This patient has clinical features of sleep apnoea. The condition is characterized by recurrent episodes of upper airway collapse and obstruction during sleep, leading to recurrent oxyhaemoglobin desaturation and arousals from sleep. Anatomical factors, such as enlarged tonsils, macroglossia and abnormal positioning of the maxilla or the mandible, are major predisposing factors to airway collapse. The site of obstruction in most patients is the soft palate, extending to the region at the base of the tongue. Sleep apnoea can be caused by either complete airway obstruction (obstructive apnoea) or partial obstruction

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(obstructive hypopnoea—i.e. slow, shallow breathing), both of which can induce sleep arousal. The frequent arousals and the inability to achieve or maintain the deeper stages of sleep lead to excessive daytime sleepiness, personality changes, memory loss and depression. Other physical signs and symptoms that support a likely diagnosis of obstructive sleep apnoea include loud snoring, witnessed apnoeic episodes, waking up not feeling refreshed, morning headaches and obesity. Polysomnography (overnight sleep study) with an Apnoea-Hypopnoea Index (AHI) score of >5-10/h—derived from the total number of apnoeas and hypopnoeas divided by total sleep time—is generally used as a cut-off level for the diagnosis of sleep apnoea.

Obstructive sleep apnoea (OSA) is recognized to be associated with increased cardiovascular morbidity and mortality. Untreated, OSA is associated with a significant 2-4-fold increase of developing fatal and non-fatal cardiovascular events. Whilst the higher cardiovascular risk was previously thought to be due to its link with obesity, recent evidence has suggested that OSA may be independently associated with the metabolic syndrome. This syndrome consists of a cluster of risk factors which includes hypertension, microalbumin-uria, dyslipidaemia, insulin resistance, glucose intolerance, central obesity and increased proatherogenic proteins. In a study by Coughlin et al.,1 metabolic syndrome was found to be nine times more likely to exist in patients with OSA compared with those without and occurs independently of obesity, smoking and age. Using mathematical models and the euglycaemic hyperinsulinaemic clamp technique to determine insulin sensitivity index, obese patients with OSA have been shown to be more insulin resistant than patients with simple obesity, independently of the degree and distribution of adiposity. Hypoxic state associated with OSA has been postulated to account for the increased vascular risk seen in patients with OSA.

More recently, data from the Sleep Heart Health Study (SHHS) have shown that sleep-disordered breathing (SDB) is independently associated with glucose intolerance and insulin resistance and may lead to type 2 diabetes mellitus. Conversely, diabetes mellitus might be a cause of SDB, mediated through autonomic neuropathy that may alter ventilatory control mechanisms. Further data from the same patient cohort showed that participants with sleep duration of less than five hours per night have a 2.5- and 1.3-fold increased risk of developing type 2 diabetes and impaired glucose tolerance.2 Because this effect was present in subjects without insomnia, voluntary sleep restriction was thought to contribute to the large public health burden of type 2 diabetes. A study involving more than 8000 subjects who participated in one of the three MONICA Augsburg surveys between 1984 and 1995 showed that difficulty in maintaining sleep was also associated with an increased risk of type 2 diabetes in both men and women from the general population. Meanwhile, results from the Nurses Health Study cohort, which followed 69 852 United States female nurses aged 40-65 years without diabetes at baseline, showed that snoring is independently associated with increased risk of developing diabetes.3 Similarly, in a Finnish population-based cohort study involving 593 subjects, habitual snoring was found to be more common in subjects with diabetes than in subjects with impaired glucose regulation or normal glucose tolerance. In this study, impaired insulin sensitivity, type 2 diabetes and smoking were all associated independently with habitual snoring, whilst high body mass index and male sex were associated independently with OSA. Epidemiological data have also shown a link between OSA and hypertension. For example, untreated OSA predisposes to an increased risk of new hypertension, whilst treatment of OSA has been shown to lower blood pressure. Possible mechanisms whereby OSA may

Fig. 5G.1 Diagnosis and management of obstructive sleep apnoea.

contribute to hypertension in obese individuals include sympathetic activation, insulin resistance, elevated angiotensin II and aldosterone levels and endothelial dysfunction.

Conservative measures such as weight loss, avoidance of alcohol 4-6 hours before bed and sleeping on one side are reasonably effective in patients with mild apnoea. In patients with moderate to severe apnoea, nasal continuous positive airway pressure (CPAP) has become the standard treatment for OSA. CPAP works by splinting the upper airway, preventing the soft tissues from collapsing. By this mechanism, it effectively eliminates the apnoeas and/or hypopnoeas, decreases the arousals, and normalizes the oxygen saturation. Emerging data suggest that this form of treatment is not only effective in improving patients' symptoms but has also been shown to improve insulin resistance, glucose metabolism and patients' cardiovascular risks.4 Flow-mediated vasodilation has been shown to improve after four weeks of nasal CPAP treatment, suggesting improvement in endothe-lial function due to CPAP treatment. In a study involving nine obese patients with type 2 diabetes, three months of CPAP treatment was shown to improve insulin sensitivity without any changes in body mass index. Another study, involving 40 patients, showed more rapid improvement in insulin sensitivity (after day two of CPAP treatment), with improved CPAP efficacy seen in subjects who are less obese. In a recent study involving 25 patients with type 2 diabetes, CPAP treatment (mean treatment duration of 83 ± 50 days) significantly reduced 1-hour post-prandial glucose levels, and in 17 patients with a baseline glycosylated haemoglobin (HbAlc) level greater than 7%, there was a significant reduction in HbAlc level (9.2% ± 2.0% to 8.6% ± 1.8%). The reduction in HbAlc level was more prominent in subjects who used CPAP for more than four hours per day. These studies suggest that SDB is pathophysiologically related to impaired glucose homeostasis, and that CPAP can be an important therapeutic approach for patients with diabetes and SDB. In a further prospective study of 54 patients with coronary artery disease (^70% coronary artery stenosis) and OSA (AHI ^15), CPAP treatment was associated with a decrease in the occurrence of new cardiovascular events, and an increase in the time to such events, compared with the group who declined CPAP treatment despite comparable baseline parameters.

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