Background-There is increasing evidence that obstructive sleep apnea (OSA) is an independent risk factor for arterial hypertension. Because there are no controlled studies showing a substantial effect of nasal continuous positive airway pressure (nCPAP) therapy on hypertension in OSA, the impact of treatment on cardiovascular sequelae has been questioned altogether. Therefore, we studied the effect of nCPAP on arterial hypertension in patients with OSA. Methods and Results-Sixty consecutive patients with moderate to severe OSA were randomly assigned to either effective or subtherapeutic nCPAP for 9 weeks on average. Nocturnal polysomnography and continuous noninvasive blood pressure recording for 19 hours was performed before and with treatment. Thirty two patients, 16 in each group, completed the study. Apneas and hypopneas were reduced by Ϸ95% and 50% in the therapeutic and subtherapeutic groups, respectively. Mean arterial blood pressure decreased by 9.9Ϯ11.4 mm Hg with effective nCPAP treatment, whereas no relevant change occurred with subtherapeutic nCPAP (Pϭ0.01). Mean, diastolic, and systolic blood pressures all decreased significantly by Ϸ10 mm Hg, both at night and during the day. Conclusions-Effective nCPAP treatment in patients with moderate to severe OSA leads to a substantial reduction in both day and night arterial blood pressure. The fact that a 50% reduction in the apnea-hypopnea index did not result in a decrease in blood pressure emphasizes the importance of highly effective treatment. The drop in mean blood pressure by 10 mm Hg would be predicted to reduce coronary heart disease event risk by 37% and stroke risk by 56%.

Snoring and sleeping apnea are reportedly associated with morbidity. We used home monitoring (MESAM IV) to measure snoring and sleep apnea in 294 men aged 40 to 65 yr from the volunteer register of the Busselton (Australia) Health Survey. In this group, 81% snored for more than 10% of the night and 22% for more than half the night; 26% had a respiratory disturbance index (RDI) > or = 5, and 10% had an RDI > or = 10. There was a relatively low correlation between percentage of night spent snoring and RDI (rho = 0.47, p < 0.005). Subjective daytime sleepiness plus RDI > or = 5 occurred in a minimum of 3%. Obesity was related to snoring, RDI, and minimum SaO2 (all p < 0.0001). There was no relationship between age and either RDI or snoring, but increased age was related to minimum SaO2 < 85% (p < 0.05). Alcohol consumption was not related to sleep-disordered breathing. Smokers snored for a greater percentage of the night than nonsmokers (41 versus 31%, p = 0.01). We conclude that, in middle-aged men, both snoring and sleep apnea are extremely common, and in this age range both are associated with obesity but not with age. However, a high percentage of snoring is not essential for the occurrence of sleep apnea, nor does it necessarily indicate that apnea is present.

We studied the effects of sleep apnea on neuroendocrine function in a cross-sectional study of 225 consecutive men undergoing sleep studies and in a longitudinal study of 43 men with severe obstructive sleep apnea before and after 3 months of successful treatment with nasal continuous positive airways pressure to eliminate upper airways obstruction. Blood samples were collected at 0600-0630 h on awakening for measurement of plasma insulin-like growth factor I (IGF-I), total and free testosterone, sex hormone-binding globulin (SHBG), LH, FSH, PRL, T4, T4-binding globulin, and cortisol. The plasma hormone levels were analyzed in relation to the severity of sleep apnea, as indicated by the desaturation index (the hourly rate of episodes of arterial oxygen desaturation greater than 4% of the stable baseline) and the mean minimal oxygen saturation during the desaturation episodes. In the cross-sectional study plasma IGF-I, free and total testosterone, and SHBG levels were significantly lower in relation to the severity of sleep apnea, whereas plasma LH, FSH, PRL, T4, T4-binding globulin, and cortisol were not. The decreases in plasma IGF-I and total and free testosterone were independent of the effects of aging and adiposity by covariance analysis. In the longitudinal study plasma IGF-I, total testosterone, and SHBG, but not free testosterone, significantly increased after 3 months of nasal continuous positive airways pressure treatment. We conclude that sleep apnea causes reversible neuroendocrine dysfunction in men, which is manifested by decreased plasma. IGF-I, testosterone, and SHBG levels. This neuroendocrine dysfunction is related to the severity of the sleep apnea, as indicated by the nadir levels of arterial oxygen desaturation and the rate of desaturation episodes. These hormonal measurements may provide biochemical markers for both the severity of sleep apnea and its response to therapeutic intervention. In addition, sleep apnea may be a previously unrecognized confounder of the neuroendocrine correlates of aging.