Relationship between epicardial adipose tissue and coronary atherosclerosis by CCTA in young adults (18-45)
- PMID: 39157644
- PMCID: PMC11327837
- DOI: 10.1016/j.ajpc.2024.100711
Relationship between epicardial adipose tissue and coronary atherosclerosis by CCTA in young adults (18-45)
Abstract
Objective: Epicardial adipose tissue (EAT) is implicated in the pathogenesis and progression of coronary artery disease (CAD). Limited data exists on the interplay between EAT and atherosclerosis in young individuals. Our study aims to explore the relationship between EAT and CAD in a young cohort.
Methods: All young (18-45 years) patients without prior CAD, referred for coronary computed tomography angiography (CCTA) from 2016 to 2022 were included. EAT volume and coronary artery calcium (CAC) were calculated from dedicated non-contrast scans. Coronary plaque presence, extent, and volume were quantified from CCTA. Multivariable logistic regression models for the presence of CAD, defined as any coronary atherosclerosis, were performed.
Results: Overall, 712 patients (39±4.8 years, 54 % female) with 45 % Hispanic, and 21 % non-Hispanic Black were included. Patients with CAD had higher EAT volume than those without (80.80 mL ± 36.00 vs 55.16 mL ± 27.92; P < 0.001). In those with CAC=0, higher EAT was associated with the presence of CAD compared to lower EAT volume (P < 0.001). An EAT volume >76 mL was associated with higher CAC (P < 0.001), segment involvement score (P < 0.001), and quantitative total, non-calcified, and low-attenuation plaque volumes (P < 0.002). At multivariable analysis, EAT volume (per 10 mL, OR: 1.21; 95 %CI: 1.12-1.30; P < 0.0001) was independently associated with the presence of CAD.
Conclusion: In a diverse cohort of young adults without history of CAD and undergoing a clinically indicated CCTA, EAT volume was independently associated with the presence of CAD. Our findings highlight EAT potential as a novel marker for CAD risk-assessment and a potential therapeutic target in young patients.
Keywords: CCTA; Coronary plaque; Epicardial adipose tissue; Young adults.
© 2024 The Author(s).
Conflict of interest statement
Annalisa Filtz, Daniel Lorenzatti, and Leandro Slipczuk are supported by institutional grants from Amgen and Philips. Damini Dey received grant support from the 10.13039/100000050National Heart, Lung, and Blood Institute, software royalties from Cedars-Sinai Medical Center, and hold a patent (US8885905B2in USA and WO patent WO2011069120A1, Method and System for Plaque Characterization). Dr Lavie is a Consultant and Promotional Speaker for Amgen, a consultant to Novartis, and on a DSMB for NovoNordisk. Michael Shapiro reports grants (to institution) from PCORI, DCRI, Amgen, Boehringer Ingelheim, 89 Bio, Esperion, Genentech, Novartis, Ionis, Merck, New Amsterdam; Scientific Advisory Boards with Amgen, Agepha, Ionis, Novartis, Precision BioScience, Novo Nordisk, New Amsterdam; and as a Consultant with Ionis, Novartis, Regeneron, Aidoc, Shanghai Pharma Biotherapeutics, Kaneka. Others have nothing to disclose.
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