Why the study?
Epicardial adipose tissue (EAT) is involved in coronary artery disease, AF, and HFpEF and is increasingly investigated as a potentially modifiable target, with exploratory evidence suggesting its response to nutrition and physical exercise is only partly explained by weight loss.
Design
Narrative review
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EAT response to intervention may exceed weight loss alone; leaves open its role as a modifiable target in CAD, AF, and HFpEF.
Epicardial adipose tissue (EAT) is an active endocrine and paracrine organ involved in coronary artery disease, atrial fibrillation (AF), and heart failure with preserved ejection fraction (HFpEF). Beyond its role as a risk marker, EAT is increasingly investigated as a potentially modifiable target, and exploratory, low-certainty evidence suggests that its response to intervention is only partly explained by weight loss. This narrative review addresses two core themes: the pathophysiology of EAT as a distinct, regionally heterogeneous adipose organ; and the effects of nutrition and physical exercise—particularly the Mediterranean diet, caloric restriction, structured training, and bariatric surgery—on EAT quantity and inflammatory quality. Pharmacological data are summarized only as a complementary comparator. Multimodality imaging—echocardiography, cardiac computed tomography (cCT), and cardiac magnetic resonance (CMR)—is discussed as the means by which EAT is measured, and minimum standards for its assessment are proposed. Finally, we outline a hypothesis-generating framework for incorporating EAT assessment into lifestyle-based cardiovascular prevention. This framework has not been validated, and whether reducing EAT improves cardiovascular outcomes independently of weight loss and other risk factors remains unknown; EAT should currently be regarded as a modifiable biomarker rather than an established therapeutic target.
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Pala et al. (2026) studied this question.
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