TY - JOUR
T1 - Effects of remote ischemic preconditioning in patients with concentric myocardial hypertrophy
T2 - A randomized, controlled trial with molecular insights
AU - Song, Young
AU - Song, Jong Wook
AU - Lee, Sak
AU - Jun, Ji Hae
AU - Kwak, Young Lan
AU - Shim, Jae Kwang
N1 - Publisher Copyright:
© 2017 Elsevier B.V.
Copyright:
Copyright 2018 Elsevier B.V., All rights reserved.
PY - 2017/12/15
Y1 - 2017/12/15
N2 - Background Efficacy of remote ischemic preconditioning (RIPC) for cardioprotection in cardiac surgery is controversial. We aimed to evaluate the clinical and molecular effects of RIPC on the concentrically hypertrophied myocardium. Methods Seventy-two aortic stenosis patients receiving aortic valve replacement (AVR) under sevoflurane anesthesia were randomly allocated to RIPC (3 cycles of 5-min inflation [300 mm Hg] and deflation on the left arm) or control (deflated cuff placement) group. The primary endpoints were 24-h area under the curve (AUC) for serum creatine kinase (CK)-MB and troponin (Tn)-T levels. The secondary endpoints were myocardial activation of cell signaling pathways, including reperfusion injury salvage kinases (RISK), signal transducer and activator of transcription (STAT), nitric oxide synthase (NOS), and apoptosis related molecules, obtained from right atrial tissue before and after cardiopulmonary bypass (CPB). Results There were no intergroup differences in 24-h AUCs of CK-MB and Tn-T. Phosphorylations of RISK pathway molecules were not enhanced by RIPC before and after CPB. Phosphorylation of STAT5 was significantly lower in the RIPC group before and after CPB. Phosphorylations of STAT3 and endothelial NOS were not enhanced by RIPC before and after CPB. Expression level of cleaved caspases-3/caspase-3 was significantly higher in the RIPC group before CPB. Conclusions RIPC did not provide clinical benefits or activate protective signaling in patients with concentric left ventricular hypertrophy undergoing AVR.
AB - Background Efficacy of remote ischemic preconditioning (RIPC) for cardioprotection in cardiac surgery is controversial. We aimed to evaluate the clinical and molecular effects of RIPC on the concentrically hypertrophied myocardium. Methods Seventy-two aortic stenosis patients receiving aortic valve replacement (AVR) under sevoflurane anesthesia were randomly allocated to RIPC (3 cycles of 5-min inflation [300 mm Hg] and deflation on the left arm) or control (deflated cuff placement) group. The primary endpoints were 24-h area under the curve (AUC) for serum creatine kinase (CK)-MB and troponin (Tn)-T levels. The secondary endpoints were myocardial activation of cell signaling pathways, including reperfusion injury salvage kinases (RISK), signal transducer and activator of transcription (STAT), nitric oxide synthase (NOS), and apoptosis related molecules, obtained from right atrial tissue before and after cardiopulmonary bypass (CPB). Results There were no intergroup differences in 24-h AUCs of CK-MB and Tn-T. Phosphorylations of RISK pathway molecules were not enhanced by RIPC before and after CPB. Phosphorylation of STAT5 was significantly lower in the RIPC group before and after CPB. Phosphorylations of STAT3 and endothelial NOS were not enhanced by RIPC before and after CPB. Expression level of cleaved caspases-3/caspase-3 was significantly higher in the RIPC group before CPB. Conclusions RIPC did not provide clinical benefits or activate protective signaling in patients with concentric left ventricular hypertrophy undergoing AVR.
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U2 - 10.1016/j.ijcard.2017.08.073
DO - 10.1016/j.ijcard.2017.08.073
M3 - Article
C2 - 28893433
AN - SCOPUS:85028924190
VL - 249
SP - 36
EP - 41
JO - International Journal of Cardiology
JF - International Journal of Cardiology
SN - 0167-5273
ER -