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Periodic limb movements during sleep (PLMS) and obstructive sleep apnea syndrome (OSAS) are two common sleep disorders. The similarity in periodicity of periodic limb movements (PLMs) and obstructive sleep apneas (OSAs) led us to hypothesize the existence of a common central generator responsible for the periodicity of both OSAs and PLMs. In order to test this hypothesis, we compared apnea periodicity before continuous positive airway pressure (CPAP) treatment with PLMs periodicity during CPAP treatment in 26 OSA patients, consecutively recorded and treated in our sleep laboratory. The investigation on CPAP was performed twice, once during the initial evaluation and once during a follow-up evaluation after 3 months of home treatment with CPAP. Our results showed that, in this sample, 16 patients out of 26 had an association of OSAS and PLMS, defined as the occurrence of at least 5 PLMs per hour of sleep. The mean apnea interval - measured as the time between the beginning of two successive apneas - was 43.1 s (+/-15.2, SD) and the mean PLM interval - calculated in the same way - was 29.6 s (+/-15.2) during the baseline night, 28.5 s (+/-15.7) during the first CPAP night, and 29.8 s (+/-14.8) during the second CPAP night. Thus, the periodicity of the two phenomena (apneas and PLMs) was different, both before and after CPAP treatment (P< 0.05). When considering the interval between the end of an event (apnea or PLM) and the beginning of the next one the mean apnea interval was 19.5 s (+/-11. 6), and the mean PLM interval was 28.1 s (+/-15.3) during the untreated night, 26.6 s (+/-16) during the first CPAP night and 27.9 s (+/-15) during the second CPAP night. The shortening of apnea intervals with this method of measuring intervals reflects the longer duration of apneas as compared to PLMs. Again the intervals between PLMs were not different between each other but the intervals between apneas were different from the intervals between PLMs (P< 0. 05) These results show that the periodicity of PLMs is different from that of OSAs, suggesting that sleep apneas and PLMs are not generated by a common central generator.

The aim of the present study was to determine survival rates of obstructive sleep apnoea patients treated with continuous positive airway pressure (CPAP) and to investigate the prognostic value of pretreatment lung function and pulmonary haemodynamics. Two hundred and ninety-six patients, exhibiting > or = 20 apnoeas plus hypopnoeas per hour of sleep, were included. Patients were treated with nasal CPAP and regularly followed up. The cumulative survival rates were 0.96 (95% confidence interval (CI): 0.94-0.99) at 3 yrs and 0.93 (95% CI: 0.91-0.97) at 5 yrs. Most patients died from cardiovascular disease. Apart from age, covariates associated with a lower survival were the presence of a heavy smoking history, a low vital capacity, a low forced expiratory volume in one second (FEV1) and a high mean pulmonary artery pressure. Only three covariates were included by forward stepwise selection in the multivariate analysis, smoking habit (>30 pack-yrs), age and FEV1. The observed survival rates of the group as a whole were similar to those of the general population matched in terms of age, sex and smoking habit, except for patients between 50 and 60 yrs old who had reduced survival. This difference disappeared when patients of the present study with an associated chronic obstructive pulmonary disease were excluded from the comparison. In conclusion, survival of obstructive sleep apnoea patients treated with nasal continuous positive airway pressure is near to that of the general population. The prognosis is worse in subgroups of patients with a history of heavy smoking and with an associated chronic obstructive pulmonary disease.

It has recently been described that the maximal respiratory effort developed at the end of an apnea (Pesmax)--which is regarded as an index of arousal threshold in patients with obstructive sleep apnea syndrome (OSA)--increases progressively during the night, probably as a consequence of associated sleep fragmentation. In order to find out whether the nocturnal trend of Pesmax may be more influenced by a sleep-dependent circadian rhythm than by sleep fragmentation, we revised the polygraphic recordings of 37 patients in whom obstructive apneas were recorded for at least 7 hours. In 15 of these patients, analysis was made for eight hours of the night. During each hour we analyzed at least 7 obstructive apneas, in which we measured the minimal esophageal pressure at the start of the apnea, the maximum value recorded at the end of the apnea (Pesmax), the difference from the minimum to the maximum (delta Pes), and the rate of increase in esophageal pressure (RPes). As indices of sleep fragmentation, we defined the number of arousals, awakenings and sleep state transitions. In the group of patients as a whole, we found a trend toward a gradual increase for apnea duration (F = 98.8, p < 0.001) and Pesmax F = 31.6, p < 0.001) which was significant from the first to the last hour. The time-dependent evolution of apnea duration and Pesmax showed that the rise in these two variables peaked during the first 3 hours of sleep, followed by a plateau and a decrease in the last hour of the night. This temporal profile was more evident when the analysis was available for 8 hours. No significant changes across the night were found for nocturnal hypoxemia and number of arousals. Considering the slope of Pesmax changes across the night, we saw that neither the apnea+hypopnea index nor the indices of sleep fragmentation affected the nocturnal trend. The present data demonstrate the presence of a nocturnal trend in arousal threshold in OSA patients independent of sleep fragmentation. The biphasic evolution of the arousal threshold may be caused by factors that influence the circadian and homeostatic processes.

