The impact of statins on coronary atherosclerosis progression and long-term cardiovascular disease risk in rheumatoid arthritis.

Objectives To evaluate whether statins lower cardiovascular disease (CVD) risk in rheumatoid arthritis (RA) and if tentative benefits are related to changes in coronary plaque burden or composition. Methods In an observational cohort study, 150 patients without CVD underwent coronary atherosclerosis evaluation (total, noncalcified, partially and fully calcified plaque) with computed tomography angiography. Prespecified cardiovascular events including cardiac death, myocardial infarction, unstable angina, revascularization, stroke, claudication, and heart failure were prospectively recorded. Change in plaque burden and composition was re-assessed in 102 patients within 6.9±0.3 years. Results Time varying statin therapy, modeled using inverse probability treatment and censoring weights, did not significantly attenuate CVD risk in RA overall (adjusted- OR = 0.39 [95%CI=0.15-1.07], p = 0.067). However, statins associated with lower CVD risk in patients with baseline CRP>0.5mg/dL (adjusted-OR=0.09 [95%CI=0.03-0.30], p 50% of follow-up time, CRP did not associate with new plaque formation (adjusted-OR=0.42 [95%CI=0.09-1.94]), in contrast to statin-naive (adjusted-OR=1.89 [95%CI=1.41-2.54]) and statin-treated 50% follow-up time predicted dissipation (adjusted-OR=5.84 [95%CI=1.29-26.55]) and calcification of prevalent noncalcified lesions (adjusted-OR=4.16 [95%CI=1.11-15.54]), as well as new calcified plaque formation in segments without baseline plaque (adjusted-OR=2.84 [95%CI=1.09-7.41]). Conclusion Statin therapy associated with lower long-term cardiovascular risk in RA patients with higher inflammation. Moreover, statin therapy modified the impact of inflammation on new coronary plaque formation and predicted both regression and calcification of prevalent noncalcified lesions.