The Journal of Clinical Hypertension (Jan 2025)

Epicardial Adipose Tissue and Left Ventricular Hypertrophy in Hypertensive Patients With Preserved Ejection Fraction: A Multicenter Retrospective Cohort Study

  • Runze Zhu,
  • Wenxian Wang,
  • Yan Gao,
  • Junchuan Liu,
  • Bowen Li,
  • Rongxue Shan,
  • Runjie Xue,
  • Xianshun Yuan,
  • Xi‐Ming Wang

DOI
https://doi.org/10.1111/jch.70003
Journal volume & issue
Vol. 27, no. 1
pp. n/a – n/a

Abstract

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ABSTRACT This study aimed to investigate the correlation of the increased volume index of epicardial adipose tissue (EAT) and left ventricular hypertrophy (LVH) in patients with Hypertension (HTN). A total of 209 HTN patients and 50 healthy controls, who underwent cardiovascular magnetic resonance (CMR) at two medical centers in China between June 2015 and October 2024, were enrolled for this study. Postprocessing and imaging analysis were conducted and EAT measurements were performed. Restricted cubic splines (RCS) were used to explore the potential relationship with LVH. Binary logistic regression models and mediation analyses were employed to evaluate the association between EAT volume and CMR parameters as well as LVH. Hypertensive patients with LVH exhibited larger indexed EAT volumes, more pronounced diffuse fibrosis, and reduced left ventricular strain compared to hypertensive patients without LVH (all p < 0.001), with results remaining stable after adjusting for confounding factors. The variables that were significant in the univariate regression were included in the multivariate logistic regression model, indicating that indexed EAT volume (p = 0.001), extracellular volume (ECV) (p = 0.012), and global longitudinal strain (GLS) (p = 0.024) were independently associated with LVH. These associations remained stable after adjusting for confounding factors. Mediation analysis further revealed that the relationship between increased EAT volume and LVH was mediated by ECV, native T1, GLS, global circumferential strain (GCS), and global radial strain (GRS) (p < 0.05). These findings imply that EAT is independently linked to LVH in hypertensive patients. The association between EAT and LVH in hypertensive patients may be mediated by myocardial fibrosis or dysfunction.

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