Epicardial Adipose Tissue, Coronary Plaque Progression, and Major Adverse Cardiovascular Events: A Multicenter Study
- PMID: 41805274
- DOI: 10.1016/j.jcmg.2026.02.003
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: Among 773 patients (mean age 62 ± 9 years; 324 women [43%]), those with CAD had significantly higher EATv than did those without CAD (95 cm3 [Q1-Q3: 72.5-127 cm3] vs 83.5 cm3 [Q1-Q3: 63-112.8 cm3]; 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.
Keywords: atherosclerosis; coronary CT; epicardial adipose tissue; percent atheroma volume; plaque progression.
Copyright © 2026 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.
Conflict of interest statement
Funding Support and Author Disclosures Drs Filtz, Lorenzatti, and Slipczuk have been supported by institutional grants from Amgen and Philips. Dr Bhatt has served on the advisory boards for Angiowave, Antlia Bioscience, Bayer, Boehringer Ingelheim, CellProthera, Cereno Scientific, E-Star Biotech, High Enroll, Janssen, Level Ex, McKinsey, Medscape Cardiology, Merck, NirvaMed, Novo Nordisk, Repair Biotechnologies, Stasys, and Tourmaline Bio; has served on the board of directors for American Heart Association New York City, Angiowave (stock options), Bristol Myers Squibb (stock), DRS.LINQ (stock options), and High Enroll (stock); has served as a consultant for Alnylam, Altimmune, Broadview Ventures, Corcept Therapeutics, Corsera, GlaxoSmithKline, Hims, SERB, SFJ, Summa Therapeutics, and Worldwide Clinical Trials; has served on data monitoring committees for Acesion Pharma, Assistance Publique–Hôpitaux de Paris, Baim Institute for Clinical Research, Boston Scientific (Chair, PEITHO trial), Cleveland Clinic, Contego Medical (Chair, PERFORMANCE 2), Duke Clinical Research Institute, Mayo Clinic, Mount Sinai School of Medicine (for the ABILITY-DM trial, funded by Concept Medical; and for ALLAY-HF, funded by Alleviant Medical), Novartis, Population Health Research Institute; Rutgers University (for the National Institutes of Health–funded MINT Trial); has received honoraria from the American College of Cardiology (Senior Associate Editor, Clinical Trials and News, ACC.org; Chair, ACC Accreditation Oversight Committee), Arnold and Porter law firm (work related to Sanofi/Bristol Myers Squibb clopidogrel litigation), Baim Institute for Clinical Research (AEGIS-II executive committee funded by CSL Behring), Belvoir Publications (Editor-in-Chief, Harvard Heart Letter), Canadian Medical and Surgical Knowledge Translation Research Group (clinical trial steering committees), CSL Behring (AHA lecture), Duke Clinical Research Institute, Engage Health Media, HMP Global (Editor-in-Chief, Journal of Invasive Cardiology), Medtelligence/ReachMD (CME steering committees), MJH Life Sciences, Oakstone CME (Course Director, Comprehensive Review of Interventional Cardiology), Philips (Becker’s Webinar on AI), Population Health Research Institute, WebMD (CME steering committees), Wiley (steering committee); has received other support from Clinical Cardiology (Deputy Editor) and Progress in Cardiovascular Diseases (Deputy Editor); owns a patent on sotagliflozin (named on a patent for sotagliflozin assigned to Brigham and Women’s Hospital, which assigned it to Lexicon; neither he nor Brigham and Women’s Hospital receive any income from this patent); has received research funding from Abbott, Acesion Pharma, Afimmune, Alnylam, Amarin, Amgen, AstraZeneca, AtriCure, Bayer, Boehringer Ingelheim, Boston Scientific, CellProthera, Cereno Scientific, Chiesi, Cleerly, CSL Behring, Faraday Pharmaceuticals, Fractyl, Idorsia, Janssen, Javelin, Lexicon, Lilly, Medtronic, Merck, MiRUS, Moderna, Novartis, Novo Nordisk, Pfizer, PhaseBio, Regeneron, Reid Hoffman Foundation, Roche, Sanofi, Stasys, and 89bio; has received royalties from Elsevier (Editor, Braunwald’s Heart Disease); and has been a site coinvestigator for Cleerly. Dr Chang holds equity in Ontact Health (ultrasound AI company). Drs Berman and Dey hold equity in Autoplaque Health. Drs Dey and Slomka hold equity in APQ Health; have received software royalties from Cedars-Sinai Medical Center; and hold a patent (US8885905B2 and WO2011069120A1, titled “Method and System for Plaque Characterization”). All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.
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