title: Simvastatin attenuates plaque inflammation: evaluation by fluorodeoxyglucose positron emission tomography.
abstract: OBJECTIVE
  We investigated whether simvastatin attenuates plaque inflammation by using 18F-fluorodeoxyglucose positron emission tomography (18FDG-PET) co-registered with computerized tomography.
  
  
  BACKGROUND
  Inflammation plays a key role in progression and destabilization of atherosclerotic plaque. 18F-fluorodeoxyglucose PET is a promising tool for visualizing inflammation of atherosclerotic plaque. Antiinflammatory action is one of the pleiotropic effects of statins.
  
  
  METHODS
  Forty-three consecutive subjects, who underwent 18FDG-PET for cancer screening and had 18FDG uptakes in the thoracic aorta and/or the carotid arteries, were randomized to either statin group receiving simvastatin (n = 21) or diet group receiving dietary management only (n = 22). The maximum standardized uptake values (SUVs) were measured in individual plaques, and were averaged for analysis of the subjectwise results. The responses were assessed after 3-month treatments.
  
  
  RESULTS
  Positron emission tomography revealed 117 and 123 18FDG-positive plaques in the statin and diet groups, respectively. Simvastatin, but not diet alone, attenuated plaque (18)FDG uptakes and decreased the SUVs (p < 0.01). Simvastatin reduced low-density lipoprotein cholesterol (LDL-C) by 30% (p < 0.01) and increased high-density lipoprotein cholesterol (HDL-C) by 15% (p < 0.01), whereas LDL-C and HDL-C levels were not changed in the diet group. In the statin group, the decrease in the SUV was well correlated with the HDL-C elevation (p < 0.01) but not with the LDL-C reduction.
  
  
  CONCLUSIONS
  18F-fluorodeoxyglucose PET visualized plaque inflammation and simvastatin attenuated it. The LDL-C-independent effects of simvastatin may participate in the beneficial effect. 18F-fluorodeoxyglucose PET has a potential for visually monitoring plaque inflammation and the therapeutic effectiveness of statins.
authors.affiliation: Department of Medicine/Cardiovascular Research Institute, Division of Cardio-Vascular Medicine, Kurume University School of Medicine, Kurume, Japan.
authors.forename: Nobuhiro
authors.initials: N
authors.lastname: Tahara
authors.forename: Hisashi
authors.initials: H
authors.lastname: Kai
authors.forename: Masatoshi
authors.initials: M
authors.lastname: Ishibashi
authors.forename: Hiroyuki
authors.initials: H
authors.lastname: Nakaura
authors.forename: Hayato
authors.initials: H
authors.lastname: Kaida
authors.forename: Kenkichi
authors.initials: K
authors.lastname: Baba
authors.forename: Naofumi
authors.initials: N
authors.lastname: Hayabuchi
authors.forename: Tsutomu
authors.initials: T
authors.lastname: Imaizumi
mesh_terms: D000368:Aged; D001013:Aorta, Thoracic / Q000000981:diagnostic imaging / Q000473:pathology; D050197:Atherosclerosis / Q000000981:diagnostic imaging* / Q000188:drug therapy* / Q000473:pathology; D016893:Carotid Stenosis / Q000000981:diagnostic imaging / Q000188:drug therapy / Q000473:pathology; D005260:Female; D019788:Fluorodeoxyglucose F18; D005500:Follow-Up Studies; D006801:Humans; D007249:Inflammation / Q000000981:diagnostic imaging / Q000188:drug therapy; D008297:Male; D008875:Middle Aged; D049268:Positron-Emission Tomography / Q000379:methods*; D011446:Prospective Studies; D019821:Simvastatin / Q000627:therapeutic use*
chemical_list: D019788:Fluorodeoxyglucose F18; D019821:Simvastatin