Key result
Epicardial fat links to ~63% higher odds of obstructive disease and vulnerable plaque in RA.
Why the study?
To evaluate epicardial adipose tissue volume and its link to coronary atherosclerosis and plaque morphology in patients with rheumatoid arthritis compared to age- and sex-matched controls.
Is epicardial adipose tissue volume associated with subclinical coronary atherosclerosis and vulnerable plaque morphology in patients with rheumatoid arthritis compared to controls?
Case-Control (n=278)
Is epicardial adipose tissue volume associated with subclinical coronary atherosclerosis and vulnerable plaque morphology in patients with rheumatoid arthritis compared to controls?
Effect estimate: OR 1.63 (95% CI 1.04-2.61)
p-value: p=≤0.048
Epicardial adipose tissue volume is associated with greater coronary plaque burden and vulnerable plaque features specifically in patients with rheumatoid arthritis, suggesting a pathogenic role in early-stage atherosclerosis in this population.
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/m 2 ). 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.
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Karpouzas et al. (2021) conducted a case-control in Rheumatoid arthritis (n=278). Epicardial adipose tissue volume (EATV) vs. Non-RA controls was evaluated on Presence of multivessel or obstructive disease (OR 1.63, 95% CI 1.04-2.61, p=≤0.048). Epicardial adipose tissue volume was associated with the presence of multivessel or obstructive disease (OR 1.63; 95% CI 1.04-2.61) and vulnerable plaque in RA patients, but not in controls.
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