Literature DB >> 11197981

An evaluation of myocardial fatty acid and glucose uptake using PET with [18F]fluoro-6-thia-heptadecanoic acid and [18F]FDG in Patients with Congestive Heart Failure.

M Taylor1, T R Wallhaus, T R Degrado, D C Russell, P Stanko, R J Nickles, C K Stone.   

Abstract

UNLABELLED: Understanding the metabolic consequences of heart failure is important in evaluating potential mechanisms for disease progression and assessing targets for therapies designed to improve myocardial metabolism in patients with heart failure. PET is uniquely suited to noninvasively evaluate myocardial metabolism. In this study, we investigated the kinetics of 14(R,S)-[18F]fluoro-6-thia-heptadecanoic acid (FTHA) and [18F]FDG in patients with stable New York Heart Association functional class III congestive heart failure and a left ventricular ejection fraction of no more than 35%.
METHODS: Twelve fasting patients underwent dynamic PET studies using [18F]FTHA and FDG. From the dynamic image data, the fractional uptake rates (Ki) were determined for [18F]FTHA and FDG. Subsequently, serum free fatty acid and glucose concentrations were used to calculate the myocardial free fatty acid and glucose uptake rates, respectively. Uptake rates were compared with reported values for [18F]FTHA and FDG in subjects with normal left ventricular function.
RESULTS: The average Ki for [18F]FTHA was 19.7 +/- 9.3 mL/100 g/min (range, 7.2-36.0 ml/100 g/min). The average myocardial fatty acid use was 19.3 +/- 2.3 mmol/100 g/min. The average Ki for FDG was 1.5 +/- 0.37 mL/100 g/min (range, 0.1-3.3 mL/100 g/min), and the average myocardial glucose use was 12.3 +/- 2.3 mmol/100 g/min.
CONCLUSION: Myocardial free fatty acid and glucose use in heart failure can be quantitatively assessed using PET with [18F]FTHA and FDG. Myocardial fatty acid uptake rates in heart failure are higher than expected for the normal heart, whereas myocardial glucose uptake rates are lower. This shift in myocardial substrate use may be an indication of impaired energy efficiency in the failing heart, providing a target for therapies directed at improving myocardial energy efficiency.

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Year:  2001        PMID: 11197981

Source DB:  PubMed          Journal:  J Nucl Med        ISSN: 0161-5505            Impact factor:   10.057


  84 in total

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3.  Exercise training improves insulin-stimulated myocardial glucose uptake in patients with dilated cardiomyopathy.

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Review 7.  Modulating fatty acid oxidation in heart failure.

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9.  TGR5 activation induces cytoprotective changes in the heart and improves myocardial adaptability to physiologic, inotropic, and pressure-induced stress in mice.

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10.  Substrate utilization by the failing human heart by direct quantification using arterio-venous blood sampling.

Authors:  Junichi Funada; Tim R Betts; Leanne Hodson; Sandy M Humphreys; Jon Timperley; Keith N Frayn; Fredrik Karpe
Journal:  PLoS One       Date:  2009-10-21       Impact factor: 3.240

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