标准化平均差（SMD）=-0.06，95%置信区间（CI）：-0.34至0.21，即IPost无影响，对通过心脏磁共振评估的结局梗死面积的随机效应模型汇总估计值进行估计。对于通过心肌坏死生物标志物估计的终点梗死面积，总体合并效应为SMD =−0.58，95%CI：−0.96至−0.19。在有把握度和无偏倚研究中，这种效应消失（SMD =0.03，95% CI：-0.48至0.55）。最后，对于结局左心室射血分数，SMD =0.47 95% CI：0.20至0.74。不幸的是，存在选择偏倚（小研究效应）。对于这一结果，荟萃回归显示，高血压的存在和纳入无偏倚研究解释了28.3%的研究异质性。通过“修剪和填充”方法进行的模拟，使用随机效应模型控制选择偏倚，稀释了效应（SMD =0.17 95%CI：-0.13至0.48）。在随访期间，除了发现充血性心力衰竭的发生率外，没有观察到IPost对ST段恢复或大多数不良临床事件的影响，这项研究的证据表明，IPost对替代和大多数临床终点没有心脏保护作用。对充血性心力衰竭发生率的可能有益作用需要通过大型临床试验来复制。
We aimed to summarize the evidence from randomized clinical trials studies examining the efficacy of ischemic postconditioning (IPost) in ST-elevation myocardial infarction. The study was a systematic review and critical appraisal, with meta-analysis of randomized clinical trials. We searched the literature. A total of 21 randomized clinical trials were identified. Both fixed effect and random effects models were used to synthesize the results of individual studies. Heterogeneity between studies was examined by subgroup and random effects meta-regression analyses, considering ptient-related and study-level variables. Publication bias, or “small-study effect”, was evaluated. Substantial heterogeneity was present. The random effects model pooled estimate for the outcome infarct size assessed by cardiac magnetic resonance was estimated by the standardized mean difference (SMD) =−0.06, 95% confidence interval (CI): −0.34 to 0.21, ie, no effect of IPost. For the end point infarct size, estimated by biomarkers of myocardial necrosis, an overall pooled effect was SMD =−0.58, 95% CI: −0.96 to −0.19. This effect disappeared in powered and nonbiased studies (SMD =0.03, 95% CI: −0.48 to 0.55). Finally, for the outcome left ventricular ejection fraction, SMD =0.47 95% CI: 0.20 to 0.74. Unfortunately, selection bias (small-study effect) was present. For this outcome, the meta-regression showed that both presence of hypertension and the inclusion of nonbiased studies explained 28.3% of the heterogeneity among the studies. Simulation by the “trim and fill” method, which controlled for selection bias using random effects model, diluted the effect (SMD =0.17 95% CI: −0.13 to 0.48). No effects by IPost on ST-segment resolution or on the majority of adverse clinical events were observed during follow up, except the incidence of congestive heart failure was found. Evidence from this study suggests no cardioprotection from IPost, on surrogate and the majority of clinical end points. A possible beneficial effect on the incidence of congestive heart failure needs to be replicated by a large clinical trial.