O bstructive sleep apnea (OSA) is a common disease that affects 2% to 4% of adult men and ≈1% to 2% of adult women, 1 and among adults aged 30 to 70 years, the prevalence of OSA increases to ≈24% to 26% in men and 17% to 28% in women.2 Repetitive asphyxia events in sleep apnea result in brain arousal, intermittent hypoxemia, and increased sympathetic nervous system activity. Both cross-sectional and longitudinal studies have demonstrated that OSA is a risk factor for hypertension that is independent of age, sex, and body mass index.3-5 Furthermore, it has been shown that OSA is an important cause of hypertension. 6,7 Several mechanisms, including increased sympathetic tone, inflammatory response, impaired arterial baroreflex sensitivity, and pleural pressure swings, induced by intermittent hypoxemia of OSA are involved in the relationship between OSA and hypertension. [8][9][10][11] Excessive daytime sleepiness (EDS) is common in patients with OSA and an important criterion for diagnosis and treatment of OSA. EDS has a prevalence of 16% to 22% in OSA in epidemiological samples, and it is the most common complaint in clinical samples. 1,12 Many studies have shown that OSA patients with subjective EDS have a higher prevalence of hypertension compared with those without EDS. [13][14][15] Furthermore, a series of clinical trials have suggested that continuous positive airway pressure (CPAP) therapy is less effective in OSA patients without EDS than those with EDS in terms of decreasing blood pressure (BP) and preventing the occurrence of hypertension. [16][17][18][19][20] These findings suggest that subjective EDS is associated with hypertension in OSA. However, in previous studies, EDS was determined by self-report, with the Epworth Sleepiness Scale (ESS) 21 being most frequently used. Lombardi et al 22 found that EDS determined by the multiple sleep latency test (MSLT) in OSA patients was associated with lower baroreflex sensitivity and higher low-to-high frequency power ratio of heart rate variability during overnight sleep compared with OSA patients without EDS. To our knowledge, this is the only existing study reflecting a possible association between objective EDS and cardiovascular events in OSA. The specific relationship between hypertension and objectively evaluated EDS has not been investigated.Abstract-Subjective daytime sleepiness is considered a significant risk factor of hypertension in patients with obstructive sleep apnea (OSA). In this study, our goal was to examine the joint effect on hypertension of OSA and objective daytime sleepiness measured by the multiple sleep latency test (MSLT). A total of 1338 Chinese patients with OSA and 484 primary snorers were included in the study. All subjects underwent 1 night polysomnography followed by MSLT. The MSLT values were classified into 3 categories: >8 minutes, 5 to 8 minutes, and <5 minutes. Hypertension was defined based either on direct blood pressure measures or on diagnosis by a physician. After controlling for confounders, OSA combined with MSLT o...
Extremes of sleep duration and obstructive sleep apnea (OSA) are both associated with hypertension. We aimed to explore whether sleep duration modifies the relationship between OSA and prevalent hypertension, using both objective and subjective measures of total sleep duration. A total of 7107 OSA patients and 1118 primary snorers were included in the study. Hypertension was defined based either on direct blood pressure measures or on diagnosis by a physician. Objective sleep duration was derived by polysomnography and subjective sleep duration was self-reported. Logistic regression models were used to estimate the associations between objective/subjective sleep duration and hypertension prevalence in OSA and primary snorers. Compared with primary snorers, OSA combined with objective sleep duration of 5 to 6 hours increased the odds of hypertension by 45% (odds ratio, 1.45; 95% confidence interval, 1.14-1.84), whereas OSA combined with objective sleep duration <5 hours further increased the odds of hypertension by 80% (odds ratio, 1.80; 95% confidence interval, 1.33-2.42). These results were independent of major confounding factors frequently associated with OSA or hypertension. In stratified analysis by sleep duration, risk of hypertension in those with extremely short sleep (<5 hours) was not significantly different between OSA and primary snorers, whereas odds were significant for OSA in the other 4 sleep duration strata (5-6, 6-7, 7-8, and >8 hours). No significance was evident using subjective sleep duration. We conclude that objective short sleep duration is associated with hypertension in OSA patients. Extremely short sleep duration in itself may actually be even more detrimental than OSA in terms of hypertension risk.
