Abstract
Fatty acid oxidation defects are being increasingly identified as causes of abnormal heart function and sudden death in children. Children with medium-chain acyl-coenzyme A (acyl-CoA) dehydrogenase defects can metabolize fatty acids labeled in the carboxylic acid end of the compound. Accordingly, our goal was to label a long-chain fatty acid in the ω-position and evaluate its myocardial kinetics. Methods: Heptadecanoic acid, a 17-carbon fatty acid, was labeled in the C-17 position with 11C by the general process of coupling 11C-methyliodide to t-butyl-15-hexadecanoate. Yield was ∼5%–10% end-of-bombardment. Subsequently, evaluation studies were performed on isolated perfused rat hearts and in intact, anesthetized dogs. The myocardial uptake and efflux of 17-11C-heptadecanoic acid were compared with those of 1-11C-palmitate. Results: With the exception of delayed efflux of tracer reflecting the temporal delay for β-oxidation, the washout of 17-11C-heptadecanoic acid from the heart mirrored that of 1-11C-palmitate in isolated rat hearts and in intact dogs with PET. Conclusion: 17-11C-Heptadecanoic acid may be a useful tracer for the identification of defects in fatty acid metabolism in subjects with medium- and short-chain fatty acid oxidation defects.
Footnotes
Received Jan. 24, 2002; revision accepted Jul. 26, 2002.
For correspondence or reprints contact: T. Lee Collier, PhD, Division of Cardiology, VC 12-238, College of Physicians and Surgeons of Columbia University, 630 W. 168th St., New York, NY 10032.
E-mail: tc311{at}columbia.edu