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Oxidative Medicine and Cellular Longevity
Volume 2015, Article ID 287058, 6 pages
http://dx.doi.org/10.1155/2015/287058
Research Article

Effects of Cyclosporine on Reperfusion Injury in Patients: A Meta-Analysis of Randomized Controlled Trials

1Department of Cardiology, The General Hospital of Chinese People’s Liberation Army, No. 28, Fuxing Road, Beijing 100853, China
2Department of Geriatric Cardiology, The General Hospital of Chinese People’s Liberation Army, No. 28, Fuxing Road, Beijing 100853, China
3Yale Cardiovascular Research Center, Department of Internal Medicine, Yale University School of Medicine, New Haven, CT 06511, USA

Received 19 October 2014; Accepted 12 January 2015

Academic Editor: Mengzhou Xue

Copyright © 2015 Kangxing Song et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

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; = 0.058), left ventricular ejection fraction (LVEF) (SMD: 0.20; 95% CI: −0.02, 0.42; = 0.079), troponin I (TnI) (SMD: −0.21; 95% CI: −0.49, 0.07; = 0.149), creatine kinase (CK) (SMD: −0.32; 95% CI: −0.98, 0.35; = 0.352), and creatine kinase-MB isoenzyme (CK-MB) (SMD: −0.06; 95% CI: −0.35, 0.23; = 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.