Arousability in sleep apnoea/hypopnoea syndrome patients.

Sleep disruption and daytime sleepiness in obstructive sleep apnoea/hypopnoea syndrome (OSAHS) patients result from recurrent apnoeas/hypopnoeas and arousals from sleep. Around 30% of apnoeas/hypopnoeas are not terminated by visible cortical arousals. The current authors tested the hypotheses that arousal induction is linked to sleep stage, oxygen desaturation, event type, event duration and time of occurrence during the night. Fifteen patients with OSAHS of varying severity were studied and all their apnoeas/hypopnoeas were evaluated. Eight of 15 patients had apnoeas/hypopnoeas in all sleep stages, and all their 610 apnoeas/hypopnoeas were analysed in the between stages comparison; data from all 15 patients were included in other comparisons. Thirty-four per cent of apnoeas/hypopnoeas during slow wave sleep (SWS) were associated with arousal, significantly less than the 77% during nonrapid eye movement (NREM) 1 and 2 and 62% during rapid eye movement (REM) sleep. Arousal induction was not affected by oxygen desaturation, event type, duration or time of the night. The apnoeal/hypopnoea index was 39 x h(-1) in REM 1 and 2, significantly higher compared to 17 x h(-1) in REM or to 11 x h(-1) in SWS sleep. In conclusion, apnoeas/hypopnoeas in slow wave sleep are associated with fewer cortically apparent, visually detected arousals.     

Mortality in severe sleep apnoea/hypopnoea syndrome patients: impact of treatment.

The aim of this study was to determine mortality in patients with sleep apnoea/hypopnoea syndrome (SAHS) according to the treatments employed and comorbidity. An historical cohort of patients with SAHS diagnosed at a university hospital between 1982 and 1992 and followed until 1996 was studied. From a total of 475 SAHS patients, 444 (94%), with a mean+/-SD apnoea/hypopnoea index at diagnosis of 55+/-27, were located and included in the study. SAHS treatments employed were: surgery (88), weight loss (134), continuous positive airway pressure (124) and 98 patients were not treated. By the end of follow-up, 49 patients had died. According to Cox regression analysis, mortality in treated patients was lower than in those not treated, but higher in those with a history of severe chronic obstructive pulmonary disease. Mortality in nontreated patients compared with that of the general population, adjusted for age and sex, showed excessive mortality, which decreased in treated patients. Stratification by age showed a greater mortality rate ratio in patients <50 yrs. These findings were maintained when mortality from cardiovascular causes was compared. In conclusion, a rise in mortality was found in nontreated sleep apnoea/hypopnoea syndrome patients compared with the general population, whereas mortality in those treated for sleep apnoea/hypopnoea syndrome did not differ significantly from that of the general population.     

Split-night versus full-night studies for sleep apnoea/hypopnoea syndrome.

Investigation and treatment of sleep apnoea/hypopnoea syndrome (SAHS) is placing increasing demands on healthcare resources. This workload may be reduced by using split-night studies instead of the standard full-nights of diagnostic polysomnography and continuous positive airway pressure (CPAP) titration. Split-night studies involve polysomnography in the first half of the night followed, if there is an abnormal frequency of apnoeas and hypopneas, by CPAP titration for the remainder of the night. The authors' database of all patients prescribed a CPAP trial 1991-1997 was used to compare long-term outcomes in all 49 (46 accepting CPAP) patients prescribed split-night studies with those in full-night patients, matched 1:2 using an apnoea/ hypopnoea index (AHI) of +/-15% and Epworth score of +/-3 units. Classical symptoms of SAHS were the main reason for the split-night studies (n=27). There were no differences between the groups in long-term CPAP use, median nightly CPAP use (split-night 6.0 h x night-1, interquartile range (IQR) 3.8-7.4, full-night; 6.2 h x night-1, IQR 3.7-7.0, p=0.9), post-treatment Epworth scores and frequency of nursing interventions/clinic visits required. The median time from referral to treatment was less for the split-night patients (13 months, IQR 11-20 months) than for full-night patients (22 months, IQR 12-34 months; p=0.003). Split-night studies, in selected patients, result in equivalent long-term continuous positive airway pressure use to full-night studies with shorter treatment times and less healthcare utilization.     