Current evidence suggests that patients with obstructive sleep apnea (OSA) may have greater pharyngeal critical pressure (Pcrit), which reflects the increase in upper airway collapsibility. The contribution of Pcrit to the severity of OSA and to the efficacious continuous positive pressure (nCPAPeff) therapy has never been extensively described and no data are available about the interaction of Pcrit, age, and anthropometric variables. To determine the relationship between Pcrit, severity of the disease, nCPAPeff, and anthropometric variables we measured Pcrit in a group of 106 patients with OSA. Pharyngeal critical pressure was derived from the relationship between maximal inspiratory flow and nasal pressure, Pcrit representing the extrapolated pressure at zero flow. Upper airway resistance (Rus) was determined as the reciprocal of the slope (DeltaPn/DeltaVImax cm H2O/L/s) in the regression equation. In a subgroup of 68 patients, during the diagnostic night, we measured as indices of respiratory effort, the maximal inspiratory esophageal pressure (Pes) at the end of apnea (Pesmax), the overall increase from the minimum to the maximum (DeltaPes), and the rate of increase of Pes during apnea (RPes). As a group, the mean Pcrit was 2.09 +/- 0.1 cm H2O (range, 0 to 4.5) and the mean Rus was 11.1 +/- 0.5 cm H2O/L/s. Although men have greater Pcrit, pharyngeal collapsibility was influenced neither by neck size nor by body mass index (BMI). Although there was a significant relationship between Pcrit and apnea plus hypopnea index (AHI) (r = 0.23, p = 0.02), neck circumference was the stronger predictor of apnea frequency, with Pcrit contributing only to the 3% of the variance. In the group of patients as a whole, a model including AHI, BMI, Rus, and Pcrit explained the 36% of the variance in nCPAPeff, with a greater contribution of AHI, Pcrit accounting for only 3% of the variation. In patients for whom the measure of respiratory effort was obtained, 42% of the variance in nCPAPeff was explained by RPes (33%) and BMI. From these results we conclude that Pcrit alone does not yield a diagnostically accurate estimation of OSA severity and nCPAPeff. Although individual collapsibility may predispose to pharyngeal collapse, upper airway occlusion may require the combination of several factors, including obesity, upper airway structure, and abnormalities in muscle control.

It has been recently described that the overnight increase in maximal end-apnoeic oesophageal pressure (P(oes,max)), considered as an index of the arousal threshold to occlusion, mostly contributes to apnoea lengthening during the night. However, the rise in apnoea duration could also be caused by changes in hypoxaemia, chemosensitivity and upper airway resistance. To better define the relative contributions of each of these factors, we examined the recordings of nine patients. Before apnoea, the mean pulmonary resistance at peak inspiratory flow (RPIF) was computed. During apnoea, all swings in oesophageal pressure (P(oes)) were measured to define the P(oes,max), the increase from the minimum to the maximum (deltaP(oes)), the rate of increase in P(oes) (RP(oes)) and the P(oes) at the first occluded breath (P(oes,1)). A gradual and significant increase in apnoea duration (p=0.02), P(oes,max) (p=0.02) and deltaP(oes) (p=0.006) was present across the night without any changes in oxygen saturation, RPIF, and P(oes,1). The slope of increase in P(oes,max), apnoea duration and deltaP(oes) was correlated with the apnoea/hypopnoea index. We conclude that in obstructive sleep apnoea, the nocturnal rise in apnoea duration is attributable more to an increase in the arousal threshold related to apnoea recurrence than to changes in chemosensitivity and upper airway resistance.

