Epicardial Adipose Tissue and Heart Failure, Friend or Foe?

Abstract

Heart failure (HF) management guidelines recommend individualized assessments based on HF phenotypes. Adiposity is a known risk factor for HF. Recently, there has been an increased interest in organ-specific adiposity, specifically the role of the epicardial adipose tissue (EAT), in HF risk. EAT is easily assessable through various imaging modalities and is anatomically and functionally connected to the myocardium. In pathological conditions, EAT secretes inflammatory cytokines, releases excessive fatty acids, and increases mechanical load on the myocardium, resulting in myocardial remodeling. EAT plays a pathophysiological role in characterizing both HF with reduced ejection fraction (HFrEF) and HF with preserved ejection fraction (HFpEF). In HFrEF, EAT volume is reduced, reflecting an impaired metabolic reservoir, whereas in HFpEF, the amount of EAT is associated with worse biomarker and hemodynamic profiles, indicating increased EAT activity. Studies have examined the possibility of therapeutically targeting EAT, and recent studies using sodium glucose cotransporter 2 inhibitors have shown potential in reducing EAT volume. However, further research is required to determine the clinical implications of reducing EAT activity in patients with HF.

New Mechanisms to Prevent Heart Failure with Preserved Ejection Fraction Using Glucagon-like Peptide-1 Receptor Agonism (GLP-1 RA) in Metabolic Syndrome and in Type 2 Diabetes: A Review

“…EAT is an extremely active endocrine organ with a high capacity for releasing and taking up free fatty acids [18]. EAT secretes inflammatory cytokines, releases excessive fatty acids, and increases the mechanical load on the myocardium, resulting in myocardial remodeling [19]. EAT can be both highly protective for the adjacent myocardium through its dynamic brown fat-like thermogenic function and deeply harmful via paracrine or vasocrine secretion of pro-inflammatory and profibrotic cytokines [20].…”

“…This is due in part to the upregulation of nuclear factor-kB (NF-kB) and c-Jun N-terminal kinase (JNK) [21]. EAT modulates the metabolic environment of the coronary arteries and myocardium and is associated with various health conditions, including coronary artery disease [19,20], metabolic syndrome [21,22], type 2 diabetes (T2D) [23,24], chronic obstructive pulmonary disease [25], obstructive sleep apnea [26], aging [27], and male sex [28]. These conditions are also risk factors for poor COVID-19 prognosis, and the infection could trigger a systemic inflammatory response [29,30].…”

“…Obesity and T2D are independently associated with increased pericardial/epicardial AT [93]. Epicardial adipose tissue (EAT), a component of VAT located in the heart, has metabolic, mechanical, and thermogenic roles [19]. EAT is twice as metabolically active as normal white AT and plays a significant role in lipolysis and free fatty acid release [94].…”