Epicardial Adipose Tissue Volume As a Marker of Subclinical Coronary Atherosclerosis in Rheumatoid Arthritis.

Objective: To assess epicardial adipose tissue volume (EATV) and its link to coronary atherosclerosis and plaque morphology in patients with rheumatoid arthritis (RA) and in age‐ and sex‐matched controls. Methods: Computed tomography angiography was used to evaluate EATV and coronary plaque in 139 RA patients and 139 non‐RA controls. All models assessing the effect of EATV on plaque were adjusted for age, sex, hypertension, diabetes, dyslipidemia, smoking status, family history of coronary artery disease, and obesity (body mass index of ≥30 kg/m2). Odds ratios (ORs) and 95% confidence intervals (95% CIs) were calculated. Results: Mean ± SD log‐transformed EATV was similar in patients with RA (4.69 ± 0.36) and controls (4.70 ± 0.42). EATV was higher in RA patients with atherosclerosis compared to those without atherosclerosis (P = 0.046). In stratified analyses, EATV was associated with the number of segments with plaque in RA patients (rate ratio 1.20 [95% CI 1.01–1.41] per 1‐SD increment of log‐unit increase in EATV) but not in controls (P for interaction = 0.089). Likewise, EATV (per 1‐SD log‐unit increase) was related to the presence of multivessel or obstructive disease (OR 1.63 [95% CI 1.04–2.61]), noncalcified plaque (OR 1.78 [95% CI 1.17–2.70]), and vulnerable plaque (OR 1.77 [95% CI 1.03–3.04]) in RA patients but not in controls (P for interaction ≤ 0.048 for each). Among RA patients, EATV was associated with the number of segments with plaque in those with RA for <10 years who did not develop any cardiovascular risk factors and who were not obese (P for interaction ≤ 0.017). Conclusion: Despite similar EATVs in RA patients and controls, EATVs were associated with greater plaque burden and presence of plaques with a noncalcified component and vulnerability features only in RA patients. EAT may be more pathogenic in RA and play a role in early‐stage atherosclerosis. Its value as a biomarker of subclinical atherosclerosis and cardiovascular risk in RA warrants further studies. [ABSTRACT FROM AUTHOR]