Can daily short-duration hypoxemia (4-8 hours) induce pulmonary hypertension and right ventricular hypertrophy? A clinical model of this type of hypoxemia does exist: isolated nocturnal hypoxemia in patients with obstructive sleep apnea syndrome (OSAS) or chronic obstructive pulmonary disease (COPD). By investigating the pulmonary hemodynamics of these patients, it should be possible to determine whether nocturnal hypoxemia alone can induce pulmonary hypertension. Although nocturnal hypoxemia (in OSAS as well as in COPD) can induce acute episodes of pulmonary hypertension, it would not appear that nocturnal hypoxemia alone would be sufficient to provoke permanent diurnal pulmonary hypertension. This is the conclusion of recent studies concerning diurnal pulmonary hemodynamics in OSAS and COPD patients exhibiting minimal hypoxemia during the day but significant nocturnal desaturation. The therapeutic consequences of these data, particularly in COPD are important: current evidence is insufficient to treat with nocturnal oxygen therapy COPD patients who have minimal diurnal hypoxemia but significant nocturnal desaturation.

The aim of this study was to investigate whether a simplified diagnostic procedure based on ambulatory monitoring with MESAM IV altered subsequent compliance with continuous positive airway pressure (CPAP) in obstructive sleep apnoea (OSA) patients. During a period of 16 months, 60 patients with symptoms evocative of OSA and positive MESAM recording were prescribed CPAP after titration with standard polysomnography. Compliance was followed during 2 yrs based on built-in time counters and was compared with the compliance in two comparison groups: an equal number of equally severely affected patients diagnosed with standard polysomnography during the 18 months (8 months before and 8 months after) preceding and following the study period and a group of 48 patients with an estimated similar apnoea/hypopnoea index but less typical clinical and/or MESAM features, diagnosed as having OSA based on polysomnography during the study period. The three groups were not different by age, body mass index, or sleepiness score. Patients diagnosed with the ambulatory procedure had higher drop-out rates (21.7% versus 10% and 6.25%; p<0.05) and lower rates of use of their CPAP (43+/-0.3 h x night(-1)) than any of the control groups (53+/-0.2 and 5.6+/-0.2 h x night(-1), p<0.05). In conclusion, there is a risk that ambulatory diagnostic procedures alter the relationship of patients to their disease and/or the medical staff so that subsequent compliance with treatment may be decreased. The greatest care concerning compliance should be taken before an ambulatory-based diagnostic procedure is implemented.

This paper is the text of a talk given at the European Respiratory Society meeting in Berlin in September 1997 in a symposium organized by the Sleep Disorders Working Group. It covers new treatments for obstructive sleep apnoea which are not established as standard treatments. Although postural treatment was proposed a long time ago, few studies have investigated its efficacy in clinical practice. However, in view of the data concerning postural sleep apnoea, it certainly deserves more consideration. Oral appliances appear to have become more popular as an alternative to continuous positive airway pressure (CPAP) when surgery is not desired or not desirable. A few controlled studies have been undertaken to establish its efficacy, which is less constant and less predictable than with CPAP. Other experimental approaches include nerve and muscle stimulation, for which preliminary results are promising. In the area of drug treatment, there is nothing new. Finally, the questions of what to do when treatment does not work and who should receive treatment are addressed.

Recent results in animals have suggested that repetition of hypoxaemic stimuli may result in a progressive increase in pulmonary arterial pressure (Ppa). The purpose of the present study was to investigate the effects of recurrent obstructive apnoeas on Ppa. We have, therefore, examined the nocturnal trend of Ppa in seven obstructive sleep apnoea syndrome (OSAS) patients and in five snorers. Mean Ppa was measured before, at the start, at the end and after the selected apnoeas. The analysis was performed for each 1 h period for at least 7 h throughout the night on at least 10 randomly selected apnoeas per hour. In snorers, 100 randomly chosen values were measured during every hour of the night. In the morning after the nocturnal study, the Ppa responses to acute hypoxia and hypercapnia were measured. No Ppa changes throughout the 7 h were found during sleep in snorers [Ppa slope:-0.002+/-0.10 mmHg x h(-1)]. In OSAS patients a small but significant increase in Ppa throughout the night was noted, affecting the values before [Ppa slope: 0.7+/-0.16 mmHg x h(-1)], at the start of apnoea [Ppa slope: 0.530.1 mmHg x h(-1)] as well as at the end [Ppa slope: 0.44+/-0.08 mmHg x h(-1)] and in the postapnoeic period [Ppa slope: 0.55+/-0.1 mmHg x h(-1)]. When we limited the analysis to nonrapid eye movement (NREM) sleep, a trend in progressive Ppa was also present, irrespective of changes in apnoea duration and apnoea desaturation. The Ppa rise during the night was not affected by diurnal Ppa pulmonary vascular response to hypoxia and hypercapnia or indices of sleep apnoea severity. We conclude that in obstructive sleep apnoea, pulmonary artery pressure progressively increases during the night, reflecting the cumulative effects of apnoeas and nocturnal hypoxaemia.

