Submitted
Abstract Submission
Longitudinal Associations of Obesity, Insulin Resistance, and Inflammation with Epicardial Fat Tissue in Older Adults: Insights from the Healthy Aging Longitudinal Study in Taiwan
Poster Presentation
Scientific Research Abstract
Obesity
Author's Information
9
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Shao-Yuan CHUANG chuangsy@nhri.edu.tw National Health Research Institutes Institute of Population Health Sciences Miaoli Taiwan *
Ming-Ting Wu wu.mingting@gmail.com Kaohsiung Veterans General Hospital Department of Radiology Kaohsiung Taiwan -
Wen-Ling Liu winnie_829@nhri.org.tw National Health Research Institutes Institute of Population Health Sciences Miaoli Taiwan -
Chia-Hung Lai chahun930@nhri.edu.tw National Health Research Institutes Institute of Population Health Sciences Miaoli Taiwan -
Chao Agnes Hsiung hsiung@nhri.edu.tw National Health Research Institutes Institute of Population Health Sciences Miaoli Taiwan -
Shu-Chun CHUANG 011002@nhri.edu.tw National Health Research Institutes Institute of Population Health Sciences Miaoli Taiwan -
I-Chien Wu icwu@nhri.edu.tw National Health Research Institutes Institute of Population Health Sciences Miaoli Taiwan -
Chih-Cheng Hsu cch@nhri.org.tw National Health Research Institutes Institute of Population Health Sciences Miaoli Taiwan -
Wayne Huey-Herng Sheu whhsheu@nhri.edu.tw National Health Research Institutes Institute of Molecular and Genomic Medicine Miaoli Taiwan -
 
 
 
 
 
 
Abstract Content
Epicardial fat tissue (EFT) has been linked to cardiovascular events and is involved in the development of coronary artery calcification (CAC). However, the long-term influence of metabolic and inflammatory risk factors on EFT remains unclear. This study aimed to investigate the longitudinal associations of obesity, insulin resistance, and inflammation with epicardial fat mass in older adults.
A total of 1252 adults aged ≥55 years (men: 608; women: 644) were recruited from the Healthy Aging Longitudinal Study in Taiwan. Epicardial fat tissue and CAC scores were assessed in 2023 using low-dose computed tomography scans. Baseline (2009–2013) and second-wave (2014–2019) data on metabolic and inflammatory indicators, as well as their longitudinal changes, were analyzed. CAC scores were calculated using the Agatston method. Linear regression analyses were conducted to examine associations between baseline and longitudinal changes in metabolic/inflammatory markers and epicardial fat mass.
Men exhibited higher epicardial fat mass compared with women (66.59 ± 33.10 vs. 62.30 ± 27.83 cm³, p = 0.0135). Baseline body mass index (BMI; r = 0.33), waist circumference (r = 0.34), systolic blood pressure (SBP; r = 0.09), diastolic blood pressure (DBP; r = 0.11), fasting glucose (r = 0.11), HbA1c (r = 0.09), HOMA-IR (r = 0.20), HDL-cholesterol (r = –0.15), triglycerides (r = 0.12), white blood counts (r = 0.13), CRP (r = 0.06), and TNF-α (r = 0.13) were significantly correlated with epicardial fat mass (All p-values < 0.05). Moreover, longitudinal changes in BMI (r = 0.11), DBP (r = –0.07), and high-sensitivity IL-6 (r = 0.06) over six years were associated with epicardial fat mass. In the multivariable model, baseline BMI (β = 2.94, p < 0.0001), HOMA-IR (β = 1.25, p = 0.0189), white blood cell counts (β = 1.47, p = 0.0101), and longitudinal changes in BMI (β = 3.62, p < 0.0001), DBP (β = –0.24, p = 0.0248), and high-sensitivity IL-6 (β = 0.68, p = 0.0797) were independently associated with epicardial fat mass. Epicardial fat tissue was also positively correlated with CAC score (r = 0.1014, p = 0.0003).
Epicardial fat tissue was positively associated with coronary artery calcification. Both obesity and inflammation had persistent effects on the development of epicardial fat tissue, while a decline in diastolic blood pressure—reflecting arterial stiffness—was also implicated in its progression.
Obesity, Insulin Resistance, and Inflammation, Epicardial Fat Tissue, retrospective design
https://storage.unitedwebnetwork.com/files/1305/db2f899086b5ffc8860163530a7230b3.jpg
Determinants of future epicardial fat tissue.
379
Shao-Yuan
CHUANG
chuangsy@nhri.edu.tw
 
Presentation Details