title: Reduced myocardial 18F-FDG uptake after calcium channel blocker administration. Initial observation for a potential new method to improve plaque detection.
abstract: OBJECTIVE
  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).
  
  
  CONCLUSIONS
  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.
authors: PET Unit, Department of Nuclear Medicine, Sant Pau Hospital, Sant Antoni Maria Claret 167, 08025, Barcelona, Spain. mc.gaeta@gmail.com
authors: Chiara
authors: C
authors: Gaeta
authors: Yolanda
authors: Y
authors: Fernández
authors: Javier
authors: J
authors: Pavía
authors: Albert
authors: A
authors: Flotats
authors: Carles
authors: C
authors: Artigas
authors: Jordi
authors: J
authors: Deportos
authors: Llanos
authors: L
authors: Geraldo
authors: Ignasi
authors: I
authors: Carrió
mesh_terms: D000818:Animals; D001692:Biological Transport / Q000187:drug effects; D002121:Calcium Channel Blockers / Q000008:administration & dosage* / Q000494:pharmacology*; D019788:Fluorodeoxyglucose F18 / Q000378:metabolism*; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D009206:Myocardium / Q000378:metabolism*; D058226:Plaque, Atherosclerotic / Q000000981:diagnostic imaging* / Q000378:metabolism*; D049268:Positron-Emission Tomography / Q000379:methods*; D014700:Verapamil / Q000008:administration & dosage / Q000494:pharmacology
chemical_list: D002121:Calcium Channel Blockers; D019788:Fluorodeoxyglucose F18; D014700:Verapamil