Human epicardial fat: what is new and what is missing?

Area of Science:

• Cardiology
• Endocrinology
• Immunology

Background:

• Epicardial adipose tissue (EAT) has proposed physiological functions including energy supply, thermoregulation, and neuroprotection.
• Pathophysiologically, EAT is implicated in cardiac arrhythmias, lipotoxic cardiomyopathy, and potentially coronary artery disease (CAD) inflammation.
• EAT volume increases with obesity and is infiltrated by inflammatory cells in CAD patients, overexpressing adipokines.

Purpose of the Study:

• To explore the physiological and pathophysiological roles of human epicardial adipose tissue (EAT).
• To investigate the association between EAT and coronary artery disease (CAD).
• To assess the potential of EAT as a cardiovascular risk factor.

Main Methods:

• Review of existing literature on EAT functions and associations with CAD.
• Analysis of EAT volume measurements (echocardiography, CT) in obese patients with and without CAD.
• Examination of inflammatory cell infiltration and gene expression in EAT from CAD patients.

Main Results:

• EAT expands in obese individuals, with or without CAD.
• EAT in CAD patients shows chronic inflammatory cell infiltration and altered adipokine gene expression.
• Cross-sectional studies link increased EAT mass to CAD burden; one prospective study suggested EAT volume predicts myocardial infarction but lacked incremental predictive value.

Conclusions:

• EAT has multiple physiological roles and may contribute to CAD pathogenesis through local inflammation.
• The precise mechanisms driving EAT expansion in CAD require further elucidation.
• Robust evidence is needed to definitively establish EAT as an independent cardiovascular risk factor.