Neurocognitive impairment in Chinese patients with obstructive sleep apnoea hypopnoea syndrome

Background and objective: Sleep‐disordered breathing is known to be associated with impairment in cognitive function. The aim of this study was to characterize neurocognitive impairment in a cohort of Chinese patients with varying severities of obstructive sleep apnoea hypopnoea syndrome (OSAHS), and to develop a sensitive instrument for routine screening of cognitive impairment. Methods: Eligible patients (n = 394) were categorized into a primary snoring group, and mild, moderate and severe OSAHS groups, based on assessment of AHI. The Montreal Cognitive Assessment (MoCA) and the Mini‐Mental State Examination (MMSE) questionnaires were administered to assess cognitive function, and the correlations between questionnaire scores and clinical and polysomnographic parameters were further evaluated by stepwise multivariate regression. Results: MoCA scores decreased progressively across the spectrum from primary snoring to severe OSAHS. Importantly, mild neurocognitive impairment as defined by a MoCA score <26 was more common in the moderate (38.6%) and severe (41.4%) OSAHS groups than in the mild OSAHS (25.0%) and primary snoring (15.2%) groups. In contrast, MMSE scores were largely normal and comparable among all four groups. Evaluation of MoCA subdomains further revealed selective reduction in memory/delayed recall, visuospatial and executive function, and attention span in the severe OSAHS group compared with the other groups. Stepwise multivariate regression analysis demonstrated that MoCA scores correlated significantly with lowest oxygen saturation (L‐SaO₂) and years of education. Conclusions: Neurocognitive impairment is common in patients with OSAHS. The MoCA is a brief and sensitive tool for the assessment of cognitive impairment in OSAHS patients, whose performance on the MMSE is in the normal range.     

Health utilities in evaluating intervention in the sleep apnoea/hypopnoea syndrome.

Formulating a rational health policy necessitates the ability to compare between different healthcare interventions and disease scenarios. Continuous positive airway pressure (CPAP) therapy with a conservative lifestyle strategy in sleep apnoea/hypopnoea syndrome (SAHS) was evaluated using health utility and quality-adjusted life years (QALYs) as outcome measures. A total 71 SAHS (apnoea/hypopnoea index > or = 15 h(-1)) patients completed a randomised, parallel group study over 3 months using utilities derived by the standard gamble approach (Usg) and European quality of life questionnaire (Euroqol) (Ueq). The severely impaired health status at baseline improved by 23% (Usg 0.32 to 0.55) adding 8 QALYs in the CPAP group, compared to a 4% improvement with 4.7 QALYs added in the lifestyle group (Usg 0.31 to 0.35). The Ueq showed a marginal change with CPAP (0.73 to 0.77) but did not demonstrate any improvement with lifestyle intervention. The health status impairment in sleep apnoea/hypopnoea syndrome patients is markedly improved by continuous positive airway pressure compared to a modest improvement with conservative lifestyle strategies using the standard gamble utility, which may be incorporated in effectiveness and economic analyses. The European quality of life questionnaire did not reflect a similar degree of impact and is probably not useful in this population.     

Evaluation of a portable device for diagnosing the sleep apnoea/hypopnoea syndrome.

Waiting times for hospital-based monitoring of the obstructive sleep apnoea/hypopnoea syndrome (OSAHS) are rising. This study tested whether Embletta, a new portable device, may accurately diagnose OSAHS at home. A synchronous comparison to polysomnography was performed in 40 patients and a comparison of home Embletta studies with in-laboratory polysomnography was performed in 61 patients. In the synchronous study, the mean difference (polysomnography-Embletta) in apnoeas+hypopnoeas (A+H) x h(-1) in bed was 2 h(-1). In comparison to the apnoea/ hypopnoea index (AHI) x h(-1) slept, the Embletta (A+H) x h(-1) in bed differed by 8 x h(-1). These data were used to construct diagnostic categories in symptomatic patients from their Embletta results: "OSAHS" (> or = 20 (A+H) x h(-1) in bed), "possible OSAHS" (10-20 (A+H) x h(-1) in bed) or "not OSAHS" (<10 (A+H) x h(-1) in bed). In the home study, the mean difference in (A+H) x h(-1) in bed was 3 x h(-1). In comparison to the polysomnographic AHI x h(-1) slept, the Embletta (A+H) x h(-1) in bed differed by 6 +/- 14 x h(-1). Using the above classification, all nine patients categorised as not OSAHS had AHI < 15 x h(-1) slept on polysomnography and all 23 with OSAHS on Embletta had an AHI > or = 15 on polysomnography, but 18 patients fell into the possible OSAHS category potentially requiring further investigation and 11 home studies failed. Most patients were satisfactorily classified by home Embletta studies but 29 out of 61 required further investigation. The study suggested a 42% saving in diagnostic costs over polysomnography if this approach were adopted.     

