Vascular endothelial dysfunction in patients with obstructive sleep apnoeasyndrome

introduction Obstructive sleep apnea syndrome (OSAS) is frequently associat ed with cardiovascular disease. We investigated endothelium-dependent and e ndothelium-independent nitric oxide-mediated vasodilatory function in normo tensive patients with OSAS using the hand vein compliance technique. Patien ts and methods Dose-response curves to the endothelium-dependent vasodilato r bradykinin were obtained in 23 male subjects with OSAS and 12 male contro l subjects of comparable age, height, and weight. Results Mean ( SD) maximu m dilation (E-max) to bradykinin was significantly lower in OSAS patients t han in controls (59.8 +/- 26.0 vs. 94.8 +/-9.5%, p<0.0001). Mean vasodilati on with nitroglycerin was not diminished in the OSAS group (90.7<plus/minus >30.5 vs. 100.3 +/- 12.9% in controls; n.s.). In 11 OSAS patients, a follow -up investigation was performed after at least 2 months of treatment with n asal continuous positive airway pressure (CPAP): Ema,, to bradykinin rose f rom 54.5 +/- 19.2% to 111.5 +/- 25.1% after treatment (p<0.001). Mean vasod ilation to nitroglycerin was unchanged. Conclusions These results suggest t hat endothelium-dependent nitric oxide-mediated vasodilation is impaired in patients with OSAS due to an impaired function in the endothelial cells. T his impairment is reversible with CPAP treatment.