Many studies have shown a relationship between obstructive sleep apnea (OSA) and accidents, but to our knowledge, none have investigated prospectively the effects of treatment with nasal continuous positive airway pressure (CPAP). CPAP was proposed to 973 patients, of whom 893 patients actually underwent CPAP. These patients were consecutively invited to enter a prospective follow-up study including a questionnaire before treatment and after 6 and 12 months of treatment; 547 patients completed the study (153 left the study, and only partial data were available for 193). The baseline questionnaire included questions concerning accidents in the previous 12 months, asking whether patients had had an accident and, if so, whether they felt that the accident(s) were related to sleepiness, and whether the patients felt that they had had near-miss accidents due to sleepiness. The questionnaires at 6 and 12 months included the same questions referring to the previous 6 months; the accidents reported on each follow-up questionnaire were cumulated and compared with the accidents during the 1-year period before treatment. The number of patients having an accident decreased with treatment for real accidents (from 60 to 36; p<0.01), as well as for near-miss accidents (from 151 to 32; p<0.01). The average number of accidents per patient also decreased, for real accidents (from 1.6+/-1.3 to 1.1+/-0.3; p<0.01) and for near-miss accidents (from 4.5+/-6.5 to 1.8+/-1.4; p<0.01). The cost, in terms of days in hospital related to accidents, decreased from 885 to 84 days. With caution due to the absence of a control group, it is suggested that treatment with CPAP decreases the number of accidents occurring in OSA patients. This result may have important implications in the evaluation of the cost/benefit ratio when treating OSA patients.

There have been very few studies assessing the long-term physiological effects of nasal continuous positive airway pressure (CPAP) for the obstructive sleep apnoea syndrome. We therefore investigated prospectively the evolution of lung function, arterial blood gases and pulmonary haemodynamics in patients with this syndrome treated with CPAP. Sixty five patients were included. The mean duration of home treatment with nasal CPAP was 64+/-6 months. Most of the patients (77%) were smokers at the baseline assessment. We observed a small, but significant, decrease in forced expiratory volume in one second (FEV1) from 80+/-21% at baseline (t0) to 76+/-21% of the predicted value at the follow-up evaluation (t5) (p<0.01). Arterial oxygen tension (P[a,O2]) for the group as a whole remained stable (9.4+/-1.5 kPa (71+/-11 mmHg) versus 9.4+/-1.2 kPa (71+/-9 mmHg)). However, P(a,O2) increased in the subgroup of patients with hypoxaemia at t0 (n=23), from 7.8+/-0.7 kPa (59+/-5 mmHg) to 8.9+/-1.2 kPa (67+/-9 mmHg). Arterial carbon dioxide tension (P[a,CO2]) for the group as a whole increased slightly, but significantly, from 5.2+/-0.7 kPa (39+/-5 mmHg) to 5.4+/-0.5 kPa (41+/-4 mmHg) (p<0.05). Mean pulmonary artery pressure (Ppa) at rest did not change (16+/-5 mmHg versus 17+/-5 mmHg; NS) nor did exercising Ppa. In the 11 patients with pulmonary hypertension at t0, Ppa was 24+/-5 mmHg at t0 versus 20+/-7 mmHg at t5 (NS). We conclude that the significant decrease of forced expiratory volume in one second after 5 yr follow-up was related to a high percentage of smokers and exsmokers in the study population. Daytime arterial oxygen tension and pulmonary artery pressure remained stable in an unselected series of 65 obstructive sleep apnoea syndrome patients treated for 5 yrs with nasal continuous positive airway pressure, unlike arterial carbon dioxide tension, which increased by a small, but significant, amount.