Due to frequent abnormal breathing events and their effects on sleep architecture, patients with obstructive sleep apnea (OSA) exhibit decreased amounts of slow wave sleep (SWS). Reduced SWS has been linked to hypertension in community-based studies. We sought to investigate whether SWS percentage modifies the association between OSA and prevalent hypertension. We studied 7107 patients with OSA and 1118 primary snorers who underwent in-laboratory polysomnography. Patients were classified into quartiles of percent SWS. Hypertension was defined based either on clinic blood pressure measures or on physician diagnosis. Multivariable logistic regression model showed a significant interaction effect of OSA and SWS on prevalent hypertension ( P =0.002). Decreased SWS was associated with higher odds for hypertension in OSA but not in primary snoring, with patients with OSA exhibiting <0.1% SWS (OR, 1.44 [95% CI, 1.21–1.70]; P =0.001) and those with 0.1% to 4.8% SWS (OR, 1.20 [95% CI, 1.03–1.40]; P =0.02) being more likely to have hypertension compared with those with >11.1% SWS. In analysis stratified by OSA severity, significant associations between percent SWS and blood pressure emerged only in moderate and severe OSA. Effect modifications by sex ( P =0.040) and age ( P =0.007) were also only evident in OSA, indicating that decreased SWS was associated with hypertension only in men and in patients <60 years old. Decreased SWS is associated with a dose-dependent increase in odds of prevalent hypertension in patients with OSA. The effects of SWS are likely to be modulated by OSA severity. SWS may be implicated in the heightened risk of cardiovascular diseases exhibited by patients with OSA.
BACKGROUND:The treatment of OSA in highland residents is not established. RESEARCH QUESTIONS: Does nocturnal oxygen supplementation (NOS) improve sleep-related breathing disturbances, nocturnal oxygenation, and cognitive performance in patients with OSA living at 3,200 m? STUDY DESIGN AND METHODS: Forty patients with OSA permanently living in Shangri-La, China at 3,200 m (median age [interquartile range], 47.0 [44.0-53.0] years; oxygen desaturation index, 38.4/h [34.2/h-52.3/h]), were randomly assigned to receive nasal NOS and sham oxygen (ambient air), for one night each, at 2 L/min, in a crossover design, separated by a washout period of 2 weeks. During treatment nights polysomnography was performed, and further outcomes were evaluated the next morning. The primary outcome was the difference in apnea-hypopnea index (AHI) between nights with NOS and nights with sham oxygen.RESULTS: During nights with sham oxygen, the median (interquartile range) total AHI was 43.4/h (31.1/h-67.5/h), the obstructive AHI was 41.9/h (28.5/h-66.8/h), and the central AHI was 0.6/h (0.1/ h-1.3/h); blood oxygenation as determined by pulse oximetry (SpO 2 ) was 87.0% (84.5%-89.0%). In intention-to-treat analysis, NOS decreased the total AHI by a median of 17.9/h (95% CI, 8.0/h-27.1/ h; P < .001), through a reduction in obstructive AHI by 16.0/h (95% CI, 6.8/h-26.0/h; P < .001) and central AHI by 0.4/h (95% CI, 0.1/h-0.9/h; P < .001). NOS also increased SpO 2 by 7.0% (95% CI, 6.0%-8.0%; P < .001). Heart rate during sleep and pulse rate in the morning after NOS were significantly reduced, but subjective sleep quality and cognitive performance showed no changes. INTERPRETATION:In highland residents with OSA, NOS significantly improved sleep-related breathing disturbances and nocturnal oxygenation. NOS also reduced heart rate during sleep and morning pulse rate. If these beneficial effects are confirmed in longer term studies, NOS may be a treatment option for highland patients with OSA who cannot be treated by CPAP.
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