Influence of setting on unattended respiratory monitoring in the sleep apnoea/hypopnoea syndrome.

The high demand for full polysomnography and the better quality of sleep at home are the main reasons for performing home sleep studies. Home respiratory monitoring has been evaluated in several studies, but the influence of setting on the results of unattended respiratory monitoring has not been assessed to date. Unattended monitoring of respiratory variables at home and in the sleep laboratory was conducted in 35 consecutive patients with suspected sleep apnoea/hypopnoea syndrome. Respiratory variables during sleep, rate of successful studies and patient preference were compared. The data acquisition failure rate was 2.8% in the sleep laboratory and 5.7% at home. The mean difference between apnoea/hypopnoea indices (AHI) obtained from home and laboratory studies was -0.21 +/- 8 (95% confidence interval 3.27-2.84). Using the method comparison approach of Bland and Altman, the limits of agreement of the mean difference between AHI home and AHI laboratory were -16.7 and 17.1. No difference was observed between the studies in time spent in different body positions. When patients were asked where they would prefer to repeat the sleep study, 53% replied at home, 28% in hospital and 19% showed no preference. It was concluded that the setting of unattended respiratory monitoring (home or sleep laboratory) influences neither the number of valid studies nor the results of the respiratory parameters measured; most patients, however, preferred home studies.     

The sleep apnoea/hypopnoea syndrome depresses waking vagal tone independent of sympathetic activation.

The modest daytime hypertension and sympathetic upregulation associated with the sleep apnoea/hypopnoea syndrome (SAHS), does not explain the relatively large increased risk of cardiac morbidity and mortality in the SAHS patients population. Therefore, efferent vagal and sympathetic activity was evaluated during wakefulness in SAHS subjects and matched healthy controls, in order to determine if vagal downregulation may play a role in the aetiology of cardiac disease in the SAHS. The awake autonomic nervous system function of 15 male subjects, with mild-to-moderate SAHS was compared to that of 14 healthy controls matched for age, body mass index, gender and blood pressure. All subjects were free from comorbidity. Vagal activity was estimated from measurements of heart rate variability high frequency power (HF) and sympathetic activity was measured from urine catecholamine excretion. The %HF power was significantly (p < 0.03) reduced in SAHS patients (10+/-1.6 (mean+/-SEM)) as compared to controls (17 +/- 3). In addition, HF power correlated with the apnoea/hypopnoea index in the SAHS subjects (R = -0.592, p = 0.02). There was no statistically significant difference in the daytime excretion of nonadrenaline between control (242 +/- 30 nmol x collection(-1)) and SAHS (316 +/- 46 nmol x collection(-1)) subjects (p = 0.38). In these sleep apnoea/hypopnoea syndrome patients there was limited evidence of increased waking levels of urine catecholamines. The principal component altering waking autonomic nervous system function, in the sleep apnoea/hypopnoea syndrome subjects, was a reduced daytime efferent vagal tone.     

Analysis of the interbeat interval increment to detect obstructive sleep apnoea/hypopnoea.

