# Sex-specific association of epicardial adipose tissue thickness and left ventricular hypertrophy in the older adults—cross-sectional results from the population-based AugUR study

**Authors:** Alexander D. Schober, Klaus J. Stark, Martina E. Zimmermann, Maria A. Heinrich, Lars S. Maier, Andreas Luchner, Iris M. Heid, Alexander Dietl

PMC · DOI: 10.3389/fcvm.2026.1705319 · Frontiers in Cardiovascular Medicine · 2026-02-18

## TL;DR

This study finds that thicker epicardial fat in older adults is linked to heart muscle thickening, especially in men.

## Contribution

The study reveals a sex-specific association between epicardial adipose tissue and left ventricular hypertrophy in older adults using population-based data.

## Key findings

- Epicardial adipose tissue thickness increases with age in older adults.
- Epicardial adipose tissue is independently associated with left ventricular mass index after adjusting for multiple factors.
- The association between epicardial adipose tissue and left ventricular hypertrophy is stronger in men than in women.

## Abstract

Our study aimed to evaluate epicardial adipose tissue (EAT) thickness in old adults, identify potential factors influencing it, and explore the association between EAT and left ventricular hypertrophy (LVH) in the older adult population.

We analyzed cross-sectional data from the population-based AugUR study, including subjects aged ≥70 years. Cardiac geometry and EAT thickness were measured by echocardiography.

Among 988 participants aged 70–95 years (55.8% men), LVH was present in 368 individuals (37.2%). EAT thickness was similar between women and men (mean ± standard deviation: 4.1 ± 2.0 mm vs. 4.2 ± 1.9 mm, p = 0.29) but increased with age group (70–79 years: 4.0 ± 1.8 mm, >79 years 4.5 ± 2.0 mm, p < 0.001). Linear regression models of potential risk factors influencing EAT thickness showed associations with age [β = 0.038 mm per year; 95% confidence interval (CI) = 0.014–0.063, p < 0.05], body mass index (BMI) (β = 0.097 mm per kg/m2, 95% CI = 0.070–0.124, p < 0.05), and low-density lipoprotein-cholesterol (LDL, β = 0.008 mm per mg/dL, 95% CI = 0.004–0.012, p < 0.05). Given the reported causal relationship between EAT and LVH in experimental studies, multivariable regression models were performed to evaluate the association between EAT thickness and left ventricular mass index (LVMi). EAT thickness was associated with LVMi independent of sex, age, BMI, LDL, smoking, hypertension, diabetes, and chronic kidney disease (LVMi ß = 2.43 g/m2/mm, 95% CI 1.26–3.59, p = <0.001; LVH OR = 1.36/mm, 95% CI 1.01–1.84, p < 0.05). This association was strong in men but not in women.

EAT thickness continues to increase with age beyond 69 years. Age, BMI, and LDL-cholesterol are associated with increasing EAT thickness. Our study strengthens the experimental hypothesis of a link between EAT and LVH by translational, population-based data. However, this association is more pronounced in men than in women.

## Full-text entities

- **Genes:** ACE (angiotensin I converting enzyme) [NCBI Gene 1636] {aka ACE1, CD143, DCP, DCP1}, REN (renin) [NCBI Gene 5972] {aka ADTKD4, HNFJ2, RTD}, GLP1R (glucagon like peptide 1 receptor) [NCBI Gene 2740] {aka GLP-1, GLP-1-R, GLP-1R}, INS (insulin) [NCBI Gene 3630] {aka IDDM, IDDM1, IDDM2, ILPR, IRDN, MODY10}, AP2B1 (adaptor related protein complex 2 subunit beta 1) [NCBI Gene 163] {aka ADTB2, AP105B, AP2-BETA, CLAPB1}, SLC5A2 (solute carrier family 5 member 2) [NCBI Gene 6524] {aka SGLT2}, CRP (C-reactive protein) [NCBI Gene 1401] {aka PTX1}
- **Diseases:** cardiomyopathies (MESH:D009202), arrhythmia (MESH:D001145), Aortic valve stenosis (MESH:D001024), LVMi (MESH:D018487), mitral valve insufficiency (MESH:D008944), ventricular mass (MESH:C536030), metabolic disease (MESH:D008659), myocardial remodeling (MESH:D064752), hyperlipidemia (MESH:D006949), fibrosis (MESH:D005355), metabolic syndrome (MESH:D024821), inflammation (MESH:D007249), chronic kidney disease (MESH:D051436), prediabetes (MESH:D011236), Valvular diseases (MESH:D006349), Diabetes (MESH:D003920), AD (MESH:D000544), CAD (MESH:D003324), cardiac adiposity (MESH:D006331), cardiac hypertrophy (MESH:D006332), remodeling (MESH:D020257), Heart failure (MESH:D006333), EAT (MESH:D018205), EF (MESH:D054144), hypertension (MESH:D006973), LVH (MESH:D017379), end systole (MESH:D003643), Age-related diseases (MESH:D010024), hypertrophy (MESH:D006984), myocardial infarction (MESH:D009203), cardiovascular disease (MESH:D002318)
- **Chemicals:** free fatty acids (MESH:D005230), testosterone (MESH:D013739), metformin (MESH:D008687), aldosterone (MESH:D000450), lipid (MESH:D008055), creatinine (MESH:D003404), DOACs (-)
- **Species:** Cavia porcellus (domestic guinea pig, species) [taxon 10141], Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

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## References

53 references — full list in the complete paper: https://tomesphere.com/paper/PMC12957171/full.md

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Source: https://tomesphere.com/paper/PMC12957171