Rosuvastatin-Induced Carotid Plaque Regression in Patients With Inflammatory Joint Diseases

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 mean6SD age of the patients was 60.86 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 mean6SD change in carotid plaque height after 18 months of treatment with rosuvastatin was 20.196 0.35 mm (P < 0.0001). The mean6SD baseline LDL cholesterol level was 4.06 0.9 mmoles/liter (154.76 34.8 mg/dl), and the mean reduction in the LDL cholesterol level was 22.3 mmoles/liter (95% confidence interval [95% CI] 22.48, 22.15) (288.9 mg/dl [95% CI 295.9, 283.1]). The mean 6 SD LDL cholesterol level during the 18 months of rosuvastatin treatment was 1.76 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. Conclusion. Intensive lipid-lowering treatment with rosuvastatin induced atherosclerotic regression ClinicalTrials.gov identifier: NCT01389388. EudraCT database no. 2008-005551-20. Supported by the South-Eastern Regional Health Authority of Norway. AstraZeneca provided the study drug. S. Rollefstad, MD, PhD, E. Ikdahl, MD, I. C. Olsen, PhD, H. B. Hammer, MD, PhD, T. K. Kvien, MD, A. G. Semb, MD, PhD: Diakonhjemmet Hospital, Oslo, Norway; J. Hisdal, PhD: Oslo University Hospital, Aker, Oslo, Norway; I. Holme, PhD: Oslo University Hospital, Ullevål, Oslo, Norway; K. T. Smerud, MSc: Smerud Medical Research International AS, Oslo, Norway; G. D. Kitas, MD, PhD, FRCP: The Dudley Group NHS Foundation Trust, West Midlands, UK; T. R. Pedersen, MD, PhD: Centre of Preventive Medicine, Oslo University Hospital, Ullevål, and University of Oslo, Oslo, Norway. Dr. Hammer has received consulting fees, speaking fees, and/ or honoraria from Pfizer, Roche, AbbVie, UCB, and Merck Sharp & Dohme (less than $10,000 each). Dr. Pedersen has received speaking fees from Amgen (less than $10,000) and consulting/speaking fees from Merck Sharp & Dohme (more than $10,000). Dr. Semb has received speaking fees, consulting fees, and/or honoraria from Merck Sharp & Dohme, Schering Plough, AbbVie, Bristol-Myers Squibb, UCB, Wyeth/ Pfizer, and Hoffmann-La Roche/Genentech (less than $10,000 each). Address correspondence to S. Rollefstad, MD, PhD, Preventive Cardio-Rheuma Clinic, Department of Rheumatology, Diakonhjemmet Hospital, PO Box 23 Vinderen, NO-0319 Oslo, Norway. E-mail: [email protected] or [email protected]. Submitted for publication October 20, 2014; accepted in revised form March 10, 2015.