Elsevier

Atherosclerosis

Volume 284, May 2019, Pages 230-236
Atherosclerosis

Association of epicardial adipose tissue attenuation with coronary atherosclerosis in patients with a high risk of coronary artery disease

https://doi.org/10.1016/j.atherosclerosis.2019.01.033Get rights and content

Highlights

  • Epicardial adipose tissue (EAT) attenuation and volume significantly correlated, but this relationship gradually diminished with increasing CAC scores

  • EAT attenuation was associated with CAD risk factors and the presence of CAD and CAC.

  • EAT attenuation was not associated with the presence of significant coronary lesions and triple-vessel plaques.

  • EAT attenuation was associated with CAC score, SIS and SSS.

Abstract

Background and aims

Density may indicate some tissue characteristics and help reveal the role of epicardial adipose tissue (EAT) in coronary artery disease (CAD). Therefore, we assessed the association of EAT density with the coronary artery plaque burden in patients presenting with chest pain.

Methods

This retrospective cohort study comprised 614 patients (mean age 61 ± 9 years, 61% males) with a high cardiovascular disease risk, who underwent cardiac computed tomography angiography. Density was reflected as attenuation.

Results

EAT attenuation was significantly associated with EAT volume with a negative Pearson's correlation coefficient and gradually increased across coronary artery calcium (CAC) scores of 0, 1–100, 101–400 and > 400. EAT attenuation was tightly associated with CAD risk factors, including age, sex, BMI, total cholesterol, neutrophil to lymphocyte ratios and CAC score. The association between EAT attenuation and CAC score was strengthened after adjusting for multivariable indices (OR 1.21, 95% CI 1.05–1.40, p = 0.01) and further adjusting for EAT volume (OR 1.26 95% CI 1.06–1.51, p<0.01). However, EAT attenuation was associated only with CAD presence (OR 1.32, 95% CI 1.02–1.69, p<0.05), CAC presence (OR 1.28, 95% CI 1.02–1.60, p<0.05), segment involvement score (OR 1.19, 95% CI 1.01–1.40, p<0.05) and segment stenosis score (OR 1.19, 95% CI 1.01–1.40, p<0.05) in the EAT volume- and multivariable-adjusted model. Additionally, EAT attenuation was not associated with significant coronary artery lesions and triple-vessel plaques.

Conclusions

Higher EAT attenuation is associated with a higher risk of CAD.

Introduction

Epicardial adipose tissue (EAT) surrounds the coronary arteries, directly connects to the arterial adventitia without fascia boundaries, has a unique transcriptome, and influences coronary artery biology via paracrine signaling [1,2]. EAT mainly exhibits a beige adipose phenotype, and its expansion via adipose cell hypertrophy and hyperplasia is associated with cardiovascular risk factors, coronary artery plaque burden, and coronary artery disease (CAD) prognosis [[3], [4], [5], [6]].

As another important attribute of EAT, changes in attenuation may be more sensitive than volume in studying cardiovascular disease [7]. Measuring the attenuation may provide information on the potential biological changes, such as fibrosis and beige-white adipose transformation [8], in the EAT of CAD patients. Based on cardiac computed tomography angiography (CCTA) images, standard software can readily quantify the tissue density, as reflected by attenuation and expressed as Hounsfield units (HUs). The adipose tissue attenuation commonly ranges between −190 HU and −30 HU [9], and the exact quantification of EAT attenuation may help explain why EAT volume expansion alone is inconsistently associated with the presence and progression of CAD in many patients.

Thus far, the role of attenuation remains largely obscure. EAT attenuation is positively connected with coronary atherosclerosis [10]; however, others have found the inverse association in asymptomatic patients [11] and patients at high risk of cardiovascular disease [12]. EAT attenuation has even been shown to not correlate with coronary aortic calcium (CAC) levels [13] and may not be an independent risk factor in subjects with suspected acute coronary syndrome [14]. In addition, few studies have systematically addressed EAT attenuation in patients with different stages of cardiovascular disease. Therefore, we investigated the association of EAT attenuation and volume with the presence and severity of CAD in a large cohort of patients presenting with chest pain.

Section snippets

Study population

A total of 812 consecutive inpatients (aged between 45 and 75 years) who underwent coronary calcium scoring (CCS) and a contrast-enhanced evaluation of coronary arteries by MDCT from July 2011 to December 2015 at Xiangya Hospital were recorded. Five of these patients had a history of prior open-heart surgery (including coronary artery bypass grafting and valve surgery), 20 patients had a history of prior percutaneous coronary intervention (PCI), 33 patients had malignancy, 7 patients had an

Baseline characteristics of the patients

The baseline characteristics of the study cohort are depicted in Table 1. Overall, 614 hospitalized patients (mean age 61 ± 9 years, 61% males) were included in this study, of whom 74% had at least a plaque presence, 47% had a significant coronary artery lesion, 19% had an LMCA plaque, and 24% had triple-vessel plaques. Most of the patients suffered mild to moderate CAD according to their CAC score, SIS and SSS, as described above.

In the univariable logistic regression analysis, age, SBP, DM2,

Discussion

In this clinical study, we examined the association of EAT attenuation derived from CTA scans with both the CAD presence, as assessed by the plaque presence, and the CAD severity, as assessed by the SIS, SSS, and CAC score. The SIS and SSS better reflected the degree of coronary artery stenosis [15], while higher CAC scores were strongly associated with a poor prognosis of CAD [18]. We found that EAT attenuation was moderately and negatively associated with EAT volume and that this association

Conflicts of interest

The author(s) declare no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

Financial support

This work was supported by a grant from the National Natural Science Foundation of China (Grant No.81572870).

Author contributions

ZH.L. contributed to the conception and design of the study; the acquisition, analysis and interpretation of the data and the drafting of the manuscript. SJ.W., YQ.W., NB.Z., J.S. and M.J. contributed to the acquisition of the data and the drafting of the manuscript. C.S. contributed to the conception and design of the study and critical revision of the manuscript for important intellectual content. FY.L. contributed to the conception and design of the study, the analysis and interpretation of

Acknowledgments

We thank Dr. Hui Zhou, department of Radiology, Xiangya Hospital, for his help in guiding the image tracing.

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