STUDY OBJECTIVES: Many patients with obstructive sleep apnea (OSA) are obese, and whether obesity itself explains the increased prevalence of cardiovascular disease in OSA is unknown. We hypothesize that OSA, independent of obesity, contributes to abnormal vascular function. DESIGN: Physiology study. SETTING: Academic medical centers. PATIENTS: Obese subjects, free of known comorbidities, were enrolled. MEASUREMENTS AND RESULTS: Vascular function was assessed with brachial artery ultrasound for flow-mediated dilation (FMD) and in skin microcirculation by laser Doppler flowmetry. Arterial stiffness was measured by arterial tonometry. Seventy-two subjects (43/72 women, 38/72 with OSA) were studied. FMD was impaired in patients with OSA, compared with control subjects (5.7% +/- 3.8% vs 8.3% +/- 4.1%, P = 0.005). In step-forward regression analysis inclusive of age, sex, and body mass index, age (P = 0.013) was a significant independent predictor of FMD. In a subgroup of subjects younger than 50 years of age (n = 59), however, OSA was the only independent predictor of FMD (P = 0.04), adjusted for known covariates. OSA did not significantly influence vascular function in the skin microcirculation. The augmentation index, a measure of arterial stiffness, was similar between the OSA and control groups (16.2% +/- 11.4% vs 20.4% +/- 10.1%, respectively, P = 0.10). In step-forward regression analysis of younger men (< or = 50 years old, 23 subjects), OSA independently predicted the augmentation index in men only (P = 0.001). CONCLUSIONS: In obesity, both OSA and aging impair endothelial function and increase arterial stiffness. The influence of OSA on vascular function is most pronounced in young subjects. OSA, therefore, may be associated with functional impairment ("a premature aging effect") on the endothelium and on arterial stiffness (in men), although skin microcirculatory function appears preserved.
STUDY OBJECTIVES: Many patients with obstructive sleep apnea (OSA) are obese, and whether obesity itself explains the increased prevalence of cardiovascular disease in OSA is unknown. We hypothesize that OSA, independent of obesity, contributes to abnormal vascular function. DESIGN: Physiology study. SETTING: Academic medical centers. PATIENTS: Obese subjects, free of known comorbidities, were enrolled. MEASUREMENTS AND RESULTS: Vascular function was assessed with brachial artery ultrasound for flow-mediated dilation (FMD) and in skin microcirculation by laser Doppler flowmetry. Arterial stiffness was measured by arterial tonometry. Seventy-two subjects (43/72 women, 38/72 with OSA) were studied. FMD was impaired in patients with OSA, compared with control subjects (5.7% +/- 3.8% vs 8.3% +/- 4.1%, P = 0.005). In step-forward regression analysis inclusive of age, sex, and body mass index, age (P = 0.013) was a significant independent predictor of FMD. In a subgroup of subjects younger than 50 years of age (n = 59), however, OSA was the only independent predictor of FMD (P = 0.04), adjusted for known covariates. OSA did not significantly influence vascular function in the skin microcirculation. The augmentation index, a measure of arterial stiffness, was similar between the OSA and control groups (16.2% +/- 11.4% vs 20.4% +/- 10.1%, respectively, P = 0.10). In step-forward regression analysis of younger men (< or = 50 years old, 23 subjects), OSA independently predicted the augmentation index in men only (P = 0.001). CONCLUSIONS: In obesity, both OSA and aging impair endothelial function and increase arterial stiffness. The influence of OSA on vascular function is most pronounced in young subjects. OSA, therefore, may be associated with functional impairment ("a premature aging effect") on the endothelium and on arterial stiffness (in men), although skin microcirculatory function appears preserved.
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