title: Effects of conventional and aggressive statin treatment on markers of endothelial function and inflammation.
abstract: BACKGROUND
  Atherosclerosis is considered to be a chronic inflammatory disorder. Several large-scale clinical studies demonstrate that markers of inflammation, such as high-sensitivity C-reactive protein (hsCRP), fibrinogen, and soluble CD40 ligand, are potent and independent predictors of vascular risk.
  
  
  OBJECTIVE
  The study was undertaken to investigate the effect of increasing the statin dose from conventional to aggressive treatment on lipids levels, inflammation, and endothelial function in patients with coronary artery disease (CAD).
  
  
  METHODS
  We randomized 97 patients to either 20 mg simvastatin or 80 mg atorvastatin. Plasma levels of lipids, hsCRP, fibrinogen, soluble adhesion molecules, and nitric oxide-total were analyzed at baseline and after 6 months of treatment.
  
  
  RESULTS
  Lipid values were significantly reduced in both treatment groups, but with significantly greater reduction in the aggressively treated group. Furthermore, aggressive statin treatment significantly decreased hsCRP and fibrinogen, while only small reductions were seen in the conventionally treated group, resulting in significant differences between the two treatment groups (p < 0.001). Nitric oxide-total increased significantly in both treatment groups, although the increase was more pronounced in the aggressively treated group (22.6 vs. 15.6%).
  
  
  CONCLUSIONS
  Aggressive statin treatment significantly improved lipid status and reduced markers of inflammation and improved endothelial function compared with conventional treatment in patients with CAD. No interaction was observed, and high-dose treatment did not offer additional benefit compared with standard-dose treatment with respect to soluble adhesion molecules.
authors.affiliation: Department of Cardiology, Rikshospitalet, Oslo, Norway. aina.hognestad@klinmed.uio.no
authors.forename: Aina
authors.initials: A
authors.lastname: Hognestad
authors.forename: Pål
authors.initials: P
authors.lastname: Aukrust
authors.forename: Ragnhild
authors.initials: R
authors.lastname: Wergeland
authors.forename: Oddvar
authors.initials: O
authors.lastname: Stokke
authors.forename: Lars
authors.initials: L
authors.lastname: Gullestad
authors.forename: Anne Grete
authors.initials: AG
authors.lastname: Semb
authors.forename: Torbjørn
authors.initials: T
authors.lastname: Holm
authors.forename: Arne K
authors.initials: AK
authors.lastname: Andreassen
authors.forename: John K
authors.initials: JK
authors.lastname: Kjekshus
mesh_terms: D001161:Arteriosclerosis / Q000188:drug therapy*; D000069059:Atorvastatin; D002097:C-Reactive Protein / Q000187:drug effects*; D002908:Chronic Disease; D003324:Coronary Artery Disease / Q000188:drug therapy; D019040:E-Selectin / Q000097:blood / Q000187:drug effects; D005260:Female; D005340:Fibrinogen / Q000187:drug effects*; D006538:Heptanoic Acids / Q000494:pharmacology / Q000627:therapeutic use*; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000494:pharmacology / Q000627:therapeutic use*; D007249:Inflammation; D008297:Male; D008875:Middle Aged; D009569:Nitric Oxide / Q000378:metabolism; D011758:Pyrroles / Q000494:pharmacology / Q000627:therapeutic use*; D019821:Simvastatin / Q000494:pharmacology / Q000627:therapeutic use*; D016896:Treatment Outcome
chemical_list: D019040:E-Selectin; D006538:Heptanoic Acids; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D011758:Pyrroles; D009569:Nitric Oxide; D005340:Fibrinogen; D002097:C-Reactive Protein; D000069059:Atorvastatin; D019821:Simvastatin