Objective: To evaluate the patients' individual characteristics predictive of the degree of respiratory effort developed during obstructive sleep apneas (OSAs)., Design: Prospective consecutive sample, collection of clinical and polysomnographic data., Setting: University teaching hospital., Patients: One hundred sixteen consecutive OSA patients with clinical symptoms of OSA and more than 20 apneas per hour of sleep., Measurements: Anthropomorphic data, daytime blood gas values, and polysomnographic data. From esophageal pressure measurements during sleep, three indexes of respiratory effort during OSAs were derived: the maximal end-apneic esophageal pressure swing (PesMax), the increase in esophageal pressure swing (deltaPes) during the apnea, and its ratio to apnea duration (RPes)., Results: The indexes of respiratory effort were significantly lower in rapid eye movement (REM) than in non-REM sleep (PesMax: 50.9+/-2.5 vs 39.6+/-1.9 cm H2O, p<0.001; deltaPes: 30.9+/-1.7 vs 23.4+/-1.4 cm H2O, p<0.001; RPes: 1.05+/-0.05 vs 0.53+/-0.03 cm H2O/s, p<0.001); therefore, a separate analysis was conducted in non-REM and in REM sleep. Indexes were also significantly lower in subgroups of older as compared to younger patients (PesMax: 55.6+/-3.5 vs 40.0+/-2.2 cm H2O, p<0.001; deltaPes: 34.2+/-2.3 vs 24.1+/-1.6 cm H2O, p=0.001; RPes: 1.21+/-0.08 vs 0.8+/-0.05 cm H2O/s, p<0.001). The three indexes were closely correlated with each other and only PesMax correlation data are reported. In non-REM sleep, age was the most important single independent correlate of PesMax (r=-0.37, p=0.000). In REM sleep, the apnea-related hypoxemia, apnea duration, and age were the main contributors to the variance of PesMax., Conclusions: Respiratory effort in response to upper airway occlusion in OSA patients is lower in REM than in non-REM sleep and decreases with increasing age.

Worsening of hypoxaemia during sleep in patients with chronic obstructive pulmonary disease has been extensively investigated in the past 20 years owing to the development of polysomnography and to the advent of reliable transcutaneous oximeters. Sleep-related hypoxaemia is characteristic of rapid-eye-movement (REM) sleep but may be present during other sleep stages. There is a strong relationship between nocturnal O2 saturation and the level of daytime PaO2: the more pronounced daytime hypoxaemia, the more severe nocturnal hypoxaemia. Sleep-related hypoxaemia is due to a variable combination of alveolar hypoventilation and ventilation-perfusion mismatching, alveolar hypoventilation being the preponderant mechanism during REM sleep. The deleterious effects of sleep-related hypoxaemia include cardiac arrhythmias, 'hypoxaemic stress' on the coronary circulation and especially, peaks of pulmonary hypertension. The treatment of nocturnal hypoxaemia is conventional O2 therapy (both nighttime and daytime) in patients who exhibit marked daytime hypoxaemia (PaO2 < 55-60 mm Hg). At present data are not sufficient for justifying the use of isolated nocturnal O2 therapy in patients with nocturnal desaturation who do not qualify for conventional O2 therapy.

Sleep-related respiratory disorders are mainly represented by the consequences of partial or total upper airway obstruction during sleep, which lead to clinical pictures ranging from "pure" snoring to full-blown obstructive sleep apnea syndrome, including obstructive sleep hypopnea syndrome and upper airway resistance syndrome. These pictures share symptoms like snoring and excessive daytime sleepiness. Beyond the social and professional impairment and the increased risk of traffic and work accidents, these patients are exposed to the complications of systemic hypertension, which is often associated, and of less frequent cardiorespiratory failure. The diagnosis is based upon polysomnography which demonstrates the ventilation abnormalities. Since stable weight loss is most often impossible to obtain, the treatment of choice is based on nasal continuous positive airway pressure during sleep. In some selected cases, facial bone surgery may be helpful.

We tested the hypothesis that the awake ventilatory response to hypoxia and hypercapnia may contribute to the variability of respiratory effort developed in response to upper airway obstruction in obstructive sleep apnea syndrome. The polygraphic recordings of 38 patients diagnosed as having obstructive sleep apnea on the basis of an apnea+hypopnea index greater than 10 were examined. All subjects received hypoxic and hypercapnic ventilatory tests the day before the nocturnal polysomnography. Thirty apneas during non-rapid eye movement (NREM) sleep and at least 10 apneas during rapid eye movement sleep were analyzed. For each considered apnea, we measured esophageal pressure (Pes) swings during the first three breaths preceding apnea and during the first three and last three occluded efforts occurring during the apnea. We considered as indices of respiratory effort the overall increase from the minimum to the maximum Pes (delta Pes), the rate of increase of Pes during apnea (RPes), and the maximal respiratory effort at the end of apnea (Pes max fin). In NREM sleep, all three indices of respiratory effort were correlated positively with the awake ventilatory response to hypoxia or hypercapnia and with the apnea index. No correlation was found between the indices of respiratory effort and body mass index, age, pulmonary function tests, awake blood gases, apnea duration, and apnea desaturation. In rapid eye movement sleep, none of the considered variables predicted the degree of respiratory effort. In conclusion, our results suggest that the degree of ventilatory response to upper airway occlusion in obstructive sleep apnea may be influenced by the sensitivity of central neural drive to chemical stimuli.

