Serial Changes in Epicardial Adipose Tissue Attenuation Identify Residual Atherosclerotic Risk Independent of LDL Lowering
8 affiliations
- 1The George Institute for Global Health, UNSW Sydney, Sydney, New South Wales, Australia; Baker Heart and Diabetes Institute, Melbourne, Victoria, Australia
- 2Baker Heart and Diabetes Institute, Melbourne, Victoria, Australia; Victorian Heart Institute, Monash University, Clayton, Victoria, Australia
- 3Baker Heart and Diabetes Institute, Melbourne, Victoria, Australia
- 4The George Institute for Global Health, UNSW Sydney, Sydney, New South Wales, Australia; Department of Cardiology, Royal Prince Alfred Hospital, Sydney, New South Wales, Australia; Department of Cardiology, St Vincent's Hospital, Sydney, New South Wales, Australia
- 5Biomedical Research Institute, Cedars Sinai Medical Center, Los Angeles, California, USA
- 6Victorian Heart Institute, Monash University, Clayton, Victoria, Australia
- 7Baker Heart and Diabetes Institute, Melbourne, Victoria, Australia; Menzies Institute for Medical Research, Hobart, Tasmania, Australia
- 8Baker Heart and Diabetes Institute, Melbourne, Victoria, Australia; Victorian Heart Institute, Monash University, Clayton, Victoria, Australia. Electronic address: [email protected]
Abstract
BACKGROUND: Coronary plaque progression persists in some patients despite effective low-density lipoprotein cholesterol (LDL-C) lowering. Epicardial adipose tissue (EAT) is a metabolically active visceral fat depot that may influence coronary atherosclerosis through inflammatory signaling. The authors hypothesized that longitudinal changes in EAT would influence plaque progression. METHODS: Plaque and EAT quantification with paired baseline and follow-up coronary computed tomography angiography was attainable in 313 asymptomatic, statin-naive participants (aged 58.8 ± 6.8 years, 44% female) in the CAUGHT-CAD (Coronary Artery calcium score: Use to Guide management of Hereditary Coronary Artery Disease) trial. Associations between longitudinal changes in EAT volume and attenuation (ΔEAT) and coronary plaque outcomes were evaluated using analysis of covariance models, with adjustment for baseline plaque burden, treatment allocation, and changes in cardiometabolic risk factors. Exploratory analyses evaluated the relationship between ΔEAT attenuation and Δ pericoronary adipose tissue (PCAT) attenuation. An LDL-C-based reference model of achieved LDL-C (Reference: <1.4 mmol/L [<55 mg/dL], 1.4-1.8 mmol/L [55-70 mg/dL], and >1.8 mmol/L [>70 mg/dL]) was used, and incremental discrimination with ΔEAT attenuation was assessed using nested model comparison and likelihood ratio testing. RESULTS: ), the addition of ΔEAT attenuation to LDL-C-based analysis of covariance models resulted in a statistically significant improvement in model fit (Δ Akaike information criterion -4.8; likelihood ratio test P = 0.012). In exploratory analyses, ΔEAT attenuation was also associated with increasing PCAT attenuation (β = 2.44 HU per SD; P < 0.001), suggesting that changes in PCAT may partly explain the observed association with plaque progression. CONCLUSIONS: The association of serial changes in EAT attenuation with coronary plaque remodeling, independent of LDL-C lowering, supports a potential mechanistic role for EAT inflammation in residual plaque progression.
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BibTeX
@article{khanna2026serial,
title = {{Serial Changes in Epicardial Adipose Tissue Attenuation Identify Residual Atherosclerotic Risk Independent of LDL Lowering}},
author = {Shaun Khanna and Edwin Xu and Cheng Hwee Soh and Sheran A. Vasanthakumar and Rhea Machado and Andrew Lin and Clare Gabrielle Arnott and Damini Dey and Stephen J Nicholls and Thomas Hugh Marwick and Nitesh Nerlekar},
journal = {JACC. Cardiovascular imaging},
year = {2026},
month = jul,
doi = {10.1016/j.jcmg.2026.05.014},
url = {https://doi.org/10.1016/j.jcmg.2026.05.014},
note = {CC BY},
}
RIS
TY - JOUR
TI - Serial Changes in Epicardial Adipose Tissue Attenuation Identify Residual Atherosclerotic Risk Independent of LDL Lowering
AU - Shaun Khanna
AU - Edwin Xu
AU - Cheng Hwee Soh
AU - Sheran A. Vasanthakumar
AU - Rhea Machado
AU - Andrew Lin
AU - Clare Gabrielle Arnott
AU - Damini Dey
AU - Stephen J Nicholls
AU - Thomas Hugh Marwick
AU - Nitesh Nerlekar
PY - 2026
DA - 2026/07/08
JO - JACC. Cardiovascular imaging
DO - 10.1016/j.jcmg.2026.05.014
UR - https://doi.org/10.1016/j.jcmg.2026.05.014
AB - BACKGROUND: Coronary plaque progression persists in some patients despite effective low-density lipoprotein cholesterol (LDL-C) lowering. Epicardial adipose tissue (EAT) is a metabolically active visceral fat depot that may influence coronary atherosclerosis through inflammatory signaling. The authors hypothesized that longitudinal changes in EAT would influence plaque progression. METHODS: Plaque and EAT quantification with paired baseline and follow-up coronary computed tomography angiography was attainable in 313 asymptomatic, statin-naive participants (aged 58.8 ± 6.8 years, 44% female) in the CAUGHT-CAD (Coronary Artery calcium score: Use to Guide management of Hereditary Coronary Artery Disease) trial. Associations between longitudinal changes in EAT volume and attenuation (ΔEAT) and coronary plaque outcomes were evaluated using analysis of covariance models, with adjustment for baseline plaque burden, treatment allocation, and changes in cardiometabolic risk factors. Exploratory analyses evaluated the relationship between ΔEAT attenuation and Δ pericoronary adipose tissue (PCAT) attenuation. An LDL-C-based reference model of achieved LDL-C (Reference: <1.4 mmol/L [<55 mg/dL], 1.4-1.8 mmol/L [55-70 mg/dL], and >1.8 mmol/L [>70 mg/dL]) was used, and incremental discrimination with ΔEAT attenuation was assessed using nested model comparison and likelihood ratio testing. RESULTS: ), the addition of ΔEAT attenuation to LDL-C-based analysis of covariance models resulted in a statistically significant improvement in model fit (Δ Akaike information criterion -4.8; likelihood ratio test P = 0.012). In exploratory analyses, ΔEAT attenuation was also associated with increasing PCAT attenuation (β = 2.44 HU per SD; P < 0.001), suggesting that changes in PCAT may partly explain the observed association with plaque progression. CONCLUSIONS: The association of serial changes in EAT attenuation with coronary plaque remodeling, independent of LDL-C lowering, supports a potential mechanistic role for EAT inflammation in residual plaque progression.
SN - 1876-7591
SN - 1936-878X
ER -