{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,1]],"date-time":"2026-10-01T01:51:25Z","timestamp":1790819485752,"version":"4.1.0"},"reference-count":49,"publisher":"Wiley","issue":"9","license":[{"start":{"date-parts":[[2020,8,7]],"date-time":"2020-08-07T00:00:00Z","timestamp":1596758400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/100004319","name":"Pfizer","doi-asserted-by":"publisher","award":["WI215017"],"award-info":[{"award-number":["WI215017"]}],"id":[{"id":"10.13039\/100004319","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["acrjournals.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Arthritis & Rheumatology"],"published-print":{"date-parts":[[2020,9]]},"abstract":"Objective<\/jats:title>To evaluate whether biologic disease\u2010modifying antirheumatic drugs (DMARD<\/jats:styled-content>s) decrease cardiovascular disease (CVD<\/jats:styled-content>) risk in rheumatoid arthritis (RA<\/jats:styled-content>) and whether biologic DMARD<\/jats:styled-content>s might have a beneficial effect on coronary plaque formation or progression.<\/jats:p><\/jats:sec>Methods<\/jats:title>In this single\u2010center observational cohort study, 150 patients underwent computed tomographic angiography for evaluation of coronary atherosclerosis (total, noncalcified, mixed\/calcified, and low\u2010attenuation plaque); 101 had repeat assessments within a mean \u00b1 SD<\/jats:styled-content> of 6.9 \u00b1 0.3 years to evaluate plaque progression. All CVD<\/jats:styled-content> events were prospectively recorded, including cardiac death, myocardial infarction, unstable angina, revascularization, stroke, claudication, and hospitalization for heart failure. The Framingham\u2010D'Agostino score was used to assess cardiovascular risk. The segment stenosis score was used to measure plaque burden. Odds ratios (OR<\/jats:styled-content>s) with 95% confidence intervals (95% CI<\/jats:styled-content>s) were calculated.<\/jats:p><\/jats:sec>Results<\/jats:title>After adjustment for the segment stenosis score, the Framingham\u2010D'Agostino score<\/jats:styled-content>, and time\u2010varying Disease Activity Score in 28 joints using the C\u2010reactive protein level using marginal structural models, current biologic DMARD<\/jats:styled-content> use was associated with lower long\u2010term CVD<\/jats:styled-content> risk (OR<\/jats:styled-content> 0.15 [95% CI<\/jats:styled-content> 0.04\u20130.60]). Noncalcified and low\u2010attenuation plaque presence moderated the effect of biologic DMARD<\/jats:styled-content>s on CVD<\/jats:styled-content> risk; specifically, biologic DMARD<\/jats:styled-content> use was associated with lower CVD<\/jats:styled-content> risk in patients with noncalcified or low\u2010attenuation plaque at baseline (OR<\/jats:styled-content> 0.21 [95% CI<\/jats:styled-content> 0.04\u20130.99] and OR<\/jats:styled-content> 0.08 [95% CI<\/jats:styled-content> 0.01\u20130.70], respectively), but not in those without noncalcified or low\u2010attenuation plaque. Per\u2010segment plaque progression analyses showed that biologic DMARD<\/jats:styled-content> exposure was associated with transition of noncalcified to mixed\/calcified plaque (OR<\/jats:styled-content> 4.00 [95% CI<\/jats:styled-content> 1.05\u201315.32]). Biologic DMARD<\/jats:styled-content> exposure predicted a lower likelihood of new plaque forming in segments without plaque among patients without mixed\/calcified plaque in other coronary segments (OR<\/jats:styled-content> 0.40 [95% CI<\/jats:styled-content> 0.17\u20130.93]), but not among those with calcification. Biologic DMARD<\/jats:styled-content> treatment also predicted low\u2010attenuation plaque loss (P<\/jats:italic> = 0.042).<\/jats:p><\/jats:sec>Conclusion<\/jats:title>Our findings indicate that in RA<\/jats:styled-content>, biologic DMARD<\/jats:styled-content> use is associated with reduced CVD<\/jats:styled-content> risk, protective calcification of noncalcified lesions, and lower likelihood of new plaque formation in patients with early atherosclerosis.<\/jats:p><\/jats:sec>","DOI":"10.1002\/art.41293","type":"journal-article","created":{"date-parts":[[2020,4,22]],"date-time":"2020-04-22T02:51:36Z","timestamp":1587523896000},"page":"1467-1475","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":75,"title":["Biologics May Prevent Cardiovascular Events in Rheumatoid Arthritis by Inhibiting Coronary Plaque Formation and Stabilizing High\u2010Risk 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