title: Effects of Cyclosporine on Reperfusion Injury in Patients: A Meta-Analysis of Randomized Controlled Trials.
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; 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.
authors.affiliation: Department of Cardiology, The General Hospital of Chinese People's Liberation Army, No. 28, Fuxing Road, Beijing 100853, China.
authors.forename: Kangxing
authors.initials: K
authors.lastname: Song
authors.affiliation: Department of Geriatric Cardiology, The General Hospital of Chinese People's Liberation Army, No. 28, Fuxing Road, Beijing 100853, China.
authors.forename: Shuxia
authors.initials: S
authors.lastname: Wang
authors.affiliation: Yale Cardiovascular Research Center, Department of Internal Medicine, Yale University School of Medicine, New Haven, CT 06511, USA.
authors.forename: Dake
authors.initials: D
authors.lastname: Qi
mesh_terms: D003402:Creatine Kinase / Q000378:metabolism; D052279:Creatine Kinase, MB Form / Q000378:metabolism; D016572:Cyclosporine / Q000494:pharmacology / Q000627:therapeutic use*; D016208:Databases, Factual; D006801:Humans; D008279:Magnetic Resonance Imaging; D033681:Mitochondrial Membrane Transport Proteins / Q000187:drug effects / Q000378:metabolism; D000083162:Mitochondrial Permeability Transition Pore; D009203:Myocardial Infarction / Q000000981:diagnostic imaging / Q000473:pathology; D015428:Myocardial Reperfusion Injury / Q000188:drug therapy*; D011859:Radiography; D016032:Randomized Controlled Trials as Topic; D019210:Troponin I / Q000378:metabolism; D016277:Ventricular Function, Left / Q000187:drug effects
chemical_list: D033681:Mitochondrial Membrane Transport Proteins; D000083162:Mitochondrial Permeability Transition Pore; D019210:Troponin I; D016572:Cyclosporine; D003402:Creatine Kinase; D052279:Creatine Kinase, MB Form