STOP-BANG–Defined high OSA risk is associated with left ventricular diastolic dysfunction in obese adults

Background Obesity is strongly associated with left ventricular diastolic dysfunction (LVDD), an early phenotype along the heart failure with preserved ejection fraction spectrum. Obstructive sleep apnea (OSA) is common in obesity and may coexist with epicardial adiposity, systemic inflammation, and autonomic imbalance; however, whether screening-defined high OSA risk is associated with LVDD in obese adults remains uncertain. Objective To evaluate associations of OSA risk, epicardial adipose tissue (EAT) thickness, systemic inflammatory indices, and heart rate variability (HRV) with LVDD in obese adults and to explore their screening-oriented discriminative performance. Methods In this single-center, cross-sectional study, consecutive adult patients presenting to the cardiology outpatient clinic between January and December 2025 were screened. Eligible participants were adults in sinus rhythm with adequate echocardiographic image quality. The final cohort included 279 participants: 113 obese adults (body mass index BMI ≥ 30 kg/m2) and 166 non-obese controls (BMI < 25 kg/m2). LVDD was assessed by transthoracic echocardiography according to the 2016 ASE/EACVI recommendations. OSA risk was evaluated using the STOP-BANG questionnaire, with high risk prespecified as a score ≥ 3. Epicardial adipose tissue (EAT) thickness and inflammatory indices, including neutrophil-to-lymphocyte ratio (NLR) and systemic immune-inflammation index (SII), were measured. LVDD prevalence comparisons were performed in the full cohort, whereas multivariable and discriminative analyses were prespecified and restricted to obese participants with definitive diastolic classification. Heart rate variability (HRV) parameters were analyzed as supportive mechanistic markers only. Results LVDD was more frequent in obese participants than in non-obese controls (43% vs 7%, p < 0.001). Within the obese subgroup, high STOP-BANG risk (≥ 3) was associated with greater EAT thickness, higher inflammatory burden, and lower HRV indices. In multivariable analyses restricted to obese participants, high STOP-BANG risk remained associated with LVDD in both the full model (OR 2.67, 95% CI 1.25–5.71; p = 0.011) and the reduced model (OR 2.55, 95% CI 1.31–5.55; p = 0.011). A reduced screening-oriented model incorporating STOP-BANG category, EAT thickness, and inflammatory indices showed acceptable discrimination for LVDD in obese adults. Conclusions In obese adults, STOP-BANG–defined high OSA risk is associated with a phenotype characterized by greater epicardial adiposity, higher inflammatory burden, autonomic impairment, and a higher prevalence of LVDD. A parsimonious model integrating STOP-BANG, EAT thickness, and inflammatory indices may support screening-oriented phenotypic characterization of obese adults with a higher likelihood of LVDD; however, these findings should not be interpreted as establishing causal inference or diagnostic confirmation of OSA. Graphical Abstract Obesity is accompanied by greater epicardial adipose tissue thickness, low-grade systemic inflammation, and higher STOP-BANG–defined OSA risk. In this cross-sectional cohort, these interrelated features were associated with a less favorable diastolic phenotype and a higher prevalence of LVDD. A parsimonious model combining EAT thickness, inflammatory indices, and STOP-BANG category may support exploratory screening-oriented phenotypic characterization of obese adults with a higher likelihood of LVDD.