Introduction & Objectives
Patients with rheumatoid arthritis (RA) experience a higher rate of cardiovascular disease (CVD) events than controls. Chronic inflammation contributes to this risk. Indeed, RA patients with greater cumulative inflammation experience higher CVD event rates, and a reduction in RA inflammation associates with lower risk. Karpouzas et al. previously reported that RA disease activity is associated with greater coronary plaque burden and plaque vulnerability. Cumulative inflammation also predicts coronary plaque progression in RA patients. And subclinical coronary plaque burden is associated with mid-term CVD events in RA patients above and beyond what traditional risk factors or the cardiovascular Framingham Risk Score (FRS) would suggest. This suggested to researchers that sustained control of inflammation with the use of biologics may lower the CVD risk in patients with RA by inhibiting coronary plaque progression.
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Explore This IssueOctober 2020
Thus, Karpouzas et al. set out to evaluate whether biologics decrease the CVD risk in RA patients and whether biologics have a beneficial effect on coronary plaque formation or progression.
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 FRS was used to assess cardiovascular risk. The segment stenosis score was used to measure plaque burden. Odds ratios (ORs) with 95% confidence intervals (95% CIs) were calculated.
After adjustment for the segment stenosis score, the FRS, and time-varying Disease Activity Score in 28 joints using the C-reactive protein level using marginal structural models, biologic 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 biologics on CVD risk. Specifically, biologic 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 exposure to biologics was associated with transition of noncalcified to mixed/calcified plaque (OR 4.00 [95% CI 1.05–15.32]). Exposure to biologics 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 treatment also predicted low-attenuation plaque loss (P=0.042).