Epicardial Adipose Tissue, Coronary Plaque Progression, and Major Adverse Cardiovascular Events A Multicenter Study

Abstract

BACKGROUND Epicardial adipose tissue (EAT) is associated with coronary artery disease (CAD), but its relationship with plaque progression (PP)-a predictor of major adverse cardiovascular events (MACE)-remains unclear. OBJECTIVES This study examines the interplay between EAT, PP, and subsequent MACE. METHODS From the PARADIGM (Progression of Atherosclerotic Plaque Determined by Computed Tomographic Angiography Imaging) registry, serial coronary computed tomography angiography assessed plaque volume (PV), percent atheroma volume (PAV), and PP. Rapid plaque progression (RPP) was defined as annual PAV increase >= 1%. EAT volume (EATv) and advanced plaque characteristics were measured. CAD was defined as any plaque. Multivariable models assessed associations between EATv, plaque, PP, and RPP. The prognostic value of PP and RPP for MACE was evaluated. RESULTS <bold> </bold>Among 773 patients (mean age 62 +/- 9 years; 324 women [43%]), those with CAD had significantly higher EATv than did those without CAD (95 cm(3) [Q1-Q3: 72.5-127 cm(3)] vs 83.5 cm(3) [Q1-Q3: 63-112.8 cm(3)]; P < 0.001). Progression of PV, PAV, and calcified and noncalcified plaque components was significantly greater in the highest (third) EATv tertile (T3) than in T1 (PV: P = 0.001; PAV: P = 0.028; calcified component: P = 0.025; noncalcified component: P = 0.022). The prevalences of PP (T1: 78.9% vs T2: 83.9% vs T3: 88.5%; P = 0.013) and RPP (T1: 25.2% vs T2: 32.3% vs T3: 36.4%; P = 0.021) also increased across EATv tertiles. In multivariable analyses, high EATv was independently associated with plaque, PP, and RPP across 2 different models adjusted for age, sex, body mass index, diabetes, dyslipidemia, hypertension, hypertriglyceridemia, smoking, and statin therapy. Patients with PP and RPP had lower 10-year MACE-free survival (log-rank; P = 0.006 and log-rank; P < 0.001, respectively). CONCLUSIONS High EATv is independently associated with CAD presence and progression, underscoring its potential as a marker for risk stratification and a therapeutic target for earlier or more intensive treatment. (c) 2026 by the American College of Cardiology Foundation.