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New and revisited approaches to preserving the reperfused myocardium.

Authors: Robert A Kloner|||David A Brown|||Marie Csete|||Wangde Dai|||James M Downey|||Roberta A Gottlieb|||Sharon L Hale|||Jianru Shi

Journal: Nature reviews. Cardiology

Publication Type: Journal Article

Date: 2017

DOI: NIHMS969246

ID: 28748958

Affiliations:

Affiliations

    Cardiovascular Research Institute, Huntington Medical Research Institutes, 99 North El Molino Avenue, Pasadena, California 91101, USA.|||Department of Human Nutrition, Foods, and Exercise, 1981 Kraft Drive, Blacksburg, Virginia 24060, USA.|||Cardiovascular Research Institute, Huntington Medical Research Institutes, 99 North El Molino Avenue, Pasadena, California 91101, USA.|||Cardiovascular Research Institute, Huntington Medical Research Institutes, 99 North El Molino Avenue, Pasadena, California 91101, USA.|||Department of Physiology and Cell Biology, University of South Alabama, 5851 USA Drive North, Mobile, Alabama 36688, USA.|||Department of Medicine, Barbra Streisand Women's Heart Center, Heart Institute of Cedars-Sinai, Cedars-Sinai Medical Center, 127 South San Vicente Boulevard, Los Angeles, California 90048, USA.|||Cardiovascular Research Institute, Huntington Medical Research Institutes, 99 North El Molino Avenue, Pasadena, California 91101, USA.|||Cardiovascular Research Institute, Huntington Medical Research Institutes, 99 North El Molino Avenue, Pasadena, California 91101, USA.

Abstract

Early coronary artery reperfusion improves outcomes for patients with ST-segment elevation myocardial infarction (STEMI), but morbidity and mortality after STEMI remain unacceptably high. The primary deficits seen in these patients include inadequate pump function, owing to rapid infarction of muscle in the first few hours of treatment, and adverse remodelling of the heart in the months that follow. Given that attempts to further reduce myocardial infarct size beyond early reperfusion in clinical trials have so far been disappointing, effective therapies are still needed to protect the reperfused myocardium. In this Review, we discuss several approaches to preserving the reperfused heart, such as therapies that target the mechanisms involved in mitochondrial bioenergetics, pyroptosis, and autophagy, as well as treatments that harness the cardioprotective properties of inhaled anaesthetic agents. We also discuss potential therapies focused on correcting the no-reflow phenomenon and its effect on healing and adverse left ventricular remodelling.


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