Vascular dysfunction in obstructive sleep apnea syndrome: associations between polysomnographic severity indices, serum endocan level, and arterial stiffness

Background Obstructive sleep apnea syndrome (OSAS) is independently associated with cardiovascular morbidity, yet simultaneous multidomain assessment of cardiovascular dysfunction within a single cohort remains limited. This study aimed to characterize endothelial dysfunction, arterial stiffness, nocturnal hemodynamic instability, and cardiac impairment in patients with moderate-to-severe OSAS and examine their correlations with polysomnographic severity indices. Patients and methods This cross-sectional observational study enrolled 52 patients with moderate-to-severe OSAS and 40 age-matched, sex-matched, and BMI-matched controls. All participants underwent serum endocan measurement, pulse wave analysis for arterial stiffness assessment, transthoracic echocardiography, and overnight polysomnography with detailed nocturnal hemodynamic analysis including pulse transit time and blood pressure dipping pattern characterization. Results OSAS patients showed significantly higher serum endocan, augmentation index, and pulse wave velocity than controls (all P < 0.001). Echocardiography demonstrated impaired left ventricular diastolic function, reduced tricuspid annular plane systolic excursion, and elevated mean pulmonary artery pressure (all P < 0.001). Abnormal blood pressure dipping occurred in 87% of OSAS patients, predominantly nondipping (56%). Reverse dippers exhibited the highest endocan levels (P = 0.022). Apnea–hypopnea index, oxygen desaturation index, and nadir oxygen saturation correlated with endocan, arterial stiffness, and nocturnal hemodynamic indices, largely independent of age and BMI. Conclusion Moderate-to-severe OSAS is associated with a broad spectrum of subclinical cardiovascular dysfunction spanning endothelial activation, arterial stiffening, nocturnal hemodynamic instability, and cardiac impairment. The identification of reverse dipping as the hemodynamic phenotype carrying the greatest endothelial burden offers a novel cardiovascular risk-stratification target in this population.