Background-There is increasing evidence that obstructive sleep apnea (OSA) is an independent risk factor for arterial hypertension. Because there are no controlled studies showing a substantial effect of nasal continuous positive airway pressure (nCPAP) therapy on hypertension in OSA, the impact of treatment on cardiovascular sequelae has been questioned altogether. Therefore, we studied the effect of nCPAP on arterial hypertension in patients with OSA. Methods and Results-Sixty consecutive patients with moderate to severe OSA were randomly assigned to either effective or subtherapeutic nCPAP for 9 weeks on average. Nocturnal polysomnography and continuous noninvasive blood pressure recording for 19 hours was performed before and with treatment. Thirty two patients, 16 in each group, completed the study. Apneas and hypopneas were reduced by Ϸ95% and 50% in the therapeutic and subtherapeutic groups, respectively. Mean arterial blood pressure decreased by 9.9Ϯ11.4 mm Hg with effective nCPAP treatment, whereas no relevant change occurred with subtherapeutic nCPAP (Pϭ0.01). Mean, diastolic, and systolic blood pressures all decreased significantly by Ϸ10 mm Hg, both at night and during the day. Conclusions-Effective nCPAP treatment in patients with moderate to severe OSA leads to a substantial reduction in both day and night arterial blood pressure. The fact that a 50% reduction in the apnea-hypopnea index did not result in a decrease in blood pressure emphasizes the importance of highly effective treatment. The drop in mean blood pressure by 10 mm Hg would be predicted to reduce coronary heart disease event risk by 37% and stroke risk by 56%.

In a systematic study we compared the performance of spectral analysis and detrended fluctuation analysis (DFA) IntroductionSleep as the absence of wakefulness and the missing ability to react on external stimuli is regarded as a unbiased test situation for the autonomic nervous system [1]. Sleep is not just a constant state controlled by metabolic needs for the body being at rest. Instead sleep consists of different well defined sleep stages which follow a well structured temporal order in normal restorative sleep. Heart rate and heart rate variability vary with the sleep stages, and their normal variability is affected in sleep disorders. It has been shown that autonomic activity changes from waking to sleep. Big differences were found between non-REM and REM sleep [2]. Sympathetic tone drops progressively from wakefulness over sleep stage 1 to 4. In contrast REM sleep was characterized by increased sympathetic tone [3]. Parasympathetic tone increases from wakefulness to non-REM sleep. Periods of wakefulness during sleep were found to have an intermediate position between non-REM and REM sleep [4].Sleep apnea affects heart rate variability during sleep described as cyclical variation of heart rate [5]. The recording of cyclical variation of heart rate together with snoring has been used in order to detect obstructive sleep apnea with ambulatory recording devices [6]. It can be assumed that the cyclical variation of heart rate can be detected by spectral analysis if the appropriate frequency range is investigated. The pattern of bradycardia and tachycardia during apnea has been attributed to an effective parasympathetic control of heart rate during sleep [7] interrupted by sympathetic activation accompanying the intermittent apnea-terminating arousals.Spectral analysis of heart rate variability is well established and provides a quantitative evaluation of sympathetic and parasympathetic activation of the heartbeat [8]. Three major oscillatory components were identified. The physiological interpretation of the verylow-frequency (VLF) component (< 0.04 Hz) is still discussed, the low-frequency (LF) component (0.04 -0.15 Hz) reflects baroreflex sympathetic control of blood pressure, and the high-frequency (HF) component (0.15 -0.4 Hz) reflects respiratory rhythm and is believed to be related to parasympathetic control of heart rate [9].Detrended fluctuation analysis (DFA) method has become a widely-used technique for the detection of long-range correlations in noisy, non-stationary time series. In the DFA method, long-range correlations between interbeat intervals separated by several beats are detected by investigating the scaling behavior of the heartbeat fluctuations on different time scales disregarding trends and non-stationarities in the data [10].This study was performed on existing sleep recordings to compare spectral analysis of heart rate and DFA in their ability to distinguish sleep stages in normal and sleep apnea subjects. We also wanted to see whether sleep apnea severity can be distinguis...

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The exact influence of sleep-related breathing disorder (SRBD) on blood pressure control remains unknown. We investigated the influence of different degrees of SRBD on daytime blood pressure and its association to documented hypertension by examining 1,190 consecutive patients referred for diagnosis of SRBD. The protocol includes clinical interview, physical examination, office blood pressure measurement, cholesterol, and blood gas analysis. Unattended home monitoring of nocturnal breathing was performed for assessment of SRBD activity (respiratory disturbance index [RDI]). RDI was independently and linearly associated with systolic blood pressure (unstandardized coefficient [B] = 0.07 +/- 0.03, p = 0.03), diastolic blood pressure (B = 0.07 +/- 0.02, p = 0 < 0.001), and heart rate (B = 0.10 +/- 0.02, p < 0.001) at rest. The relative risk for hypertension (blood pressure >/= 160/95 mm Hg) increased with SRBD severity (odds ratio [OR], 4.15 for RDI >/= 40 versus < 5 [95% CI, 2.7 to 6.5]). This relative risk was also elevated in younger ( 50 yr) (OR, 7.15 versus 2.70 for RDI >/= 40 versus < 5). These cross-sectional clinical data suggest a relationship between SRBD severity and systolic blood pressure, diastolic blood pressure, and heart rate after control for confounders such as body mass index (BMI), age, alcohol/nicotine consumption, cholesterol level, and daytime PO(2) and PCO(2). SRBD is an independent risk factor for systemic hypertension with an increased likelihood in subjects