title: Effect of intensive versus moderate lipid-lowering therapy on epicardial adipose tissue in hyperlipidemic post-menopausal women: a substudy of the BELLES trial (Beyond Endorsed Lipid Lowering with EBT Scanning).
abstract: OBJECTIVE
  This study sought to evaluate the effect of intensive and moderate statin therapy on epicardial adipose tissue (EAT).
  
  
  BACKGROUND
  EAT has been associated with coronary artery disease severity and outcome. It is currently unknown whether EAT volume changes over time when patients are exposed to statin therapy.
  
  
  METHODS
  Subanalysis of a randomized study of atorvastatin 80 mg/day versus pravastatin 40 mg/day for 1 year in a clinical trial designed to assess the progression of coronary artery calcium (CAC) in hyperlipidemic post-menopausal women. Patients underwent cardiac computed tomography scans at the start and end of the trial period.
  
  
  RESULTS
  Of 420 patients, 194 received atorvastatin and 226 pravastatin; the median low-density lipoprotein change was -53.3% and -28.3% with atorvastatin and pravastatin, respectively (p < 0.001). Baseline EAT correlated with age, body mass index, hypertension, diabetes mellitus, high-density lipoprotein, triglyceride levels, and CAC (p < 0.001). At the end of follow-up, EAT regressed more in the atorvastatin than in the pravastatin group (median, -3.38% vs. -0.83%, p = 0.025). The EAT percent change from baseline was significant in the atorvastatin, but not the pravastatin group (p < 0.001 and p = 0.2, respectively). There was no correlation between lipid lowering and EAT regression. CAC progressed significantly in both groups from baseline.
  
  
  CONCLUSIONS
  In hyperlipidemic post-menopausal women, statin therapy induced EAT regression, although intensive therapy was more effective than moderate-intensity therapy. This effect does not seem linked to low-density lipoprotein lowering and may be secondary to other actions of statins such as anti-inflammatory effects.
authors.affiliation: Division of Cardiology, Department of Medicine, Emory University, Atlanta, Georgia, USA.
authors.forename: Nikolaos
authors.initials: N
authors.lastname: Alexopoulos
authors.forename: Bekir H
authors.initials: BH
authors.lastname: Melek
authors.forename: Chesnal D
authors.initials: CD
authors.lastname: Arepalli
authors.forename: Gregory-Randell
authors.initials: GR
authors.lastname: Hartlage
authors.forename: Zhengjia
authors.initials: Z
authors.lastname: Chen
authors.forename: Sungjin
authors.initials: S
authors.lastname: Kim
authors.forename: Arthur E
authors.initials: AE
authors.lastname: Stillman
authors.forename: Paolo
authors.initials: P
authors.lastname: Raggi
mesh_terms: D000273:Adipose Tissue / Q000187:drug effects*; D000368:Aged; D000369:Aged, 80 and over; D050197:Atherosclerosis / Q000209:etiology / Q000517:prevention & control*; D000069059:Atorvastatin; D003324:Coronary Artery Disease / Q000517:prevention & control; D005260:Female; D006538:Heptanoic Acids / Q000008:administration & dosage; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000008:administration & dosage*; D006949:Hyperlipidemias / Q000150:complications* / Q000188:drug therapy; D008875:Middle Aged; D017698:Postmenopause / Q000187:drug effects; D017035:Pravastatin / Q000008:administration & dosage; D011758:Pyrroles / Q000008:administration & dosage; D061205:Vascular Calcification / Q000517:prevention & control
chemical_list: D006538:Heptanoic Acids; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D011758:Pyrroles; D000069059:Atorvastatin; D017035:Pravastatin