Serial Changes in Epicardial Adipose Tissue Attenuation Identify Residual Atherosclerotic Risk Independent of LDL Lowering

IF 19 1区 医学 Q1 CARDIAC & CARDIOVASCULAR SYSTEMS
JACC. Cardiovascular imaging Pub Date : 2026-09-01 Epub Date: 2026-07-08 DOI:10.1016/j.jcmg.2026.05.014
Shaun Khanna MBBS, MMed, Edwin Xu MD, Cheng Hwee Soh BSc (Biomed), PhD, Sheran Vasanthakumar MBBS, Rhea Machado MD, Andrew Lin MBBS, PhD, Clare Arnott MBBS, PhD, Damini Dey PhD, Stephen J. Nicholls MBBS, PhD, Thomas H. Marwick MBBS, MPH, PhD, Nitesh Nerlekar MBBS, MPH, PhD
{"title":"Serial Changes in Epicardial Adipose Tissue Attenuation Identify Residual Atherosclerotic Risk Independent of LDL Lowering","authors":"Shaun Khanna MBBS, MMed,&nbsp;Edwin Xu MD,&nbsp;Cheng Hwee Soh BSc (Biomed), PhD,&nbsp;Sheran Vasanthakumar MBBS,&nbsp;Rhea Machado MD,&nbsp;Andrew Lin MBBS, PhD,&nbsp;Clare Arnott MBBS, PhD,&nbsp;Damini Dey PhD,&nbsp;Stephen J. Nicholls MBBS, PhD,&nbsp;Thomas H. Marwick MBBS, MPH, PhD,&nbsp;Nitesh Nerlekar MBBS, MPH, PhD","doi":"10.1016/j.jcmg.2026.05.014","DOIUrl":null,"url":null,"abstract":"<div><h3>Background</h3><div>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.</div></div><div><h3>Methods</h3><div>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: &lt;1.4 mmol/L [&lt;55 mg/dL], 1.4-1.8 mmol/L [55-70 mg/dL], and &gt;1.8 mmol/L [&gt;70 mg/dL]) was used, and incremental discrimination with ΔEAT attenuation was assessed using nested model comparison and likelihood ratio testing.</div></div><div><h3>Results</h3><div>Higher ΔEAT attenuation, but not EAT volume change, remained independently associated with progression of noncalcified plaque (NCP) and adverse plaque remodeling. Per 1-SD increase in ΔEAT attenuation, NCP volume was higher by 4.21 mm<sup>3</sup> (95% CI: 0.67-7.74; <em>P</em> = 0.020), fibrous plaque volume by 3.55 mm<sup>3</sup> (95% CI: 0.67-6.43; <em>P</em> = 0.016), and NCP percent atheroma volume by 1.08% (95% CI: 0.47-1.69; <em>P</em> &lt; 0.001). In participants with high baseline EAT volume (tertile 3 ≥67.1 cm<sup>3</sup>), 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 <em>P</em> = 0.012). In exploratory analyses, ΔEAT attenuation was also associated with increasing PCAT attenuation (β = 2.44 HU per SD; <em>P</em> &lt; 0.001), suggesting that changes in PCAT may partly explain the observed association with plaque progression.</div></div><div><h3>Conclusions</h3><div>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.</div></div>","PeriodicalId":14767,"journal":{"name":"JACC. Cardiovascular imaging","volume":"19 9","pages":"Pages 1077-1089"},"PeriodicalIF":19.0000,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"JACC. Cardiovascular imaging","FirstCategoryId":"3","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S1936878X26002767","RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2026/7/8 0:00:00","PubModel":"Epub","JCR":"Q1","JCRName":"CARDIAC & CARDIOVASCULAR SYSTEMS","Score":null,"Total":0}
引用次数: 0