The prevalence of obstructive sleep apnoea/hypopnoea syndrome (OSAHS) is underestimated and its diagnosis is costly and restricted to specialised sleep laboratories. The frequency component of interbeat interval increment (III) has been proposed as a simple and inexpensive diagnostic tool in OSAHS. In a set of 150 patients with clinically suspected sleep-related breathing disorder, the actual predictive accuracy of the power spectral density of the III of the very low frequencies (%VLFI) was analysed by comparing with the apnoea/hypopnoea index (AHI), as assessed by synchronised polysomnography. OSAHS was defined in 100 patients according to an AHI>or=15 events.h(-1). Receiver operator characteristic curves built for %VLFI confirmed that this variable was able to separate OSAHS positive from OSAHS negative with statistical significance. Using an appropriate threshold (>4%), %VLFI demonstrated a positive predictive value of 80%. Misclassification of false-positive subjects occurred when the patient presented significant sleep discontinuity and sleep fragmentation (sleep fragmentation index>or=50 events.h(-1)) related to insomnia or periodic limb movements. A power spectral density of the interbeat interval increment of very low frequencies>4% allowed correct classification of obstructive sleep apnoea/hypopnoea syndrome when the clinical history suggested sleep-related breathing disorders and when moderate-to-severe cases are considered. Higher power spectral density of the interbeat interval increment of very low frequencies may also indicate disrupted sleep in the absence of clear clinical symptoms of sleep apnoea/hypopnoea syndrome.     

Clinical audit of subjects with snoring & sleep apnoea/hypopnoea syndrome fitted with mandibular repositioning splint

Snoring and obstructive sleep apnoea/hypopnoea syndrome (OSAHS) are often treated with mandibular repositioning splints (MRS), but the efficacy and satisfaction of them has not been comprehensively addressed. A survey on the use of and satisfaction with MRS was posted to 177 patients referred by a hospital orthodontic department for custom-fitting of a MRS. Data were analysed using non-parametric techniques. The response rate was 81% (n=144). Responders (30F, 114M) had mean (SD) age of 51 (11) years, apnoea+hypopnoea index (AHI) of 24 (21) per hr and Epworth Score of 10 (5) at diagnosis, and had been supplied with their MRS a median 7 (IQR 5-11) months previously. Fifty of the 144 patients (35%) had been offered continuous positive airway pressure (CPAP) treatment but had declined or abandoned this. Self-reported MRS use was 5 (2) h/night, with 74 of the 144 patients (51%) continuing to use MRS at least occasionally at a median 7 months after fitting. Survival analysis showed 12% still using MRS at 12 months. Epworth score fell slightly with MRS therapy [-2.4 (3.5); P=0.005] and 7 daytime and 2 nocturnal symptoms improved in MRS users (all P<0.05). Marital satisfaction did not change with MRS. Problems preventing MRS use in 70 non-users included: non-retention (n=12), sore mouth (n=13) or jaw (n=7), difficulties falling asleep (n=10) or breathing (n=7), excessive salivation (n=4), dental damage (n=4) and other problems (n=3). Continued use of MRS therapy was associated with a higher number of teeth, low marital satisfaction perceived by partners and greater improvement in symptoms reported by patients and partners. Continuance with MRS may be low and linked to tolerance problems.     

Platelet function in patients with obstructive sleep apnoea syndrome.

Patients with obstructive sleep apnoea syndrome (OSAS) are subject to an increased cardiovascular morbidity including myocardial infarction and stroke. Platelets play an important role in the pathogenesis and triggering of acute cardiovascular syndromes. So far, the influence of OSAS on platelet function is not fully understood. Platelet aggregability to epinephrine, collagen, arachidonic acid, and adenosine diphosphate in vitro was measured in 17 consecutive male patients (53.0+/-2.1 yrs) with polysomnographically verified OSAS and compared with that of 15 male controls (50.1+/-3.6 yrs) at 20:00 h, 24:00 h, and 06:00 h. In addition, the long-term effects of continuous positive airway pressure (CPAP) therapy on platelet aggregability was assessed after 6 months. Platelet aggregation in vitro induced by epinephrine showed a slight increase overnight in the untreated OSAS patients (NS) whereas it decreased slightly (NS) in the controls and in the treated OSAS patients. Pretherapeutic platelet aggregability was significantly lowered by CPAP therapy both at 24:00 h (64.0+/-6.5 versus 55.3+/-6.7%, p<0.05) and at 06:00 h (64.1+/-6.5 versus 45.8+/-7.6%; p=0.01). Platelet aggregability during sleep in the controls resembled that found in patients with OSAS during CPAP therapy. The results suggest that obstructive sleep apnoea syndrome contributes, at least in part, to platelet dysfunction and that long-term continuous positive airway pressure treatment may reduce platelet aggregability.     