A prospective study aimed at objectively evaluating compliance with nasal continuous positive airway pressure (CPAP) treatment was conducted in 728 obstructive sleep apnea [OSA; apnea/hypopnea index (AHI) > 15 events/hour] patients and 98 nonapneic snorers (AHI < or = 15 events/hour). Five-hundred seventy-five OSA patients and 33 nonapneic snorers underwent CPAP therapy and were followed-up for an average of 1,176 +/- 38 days (27 to 4,203 days). Compliance to treatment was measured by the mean rate of use of the CPAP device obtained from a built-in time counter. Acceptance of treatment was measured using Kaplan-Meier's model. The acceptance of CPAP was greater than 90% at 3 years and greater than 85% at 7 years in OSA patients. It was greater than 60% at 3 years in nonapneic snorers. The mean rate of CPAP use was 5.7 +/- 1.8 hours/day in OSA patients and 5.6 +/- 1.4 hours/day in snorers who were still on CPAP on October 1, 1995. It was correlated positively with age, body mass index, and AHI, and it was correlated negatively with daytime partial pressure of oxygen (PaO2), forced expiratory volume in 1 second (FEV1), and vital capacity in the group of OSA patients. This study shows that CPAP therapy is reasonably accepted by OSA patients as well as by nonapneic snorers. Both within and between groups, objective disease severity (as measured by the respiratory event index and daytime and nighttime hypoxemia), rather than patients' symptoms or complaints, seemed to play a role in the quality of compliance to treatment.

Apneas generally reappear in patients with obstructive sleep apnea (OSA) when treatment with continuous positive airway pressure (CPAP) is interrupted. However, a single-night treatment interruption may be associated with a lesser severity of sleep apneas than before treatment. We hypothesized that this decrease in severity of sleep apneas reflects changes in the respiratory response to upper airway obstruction. Therefore, we compared indexes of respiratory effort during sleep in 25 patients with OSA before and after 1 year of CPAP treatment. Respiratory effort was assessed by means of an esophageal balloon. After 1 year of CPAP treatment, there was a decrease in the maximal end-apneic esophageal pressure swings (Pes) (from 56.7 +/- 5.4 to 30.3 +/- 2.6 cm H2O; p = 0.000; mean +/- SEM), in the overall increase in Pes during an apnea (35.2 +/- 3.6 vs 16.5 +/- 1.5 cm H2O; p = 0.000), as well as the rate of increase in Pes (1.1 +/- 0.1 vs 0.6 +/- 0.1 cm H2O/s; p = 0.000). Although body mass index (BMI) did not change significantly, the individual changes in BMI significantly correlated with the changes in respiratory effort after 1 year of CPAP treatment. Apnea duration and apnea-related oxygen desaturation also decreased significantly. We conclude that long-term CPAP treatment induces changes in respiratory control that persist at least on the first night of treatment interruption.

"Cor pulmonale" is a classic feature of the "Pickwickian syndrome". Earlier studies have reported a high prevalence of pulmonary hypertension (PH) in obstructive sleep apnoea (OSA) patients, but this has not been confirmed by recent studies with a more adequate methodology, including larger groups of patients. The first part of this review is devoted to the prevalence of PH in OSA; most recent studies agree on prevalence of 15-20%. The second (and major) part of the study deals with the causes and mechanisms of PH in OSA. Pulmonary hypertension is rarely observed in the absence of day-time hypoxaemia, and the severity of nocturnal events (apnoea index (AI), apnoea+ hypopnoea index (AHI) does not appear to be the determining factor of PH. Diurnal arterial blood gas disturbances and PH are most often explained by the presence of severe obesity (obesity-hypoventilation syndrome) and, principally, by association of OSA with chronic obstructive pulmonary disease (the so called "overlap syndrome"). Bronchial obstruction is generally of mild-to-moderate degree and may be asymptomatic. The final part of the review analyses the therapeutic consequences of the presence of PH in OSA patients. Pulmonary hypertension, which is generally mild-to-moderate, does not need a specific treatment. When nasal continuous positive airway pressure (CPAP) fails to correct sleep-related hypoxaemia, supplementary oxygen must be administered. In patients with marked daytime hypoxaemia (arterial oxygen tension (Pa,O2), < or = 7.3 kPa (55 mmHg) conventional O2 therapy (nocturnal + diurnal) is required.

