Epicardial adipose tissue volume is associated with impaired left atrial mechanics in hypertensive overweight/obese patients: the potential mediating role of insulin resistance
Abstract
Background: Epicardial adipose tissue (EAT) is implicated in cardiovascular disease, but its specific impact on left atrial (LA) mechanics in hypertensive overweight/obese patients remains unclear. We investigated the association between EAT volume (EATV) and LA dysfunction in this high-risk population. Methods: ). LA strain analysis, including reservoir strain (LAs-s), conduit strain (LAs-e), booster strain (LAs-a), and LA stiffness index (LASI), were assessed by two-dimensional speckle tracking echocardiography. The triglyceride glucose-body mass index (TyG-BMI) was calculated to reflect the insulin resistance. Multivariable regression and mediation analyses evaluated associations between EATV and LA mechanics. Results: The high-EATV group had significantly higher TyG-BMI and longer hypertension duration. Despite comparable conventional echocardiographic parameters, this group demonstrated impaired LA mechanics, evidenced by reduced LAs-s, LAs-e, and LAs-a, alongside elevated LASI. EATV was inversely correlated with LA strains (LAs-s, LAs-e, LAs-a) but positively correlated with both TyG-BMI and LASI. After multivariable adjustment, EATV remained independently associated with LAs-s, LAs-a, and LASI. Mediation analysis indicated that TyG-BMI explained 12.87% of the association between EATV and LAs-s, and 10.00% of the association between EATV and LASI. Conclusion: Increased EATV is independently associated with impaired LA mechanics in hypertensive overweight/obese patients. Insulin resistance, assessed by TyG-BMI, may partly explain these associations, linking epicardial adiposity to early atrial dysfunction.
Fields of Study & Subjects
Cardiovascular Disease and Adiposity
Cardiovascular Function and Risk Factors
Cardiac Fibrosis and Remodeling
Publication details
- Journal / source
- Frontiers in Nutrition
- Volume
- 13
- Pages
- 1778193–1778193
- Publication date
- 23 February 2026
- Language
- EN