Obstructive sleep apnea and hypopnea syndrome in patients admitted in a tertiary hospital in Cameroon: Prevalence and associated factors.

PURPOSE: Obstructive sleep apnea and hypopnea syndrome (OSAHS) is poorly documented in Sub-Saharan Africa, especially in the hospital setting. The aim of this study was to determine its prevalence and to investigate the associated factors in patients admitted in a tertiary referral hospital in Cameroon. METHODS: In this cross-sectional study conducted in the Cardiology, Endocrinology and Neurology departments of the Yaounde Central Hospital; all patients aged 21 and older were included consecutively. A sample of randomly selected patients was recorded using a portable sleep monitoring device (PMD). OSAHS was defined as apnea-hypopnea index (AHI) ≥ 5/hour (with > 50% of events being obstructive) and moderate to severe OSAHS as an AHI > 15/hour. Logistic regression was used to identify factors associated to OSAHS. RESULTS: Of the 359 patients included, 202 (56.3%) patients were women. The mean age (standard deviation) was 58 (16) years. The prevalence of OSAHS assessed by PMD (95% CI) was 57.7% (48.5-66.9%), 53.8% in men and 62.7% in women (p = 0.44). The median (25th-75th percentiles) AHI, body mass index and Epworth Sleepiness Scale score of OSAHS patients were 17 (10.6-26.9)/hour, 27.4 (24.7-31.6) kg/m2 and 7 (5-9) respectively. The only factor associated to moderate to severe OSAHS was hypertension [odds ratio (95% CI)]: 3.24 (1.08-9.72), p = 0.036. CONCLUSION: OSAHS is a common condition in patients in this health care centre of Cameroon. In the hospital setting, screening for OSAHS in patients with hypertension is recommended.

Complex sleep apnea at auto-titrating CPAP initiation: prevalence, significance and predictive factors.

INTRODUCTION: Obstructive sleep apnea (OSA) patients may develop central respiratory events under continuous positive airway pressure (CPAP), referred to as complex sleep apnea (CompSA). OBJECTIVE: We aimed to assess prevalence and predictive factors of complex apnea and to evaluate treatment response to CPAP. METHODS: Within a retrospective cohort study, we assessed clinical data of OSA patients, attending the sleep lab during a 15-months period. Included participants underwent two consecutive polysomnographies; baseline diagnosis and treatment trial. Complex apnea patients, defined by a central apnea index ≥ 5 per hour during pressure auto-titration, were compared to remainders. RESULTS: Among 263 included patients, the prevalence of complex apnea was 9.1%. The mean apnea hypopnea index only dropped from 52.7 to 39.9 per hour in CompSA patients, while it improved from 40.9 to 7.3 in patients without CompSA. Although a decreased sleep-fragmentation under CPAP was observable in both groups, the enhancement of Non-REM sleep was superior in patients without CompSA. The CompSA patients showed higher median apnea-hypopnea, mixed apnea and central apnea indices at baseline and displayed higher rates of comorbid heart failure and obstructive pulmonary disease, but no higher severity of associated daytime fatigue and sleepiness symptoms. CONCLUSION: Despite evidenced partial improvement of obstructive events, nocturnal hypoxemia and sleep fragmentation, the occurrence of complex apnea presented here as a clear therapeutic failure of auto-titrating CPAP and was associated with heart failure, COPD and higher central and mixed apnea indices at baseline.

Long-term CPAP treatment partially improves the link between cardiac vagal influence and delta sleep.

