Editorial Commentary Somnolence The Silent Partner in the Sleep Apnea–Hypertension Relationship Naima Covassin, Virend K. Somers See related article, pp xx–xx

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minutes had 1.95 and 2.11 times higher odds for prevalent hypertension than non-OSA counterparts with an objective sleep latency >8 minutes. The increased likelihood of hypertension in objectively sleepy OSA patients was evident across sex, age, and body mass index groups, indicating that the relation is not modified by traditional risk factors. Importantly, when OSA patients were stratified based on presence or absence of subjective EDS as measured by Epworth Sleepiness Scale, the association between objective EDS and hypertension was retained in both strata. Linear trends were noted between blood pressure and MSLT categories, again restricted to the OSA group. These novel findings suggest that objective sleepiness may be a sensitive, independent indicator of risk of hypertension in OSA population. Its predictive significance irrespective of self-reported or perceived sleepiness deserves further comment. It is well known that the agreement between subjective and objective methods to ascertain EDS is rather poor. This is assumed to be a reflection of the multifaceted and variable nature of sleepiness, which may not be fully captured by any single instrument. Although self-reports, such as the Epworth Sleepiness Scale, estimate sleepiness by targeting cognitive– behavioral components, tests such as the MSLT determine the physiological propensity to fall asleep. The likely relationship between the physiological drive to sleep and MSLT-derived EDS may also account for its closer link to hypertension and other biological markers of risks, as observed by Ren et al and in previous research.6,9 Importantly, the relation between objective EDS and hypertension reported by Ren et al6 was confined to the OSA group, a finding suggesting that there are unique, diseasespecific mechanisms linking EDS and high blood pressure in this population. Indeed, the recurrent episodes of hypoxemia, hypercapnia, arousals from sleep, and swings in intrathoracic pressure induced by apneic events activate a cluster of pathogenic responses that, over time, lead to blood pressure elevation and promote daytime hypersomnolence (Figure).3 Whether sleepiness is a marker or mediator of hypertension risk in OSA cannot be definitively answered by this study. However, rather than lying in the causal pathway between OSA and hypertension, EDS is more likely another clinical complication and, like hypertension, may be a downstream consequence of the sleep disorder. Bearing in mind that both hypertension and EDS are frequent but not ubiquitous manifestations in OSA patients, hypersomnolence may be regarded not only as a mere marker of disease severity, but also as an expression of the individual vulnerability to the adverse

vidence implicating obstructive sleep apnea (OSA) in blood pressure elevation is compelling, such that OSA is acknowledged as a risk factor in the major guidelines for prevention and management of hypertension.1,2 Nevertheless, not every patient with OSA will develop comorbid hypertension. Traditional markers of disease severity, such as apnea– hypopnea index and degree of nocturnal desaturation, as well as coexisting conditions, including obesity and old age, have been implicated as determinants of enhanced vulnerability.3 More recently, excessive daytime sleepiness (EDS), a common but not pervasive symptom of OSA, has emerged as a nonconventional indicator for identifying high-risk OSA subjects. However, the available literature on the prognostic role of hypersomnolence for clinical outcomes, including hypertension, is controversial.4,5 This discrepancy may be ascribed to the various approaches used to determine EDS, as suggested by Ren et al6 in this issue of Hypertension. These investigators examined the association between prevalent hypertension and EDS in a large, well-characterized Chinese population. The sample consisted of referrals to the sleep clinic for suspected OSA, which was assessed by inlaboratory polysomnography. The use of the gold standard diagnostic method for OSA, in lieu of questionnaires or portable monitors, is a strength of the article. Another important feature is the dual assessment of sleepiness performed in the study. All subjects completed a self-report measure (Epworth Sleepiness Scale7) and a sleep laboratory test (Multiple Sleep Latency Test [MSLT]8) and were then classified based on the average sleep latency (the time taken to fall asleep) exhibited at the MSLT, as an index of EDS. The MSLT consists of 4 to 5 nap opportunities spread across the day, with the subject monitored continuously by polysomnography. The average sleep onset latency in all naps is computed to provide a quantitative estimate of somnolence. After correcting for established risk factors, multivariate analysis showed that those who had OSA and manifested a mean sleep latency at the MSLT of 5 to 8 minutes or

Somnolence: The Silent Partner in the Sleep Apnea-Hypertension Relationship.

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