Metabolic Complexities in Cardiac Imaging

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For patients with advanced ischemic heart disease, positron emission tomography (PET) is a reimbursable method for identifying those suitable for revascularization. This will probably increase the use of PET in deciding whether potentially life-enhancing, but costly, interventions will be performed. In this issue of Circulation , an important article by Taegtmeyer and colleagues1 shows that it may not be possible to use the seductive, computer-derived colored images produced by PET as a quantitative measure of myocardial metabolic rate. These researchers have shown that accumulation of [2-18F]fluoro-2-deoxy-d-glucose (FDG), a widely used PET tracer, does not give an accurate measure of glucose metabolism under many of the physiological, metabolic, and hormonal conditions experienced by the heart. Modeling of FDG as a glucose analogue for glycolysis in the heart comes in large part from work in brain metabolism,2 where glucose is the major metabolic fuel and glycogen synthesis from glucose is essentially nil. In contrast, the heart is omnivorous in its choice of metabolic fuels, with a preference for fatty acids and with considerable glycogen synthesis and degradation.3 4 Consequently, expressions such as “myocardial glucose metabolism” and “myocardial glucose utilization” were coined in part out of recognition that FDG flux rates are unable to distinguish glycogen synthesis from glycolysis. In the heart, therefore, a measure of the rate of FDG accumulation may be just that—a measure of FDG accumulation and not a measure of metabolic rate. If one is to interpret the meaning of a change in FDG accumulation over time, a number of assumptions governing the rates of the reactions of glucose transport and phosphorylation must be met. The major reactions determining the extent of the intracellular use of glucose and FDG are transport into the cell, phosphorylation in the hexokinase reaction, dephosphorylation of glucose-6-phosphate …