Effects of remote ischemic preconditioning in patients with concentric myocardial hypertrophy: A randomized, controlled trial with molecular insights

Young Song, Jong Wook Song, Sak Lee, Ji Hae Jun, Younglan Kwak, Jae Kwang Shim

Research output: Contribution to journalArticle

5 Citations (Scopus)

Abstract

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.

Original languageEnglish
Pages (from-to)36-41
Number of pages6
JournalInternational Journal of Cardiology
Volume249
DOIs
Publication statusPublished - 2017 Dec 15

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Ischemic Preconditioning
Hypertrophy
Randomized Controlled Trials
Cardiopulmonary Bypass
MB Form Creatine Kinase
Troponin T
Phosphorylation
Reperfusion Injury
Aortic Valve
Caspase 3
Area Under Curve
Phosphotransferases
Nitric Oxide Synthase Type III
Aortic Valve Stenosis
Economic Inflation
Left Ventricular Hypertrophy
Transducers
Nitric Oxide Synthase
Thoracic Surgery
Myocardium

All Science Journal Classification (ASJC) codes

  • Cardiology and Cardiovascular Medicine

Cite this

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title = "Effects of remote ischemic preconditioning in patients with concentric myocardial hypertrophy: A randomized, controlled trial with molecular insights",
abstract = "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.",
author = "Young Song and Song, {Jong Wook} and Sak Lee and Jun, {Ji Hae} and Younglan Kwak and Shim, {Jae Kwang}",
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Effects of remote ischemic preconditioning in patients with concentric myocardial hypertrophy : A randomized, controlled trial with molecular insights. / Song, Young; Song, Jong Wook; Lee, Sak; Jun, Ji Hae; Kwak, Younglan; Shim, Jae Kwang.

In: International Journal of Cardiology, Vol. 249, 15.12.2017, p. 36-41.

Research output: Contribution to journalArticle

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, Younglan

AU - Shim, Jae Kwang

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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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