Obstructive Sleep Apnea

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Obese women with PCOS are at increased risk for obstructive sleep apnea (OSA) (56). Based on the increased prevalence of OSA in men, and recent evidence that androgens may play a role in the male predominance, overnight polysomnog-raphy was performed in obese women with PCOS and age/weight-matched controls (56). Women with PCOS had a significantly higher apnea-hypopnea index | (AHI), and were more likely to suffer from symptomatic OSA syndrome. The AHI correlated with waist-hip ratio, as well as total and free testosterone levels. g Vgontzas et al. (57) also reported that sleep-disordered breathing (SDB) and ex- <j cessive daytime sleepiness are more frequent in women with PCOS than in pre-menopausal controls. Insulin resistance appeared to be a risk factor for SDB in J women with PCOS. Q Whether there is a causal relationship between OSA and cardiovascular

& u morbidity and mortality is uncertain. However, recent evidence suggests that OSA may indirectly increase the risk of cardiovascular morbidity and mortality. The Wisconsin Sleep Cohort Study documented that an apnea index of five or more events per hour resulted in significantly higher systemic pressures than in snorers or normals (58). Lavie et al. (59) demonstrated a similar association between an increased apnea-hypopnea index and systolic and diastolic blood pressures during waketime hours. Furthermore, a 10% decrement in oxygen saturation during sleep was linearly associated with an increased risk of systemic hypertension (59). Several recent studies have demonstrated that OSA alone is not sufficient to cause persistently elevated pulmonary arterial pressures. Daytime hy-poxia, resulting from obesity or underlying lung disease, is also necessary for the development of sustained pulmonary hypertension. The most common and significant cardiac rhythm abnormalities associated with OSA are severe brady-cardia and ventricular asystole greater than 10 s (60). The physiological abnormalities associated with OSA, including hypoventilation, hypoxemia, respiratory acidosis, and vigorous inspiratory effort against a closed airway, result in para-sympathetic stimulation and the resultant rhythm disturbances. Finally, there is little direct evidence to support the hypothesis that OSA contributes to vascular morbidity including myocardial infarction and stroke. It thus appears that obese women with PCOS are at increased risk for OSA, and that they should be questioned carefully regarding potential symptoms of sleep-disordered breathing. It remains speculative as to whether obstructive sleep apnea predisposes women with PCOS to a higher risk of systemic hypertension, and subsequent cardiovascular morbidity and mortality.

In conclusion, the metabolic alterations seen in PCOS appear to impart an increase in risk for the development of glucose intolerance and diabetes as well as lipid abnormalities and macrovascular disease. Advances in our understanding of the pathogenesis of the insulin resistance that underlies the development of these complications has provided the impetus for use of novel therapies, chief among them the insulin-lowering medications. The ultimate role of these agents in the treatment of PCOS and its metabolic sequelae remains to be determined.

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