BACKGROUND: Continuous positive airway pressure (CPAP) treatment improves the risk of cardiovascular events in patients suffering from severe sleep apnea-hypopnea syndrome (SAHS) but its effect on the link between delta power band that is related to deep sleep and the relative cardiac vagal component of heart rate variability, HF(nu) of HRV, is unknown. Therefore, we tested the hypothesis that CPAP restores the link between cardiac autonomic activity and delta sleep across the night. METHODS: Eight patients suffering from severe SAHS before and after 4 ± 3 years of nasal CPAP treatment were matched with fourteen healthy controls. Sleep EEG and ECG were analysed to obtain spectral sleep and HRV components. Coherence analysis was applied between HF(nu) and delta power bands across the first three sleep cycles. RESULTS: Sleep characteristics and spectral HRV components were similar between untreated patients, treated patients and controls, with the exception of decreased Rapid Eye Movement duration in untreated patients. Coherence and gain values between HF(nu) and delta EEG variability were decreased in untreated patients while gain values normalized in treated patients. In patients before and during long-term CPAP treatment, phase shift and delay between modifications in HF(nu) and delta EEG variability did not differ from controls but were not different from zero. In healthy men, changes in cardiac vagal activity appeared 9 ± 7 minutes before modifications in delta sleep. CONCLUSIONS: Long-term nasal CPAP restored, in severe SAHS, the information between cardiovascular and sleep brainstem structures by increasing gain, but did not improve its tightness or time shift.

Body position and breathing abnormalities during sleep: a systematic study.

BACKGROUND: Until now, studies about body position and nocturnal breathing abnormalities have been restricted to comparing supine versus lateral positions. OBJECTIVES: In this retrospective study, we systematically evaluated the effect of body position on nocturnal breathing in 105 patients with a sleep apnea hypopnea syndrome (SAHS). METHODS: All the patients had an apnea hypopnea index > 10/h, as judged from polysomnography performed in the sleep laboratory. A thoracic sensor allowed to detect nine distinct body positions: supine (S), supine right (SR), right (R), prone right (PR), prone (P), prone left (PL), left (L), supine left (SL) and sitting upward (UP). Respiratory variables (number of obstructive, central and mixed apneas, of hypopneas and of desaturations, all expressed as an index per hour of total sleep time) were evaluated versus the body positions, using the non-parametric Kruskal-Wallis H method. Pairwise comparisons were performed using Mann-Whitney U tests. RESULTS: Most of the total sleep time (45%) was spent supine. A significant effect of body position was found for all the respiratory variables. Breathing was better in the intermediate SR and SL positions than S, and also better in PR and PL positions than, respectively, R and L. All the respiratory variables gradually improved when gradualling moving from the S to the P position. CONCLUSIONS: A nine position sensor, able to define intermediate positions in addition to the basic cardinal positions, is useful in the sleep laboratory. Using such a sensor, we found in SAHS patients that nocturnal breathing improves as a continuum from the S to the P position.

Scale-free dynamics of the synchronization between sleep EEG power bands and the high frequency component of heart rate variability in normal men and patients with sleep apnea-hypopnea syndrome.

OBJECTIVE: To investigate the dynamics of the synchronization between heart rate variability and sleep electroencephalogram power spectra and the effect of sleep apnea-hypopnea syndrome. METHODS: Heart rate and sleep electroencephalogram signals were recorded in controls and patients with sleep apnea-hypopnea syndrome that were matched for age, gender, sleep parameters, and blood pressure. Spectral analysis was applied to electrocardiogram and electroencephalogram sleep recordings to obtain power values every 20s. Synchronization likelihood was computed between time series of the normalized high frequency spectral component of RR-intervals and all electroencephalographic frequency bands. Detrended fluctuation analysis was applied to the synchronizations in order to qualify their dynamic behaviors. RESULTS: For all sleep bands, the fluctuations of the synchronization between sleep EEG and heart activity appear scale free and the scaling exponent is close to one as for 1/f noise. We could not detect any effect due to sleep apnea-hypopnea syndrome. CONCLUSIONS: The synchronizations between the high frequency component of heart rate variability and all sleep power bands exhibited robust fluctuations characterized by self-similar temporal behavior of 1/f noise type. No effects of sleep apnea-hypopnea syndrome were observed in these synchronizations. SIGNIFICANCE: Sleep apnea-hypopnea syndrome does not affect the interdependence between the high frequency component of heart rate variability and all sleep power bands as measured by synchronization likelihood.

Does endothelin play a role in chemoreception during acute hypoxia in normal men?

