Abstract

BackgroundPrevious studies have shown that excessive abdominal visceral adipose tissue (AVAT) and epicardial adipose tissue (EAT) are risk factors of cardiometabolic disease; we hypothesized there is differential contribution of abdominal and cardiac fat deposits to the cardiometabolic profiles.MethodsTwo hundred eight consecutive subjects with clinical suspicion of coronary artery disease (CAD) who underwent cardiac and abdominal CT for Agatston score and abdominal visceral fat measurement were retrospectively analyzed. Regional thickness of EAT (EATth), total volume of EAT, total volume of paracardial adipose tissue (PAT) and total volume of AVAT from L2 to L5 level were measured. The relationships between abdominal and cardiac adipose tissue measurements, the number of components of metabolic syndrome, and the severity of Agatston score on a four ranking scale (0, 1–10,11–100, 101–400, >400) were investigated.ResultsThe amounts of AVAT, EAT, PAT and EATth-LAVG showed a significant linear trend with increasing number (0–5) of components in metabolic syndrome (AVAT, EAT and PAT P for trend <0.0001; EATth-LVAG P for trend <0.001). EATth at left atrioventricular groove (EATth-LAVG) showed significant linear trend with the severity of Agatston score on a four ranking scale (P for trend <0.0001). In multivariate binary regression analysis, total volume of AVAT was the sole adiposity predictor for metabolic syndrome independent to age, gender, and waist circumference (odds ratio of 1.20, 95 % CI 1.08–1.32, p < 0.001) while total volume of EAT, PAT, and EATth-LAVG were not. In contrary, EATth-LAVG was the sole adiposity predictor for Agatston score >400 (odds ratio of 1.11, 95 % CI 1.034–1.184, p = 0.004).ConclusionsExcessive total volume of AVAT appears to be preferentially associated with metabolic syndrome; while EAT, esp. EATth-LAVG is preferentially associated with coronary artery disease. This differential effect of the two adiposities deserves a large-scale cohort study for further investigation.

Highlights

  • Previous studies have shown that excessive abdominal visceral adipose tissue (AVAT) and epicardial adipose tissue (EAT) are risk factors of cardiometabolic disease; we hypothesized there is differential contribution of abdominal and cardiac fat deposits to the cardiometabolic profiles

  • Correlations between cardiometabolic risk and adipose tissue measurements As shown in Fig. 2a, total volume of AVAT, EAT, paracardial adipose tissue (PAT) and EATth-left atrioventricular groove (LAVG) significantly increased as the number of the metabolic syndrome components increased (p for trend

  • Data are presented as mean ± SD or median, depending on distribution BMI body mass index, HDL high density lipoprotein, AVAT abdominal visceral adipose tissue, SAT abdominal subcutaneous adipose tissue, EAT epicardial adipose tissue, PAT paracardial adipose tissue, EATth-LAVG EAT thickness at left AV(atrioventricular) groove, EATth-RAVG EAT thickness at right AV(atrioventricular) groove, EATth-AIVG EAT thickness at anterior IV groove significantly increased with the severity of Agatston score on a four ranking scale (p for trend

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Summary

Introduction

Previous studies have shown that excessive abdominal visceral adipose tissue (AVAT) and epicardial adipose tissue (EAT) are risk factors of cardiometabolic disease; we hypothesized there is differential contribution of abdominal and cardiac fat deposits to the cardiometabolic profiles. Abdominal visceral fat is believed to be intrinsically different from cardiac visceral fat Both excessive abdominal adiposity and cardiac adiposity are essential contributors to the development of the cardiometabolic risks. They tend to occur together, their quantitative relationship and their respective roles in various cardiometabolic components remain unclear. There is a lack of studies aiming at systematic investigation, using precise measurement techniques, of the relative importance of excessive abdominal and cardiac fat accumulation in explaining the variation of the components of the cardiometabolic risks. Different types of regional-specific or total volume of EAT depot may play differential roles in the progression of coronary artery atherosclerosis; this issue has not been well addressed [16, 18,19,20]

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