The association of nocturnal hypoxemia with arterial stiffness and endothelial dysfunction in male patients with obstructive sleep apnea syndrome.

BACKGROUND Obstructive sleep apnea syndrome (OSAS) is associated with cardiovascular complications, and atherosclerosis is considered to mediate this association. Arterial stiffness and endothelial dysfunction are widely accepted as early markers of atherosclerosis. OBJECTIVES The purpose of this study was to investigate the influence of sleep apnea on arterial stiffness and endothelial dysfunction. METHODS We enrolled 83 OSAS patients including 39 with mild to moderate degree (apnea hypopnea index, AHI >or=5, AHI <30) and 44 with severe degree sleep apnea (AHI >or=30) and 29 normal control subjects (AHI <5). After finishing polysomnography, carotid-femoral pulse wave velocity (cfPWV) and flow-mediated dilation (FMD) were measured using noninvasive devices. RESULTS In patients with severe degree of OSAS, cfPWV was significantly higher than mild to moderate degree of OSAS or normal control subjects. Also, the severe OSAS group showed lower FMD than the normal control group (all p < 0.01). The cfPWV was significantly correlated with FMD (r = -0.26, p < 0.01). Age (beta = 0.33, p < 0.01) and percentage of time below 90% O(2) saturation (beta = 0.34, p < 0.01) were the significant variables to determine cfPWV (adjusted R(2) = 21%, p < 0.01) in multivariate analysis, and the lowest O(2) saturation was a significant determinant for FMD (beta = 0.25, adjusted R(2) = 6%, p < 0.01). CONCLUSIONS Nocturnal hypoxemia may alter arterial elasticity and endothelial function in OSAS patients, and those impairments could increase the risk of cardiovascular complications.