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Epicardial adipose tissue: anatomic, biomolecular and clinical relationships with the heart

Abstract

A growing amount of evidence suggests that regional fat distribution plays an important part in the development of an unfavorable metabolic and cardiovascular risk profile. Epicardial fat is a metabolically active organ that generates various bioactive molecules, which might significantly affect cardiac function. This small, visceral fat depot is now recognized as a rich source of free fatty acids and a number of bioactive molecules, such as adiponectin, resistin and inflammatory cytokines, which could affect the coronary artery response. The observed increases in concentrations of inflammatory factors in patients who have undergone coronary artery bypass grafting remain to be confirmed in healthy individuals. Furthermore, epicardial adipose mass might reflect intra-abdominal visceral fat. Therefore, we propose that echocardiographic assessment of this tissue could serve as a reliable marker of visceral adiposity. Epicardial adipose tissue is also clinically related to left ventricular mass and other features of the metabolic syndrome, such as concentrations of LDL cholesterol, fasting insulin and adiponectin, and arterial blood pressure. Echocardiographic assessment of epicardial fat could be a simple and practical tool for cardiovascular risk stratification in clinical practice and research. In this paper, we briefly review the rapidly emerging evidence pointing to a specific role of epicardial adipose tissue both as a cardiac risk marker and as a potentially active player in the development of cardiac pathology.

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Figure 1: Macroscopic appearance of epicardial fat.
Figure 2: Microscopic appearance of epicardial fat.
Figure 3: Echocardiographic imaging of epicardial adipose tissue.
Figure 4: MRI of epicardial adipose tissue.

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Correspondence to Gianluca Iacobellis.

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Iacobellis, G., Corradi, D. & Sharma, A. Epicardial adipose tissue: anatomic, biomolecular and clinical relationships with the heart. Nat Rev Cardiol 2, 536–543 (2005). https://doi.org/10.1038/ncpcardio0319

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