Premium
Evaluation of 14( R , S )‐[ 18 F]fluoro‐6‐thia‐heptadecanoic acid (FTHA) as a positron emission tomography fatty acid tracer of beta‐oxidation in the heart
Author(s) -
Pooley Robert A.
Publication year - 1996
Publication title -
medical physics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.473
H-Index - 180
eISSN - 2473-4209
pISSN - 0094-2405
DOI - 10.1118/1.597823
Subject(s) - perfusion , chemistry , in vivo , nuclear medicine , fatty acid , medicine , biochemistry , biology , microbiology and biotechnology
The radiolabeled long‐chain fatty acid analog, 14( R , S )‐[ 18 F]fluoro‐6‐thia‐heptadecanoic acid (FTHA), was designed (DeGrado, 1991) to undergo metabolic trapping subsequent to its commitment to the beta‐oxidation (β‐ox) pathway. FTHA was evaluated under various conditions in two animal models for heart research: isolated perfused working rat heart and open‐chest extracorporeally perfused swine heart. FTHA was infused into working rat hearts. Linear radioactivity accumulation was measured by external coincidence detection; the slope was used to determine an estimate for the rate of β‐ox and was compared to the rate determined from the standard tracer, 3 H‐palmitate ( 3 H‐PA). Experiments were conducted under conditions of low and high workload, fed and fasted states, suppression of β‐ox, and various perfusate concentrations of palmitate and glucose. Swine LAD artery was cannulated and perfused from the femoral artery through a perfusion pump. FTHA and 3 H‐PA were simultaneously infused during three 15 min segments of hyperemia, control, and β‐ox suppression. Blood samples were collected and assayed for 3 H 2 O and 18 F concentrations. Results indicate that FTHA uptake is specifically sensitive to β‐ox, sensitive to changes in energy demand, independent of flow, and can accurately determine in vivo rates of β‐ox in the normal clinical range of fatty acid concentrations. At concentrations higher than this range, FTHA showed a decreased sensitivity to β‐ox, indicating the required use of a correction factor in the clinic.