To test the hypothesis that respiratory effort during obstructive apneas contributes, together with hypoxemia and sleep fragmentation, to excessive daytime sleepiness, we investigated the relationship between daytime sleepiness and polysomnographic variables in 44 patients with obstructive sleep apnea (OSA). In all patients, daytime sleep propensity was assessed by an 11-item standardized self-questionnaire yielding a sleepiness score and by a modified sleep latency test yielding a mean sleep latency. Respiratory effort during apneas was evaluated by measuring esophageal pressure swings using an esophageal balloon. Within each apneic cycle, we measured the esophageal pressure swings during the first three and the last three occluded efforts during the apnea to define the overall increase, its ratio to apnea duration, and the maximal effort developed during obstruction. In the group of patients as a whole, the sleepiness score was negatively correlated with the mean sleep latency (r=-0.38, p=0.01). The sleepiness score was correlated with the indexes of respiratory effort during apneas (ie, the overall increase, its ratio to apnea duration, and the maximal end-apneic swing in esophageal pressure) and with the apnea+hypopnea index. The mean sleep latency was correlated with all indexes of nocturnal hypoxemia (ie, the mean lowest oxyhemoglobin saturation [SaO2] and the index of apnea associated with a fall in SaO2 below 90% and 80%). We conclude that the degree of respiratory effort during obstructive apneas contributes to self-rated sleep propensity in patients with OSA.

We have investigated pulmonary hemodynamics in a large series of consecutive, unselected patients with obstructive sleep apnea syndrome (OSAS). The aims of this study were to evaluate the frequency of pulmonary artery hypertension (PH) in OSAS and to analyze, as far as possible, its mechanisms. Two hundred twenty patients were included on the basis of a polysomnographic diagnosis of OSAS (apnea+hypopnea index > 20). PH, defined by a resting mean pulmonary artery mean pressure (PAP) of at least 20 mm Hg, was observed in 37 of 220 patients (17%). Patients with PH differed from the others with regard to pulmonary volumes (vital capacity [VC], FEV1) and the FEV1/VC ratio that were significantly lower (p < 0.001); PaO2 (64.4 +/- 9.3 vs 74.7 +/- 10.1 mm Hg; p < 0.001); PaCO2 (43.8 +/- 5.4 vs 37.6 +/- 3.9 mm Hg; p < 0.001), apnea+hypopnea index (100 +/- 33 vs 74 +/- 32; p < 0.001), and mean nocturnal arterial oxygen saturation (SaO2) (88 +/- 6% vs 94 +/- 2%; p < 0.001). Patients with PH were also more overweight (p < 0.001). Multiple regression analysis showed that 50% of the variance of PAP could be predicted by an equation including PaCO2 (accounting for 32% of the variance), FEV1 (12%), airway resistance (4%), and mean nocturnal SaO2 (2%). In conclusion, PH is observed, in agreement with previous studies, in less than 20% of OSAS patients. PH is strongly linked to the presence of an obstructive (rather than restrictive) ventilatory pattern, hypoxemia, and hypercapnia, and is generally accounted for by an associated obstructive airways disease. In this regard, the severity of OSAS plays only a minor role.

Daytime sleepiness is one of the major symptoms of obstructive sleep apnea. However, its definition raises problems, since it may be based on either subjective feeling (evaluated by means of questionnaires or analog visual scales), physiological drive or need (inferred by a sleep latency) or on the concept of sleep propensity defined as the probability of falling asleep (measured by the occurrence of sleep in various circumstances of daily life). Data from the literature suggest that sleep fragmentation and hypoxemia, both related to sleep apneas, cause daytime sleepiness. Our own data show that sleep propensity in a group of 44 patients with obstructive sleep apnea was correlated with the increase in esophageal pressure swings during obstructive apneas. This result suggests that the increased respiratory effort against occluded upper airways also contributes to daytime sleepiness in patients with obstructive sleep apnea.

We investigated whether cephalometric measurements, nocturnal indices of negative intrathoracic pressure, or the frequency of sleep-related breathing disorders were related to the level of effective continuous positive airway pressure (CPAP) in patients with obstructive sleep apnea (OSA). We examined 22 OSA patients who underwent two consecutive polysomnographic recordings, the first for diagnosis and the second for CPAP titration. Cephalometric measurements, spirometric data, and blood-gas analysis results were available for all subjects. In the diagnostic polysomnography, at least 30 apneas were analyzed during non-rapid-eye-movement (NREM) sleep and 10 apneas during rapid eye movement (REM) sleep for each patient. Swings in esophageal pressure (Pes) during the preapneic period and during the beginning and the end of obstructive apneas were calculated as the average of three consecutive breaths (or ineffective efforts). The difference in Pes from the minimal initial to the maximal final apneic respiratory effort (DPes) and the rate of increase in Pes (RPes = DPes/apnea duration) during apnea were computed. Within an apnea, the lowest Pes always occurred during the first three occluded breaths and the highest during the last three, with a more marked difference in NREM sleep. The level of effective CPAP was correlated with the length of the soft palate (r = 0.69, p = 0.000), RPes (r = 0.55, p = 0.008), and DPes (r = 0.49, p = 0.02). The correlations of effective CPAP level with body mass index and apnea + hypopnea index were not significant. A model including length of the uvula, DPes, and RPes accounted for 56 to 59% of the variability in effective CPAP.(ABSTRACT TRUNCATED AT 250 WORDS)

