Consequences of hypoxia-reoxygenation phenomena in patients with obstructive sleep apnea syndrome

BACKGROUND AND OBJECTIVES: Obstructive sleep apnea syndrome (OSAS) is a common disorder characterized by numerous episodes of absence of respiratory flow during sleep, which can be followed by a decrease in SaO(2), which is rapidly normalized when ventilation resumes. We hypothesize that this hypoxia–reoxygenation phenomena may affect the generation of vascular endothelial growth factor (VEGF), erythropoietin (EPO), endothelin-1 (ENDO-1), and inducible nitric oxide synthase (iNOS). DESIGN AND SETTING: Prospective, patients referred to sleep disorders center. PATIENTS AND METHODS: The presence and severity of OSAS were determined using the standard overnight polysomnography. Diagnosis of OSAS was made when the apnea-hypopnea index (AHI) was ≥15, independent of the appearance of symptoms. Serum levels of VEGF, EPO, ENDO-1, and nitrite–nitrate were measured after overnight fasting in 69 patients with OSAS and in 17 healthy control subjects. Serum levels of VEGF and nitrite–nitrate were measured again after 12 weeks of treatment with continuous positive airway pressure (CPAP) in OSAS patients. RESULTS: Serum VEGF levels were found to be significantly higher and nitrite-nitrate levels were found to be significantly lower in OSAS patients than in controls (P=.003, .008, respectively), but no differences in EPO and ENDO-1 levels were found between the groups. We demonstrated that in OSAS patients, the serum VEGF levels were decreased and nitrate levels were increased after 12 weeks of CPAP treatment (P=.001, .002, respectively). CONCLUSION: According to our data, it is likely that hypoxia–reoxygenation phenomena affect the VEGF and nitrite–nitrate levels, which may be pathogenic factors in generating cardiovascular complications in OSAS.