4.7 Article

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

Journal

RHEUMATOLOGY
Volume 61, Issue 5, Pages 1857-1866

Publisher

OXFORD UNIV PRESS
DOI: 10.1093/rheumatology/keab642

Keywords

rheumatoid arthritis; cardiovascular disease; atherosclerosis progression; computed tomography; statins

Categories

Funding

  1. American Heart Association [AHA-09CRP2251004]
  2. Pfizer [WI215017]

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In this study, statin therapy was associated with lower long-term cardiovascular risk in rheumatoid arthritis patients, especially those with higher inflammation levels. Additionally, statin therapy modified the impact of inflammation on new coronary plaque formation and predicted regression and calcification of prevalent noncalcified lesions.
Objectives To evaluate whether statins lower cardiovascular disease (CVD) risk in 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 CT 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 odds ratio (OR) = 0.39 (95% CI: 0.15, 1.07), P =0.067]. However, statins associated with lower CVD risk in patients with baseline CRP > 0.5 mg/dl [adjusted OR = 0.09 (95%CI: 0.03, 0.30), P <0.001] but not in those with CRP < 0.5 mg/dl (P-interaction = 0.023), after controlling for Framingham-CVD score and time-varying bDMARD use. In patients treated with statin >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% time [adjusted-OR = 1.41 (95% CI: 1.03, 1.95), P-interaction = 0.029]. Statin therapy >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.

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