PURPOSE: Physiological glucose uptake by the myocardium may hamper visualization of coronary atherosclerotic plaques in (18)F-FDG PET studies. Intracellular myocardial calcium relates to glucose influx. We assessed whether administration of a calcium channel blocker such as verapamil could decrease myocardial (18)F-FDG uptake in mice. METHODS: Experiments were conducted on ten male C57BL/6JOlaHsd mice. The mice were studied by (18)F-FDG PET/CT under basal conditions and after a single administration of verapamil injected 1 h prior to (18)F-FDG administration at doses of 1 mg/kg (group A, n = 5) and 20 mg/kg (group B, n = 5). PET scanning was started 60 min after injection of (18)F-FDG employing a dedicated small-animal PET/CT system (ARGUS-CT). In each mouse, post-verapamil PET images were coregistered with the basal PET images. Volumetric regions of interest (VOI) were drawn on the basal study containing the myocardium of the whole left ventricle and quantitatively compared with the same VOI applied to the post-verapamil scan. The SUV(mean) was used to express the mean myocardial (18)F-FDG uptake. The relative coefficient of variation (RV) between the basal and post-verapamil conditions was calculated. RESULTS: Verapamil administration decreased myocardial (18)F-FDG uptake in all animals. The median (range) SUV(mean) values in group A were 2.6 (1.6-4.1) under basal conditions and 1.7 (1.1-2.9) after verapamil administration (p = 0.043), and in group B were 1.6 (1.3-2.0) under basal conditions and 1.0 (0.9-1.4) after verapamil administration (p = 0.043). The median (range) RV values were -31% (-5%, -50%) in group A, and -37% (-10%, -51%) in group B (p = 0.6). CONCLUSION: In this animal model there was a significant reduction in (18)F-FDG uptake in the myocardium following verapamil administration. This type of intervention could facilitate the definition of coronary atherosclerotic plaque inflammation on (18)F-FDG PET scans.
PURPOSE: Physiological glucose uptake by the myocardium may hamper visualization of coronary atherosclerotic plaques in (18)F-FDG PET studies. Intracellular myocardial calcium relates to glucose influx. We assessed whether administration of a calcium channel blocker such as verapamil could decrease myocardial (18)F-FDG uptake in mice. METHODS: Experiments were conducted on ten male C57BL/6JOlaHsd mice. The mice were studied by (18)F-FDG PET/CT under basal conditions and after a single administration of verapamil injected 1 h prior to (18)F-FDG administration at doses of 1 mg/kg (group A, n = 5) and 20 mg/kg (group B, n = 5). PET scanning was started 60 min after injection of (18)F-FDG employing a dedicated small-animal PET/CT system (ARGUS-CT). In each mouse, post-verapamil PET images were coregistered with the basal PET images. Volumetric regions of interest (VOI) were drawn on the basal study containing the myocardium of the whole left ventricle and quantitatively compared with the same VOI applied to the post-verapamil scan. The SUV(mean) was used to express the mean myocardial (18)F-FDG uptake. The relative coefficient of variation (RV) between the basal and post-verapamil conditions was calculated. RESULTS:Verapamil administration decreased myocardial (18)F-FDG uptake in all animals. The median (range) SUV(mean) values in group A were 2.6 (1.6-4.1) under basal conditions and 1.7 (1.1-2.9) after verapamil administration (p = 0.043), and in group B were 1.6 (1.3-2.0) under basal conditions and 1.0 (0.9-1.4) after verapamil administration (p = 0.043). The median (range) RV values were -31% (-5%, -50%) in group A, and -37% (-10%, -51%) in group B (p = 0.6). CONCLUSION: In this animal model there was a significant reduction in (18)F-FDG uptake in the myocardium following verapamil administration. This type of intervention could facilitate the definition of coronary atherosclerotic plaque inflammation on (18)F-FDG PET scans.
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