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Journal of Nuclear Medicine Vol. 45 No. 11 1885-1891
© 2004 by Society of Nuclear Medicine


Clinical Investigations

Reduced Oxidative Metabolic Response in Dysfunctional Myocardium with Preserved Glucose Metabolism but with Impaired Contractile Reserve

Keiichiro Yoshinaga, MD1, Chietsugu Katoh, MD2, Rob S.B. Beanlands, MD3, Kazuyuki Noriyasu, MD4, Kaoru Komuro, MD4, Satoshi Yamada, MD4, Yuji Kuge, PhD2, Koichi Morita, MD1, Akira Kitabatake, MD4 and Nagara Tamaki, MD1

1 Department of Nuclear Medicine, Hokkaido University Graduate School of Medicine, Sapporo, Japan
2 Department of Tracer Kinetics, Hokkaido University Graduate School of Medicine, Sapporo, Japan
3 Division of Cardiology, University of Ottawa Heart Institute, Ottawa, Ontario, Canada
4 Department of Cardiovascular Medicine, Hokkaido University Graduate School of Medicine, Sapporo, Japan

The recovery of function in myocardium defined as viable by 18F-FDG PET may differ from that defined by dobutamine stress echocardiography (DSE). The aim of this study was to investigate the difference in the oxidative metabolic response between myocardial segments with preserved contractile reserve (CR) and those without CR, in segments with and without preserved glucose metabolism (GM), using 11C-acetate PET. Methods: Twenty patients with previous myocardial infarction (left ventricular ejection fraction, 37.1% ± 16.5%) underwent dynamic 11C-acetate PET at rest and during dobutamine (7.5 µg/kg/min) infusion. GM was evaluated using 18F-FDG PET and CR was evaluated using DSE. Dysfunctional segments were divided into 3 groups: group A (n = 26) with preserved CR and GM, group B (n = 15) without CR but with preserved GM, and group C (n = 41) without CR and without preserved GM. Results: Resting oxidative metabolism (k mono = monoexponential clearance rate) was preserved in group A and group B (0.052 ± 0.011/min vs. 0.051 ± 0.012/min, P = not significant) but was reduced in group C (0.040 ± 0.015/min) (P < 0.03 vs. group A and group B). The change in k mono, as a measure of the metabolic response to low-dose dobutamine, was significantly higher in group A (0.018 ± 0.012) than that in group B (0.0075 ± 0.0096, P < 0.03) and group C (0.0080 ± 0.012, P < 0.005). Conclusion: Viable segments based on 18F-FDG PET have preserved resting oxidative metabolism. However, segments without CR but with preserved GM show a reduction in the oxidative metabolic response to low-dose dobutamine infusion. The decrease in CR may be related to the reduction in the metabolic response to inotropic stimulation despite preservation of tissue viability on 18F-FDG PET.

Key Words: oxidative metabolism • coronary disease • tomography • dobutamine • hibernation


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