Cardiovascular risk factors in patients with obstructive sleep apnoea syndrome.

Cardiovascular disorders are common in patients with obstructive sleep apnoea syndrome (OSAS) but there is debate as to whether OSAS is an independent risk factor for their development, since OSAS may be associated with other disorders and risk factors that predispose to cardiovascular disease. In an effort to quantify the risk of OSAS patients for cardiovascular disease arising from these other factors, the authors assessed the future risk for cardiovascular disease among a group of 114 consecutive patients with established OSAS prior to nasal continuous positive airway pressure therapy, using an established method of risk prediction employed in the Framingham studies. Patients were 100 males, aged (mean+/-SD) 52+/-9.0 yrs, and 14 females, aged 51+/-10.4 yrs, with an apnoea/hypopnoea index of 45+/-22 x h(-1). Based on either a prior diagnosis, or a mean of three resting blood pressure recordings >140 mmHg systolic and/or 90 diastolic, 68% of patients were hypertensive. Only 18% were current smokers, while 16% had either diabetes mellitus or impaired glucose tolerance, and 63% had elevated fasting cholesterol and/or triglyceride levels. The estimated 10-yr risk of a coronary heart disease (CHD) event in males was (mean+/-SEM) 13.9+/-0.9%, 95% confidence interval (95% CI) 12.1-16.0, and for a stroke was 12.3+/-1.4%; 95% CI 9.4-15.1, with a combined 10 yr risk for stroke and CHD events of 32.9+/-2.7%; 95% CI 27.8-38.5 in males aged >53 yrs. These findings indicate that obstructive sleep apnoea syndrome patients are at high risk of future cardiovascular disease from factors other than obstructive sleep apnoea syndrome, and may help explain the difficulties in identifying a potential independent risk from obstructive sleep apnoea syndrome.     

Progression of obstructive sleep apnoea syndrome in Japanese patients

Sleep and Breathing - The aggravation of obstructive sleep apnoea syndrome (OSAS) is reportedly associated with weight gain. The present study investigated the factors associated with worsening of...     

QT interval dispersion in obstructive sleep apnoea syndrome patients without hypertension.

QT interval dispersion (QT(d)) reflects inhomogeneity of repolarisation. Delayed cardiac repolarisation leading to the prolongation of the QT interval is a well-characterised precursor of arrhythmias. Obstructive sleep apnoea syndrome (OSAS) can cause cardiovascular complications, such as arrhythmias, myocardial infarction, and systemic and pulmonary hypertension. The aim of this study was to assess QT(d) in OSAS patients without hypertension. A total of 49 subjects without hypertension, diabetes mellitus, any cardiac or pulmonary diseases, or any hormonal, hepatic, renal or electrolyte disorders were referred for evaluation of OSAS. An overnight polysomnography and a standard 12-lead ECG were performed in each subject. According to the apnoea-hypopnoea index (AHI), subjects were divided into control subjects (AHI <5, n = 20) and moderate-severe OSAS patients (AHI > or =15, n = 29). QT(d) (defined as the difference between the maximum and minimum QT interval) and QT-corrected interval dispersion (QT(cd)) were calculated using Bazzet's formula. In conclusion, the QT(cd) was significantly higher in OSAS patients (56.1+/-9.3 ms) than in controls (36.3+/-4.5 ms). A strong positive correlation was shown between QT(cd) and AHI. In addition, a significantly positive correlation was shown between QT(cd) and the desaturation index (DI). The AHI and DI were significantly related to QT(cd) as an independent variable using stepwise regression analysis. The QT-corrected interval dispersion is increased in obstructive sleep apnoea syndrome patients without hypertension, and it may reflect obstructive sleep apnoea syndrome severity.     

