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CLINICAL INVESTIGATIONS |
William S. Middleton Memorial Veterans Hospital, Madison; Departments of Medical Physics and Medicine, University of Wisconsin-Madison, Madison, Wisconsin; and Department of Medical Physics, Duke University, Durham, North Carolina
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.
Key Words: PET • myocardial metabolism • 14(R,S)-[18F]fluoro-6-thia-heptadecanoic acid
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