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01 · ABSTRACT

Abstract

Objective. Epicardial adipose tissue volume (EATv) associated with coronary atherosclerosis burden, noncalcified plaque and vulnerable plaque characteristics in patients with rheumatoid arthritis. We here evaluate the influence of EATv on plaque progression and factors that modify this relationship.

Methods. We assessed 100 patients without cardiovascular disease and a screening computed tomography angiography for EATv and coronary atherosclerosis who underwent surveillance evaluation for atherosclerosis progression 6.9±0.3 years later. The main outcome was new plaque formation. Robust multivariable logistic regression evaluated the effect of high versus low EATv (based on median) on likelihood of new plaque formation and the moderating effects of prespecified predictors.

Results. High EATv (>107 cm3) predicted new plaque formation, odds ratio (OR) 2.77 (95% confidence interval [95% CI] 1.43-5.37), however, significance was lost in the multivariable model. High EATv associated with new higher-risk noncalcified and mixed plaque after adjusting for cardiovascular risk score, obesity, segment location, time-averaged C-reactive protein, duration of biologic and statin use and cumulative prednisone dose, adjusted OR 2.57, 95% CI 1.02-6.48. High EATv predicted new plaque in patients with disease duration <10 versus >10 years (adjusted OR 5.75, 95% CI 1.77-18.67), with 1 risk factors versus >1 (adjusted OR 3.40, 95% CI 1.46-7.90), those without baseline calcification (adjusted OR 2.65, 95% CI 1.11-6.31) and those with statin treatment for <1 versus >1 year (adjusted OR 3.33, 95% CI 1.13-9.77).

Conclusion. Baseline EATv predicted new higher-risk noncalcified and mixed coronary plaque in rheumatoid arthritis. Notably, EATv conditionally promoted new plaque in patients with earlier disease, low risk factor burden, with no or early atherosclerosis and limited statin exposure. A larger prospective evaluation of EATv as a biomarker of coronary atherosclerosis in rheumatoid arthritis may therefore be warranted.

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02 · PUBLICATION RECORD

Article details

JournalMedical Research Archives
IssueVol 13 No 2 (2025): Vol.13 issue 2 February 2025
SectionResearch Articles
Published26 February 2025
DOI10.18103/mra.v13i2.6246
ISSN2375-1924
03 · RIGHTS & REUSE

Rights & reuse

This article is published under a Creative Commons Attribution License (CC BY 3.0) and may be shared or distributed by anyone as long as attribution is given to the journal.

Authors & affiliations

GK

George A Karpouzas

Division of Rheumatology, The Lundquist Institute for Biomedical Innovation at Harbor-UCLA Medical Center, 1124 West Carson Street, Torrance, CA 90502, USA.

PR

Panteha Rezaeian

Division of Cardiology, The Lundquist Institute for Biomedical Innovation at Harbor-UCLA Medical Center, 1124 West Carson Street, Torrance, CA 90502, USA.

EH

Elizabeth Hernandez

Division of Rheumatology, The Lundquist Institute for Biomedical Innovation at Harbor-UCLA Medical Center, 1124 West Carson Street, Torrance, CA 90502, USA.

MB

Matthew J Budoff

Division of Cardiology, The Lundquist Institute for Biomedical Innovation at Harbor-UCLA Medical Center, 1124 West Carson Street, Torrance, CA 90502, USA.

SO

Sarah R Ormseth

Division of Rheumatology, The Lundquist Institute for Biomedical Innovation at Harbor-UCLA Medical Center, 1124 West Carson Street, Torrance, CA 90502, USA.

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