Quantitative Relation Between Myocardial Viability and Improvement in Heart Failure Symptoms After Revascularization in Patients With Ischemic Cardiomyopathy

Carli, Marcelo F. Di; Asgarzadie, Farbod; Schelbert, Heinrich R.; Brunken, Richard C.; Laks, Hillel; Phelps, Michael E.; Maddahi, Jamshid

doi:10.1161/01.cir.92.12.3436

Cited by 412 publications

(145 citation statements)

References 27 publications

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“…Discerning the etiology of LV dysfunction is often the first step in management. Underlying coronary artery disease (CAD) and ischemia are responsible for approximately two-thirds of all systolic dysfunction [1] and delineating it from nonischemic causes has essential therapeutic [2,3,4] and prognostic [5,6,7,8] implications. The electrocardiogram (ECG) [9], presence of anginal chest pain [10], and elevated troponins [11] are unable to accurately differentiate ischemic from nonischemic cardiomyopathy (NICM).…”

Section: Introductionmentioning

confidence: 99%

Can late gadolinium enhancement by cardiovascular magnetic resonance identify coronary artery disease as the etiology of new onset congestive heart failure?

Schietinger

Vörös

Isbell

et al. 2007

Int J Cardiovasc Imaging

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Background-New left ventricular systolic dysfunction affects 500,000 Americans and coronary artery disease (CAD) is responsible for two-thirds of cases. Identifying CAD has both prognostic and therapeutic implications. We evaluated the ability of late gadolinium enhancement (LGE) by cardiovascular magnetic resonance imaging (CMR) to detect CAD as the etiology of recent onset congestive heart failure (CHF).

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Section: Introductionmentioning

confidence: 99%

Can late gadolinium enhancement by cardiovascular magnetic resonance identify coronary artery disease as the etiology of new onset congestive heart failure?

Schietinger

Vörös

Isbell

et al. 2007

Int J Cardiovasc Imaging

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“…More than three decades ago, Neely and colleagues (35,37) showed that ischemia reduces glucose uptake and glycolysis. However, those results contrast with positron emission tomography studies that show an increase in the uptake of 18 F-deoxyglucose in relation to coronary flow in patients with coronary artery disease (10,32). Similar observations in vivo (50) and ex vivo (40,45) were attributed to a translocation of GLUT4 to the cell surface, due to ischemiainduced activation of adenosine 5Ј-monophosphate-activated protein kinase (AMPK) (39).…”

mentioning

confidence: 76%

Ischemia-induced activation of AMPK does not increase glucose uptake in glycogen-replete isolated working rat hearts

Omar¹,

Fraser²,

Clanachan³

2008

American Journal of Physiology-Heart and Circulatory Physiology

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Omar MA, Fraser H, Clanachan AS. Ischemia-induced activation of AMPK does not increase glucose uptake in glycogenreplete isolated working rat hearts. Am J Physiol Heart Circ Physiol 294: H1266-H1273, 2008. First published January 4, 2008 doi:10.1152/ajpheart.01087.2007.-Alterations in myocardial glucose metabolism are a key determinant of ischemia-induced depression of left ventricular mechanical function. Since myocardial glycogen is an important source of endogenous glucose, we compared the effects of ischemia on glucose uptake and utilization in isolated working rat hearts in which glycogen content was either replete (G replete, 114 mol/g dry wt) or partially depleted (G depleted, 71 mol/g dry wt). The effects of low-flow ischemia (LFI, 0.5 ml/min) on glucose uptake, glycogen turnover (glycogenolysis and glycogen synthesis), glycolysis, adenosine 5Ј-monophosphate-activated protein kinase (AMPK) activity, and GLUT4 translocation were measured. Relative to preischemic values, LFI caused a time-dependent reduction in glycogen content in both G-replete and G-depleted groups due to an acceleration of glycogenolysis (by 12-fold and 6-fold, respectively). In G-replete hearts, LFI (15 min) decreased glucose uptake (by 59%) and did not affect GLUT4 translocation. In G-depleted hearts, LFI also decreased initially glucose uptake (by 90%) and glycogen synthesis, but after 15 min, when glycogenolysis slowed due to exhaustion of glycogen content, glucose uptake increased (by 31%) in association with an increase in GLUT4 translocation. After 60 min of LFI, glucose uptake, glycogenolysis, and glycolysis recovered to near-preischemic values in both groups. LFI increased AMPK activity in a time-dependent manner in both groups (by 6-fold and 4-fold, respectively). Thus, when glycogen stores are replete before ischemia, ischemia-induced AMPK activation is not sufficient to increase glucose uptake. Under these conditions, an acceleration of glycogen degradation provides sufficient endogenous substrate for glycolysis during ischemia. low-flow ischemia; glucose uptake; glycogen metabolism; glucose metabolism; adenosine-5Ј-monophosphate-activated protein kinase UNDER AEROBIC CONDITIONS, ϳ95% of the energy requirement of cardiac muscle is derived from the mitochondrial oxidation of fatty acids and carbohydrates, whereas the remainder is provided by glycolysis. However, during ischemia, oxygen (O 2 ) deprivation inhibits oxidative metabolism and glycolysis becomes a major source of myocardial ATP production (44). Thus myocardial carbohydrate availability and metabolism are critical determinants of ischemic injury and postischemic left ventricular (LV) mechanical function.Glucose transport, the first step of myocardial glucose utilization, involves the facilitated diffusion of glucose across the sarcolemmal membrane. The rate of glucose transport is determined by the transmembrane concentration gradient of glucose as well as the abundance and affinity of glucose transporter proteins, GLUT1 and GLUT4 (27). Following transport, gluco...

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“…The presence of myocardial viability appears to help to predict those patients most likely to manifest improved symptoms and reversibility of chronic LV dysfunction (33)(34)(35)(36)(37)(38)(39)(40). The assessment of myocardial viability is therefore important to identify patients with a significant amount of viable, dysfunctional myocardium that is likely to recover function if revascularized with adequate blood flow.…”

Section: The Role Of Evaluation Of Myocardial Viabilitymentioning

confidence: 99%

“…The assessment of myocardial viability is therefore important to identify patients with a significant amount of viable, dysfunctional myocardium that is likely to recover function if revascularized with adequate blood flow. A variety of imaging techniques have helped to characterize the presence of viable but dysfunctional myocardial tissue, for example, myocardial perfusion imaging with radionuclide flow tracers, positron emission tomography (PET) imaging with 18 F-fluorodeoxyglucose, and assessment of inotropic reserve through echocardiographic or nuclear imaging under catecholamine stimulation (33)(34)(35)(36)(37)(38)(39)(40).…”

Section: The Role Of Evaluation Of Myocardial Viabilitymentioning

confidence: 99%

The heart failure challenge: Optimizing medical and surgical management

Racine

Rouleau

2006

Canadian Journal of Cardiology

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Quantitative Relation Between Myocardial Viability and Improvement in Heart Failure Symptoms After Revascularization in Patients With Ischemic Cardiomyopathy

Cited by 412 publications

References 27 publications

Can late gadolinium enhancement by cardiovascular magnetic resonance identify coronary artery disease as the etiology of new onset congestive heart failure?

Can late gadolinium enhancement by cardiovascular magnetic resonance identify coronary artery disease as the etiology of new onset congestive heart failure?

Ischemia-induced activation of AMPK does not increase glucose uptake in glycogen-replete isolated working rat hearts

The heart failure challenge: Optimizing medical and surgical management

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