title: Effects of rosuvastatin on subclinical atherosclerosis and arterial stiffness in rheumatoid arthritis: a randomized controlled pilot trial.
abstract: OBJECTIVE
  To ascertain the effect of rosuvastatin on carotid atherosclerosis and arterial stiffness in patients with rheumatoid arthritis (RA).
  
  
  METHODS
  Fifty RA patients were randomized in a double-blind placebo-controlled trial to receive 10 mg rosuvastatin (n = 24) or placebo (n = 26). Patients were followed prospectively every 3 months for 12 months. Intima-media thickness (IMT), augmentation index (AIx), and subendocardial viability ratio (SEVR) were measured at baseline, 6 and 12 months.
  
  
  RESULTS
  Rosuvastatin resulted in statistically significant reductions of total cholesterol (TC), low density lipoprotein cholesterol (LDL-C), apolipoprotein B (Apo B), and urate levels vs. placebo. However, rosuvastatin had no significant effect on changes in inflammatory markers, including C-reactive protein (CRP) levels [from 2.9 (1.4-11.0) to 3.1 (0.9-13.3) mg/L in the rosuvastatin group compared with from 5.8 (2.6-14.2) to 4.4 (1.2-12.3) mg/L in the placebo group]. Nonetheless, a significant improvement in the Disease Activity Score (DAS) and a reduction in fibrinogen level was observed at 6 and 12 months compared with baseline in the rosuvastatin group. The treatment group exhibited a significant increase in SEVR (from 157 ± 28% to 163 ± 33% in the rosuvastatin group compared with from 143 ± 18% to 143 ± 26% in the placebo group, p = 0.023), but no significant effect was observed in the changes in IMT and AIx.
  
  
  CONCLUSIONS
  Our data suggest that rosuvastatin has a modest anti-inflammatory effect in RA patients with low disease activity in terms of reduction in DAS and fibrinogen level. Rosuvastastin may also improve subendocardial perfusion and lower the urate level.
authors.affiliation: Department of Medicine and Therapeutics, The Prince of Wales Hospital, Shatin, Hong Kong, PR China. tamls_813@yahoo.com
authors.forename: L-S
authors.initials: LS
authors.lastname: Tam
authors.forename: E K
authors.initials: EK
authors.lastname: Li
authors.forename: Q
authors.initials: Q
authors.lastname: Shang
authors.forename: B
authors.initials: B
authors.lastname: Tomlinson
authors.forename: V W
authors.initials: VW
authors.lastname: Lee
authors.forename: K K
authors.initials: KK
authors.lastname: Lee
authors.forename: M
authors.initials: M
authors.lastname: Li
authors.forename: W Pang
authors.initials: WP
authors.lastname: Kuan
authors.forename: T K
authors.initials: TK
authors.lastname: Li
authors.forename: L
authors.initials: L
authors.lastname: Tseung
authors.forename: G W K
authors.initials: GW
authors.lastname: Yip
authors.forename: B
authors.initials: B
authors.lastname: Freedman
authors.forename: C-M
authors.initials: CM
authors.lastname: Yu
mesh_terms: D001055:Apolipoproteins B / Q000097:blood; D001172:Arthritis, Rheumatoid / Q000188:drug therapy* / Q000503:physiopathology; D050197:Atherosclerosis / Q000188:drug therapy* / Q000503:physiopathology; D059168:Carotid Intima-Media Thickness; D016893:Carotid Stenosis / Q000000981:diagnostic imaging; D002784:Cholesterol / Q000097:blood; D018450:Disease Progression; D004311:Double-Blind Method; D005260:Female; D005464:Fluorobenzenes / Q000627:therapeutic use*; D005500:Follow-Up Studies; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000627:therapeutic use*; D008297:Male; D008875:Middle Aged; D010865:Pilot Projects; D011446:Prospective Studies; D011743:Pyrimidines / Q000627:therapeutic use*; D012307:Risk Factors; D000068718:Rosuvastatin Calcium; D012720:Severity of Illness Index; D013449:Sulfonamides / Q000627:therapeutic use*; D016896:Treatment Outcome; D059289:Vascular Stiffness / Q000187:drug effects* / Q000502:physiology
chemical_list: D001055:Apolipoproteins B; D005464:Fluorobenzenes; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D011743:Pyrimidines; D013449:Sulfonamides; D000068718:Rosuvastatin Calcium; D002784:Cholesterol