BACKGROUND: The peripheral chemoreceptors are the dominant reflex mechanism responsible for the rise in ventilation and muscle sympathetic nerve activity (MSNA) in response to hypoxia. Animal studies have suggested that endothelin (ET) plays an important role in chemosensitivity. Moreover, several human clinical conditions in which circulating ET levels are increased are accompanied by enhanced chemoreflex sensitivity. Whether ET plays a role in normal human chemosensitivity is unknown. METHODS: We determined whether bosentan, a nonspecific ET receptor antagonist, would decrease chemoreflex sensitivity in 14 healthy subjects. We assessed the effects of bosentan on the response to isocapnic hypoxia, using a randomized, crossover, double-blinded study design. RESULTS: Bosentan increased mean (+/- SEM) plasma ET levels from 1.97 +/- 0.28 to 2.53 +/- 0.23 pg/mL (p = 0.01). Hypoxia increased mean minute ventilation from 6.7 +/- 0.3 to 8+/0.4 L/min (p < 0.01), mean MSNA from 100 to 111 +/- 5% (p < 0.01), mean heart rate from 67 +/- 3 to 86 +/- 3 beats/min (p < 0.01), and mean systolic BP from 116 +/- 3 to 122 +/- 3 mm Hg (p < 0.01). However, none of these responses differed between therapy with bosentan and therapy with placebo (p = 0.26). Bosentan did not affect the mean MSNA responses to the apneas, during normoxia (change from baseline: placebo, 259 +/- 58%; bosentan, 201 +/- 28%; p = 0.17) or during hypoxia (change from baseline: placebo, 469 +/- 139%; bosentan, 329 +/- 46%; p = 0.24). The durations of the voluntary end-expiratory apneas in normoxia and hypoxia, and the subsequent reductions in oxygen saturation, were also similar with therapy using bosentan and placebo (p = 0.42). CONCLUSION: In healthy men, ET does not play an important role in peripheral chemoreceptor activation by acute hypoxia.

Constant vs auto-continuous positive airway pressure in patients with sleep apnea hypopnea syndrome and a high variability in pressure requirement.

STUDY OBJECTIVES: Auto-continuous positive airway pressure (CPAP) has been reported to have no more efficacy than constant CPAP in unselected patients with sleep apnea hypopnea syndrome (SAHS). The aim of this study was to evaluate patients judged to be good candidates for auto-CPAP because of a high within-night variability in pressure requirement. DESIGN: Single-blind, randomized, cross-over study (2 x 8 weeks) to compare auto-CPAP with constant CPAP. PATIENTS: Outpatients with moderate-to-severe SAHS attending the chest clinic. INTERVENTIONS: Patients were equipped at home in the auto-CPAP mode (model GK418A; Malinckrodt; Nancy, France), using a 4- to 14-cm H(2)O pressure range. Those individuals having a high within-night variability in pressure requirement, assessed at the end of a 14-day run-in period, were included in the cross-over study. Auto-CPAP was compared with constant CPAP (according to a titration night in the sleep laboratory) in terms of compliance, efficacy on apneas (assessed from the pressure monitor), and sleepiness (assessed on the Epworth sleepiness scale). MEASUREMENTS AND RESULTS: Of 90 consecutive patients with SAHS, 27 patients were selected for a within-night variability in pressure requirement exceeding a given threshold. After completion of the cross-over, 24 patients were evaluable. The median percentage of nights the machine was used was 95.5% (range, 45 to 100%) on constant CPAP, and 96.5% (range, 40 to 100%) on auto-CPAP; the median apnea index recorded by the device was 0.40/h (range, 0 to 2.40/h) on constant CPAP, and 0.45/h (range, 0 to 5.80/h) on auto-CPAP (differences not significant). The mean Epworth sleepiness score was significantly (p < 0.01) lower on auto-CPAP (5.1; SD, 2.8) than on constant CPAP (6.1; SD, 2.8). CONCLUSIONS: In patients selected for a high within-night variability in pressure requirement, auto-CPAP administered via a GK418A device was equivalent to constant CPAP based on a titration night in the sleep laboratory. Subjective ratings for sleepiness were slightly lower on auto-CPAP.