Song Kangxing, Wang Shuxia, Qi Dake
Department of Cardiology, The General Hospital of Chinese People's Liberation Army, No. 28, Fuxing Road, Beijing 100853, China.
Department of Geriatric Cardiology, The General Hospital of Chinese People's Liberation Army, No. 28, Fuxing Road, Beijing 100853, China.
Oxid Med Cell Longev. 2015;2015:287058. doi: 10.1155/2015/287058. Epub 2015 Jun 16.
Mitochondrial permeability transition pore (mPTP) opening due to its role in regulating ROS generation contributes to cardiac reperfusion injury. In animals, cyclosporine (cyclosporine A, CsA), an inhibitor of mPTP, has been found to prevent reperfusion injury following acute myocardial infarction. However, the effects of CsA in reperfusion injury in clinical patients are not elucidated. We performed a meta-analysis using published clinical studies and electronic databases. Relevant data were extracted using standardized algorithms and additional data were obtained directly from investigators as indicated. Five randomized controlled blind trials were included in our meta-analysis. The clinical outcomes including infarct size (SMD: -0.41; 95% CI: -0.81, 0.01; P = 0.058), left ventricular ejection fraction (LVEF) (SMD: 0.20; 95% CI: -0.02, 0.42; P = 0.079), troponin I (TnI) (SMD: -0.21; 95% CI: -0.49, 0.07; P = 0.149), creatine kinase (CK) (SMD: -0.32; 95% CI: -0.98, 0.35; P = 0.352), and creatine kinase-MB isoenzyme (CK-MB) (SMD: -0.06; 95% CI: -0.35, 0.23; P = 0.689) suggested that there is no significant difference on cardiac function and injury with or without CsA treatment. Our results indicated that, unlike the positive effects of CsA in animal models, CsA administration may not protect heart from reperfusion injury in clinical patients with myocardial infarction.
线粒体通透性转换孔（mPTP）开放因其在调节活性氧生成中的作用而导致心脏再灌注损伤。在动物实验中，已发现mPTP抑制剂环孢素（环孢素A，CsA）可预防急性心肌梗死后的再灌注损伤。然而，CsA在临床患者再灌注损伤中的作用尚未阐明。我们使用已发表的临床研究和电子数据库进行了一项荟萃分析。使用标准化算法提取相关数据，并按指示直接从研究人员处获取其他数据。我们的荟萃分析纳入了五项随机对照盲法试验。临床结果包括梗死面积（标准化均数差：-0.41；95%可信区间：-0.81，0.01；P = 0.058）、左心室射血分数（LVEF）（标准化均数差：0.20；95%可信区间：-0.02，0.42；P = 0.079）、肌钙蛋白I（TnI）（标准化均数差：-0.21；95%可信区间：-0.49，0.07；P = 0.149）、肌酸激酶（CK）（标准化均数差：-0.32；95%可信区间：-0.98，0.35；P = 0.352）和肌酸激酶-MB同工酶（CK-MB）（标准化均数差：-0.06；95%可信区间：-0.35，0.23；P = 0.689），表明CsA治疗与否在心脏功能和损伤方面无显著差异。我们的结果表明，与CsA在动物模型中的积极作用不同，在心肌梗死临床患者中给予CsA可能无法保护心脏免受再灌注损伤。
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