Relationship between epicardial adipose tissue attenuation and coronary artery disease in type 2 diabetes mellitus patients : Journal of Cardiovascular Medicine

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Original articles: Focus on: Epicardial adipose tissue in cardiovascular diseases

Relationship between epicardial adipose tissue attenuation and coronary artery disease in type 2 diabetes mellitus patients

Liu, Zihou; Neuber, Sebastian; Klose, Kristin; Jiang, Meng; Kelle, Sebastian; Zhou, Ningbo; Wang, Shunjun; Stamm, Christof; Luo, Fanyan

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Journal of Cardiovascular Medicine 24(4):p 244-252, April 2023. | DOI: 10.2459/JCM.0000000000001454

Abstract

Background and aims 

High epicardial adipose tissue (EAT) attenuation is a key characteristic of adipose tissue dysfunction and associated with coronary artery disease (CAD). As little is known about the modulation of EAT attenuation by metabolic disorders, we investigated the association between EAT attenuation and CAD risk factors, CAD presence and CAD severity in type 2 diabetes mellitus (T2DM) patients.

Methods 

We included 276 inpatients with T2DM and 305 control patients with normal glucose metabolism (NGM), who underwent cardiac computed tomography angiography (CCTA) and coronary artery calcium (CAC) scoring. EAT attenuation and volume were evaluated by contrast-enhanced CCTA image analysis. Furthermore, segment stenosis scores (SSSs) of the left main coronary artery (LMCA), left anterior descending artery (LAD), left circumflex artery (LCX), right coronary artery (RCA), diagonal/intermediate branch (D/I) and obtuse marginal branch (OM) were calculated to assess CAD severity.

Results 

T2DM patients showed higher significant CAC scores, coronary plaque prevalence, total SSSs and LMCA-SSSs, LAD-SSSs, LCX-SSSs, RCA-SSSs and D/I-SSSs compared with NGM controls. In contrast to NGM controls, EAT volume was significantly increased in T2DM patients, whereas EAT attenuation was similar. In T2DM patients, EAT attenuation was associated with discrete CAD risk factors, the presence of coronary and triple-vessel plaques, as well as LAD-SSSs, LCX-SSSs, RCA-SSSs and total SSSs. In addition, EAT attenuation was only associated with the total SSS of calcified plaques, but not with noncalcified plaques.

Conclusion 

In T2DM patients, high EAT attenuation is associated with the presence and severity of CAD in general and with coronary stenosis caused by calcified plaques in particular.

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