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Article #81

SUMMARY     This report is based on data drawn from the Wisconsin Sleep Cohort Study. This is a long-term follow-up study of a large sample of 709 subjects drawn randomly (not defined by presence or absence of sleep-disordered breathing) from a group of state employees responding to an initial questionnaire and undergoing at least two sleep studies, at four-year intervals, thereafter being continued in similar follow-up every four years.     These subject were about half (45%) female, averaging 46 years of age, with initial apnea-hypopnea indices averaging 4/hour. About one-quarter had AHIs greater of 5 or greater and a similar proportion had hypertension at intake. The authors note that such a proportion of randomly selected people who show at least minimal AHI criteria for mild sleep apnea is high, as is the prevalence of hypertension in this sample. The protocol excluded people under medical treatment for sleep-disordered breathing.     The outcome variable of interest was the presence of hypertension at follow-up. This was tested for a predictive relationship with initial degree of sleep-disordered breathing as measured by the AHI (classified as 0/hr, 0.1-4.9/hr, 5.0-14.9/hr and 15 or more per hr) at baseline. Statistical analyses separated this relationship from the effects of initial, baseline hypertension status, body-mass index, neck and waist circumference, age, sex, and weekly use of alcohol and cigarettes.     The results showed that the degree of sleep-disordered breathing at baseline did predict the presence of hypertension four years later, independently of the potential confounding factors noted just above. As the baseline severity of sleep-disordered breathing rose (from 0/hr to 0.1-4.9/hr, to 5.0 to 14.9/hr, to 15 or more per hour), so the probability of later hypertensive rose accordingly, increasing (compared to subjects with AHIs of 0/hr) by 42% for those with AHIs of 0.1 to 4.9/hr, up to 2-3X for those with AHIs greater 0f 15 or more/hr. The authors describe this as a "dose-response relationship" between initial sleep-disordered breathing and subsequent hypertension.     The authors caution that differential drop-out rates of different types of subjects--if this occurred--might have affected their results, but note that the subjects who dropped out resembled closely those who continued in follow-up.     The authors assess the results of their study as providing added support for a causal relationship of sleep-disordered breathing to hypertension, derived from a larger-scale, better-designed study than those which had gone before.

Here is another straightforward, credible study confirming previous findings with a larger sample and better design. People with sleep apnea, many already convinced of the causal relationship of sleep-disordered breathing to hypertension, may wonder why I have included this article.     I include this mainly to illustrate what might be called state-of-the-art research, as definitive as such studies get in this realm of epidemiological, population-based follow-up. You should know that, among professional medical journals, The New England Journal of Medicine enjoys a measure of prestige if not pre-eminence. Those reports it does publish would often represent state-of-the-art research with the most nearly definitive results available.     In contrast, research of a more preliminary nature, besides studying smaller subject samples, would typically draw these samples from groups of patients with sleep apnea, not large population samples where sleep apnea exists in only a minority of participants. Moreover, they would rarely aim for such ambitious follow-up as every four years. Their statistical analyses, while controlling for one or another "confounding factor," would eliminate a smaller set of factors, necessitated by their smaller group of subjects.     In short, especially where the finding is so critical to health care planning for patients, professionals, and public health services, it is important to see what aspects of one study make its results weightier than those of another, which might be more severely limited in its implications by reason of its deficiencies.     So, does this study "prove" the relationship? It depends on your perspective. The authors themselves, careful of editorial criticism, claim only that they have found "an association" which "suggests that sleep-disordered breathing is likely to be a risk factor for hypertension and consequent cardiovascular morbidity in the general population."     As for myself, I needed no further convincing after my own, personal experience. First diagnosed and treated for hypertension over 10 years ago, I took a variety of antihypertensive medications, with limited success and some side-effects, until I first started on CPAP about 8 years ago. Thereafter I never again had hypertension, despite stopping antihypertensive medication years ago, and even despite gaining considerable weight from medications of a different type that I ended up on later. But scientists take more convincing than my own case report!

"Thou has nor youth nor age; But, as it were, an after-dinner's sleep, Dreaming on both." William Shakespeare, 1564-1616

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