Long-term follow-up of untreated patients with sleep apnoea syndrome

Obstructive sleep apnoea (OSA) is a common disorder with numerous potential sequelae. Although the majority of these consequences can be reduced with appropriate treatment, only limited data exist regarding the natural progression ofthis disorder in untreated individuals. We hereby report a long-term follow-up of all untreated patients (n = 40) followed-up in the Technion Sleep Clinic, using both subjective and objective measurements. In addition, we report a long-term follow-up of 11 patients who attempted dietary weight loss. The average time interval between the first and second polysomnographies for the untreated group was 5.0 +/- 2.8 yrs, and 2.5 +/- 2.3 yrs for the weight reduction group. There was no significant change in Body Mass Index (BMI) or Respiratory Disturbance Index (RDI) between the two Polysomnographic (PSG) evaluations in the untreated patients. However, eight patients developed hypertension (n=5) or ischaemic heart disease (IHD) (n=3) between the two evaluations. RDI, age and BMI at the time ofthe initial evaluation were not predictive of changes in RDI, snoring intensity or minimal oxygen saturation. However, the patients who developed hypertension/IHD had significantly higher RDI than the patients who did not (46 +/- 27 vs. 23 +/- 17 h(-1), P < 0.005). In the weight-loss group, BMI decreased by a mean of 3.1 kg m(-2), and RDI decreased by 20events h(-1), P<0.05 for both.There was a significant correlation between the weight loss and improvement in RDI (R = 0.75, P = 0.005). We conclude that in untreated obstructive sleep apnoea patients RDI does not necessarily increase over time, but associated hypertension or ischaemic heart disease may develop.When weight loss is successfully achieved, sleep apnoea significantly improves with a high correlation between the extent of weight loss and the improvement in apnoea status.     

Endothelial injury markers before and after nasal continuous positive airway pressure treatment for obstructive sleep apnoea hypopnoea syndrome

Purpose

The purpose of this study was to evaluate whether serum amyloid A (SAA), C-reactive protein (CRP), vascular cell adhesion molecule-1 (VCAM-1) and intercellular adhesion molecule-1 (ICAM-1) levels are elevated in obstructive sleep apnoea hypopnoea syndrome (OSAHS), and whether they change following acute- and medium-term CPAP treatment.

Methods

Consecutive subjects (n?=?40) referred to the Sleep Disordered Breathing Unit were included in the research. Sera were sampled in the afternoon prior to an in-hospital limited-channel sleep study and on the next morning. Those diagnosed with OSAHS were commenced on CPAP and had further blood samples collected in the morning after the first night and then after a month of treatment.

Results

We had 20 subjects with moderate/severe OSAHS (mean ± SD), 4 % desaturation rate (4 % DR) 44.3?±?31.4 events/h, and 20 comparator subjects with symptoms but negative sleep studies, 4 % DR 5.6?±?2.9 events/h. There was no difference in the morning and afternoon vascular injury marker levels between the OSAHS and comparator groups. However, CRP (6.52?±?9.53 vs. 5.58?±?8.47, p?=?0.04) and VCAM-1 (366.30?±?90.11 vs. 339.60?±?95.87, p?=?0.02) levels showed significant diurnal variation within the OSAHS group with higher afternoon levels compared to morning measurements. There were no changes in any of the vascular injury marker levels following CPAP.

Conclusions

This study demonstrates that OSAHS leads to endothelial dysfunction as reflected by higher afternoon than morning CRP and VCAM-1 levels. However, despite a good CPAP compliance, a month of treatment does not decrease vascular injury marker levels.     

Hypercapnia in obstructive sleep apnoea syndrome

BACKGROUND: The reports on the prevalence of hypercapnia in Obstructive Sleep Apnoea Syndrome (OSAS) are conflicting. We studied the prevalence of hypercapnia in a population of OSAS patients referred to a Department of Respiratory Medicine and the mechanism of the respiratory failure in OSAS associated with Obesity Hypoventilation Syndrome (OHS) or with Chronic Obstructive Pulmonary Disease (COPD) (Overlap syndrome). METHODS: We studied 219 consecutive OSAS patients during a period of 3 years. We recorded age and anthropomorphic data and performed polysomnography and pulmonary function tests. In relation to the value of PaCO(2), the patients were divided in hypercapnic (PaCO(2)>45 mmHg) patients and normocapnic patients. They were also divided into three groups in relation to the presence of "simple" or "pure" OSAS, to the presence of OSAS associated with COPD, to the presence of OSAS associated with OHS. RESULTS: Seventeen per cent of the patients were hypercapnic. They were significantly heavier, had more severe lung function test abnormalities and more severe nocturnal oxyhemoglobin desaturations than the normocapnic ones, while Forced Expiratory Volume in one second as a percentage of Forced Vital Capacity (FEV1/FVC %) and Apnoea/Hypopnoea Index (AHI) were similar. OHS patients (13%) were significantly younger and heavier, had lower PaO(2) and higher PaCO(2) than "simple" OSAS patients (77%) and Overlap patients (10%) and had more severe restrictive defect. There was no difference in terms of AHI among the three groups, but nocturnal oxyhemoglobin desaturations were more severe in OHS group. In OHS group hypercapnia was correlated to FVC% of predicted and FEV1% of predicted and to the mean nocturnal oxyhemoglobin saturation; in Overlap patients PaCO(2) was correlated to Forced Expiratory Flow rate at low Vital Capacity. CONCLUSION: Seventeen per cent of OSAS patients referred to a Department of Respiratory Medicine were hypercapnic. Hypercapnia in OHS patients correlates to the restrictive ventilatory defect whereas in Overlap patients it seems to correlate to peripheral airways obstruction. The distinction between patients with "simple" or "pure" OSAS and patients affected by OSAS associated with OHS or COPD could be important not only for clinical and prognostic implications, but also for the consequences in terms of ventilatory treatment.     

