• Silje K Namtvedt, Jonny Hisdal, Anna Randby, Stefan Agewall, Einar Stranden, Virend K Somers, Helge Røsjø, and Torbjørn Omland.
• Department of Internal Medicine, Division of Medicine, Akershus University Hospital, Lorenskog, Norway.
• Heart. 2013 Jan 1;99(1):30-4.

ObjectiveObstructive sleep apnoea (OSA) and obesity are both associated with endothelial dysfunction, which precedes the development of atherosclerosis. As obesity is highly prevalent in OSA, we wanted to test the hypothesis that OSA is associated with endothelial dysfunction independently of obesity.DesignCross-sectional, population-based study.SettingNorwegian university hospital.PatientsSeventy-one subjects (median age 44 years, 35% female) were recruited from a population-based study in Norway. Participants were categorised as obese (body mass index (BMI) ≥30 kg/m(2)), non-obese (BMI<30 kg/m(2)) with OSA (apnoea-hypopnoea index (AHI)≥10), or non-obese without OSA (AHI<5).InterventionsNone.Main Outcome MeasuresEndothelial function measured by brachial artery ultrasound and expressed as percentage of flow-mediated dilation (FMD%).ResultsWhen non-obese subjects without OSA were used as the reference (FMD% (mean±SD) 10.1±6.3), endothelial function was found to be impaired in subjects with OSA (FMD% 6.4±3.2) (p=0.003). FMD% did not differ between obese (6.0±3.4) and non-obese (6.7±3.1) OSA subjects (p=0.3). By univariate linear regression analysis, AHI, BMI, gender and baseline brachial artery diameter were significantly associated with FMD%. When these variables were entered into a multivariate model, only AHI was significantly associated with FMD%.ConclusionsOSA is associated with endothelial dysfunction independently of obesity and conventional risk factors.

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