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Circ Res. 2017 Mar 31;120(7):1197-1212. doi: 10.1161/CIRCRESAHA.116.307898.

Myocardial Viability: Survival Mechanisms and Molecular Imaging Targets in Acute and Chronic Ischemia.

Author information

1
From the Department of Medicine (Cardiology Division), Massachusetts General Hospital, Harvard Medical School, Boston (H.G.); and Department of Diagnostic Radiology and Nuclear Medicine, University of Maryland School of Medicine, Baltimore (V.D.).
2
From the Department of Medicine (Cardiology Division), Massachusetts General Hospital, Harvard Medical School, Boston (H.G.); and Department of Diagnostic Radiology and Nuclear Medicine, University of Maryland School of Medicine, Baltimore (V.D.). vdilsizian@umm.edu.

Abstract

Myocardial responses to acute ischemia/reperfusion and to chronic ischemic conditions have been studied extensively at all levels of organization. These include subcellular (eg, mitochondria in vitro); intact, large animal models (eg, swine with chronic coronary stenosis); as well as human subjects. Investigations in humans have used positron emission tomographic metabolic and myocardial blood flow measurements, assessment of gene expression and anatomic description of myocardium obtained at the time of coronary artery revascularization, ventricular assist device placement, or heart transplantation. A multitude of genetic, molecular, and metabolic pathways have been identified, which may promote either myocyte survival or death or, most interestingly, both. Many of these potential mediators in both acute ischemia/reperfusion and adaptations to chronic ischemic conditions involve the mitochondria, which play a central role in cellular energy production and homeostasis. The present review is focused on operative survival mechanisms and potential myocardial viability molecular imaging targets in acute and chronic ischemia, especially those which impact mitochondrial function.

KEYWORDS:

fluorodeoxyglucose; gene programs; mitochondria; molecular imaging; myocardial blood flow; myocardium; oxidant stress; renin–angiotensin–aldosterone system

PMID:
28360350
DOI:
10.1161/CIRCRESAHA.116.307898
[Indexed for MEDLINE]

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