The Cardiometabolic Triad: Obesity, Sleep-Disordered Breathing, and Epicardial Adipose Tissue as Interacting Determinants of Cardiovascular Remodeling

Obesity, sleep-disordered breathing (SDB), and epicardial adipose tissue (EAT) are increasingly recognized as interconnected contributors to cardiometabolic and cardiovascular disease, although they are often addressed as distinct clinical conditions. This narrative review aims to integrate current evidence on the reciprocal pathophysiological interactions linking these entities and their contribution to cardiovascular remodeling. A comprehensive literature search up to May 2025 was performed, focusing on clinical, imaging, and mechanistic studies examining obesity, SDB, EAT, and cardiovascular outcomes. Available data indicate that obesity promotes visceral and epicardial fat expansion, systemic inflammation, and altered cardiopulmonary mechanics, thereby facilitating the development of SDB. In turn, intermittent hypoxia and sympathetic activation associated with SDB further aggravate adipose tissue dysfunction and inflammatory activation of EAT. As a metabolically active fat depot in direct anatomical continuity with the myocardium and coronary arteries, EAT contributes to myocardial fibrosis, atrial remodeling, diastolic dysfunction, and coronary atherosclerosis through paracrine inflammatory and neurohumoral pathways. The convergence of these mechanisms delineates a high-risk cardiometabolic phenotype associated with atrial fibrillation, coronary artery disease, and heart failure with preserved ejection fraction. Recognizing obesity, SDB, and EAT as components of an integrated cardiometabolic system may support improved phenotypic stratification and inform more comprehensive approaches to residual cardiovascular risk.