Cardiac magnetic resonance quantification of epicardial adipose tissue identifies subclinical cardiac dysfunction in asymptomatic obesity: A multicenter cross‐sectional study

Abstract Emerging evidence suggests that epicardial adipose tissue (EAT) contributes to the pathophysiology of obesity‐related heart failure. However, the relationship between EAT and subclinical cardiac dysfunction in obese individuals without cardiac symptoms or known cardiac disease remains largely unknown. This study enrolled 87 asymptomatic obese adults and 30 healthy nonobese controls in the prospective multicenter study (EARLY‐MYO‐OBESITY, NCT05277779), and explored the association between EAT and subclinical cardiac dysfunction by assessing EAT volume, cardiac morphology, function, and tissue characteristics through cardiac magnetic resonance (CMR). Compared to controls, obese participants exhibited elevated EAT volume alongside systolic and diastolic dysfunction, manifested by significant reductions in left ventricular global longitudinal peak systolic strain (LVGLS) and early diastolic longitudinal strain rate (e'SR). Linear regression revealed that EAT volume was independently associated with decreased LVGLS (unstandardized β coefficient −0.118, p < .001) and e'SR (unstandardized β coefficient −0.008, p < .001). After multivariable adjustment, EAT volume remained independently associated with LVGLS (unstandardized β coefficient −0.092, p < .001) and e'SR (unstandardized β coefficient −0.006, p = .002). Furthermore, EAT volume independently predicted cardiac dysfunction defined by LVGLS < 15% (odds ratio 1.095, p < .001) and e'SR < 0.57 s −1 (odds ratio 1.064, p < .001). This study establishes that increased EAT volume is independently associated with subclinical cardiac dysfunction in asymptomatic obese individuals. Despite similar left ventricular ejection fraction, obese individuals with elevated EAT volume exhibit more pronounced impairment in both systolic and diastolic function, which may represent a distinct pathophysiological feature in heart failure progression.