Abstract

Recently available data from a number of studies provide convincing evidence that obstructive sleep apnea hypopnea (OSAH) is an independent risk factor for the development of cardiovascular disease (CVD) and for increased mortality.1–3 Even if the prevalence of OSAH is assumed to be 2% to 4% in the general population, an arguably conservative estimate, OSAH is a significant public health concern. Initial consideration of these findings would suggest that we as Sleep Medicine practitioners should be as diligent in identifying and prescribing treatment for OSAH as internists and family practitioners are for treatment of elevated lipids and hypertension. As much as this strategy is attractive from a scientific perspective, there are some important gaps in our knowledge with respect to the impact of OSAH on all segments of the population as well as practical barriers that preclude implementation. Although recent prospective observational studies have demonstrated that OSAH appears to be an independent risk factor for CVD and increased mortality,2,3 it is not clear that the impact is uniform across all segments of the population. Data presented last year by the Sleep Heart Health Study indicate that the impact of OSAH on mortality and incident CVD is primarily found in men less than 70 years of age, with little effect in women and older men.4 The absence of an adverse impact on older men is consistent with a previous study in a large clinical cohort.1 Furthermore, longitudinal studies of clinical populations demonstrating an adverse impact of OSAH on CVD and mortality have been performed in cohorts comprised predominantly or entirely of men.1,5,6 Thus, it can be argued that the adverse impact on mortality and incident CVD, if any, of OSAH on women, and perhaps older men remains to be determined. Perhaps an equally vexing issue for Sleep Medicine practitioners is the question of who to treat. Review of the data from several longitudinal studies suggest that the mortality and CVD risks for persons with an AHI < 15 may be very low or absent. For example, in the frequently cited study by Marin et al, increased risk of incident CVD and mortality appeared to be present only in those with an AHI ≥ 30.5 Moreover, in the Busselton study, an increase in all-cause mortality was associated only with a RDI ≥ 15.2 Many individuals with OSAH are not sleepy or feel unrested7 and present for medical attention for other reasons. Can we justify treatment of mild OSAH in those with the absence of these symptoms given the lack of definitive evidence of an adverse CVD or mortality impact in this group? In particular, should older persons and women with mild OSAH be treated? The question of who to treat would be less of an issue if available treatment modalities were plentiful and highly effective. Unfortunately, neither is the case. There are 4 commonly employed therapeutic modalities for OSAH: weight loss, upper airway surgery, oral appliances, and positive airway pressure (PAP). Excluding surgical procedures for weight loss, diet programs have not been highly effective. Upper airway surgery is only modestly efficacious at best, and even less effective.8 Oral appliances and PAP therapy are highly efficacious, but their clinical effectiveness rates are less than desirable.9,10 Long-term use of PAP therapy in some studies is reported to be only ∼60%.10 This latter observation is now reflected in Medicare regulations, which require documentation of both treatment compliance and improvement in symptoms for continued reimbursement for PAP therapy. The aforementioned realities present significant challenges to the field of Sleep Medicine. One of our most important disease conditions is highly prevalent in the general population, but it is unclear whether all persons should be treated. Moreover, available treatment modalities are limited and are not highly effective. Recently published studies have provided important information concerning the health impact of OSA, but we are not there yet' Many unresolved issues remain. Additional research and development will be required from both the scientific community and industry to effectively treat the epidemic of OSA.

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