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

Higher ΔEAT attenuation, but not EAT volume change, remained independently associated with progression of noncalcified plaque (NCP) and adverse plaque remodeling. Per 1-SD increase in ΔEAT attenuation, NCP volume was higher by 4.21 mm3 (95% CI: 0.67-7.74; P = 0.020), fibrous plaque volume by 3.55 mm3 (95% CI: 0.67-6.43; P = 0.016), and NCP percent atheroma volume by 1.08% (95% CI: 0.47-1.69; P < 0.001). In participants with high baseline EAT volume (tertile 3 ≥67.1 cm3), 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.
心外膜脂肪组织衰减的一系列变化确定了独立于LDL降低的残余动脉粥样硬化风险:一项对冠心病试验的事后分析。
背景:尽管有效降低了低密度脂蛋白胆固醇(LDL-C),一些患者的冠状动脉斑块仍持续进展。心外膜脂肪组织(EAT)是一个代谢活跃的内脏脂肪库,可能通过炎症信号影响冠状动脉粥样硬化。作者假设EAT的纵向变化会影响斑块的进展。方法:在冠心病(冠状动脉钙评分:用于指导遗传性冠状动脉疾病的治疗)试验中,313名无症状、未使用他汀类药物的受试者(年龄58.8±6.8岁,44%为男性)进行了基线和随访冠状动脉计算机断层血管造影的定量分析和EAT。通过协方差模型分析,调整基线斑块负担、治疗分配和心脏代谢危险因素的变化,评估EAT体积和衰减的纵向变化(ΔEAT)与冠状动脉斑块结果之间的关系。探索性分析评估了ΔEAT衰减和Δpericoronary脂肪组织(PCAT)衰减之间的关系。采用基于LDL-C的参考模型(参考值1.8 mmol/L [>70 mg/dL]),通过嵌套模型比较和似然比检验评估ΔEAT衰减的增量判别。结果较高的ΔEAT衰减,而不是EAT体积变化,仍然与非钙化斑块(NCP)的进展和不良斑块重构独立相关。ΔEAT衰减每增加1 sd, NCP体积增加4.21 mm3 (95% CI: 0.67-7.74; P = 0.020),纤维斑块体积增加3.55 mm3 (95% CI: 0.67-6.43; P = 0.016), NCP百分比动脉粥样硬化体积增加1.08% (95% CI: 0.47-1.69; P < 0.001)。在基线EAT容量高的参与者(三分位数≥67.1 cm3)中,在基于ldl - c的协方差模型分析中加入ΔEAT衰减后,模型拟合有统计学意义的改善(ΔAkaike信息准则-4.8;似然比检验P = 0.012)。在探索性分析中,ΔEAT衰减也与PCAT衰减增加相关(β = 2.44 HU / SD; P < 0.001),这表明PCAT的变化可能部分解释了观察到的与斑块进展的关联。结论:与LDL-C降低无关的EAT衰减与冠状动脉斑块重构的一系列变化,支持了EAT炎症在残余斑块进展中的潜在机制作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 求助全文
来源期刊
JACC. Cardiovascular imaging
JACC. Cardiovascular imaging CARDIAC & CARDIOVASCULAR SYSTEMS-RADIOLOGY, NUCLEAR MEDICINE & MEDICAL IMAGING
CiteScore
24.90
自引率
5.70%
发文量
330
审稿时长
4-8 weeks
期刊介绍: JACC: Cardiovascular Imaging, part of the prestigious Journal of the American College of Cardiology (JACC) family, offers readers a comprehensive perspective on all aspects of cardiovascular imaging. This specialist journal covers original clinical research on both non-invasive and invasive imaging techniques, including echocardiography, CT, CMR, nuclear, optical imaging, and cine-angiography. JACC. Cardiovascular imaging highlights advances in basic science and molecular imaging that are expected to significantly impact clinical practice in the next decade. This influence encompasses improvements in diagnostic performance, enhanced understanding of the pathogenetic basis of diseases, and advancements in therapy. In addition to cutting-edge research,the content of JACC: Cardiovascular Imaging emphasizes practical aspects for the practicing cardiologist, including advocacy and practice management.The journal also features state-of-the-art reviews, ensuring a well-rounded and insightful resource for professionals in the field of cardiovascular imaging.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:604180095
Book学术官方微信
小红书