title: Rosuvastatin-Induced Carotid Plaque Regression in Patients With Inflammatory Joint Diseases: The Rosuvastatin in Rheumatoid Arthritis, Ankylosing Spondylitis and Other Inflammatory Joint Diseases Study.
abstract: OBJECTIVE
  Patients with rheumatoid arthritis (RA) and carotid artery plaques have an increased risk of acute coronary syndromes. Statin treatment with the goal of achieving a low-density lipoprotein (LDL) cholesterol level of ≤1.8 mmoles/liter (≤70 mg/dl) is recommended for individuals in the general population who have carotid plaques. The aim of the ROsuvastatin in Rheumatoid Arthritis, Ankylosing Spondylitis and other inflammatory joint diseases (RORA-AS) study was to evaluate the effect of 18 months of intensive lipid-lowering treatment with rosuvastatin with regard to change in carotid plaque height.
  
  
  METHODS
  Eighty-six patients (60.5% of whom were female) with carotid plaques and inflammatory joint disease (55 with RA, 21 with AS, and 10 with psoriatic arthritis) were treated with rosuvastatin to obtain the LDL cholesterol goal. Carotid plaque height was evaluated by B-mode ultrasonography.
  
  
  RESULTS
  The mean ± SD age of the patients was 60.8 ± 8.5 years, and the median compliance with rosuvastatin treatment was 97.9% (interquartile range [IQR] 96.0-99.4). At baseline, the median number and height of the carotid plaques were 1.0 (range 1-8) and 1.80 mm (IQR 1.60-2.10), respectively. The mean ± SD change in carotid plaque height after 18 months of treatment with rosuvastatin was -0.19 ± 0.35 mm (P < 0.0001). The mean ± SD baseline LDL cholesterol level was 4.0 ± 0.9 mmoles/liter (154.7 ± 34.8 mg/dl), and the mean reduction in the LDL cholesterol level was -2.3 mmoles/liter (95% confidence interval [95% CI] -2.48, -2.15) (-88.9 mg/dl [95% CI -95.9, -83.1]). The mean ± SD LDL cholesterol level during the 18 months of rosuvastatin treatment was 1.7 ± 0.4 mmoles/liter (area under the curve). After adjustment for age/sex/blood pressure, no linear relationship between a reduction in carotid plaque height and the level of LDL cholesterol exposure during the study period was observed. Attainment of the LDL cholesterol goal of ≤1.8 mmoles/liter (≤70 mg/dl) or the amount of change in the LDL cholesterol level during the study period did not influence the degree of carotid plaque height reduction.
  
  
  CONCLUSIONS
  Intensive lipid-lowering treatment with rosuvastatin induced atherosclerotic regression and reduced the LDL cholesterol level significantly in patients with inflammatory joint disease.
authors.affiliation: Diakonhjemmet Hospital, Oslo, Norway.
authors.forename: S
authors.initials: S
authors.lastname: Rollefstad
authors.affiliation: Diakonhjemmet Hospital, Oslo, Norway.
authors.forename: E
authors.initials: E
authors.lastname: Ikdahl
authors.affiliation: Oslo University Hospital, Aker, Oslo, Norway.
authors.forename: J
authors.initials: J
authors.lastname: Hisdal
authors.affiliation: Diakonhjemmet Hospital, Oslo, Norway.
authors.forename: I C
authors.initials: IC
authors.lastname: Olsen
authors.affiliation: Oslo University Hospital, Ullevål, Oslo, Norway.
authors.forename: I
authors.initials: I
authors.lastname: Holme
authors.affiliation: Diakonhjemmet Hospital, Oslo, Norway.
authors.forename: H B
authors.initials: HB
authors.lastname: Hammer
authors.affiliation: Smerud Medical Research International AS, Oslo, Norway.
authors.forename: K T
authors.initials: KT
authors.lastname: Smerud
authors.affiliation: The Dudley Group NHS Foundation Trust, West Midlands, UK.
authors.forename: G D
authors.initials: GD
authors.lastname: Kitas
authors.affiliation: Centre of Preventive Medicine, Oslo University Hospital, Ullevål, and University of Oslo, Oslo, Norway.
authors.forename: T R
authors.initials: TR
authors.lastname: Pedersen
authors.affiliation: Diakonhjemmet Hospital, Oslo, Norway.
authors.forename: T K
authors.initials: TK
authors.lastname: Kvien
authors.affiliation: Diakonhjemmet Hospital, Oslo, Norway.
authors.forename: A G
authors.initials: AG
authors.lastname: Semb
mesh_terms: D054058:Acute Coronary Syndrome / Q000453:epidemiology; D000368:Aged; D015535:Arthritis, Psoriatic / Q000150:complications*; D001172:Arthritis, Rheumatoid / Q000150:complications*; D016893:Carotid Stenosis / Q000097:blood / Q000000981:diagnostic imaging / Q000517:prevention & control*; D008078:Cholesterol, LDL / Q000097:blood; D005260:Female; D005464:Fluorobenzenes / Q000627:therapeutic use*; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000627:therapeutic use*; D016015:Logistic Models; D008297:Male; D008875:Middle Aged; D011446:Prospective Studies; D011743:Pyrimidines / Q000627:therapeutic use*; D012307:Risk Factors; D000068718:Rosuvastatin Calcium; D013167:Spondylitis, Ankylosing / Q000150:complications*; D013449:Sulfonamides / Q000627:therapeutic use*; D016896:Treatment Outcome; D018084:Ultrasonography, Interventional
chemical_list: D008078:Cholesterol, LDL; D005464:Fluorobenzenes; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D011743:Pyrimidines; D013449:Sulfonamides; D000068718:Rosuvastatin Calcium