# Epicardial adipose tissue volume is associated with impaired left atrial mechanics in hypertensive overweight/obese patients: the potential mediating role of insulin resistance

## TL;DR

Excess heart fat is linked to worse heart function in overweight/obese people with high blood pressure, possibly due to insulin resistance.

## Contribution

Shows that epicardial fat independently affects left atrial mechanics, partially mediated by insulin resistance in hypertensive patients.

## Key findings

- Higher EAT volume correlates with reduced LA strain and increased stiffness in overweight/obese hypertensive patients.
- TyG-BMI explains part of the relationship between EAT volume and impaired LA mechanics.
- EAT volume remains a significant predictor of LA dysfunction after adjusting for other factors.

## Abstract

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.

In this cross-sectional study, 264 hypertensive overweight/obese patients (body mass index ≥24 kg/m2) underwent coronary computed tomography angiography (CCTA) for EATV quantification. Participants were stratified into low- and high-EATV groups by the median value (72.67 cm3). 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.

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.

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.