Skeletal muscle changes in patients with obstructive sleep apnoea syndrome

Previous studies have shown that chronic hypoxia leads to changes in skeletal muscle structure (fibre size and type) and activities of several bioenergetic enzymes. Whether this occurs also in conditions characterised by intermittent hypoxia, such as the obstructive sleep apnoea syndrome (OSAS), is unknown. To explore this possibility, we obtained a needle biopsy of the quadriceps femoris in 12 consecutive stable outpatients with severe OSAS (52 +/- 9 year, apnoea-hypopnoea index 70 +/- 14 h(-1)) (x +/- SD) and in six healthy volunteers (49 +/- 8 year), where we quantified fibre type, size and protein content, as well as phosphofructo-kinase (PFK) and cytochrome oxidase (CytOx) activities. We found that fibre-type distribution was similar in patients and controls. In contrast, the diameter of type II fibres (74 +/- 10 microm vs. 56 +/- 11 microm, P < 0.05) and protein content (100 +/- 14 vs. 88 +/- 8 microg/mg) was higher in patients with OSAS. Likewise, we observed upregulation of CytOx (0.93 +/- 0.38 vs. 0.40 +/- 0.22 microkat/mg protein, P < 0.01) and PFK activities (5.35 +/- 4.8 vs. 1.3 +/- 1.3 microkat/ mg protein, P < 0.05) in patients with OSAS. These results show that, paralleling which occurs in conditions characterised by continuous hypoxia, patients with OSAS (and intermittent hypoxia) also show structural and bioenergetic changes in their skeletal muscle.     

Evidence for left ventricular dysfunction in patients with obstructive sleep apnoea syndrome.

There is limited information on the development of left ventricular (LV) dysfunction in patients with obstructive sleep apnoea (OSA) in the absence of lung and cardiac comorbidity. This study aimed to investigate whether OSA patients without heart morbidity develop LV dysfunction, and to assess the effect of continuous positive airway pressure (CPAP) on LV function. Twenty-nine OSA patients and 12 control subjects were studied using technetium-99m ventriculography to estimate LV ejection fraction (LVEF), LV peak emptying rate (LVPER), time to peak emptying rate (TPER), peak filling rate (LVPFR) and time to peak filling rate (TPFR) before and after 6 months of treatment with CPAP. A significantly lower LVEF was found in OSA patients, compared to control subjects, (53+/-7 versus 61+/-6%) along with a reduced LVPER (2.82+/-0.58 versus 3.82+/-0.77 end-diastolic volumes x s(-1)). Furthermore, OSA patients had significantly lower LVPFR (2.67+/-0.71 versus 3.93+/-0.58 end-diastolic volumes x s(-1)) and delayed TPFR (0.19+/-0.04 versus 0.15+/-0.03 s) in comparison with the control group. Six-months of CPAP treatment was effective in significantly improving LVEF, LVPER, LVPFR and TPFR. In conclusion, obstructive sleep apnoea patients without any cardiovascular disease seem to develop left ventricular systolic and diastolic dysfunction, which may be reversed, either partially or completely, after 6 months of continuous positive airway pressure treatment.