Statin May Put the Brakes on Artery Hardening in AS, RA

April 15, 2015
Rita Baron-Faust

Patients with rheumatoid arthritis face an increased risk for acute coronary syndromes, but a popular statin seems to reduce asymptomatic carotid plaques.

Rollefstad S, Ikdahl E, J. Hisdal J, et al., Rosuvastatin induced carotid plaque regression in patients with inflammatory joint diseases: The RORA-AS study.Arthritis & Rheumatology. Accepted Article. doi: 10.1002/art.39114 [Online March 21, 2015]

Intensive treatment with rosuvastatin (Crestor) appears to induce regression of atherosclerotic plaques in carotid arteries and significantly lowers “bad” cholesterol in patients with inflammatory arthritis, Norwegian researchers say.

Eighty-six patients with rheumatoid arthritis (RA), ankylosing spondylitis (AS), and psoriatic arthritis (PsA) took part in the 18-month intervention study. None were on statins but all had asymptomatic carotid plaques identified on ultrasound.

More than half the patients were women, ages 50 to 80. They received age-titrated doses of rosuvastatin with the aim of reducing low-density lipoprotein cholesterol (LDL-c) to under 1.8 mmol/L (below 70 mg/dl).

Almost 62% hit the LDL-c goal and experienced a reduction in the height of their carotid plaques based on ultrasonography.

Attainment of the LDL-c goal, or the amount of change in LDL-c, does not appear to influence the degree of carotid plaque height reduction, suggesting that intensive drug treatment is responsible for regression of atherosclerotic plaques.

Those with the highest carotid plaques, and the youngest patients, had the biggest reduction in plaques, as did patients on synthetic disease modifying antirheumatic drugs (DMARDs) monotherapy, and non-users of DMARDs. Users of biological DMARDs saw no changes.

The authors report no change in disease activity for either the RA patients, as measured by disease activity in 28 joints (DAS28), or the AS patients, based on the Ankylosing Spondylitis Disease Activity Score (ASDAS).

The latter result is in step with results from previous studies, “since disease activity is a composite measure which includes inflammatory biomarkers,” the authors note.

Study limitations include the lack of a placebo group (the statin users acted as their own controls). But the researchers stress that “placebo treated patients would most likely not obtain a spontaneous regression of the atherosclerotic plaque.”