From Adiposity to Diastolic Dysfunction: The Integrated Role of Epicardial Fat, Autonomic Dysregulation, and Morning Blood Pressure Surge in Obesity

Objective Although the association between obesity and left ventricular diastolic dysfunction (LVDD) is well established, the concurrent associations of epicardial adipose tissue (EAT), sleep‐trough (prewaking) morning blood pressure surge (MBPS), and autonomic imbalance with LVDD have not been fully elucidated. This study aimed to evaluate the associations of EAT thickness, MBPS, and heart rate variability (HRV) parameters with LVDD in obese adults and to assess the cross‐sectional discriminatory performance of these multimodal markers. Methods This cross‐sectional study included 240 individuals, comprising 120 obese participants (body mass index ≥ 30 kg/m 2 ) and 120 age‐ and sex‐matched normal‐weight controls (body mass index 18.5–24.9 kg/m 2 ). All participants underwent transthoracic echocardiography, 24‐h ambulatory blood pressure monitoring, and 24‐h Holter electrocardiographic analysis, with HRV data available for the entire cohort ( n = 240). EAT thickness was measured echocardiographically, and LVDD was classified using contemporary guideline‐based echocardiographic criteria. SDNN was predefined as the primary autonomic marker, while RMSSD and the LF/HF ratio were reported as supportive indices. Associations with LVDD (≥ Grade I) were evaluated using correlation analysis, multivariable logistic regression, and receiver operating characteristic analyses. Cross‐sectional discrimination analysis and performance assessment were performed within the obese subgroup ( n = 120). Results Compared with controls, obese participants exhibited greater EAT thickness (6.5 ± 1.7 vs. 4.0 ± 1.2 mm), higher MBPS (33 ± 10 vs. 21 ± 7 mmHg), increased LF/HF ratio, and lower SDNN and RMSSD values (all p < 0.001). The prevalence of LVDD was significantly higher in obese individuals than in controls (45% vs. 15%, p < 0.001). In multivariable analysis, EAT thickness (odds ratio [OR] = 1.20 per 1 mm; 95% confidence interval [CI] 1.08–1.34), MBPS (OR = 1.35 per 10 mmHg; 95% CI 1.10–1.65), and SDNN (OR = 0.88 per 10 ms; 95% CI 0.80–0.97) were independently associated with LVDD. The parsimonious model demonstrated discrimination and calibration comparable to or superior to the full clinical model (AUC: 0.89 vs. 0.85). Conclusion In obese adults, increased epicardial adiposity, exaggerated MBPS, and autonomic dysfunction coexist with LVDD. Integrated assessment of structural (EAT), hemodynamic (MBPS), and autonomic (SDNN) markers may facilitate cross‐sectional identification of LVDD and improve phenotypic characterization in obesity.