Framingham Risk Score

Revascularization

Arterial disease

Claudication

Cohort

Cardiology

Rheumatoid arthritis

Coronary artery disease

Framingham Heart Study

Vascular disease

Unstable angina

Myocardial infarction

Internal medicine

Confidence interval

Odds ratio

Medicine

Disease

Vulnerable plaque

Arthritis & Rheumatology

Objective To evaluate whether biologic disease‐modifying antirheumatic drugs ( DMARD s) decrease cardiovascular disease ( CVD ) risk in rheumatoid arthritis ( RA ) and whether biologic DMARD s might have a beneficial effect on coronary plaque formation or progression. Methods In this single‐center observational cohort study, 150 patients underwent computed tomographic angiography for evaluation of coronary atherosclerosis (total, noncalcified, mixed/calcified, and low‐attenuation plaque); 101 had repeat assessments within a mean ± SD of 6.9 ± 0.3 years to evaluate plaque progression. All CVD events were prospectively recorded, including cardiac death, myocardial infarction, unstable angina, revascularization, stroke, claudication, and hospitalization for heart failure. The Framingham‐D'Agostino score was used to assess cardiovascular risk. The segment stenosis score was used to measure plaque burden. Odds ratios ( OR s) with 95% confidence intervals (95% CI s) were calculated. Results After adjustment for the segment stenosis score, the Framingham‐D'Agostino score , and time‐varying Disease Activity Score in 28 joints using the C‐reactive protein level using marginal structural models, current biologic DMARD use was associated with lower long‐term CVD risk ( OR 0.15 [95% CI 0.04–0.60]). Noncalcified and low‐attenuation plaque presence moderated the effect of biologic DMARD s on CVD risk; specifically, biologic DMARD use was associated with lower CVD risk in patients with noncalcified or low‐attenuation plaque at baseline ( OR 0.21 [95% CI 0.04–0.99] and OR 0.08 [95% CI 0.01–0.70], respectively), but not in those without noncalcified or low‐attenuation plaque. Per‐segment plaque progression analyses showed that biologic DMARD exposure was associated with transition of noncalcified to mixed/calcified plaque ( OR 4.00 [95% CI 1.05–15.32]). Biologic DMARD exposure predicted a lower likelihood of new plaque forming in segments without plaque among patients without mixed/calcified plaque in other coronary segments ( OR 0.40 [95% CI 0.17–0.93]), but not among those with calcification. Biologic DMARD treatment also predicted low‐attenuation plaque loss ( P = 0.042). Conclusion Our findings indicate that in RA , biologic DMARD use is associated with reduced CVD risk, protective calcification of noncalcified lesions, and lower likelihood of new plaque formation in patients with early atherosclerosis.

Biologics May Prevent Cardiovascular Events in Rheumatoid Arthritis by Inhibiting Coronary Plaque Formation and Stabilizing High‐Risk Lesions