Impact of epicardial adipose tissue volume and hypertension on left ventricular hypertrophy in preclinical heart failure patients with metabolic syndrome

Left ventricular hypertrophy (LVH) is a critical risk factor for cardiovascular diseases, yet the interplay between metabolic disorders and hypertension in its pathogenesis remains underexplored. This retrospective study investigated the independent and synergistic roles of epicardial adipose tissue (EAT) volume and hypertension in driving LVH among 253 preclinical heart failure patients with metabolic syndrome (MetS). EAT volume was measured via non-contrast computed tomography (CT). Analysis of covariance (ANCOVA) was employed to assess the contributions of metabolic factors and hypertension to LVH. Mediation analysis was conducted to evaluate whether the effect of EAT on LVH is mediated through blood pressure. Patients with LVH (median age 33 years) exhibited significantly higher prevalence of hypertension (70.9% vs. 36.5%, P < 0.001) and elevated metabolic indices, including fasting glucose, TyG index, and EAT volume (126 vs. 112 cm³, P = 0.005), compared to non-LVH counterparts. Covariance analysis revealed hypertension accounted for 13.5% of LV mass variance, while EAT volume independently contributed 16.5%. Notably, metabolic factors of Mets-IR, uric acid, and body fat mass further modulated hypertension-associated LV remodeling. Mediation analysis demonstrated systolic and diastolic blood pressure partially mediated the EAT-LV mass relationship (mediation effect: 13.2% and 9%, respectively). These findings underscore EAT volume as a strong mediator of metabolic-driven cardiac hypertrophy in preclinical heart failure patients with MetS. • Metabolic related cardiac damage is overlooked in clinical practice in preclinical heart failure patients with metabolic syndrome (MetS). • EAT volume measured by non-contrast CT is a strong metabolic risk factor mediating LVH in preclinical heart failure patients with MetS. • It is important to consider metabolic treatment strategies in LVH during preclinical heart failure.