Public health aspects of obstructive sleep apnoea.

The following three articles in this issue of Thorax summarise the contributions to a lively symposium on public health aspects of obstructive sleep apnoea (OSA) which I had the pleasure of chairing at the meeting of the British Thoracic Society in December 1997. The symposium followed the publication in the BMJ of a systematic review by Wright and colleagues on the health eVects of obstructive sleep apnoea and the eVectiveness of continuous positive airway pressure. Their main conclusions were that the relevance of sleep apnoea to public health had been exaggerated and the eVectiveness of treatment with continuous positive airway pressure (CPAP) had been poorly evaluated. The authors questioned whether sleep apnoea was “a separate disease entity or a marker or a symptom of obesity and ageing” and they suggested that the morbidity associated with sleep apnoea was due to confounding factors, particularly obesity. In relation to CPAP treatment, they concluded that the quality of controlled trials was “poor” and that no studies had included “an adequate placebo”. Anecdotal evidence from several centres suggests that the final sentence of their paper: “Calls for widespread investment in health service provision in this topic may be premature” has been taken to heart in considerable measure by purchasing authorities throughout the UK and further afield. The juxtaposition in the paper by Wright et al of reviews of the cardiovascular morbidity and mortality possibly associated with sleep apnoea and the eYcacy of treatment with CPAP could easily lead the clinically naive purchaser to infer that CPAP treatment is used to prevent such long term vascular consequences. As Davies points out, this is not the case—the aim of treatment is to control the morbidity associated with disabling sleepiness. As it happens, a similar review of CPAP treatment was carried out almost simultaneously by the Australian National Health and Medical Research Council. Wright and Sheldon correctly point out that nine of the 10 recommendations in the Australian report agreed with their own. The diVerence, of course, lay in the all important first recommendation in the Australian report that CPAP treatment was indicated for symptomatic patients with OSA. Some estimates of the potential impact of sleep apnoea and the consequent financial implications have sent shudders down the public health spine and the case of patients with disabling sleep apnoea may not have been helped by such extravagant claims. Nonetheless, it is now abundantly clear that symptomatic OSA is very common and undoubtedly a cause of considerable cumulative morbidity, albeit not necessarily vascular morbidity. Wright and Sheldon pose important specific questions. Firstly, “what is sleep apnoea and how common is it?”, pointing out that immediately we run into problems of changing definitions. A major diYculty in this area is the lack of a robust method of categorising patients with OSA and related conditions. This is less important in sleepy patients with a very high apnoea/hypopnoea index (AHI), but there are also patients with high AHI values and few symptoms (who are likely to be picked up in epidemiological studies) and a larger group within the hospital population with troublesome symptoms and little apparent “abnormality” in terms of AHI. The problems of imprecise definition of disease will not be unfamiliar to respiratory physicians who have struggled for nearly half a century to distinguish between asthma and COPD! Wright and Sheldon conclude reasonably that the definition should be developed in the context of the impact of treatment. They then address the question: “is there a causal link between sleep apnoea and morbidity and mortality?”, defining the criteria which should be used in answering such a question and raising the important role of confounding factors, particularly obesity. There is considerable agreement between them and Davies on the unconvincing nature of much of the evidence linkingOSA with sustained daytime hypertension, ischaemic heart disease, and stroke. Davies makes the additional important point that mean nocturnal blood pressure is clearly raised in patients with untreated OSA, a point which should not be dismissed in view of the evidence in essential hypertension that nocturnal blood pressure has an independent adverse prognostic eVect. Recent data from the large epidemiological study in Wisconsin oVer the most convincing evidence to date that OSA may indeed have an independent eVect on daytime blood pressure, but it seems unlikely to be as large an eVect as that associated with other important risk factors such as obesity. Turning to treatment, Wright and Sheldon restate their criticisms of the only randomised controlled study of treatment published at the time of their original review. Not surprisingly, Douglas oVers a detailed and robust defence of this study and he usefully summarises four further studies subsequently published in full or as an abstract, one of which is published in this issue of Thorax. Wright and Sheldon’s main criticism of the Edinburgh studies continues to be the placebo used (a tablet), but they underestimate the diYculty of finding an appropriate placebo for such studies. Unlike conventional randomised control trials of pharmacological treatment, there is no satisfactory placebo for nasal CPAP. Clearly a tablet is less than ideal but, for the reasons expounded by Douglas, nor is “sham CPAP” perfect. Thorax 1998;53:408–409 408