The association of chronic obstructive pulmonary disease (COPD) and sleep apnea syndrome (SAS), which are both frequent diseases, is likely to occur in a number of patients. We have prospectively investigated a large series (n = 265) of patients who were selected solely on the basis of a confirmed diagnosis of SAS (apnea + hypopnea index > 20/hr). An obstructive spirographic pattern, defined by an FEV1/VC ratio < or = 60%, was observed in 30 of 265 patients (11%). These patients (subgroup "overlap") were older (58 +/- 9) versus 53 +/- 10 yr, p = 0.01) than the remainder of the study population, and all were male patients. Body mass index (BMI) was identical in overlap patients to that in the remainder. Vital capacity and FEV1 were lower, by definition, in the overlap group. PaO2 was lower (66 +/- 10 versus 74 +/- 10 mm Hg, p < 0.001) and PaCO2 higher (42 +/- 6 versus 38 +/- 4 mm Hg, p < 0.001) in the overlap group. Hypoxemia (Pao2, < or = 65 mm Hg) was observed in 17 of 30 overlap patients and in 54 of 235 of the remainder. Hypercapnia (Paco2 > or = 45 mm Hg) was observed in 8 of 30 overlap patients and in 19 of 235 of the remainder. The pulmonary artery mean pressure (PAP) was higher in overlap patients both at rest (20 +/- 6 versus 15 +/- 5 mm Hg, p < 0.01) and during steady-state exercise (37 +/- 12 versus 29 +/- 10 mm Hg, p = 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

In its most frequent form, in which obstructive apneas are predominant, the sleep apnea syndrome appears more and more as a frequent disorder. Clinically, it can be easily suspected in a patient presenting with snoring and daytime sleepiness, provided that these symptoms are systematically sought. A firm diagnosis relies on polysomnographic recordings. Beyond these symptoms, which are social and professional handicaps, the severity of the disorder is related to its cardiovascular long-term complications. The standard treatment is based upon nasal continuous positive airway pressure, which is safe and efficient but constraining. Surgical treatments, which are not as safe nor as efficient, can be proposed when continuous positive airway pressure is not accepted.

The principal nocturnal GH peak normally coincides with the first episode of slow wave sleep (SWS). Obstructive sleep apnea (OSA) patients have low nocturnal GH levels which may be explained by their poor quality fragmented sleep but other factors are possibly involved. Obesity is frequently associated with OSA, and obese patients also manifest reduced GH secretion. The mechanisms reducing GH levels in obese subjects are not understood, but hyperinsulinaemia is a suggested factor. In this study nocturnal plasma and secretory GH profiles of OSA patients were examined in relation to the quality and quantity of sleep, together with plasma glucose and insulin levels. Eight OSA patients, (BMI 32.7 +/- 2.3 kg/m2), underwent 2 night studies. For one night no treatment was given and for the other continuous positive airway pressure (CPAP) treatment was administered for the first time. Blood was collected continuously throughout each night and plasma GH, insulin and glucose profiles established in 10 min interval samples. From the plasma data a deconvolution model was used to calculate GH secretion rates. Sleep was recorded during the studies. For the non-treatment night GH levels were low and increased significantly with treatment, p = 0.008 for plasma levels and p = 0.02 for secretion rates. Treatment significantly decreased the cumulative apnea duration and increased the quantity of SWS and Rapid Eye Movement (REM) sleep (p = 0.008), but the mean insulin and glucose profiles did not differ between the two nights. Individual GH plasma and secretion rates, on treatment, showed a tendency to correlate with the amount of SWS (p = 0.09).(ABSTRACT TRUNCATED AT 250 WORDS)

A questionnaire was given to 102 obstructive sleep apnea patients and 86 controls. A somnolence index was defined by averaging the scores of the answers to eleven questions concerning sleepiness. This index separated patients and controls (P < 0.0001). It was correlated with the apnea + hypopnea index (r = 0.32, P < 0.001), the body mass index (r = 0.45, P < 0.001) and with an objective measurement of sleepiness obtained from a modified multiple sleep latency test (r = -0.54, P < 0.001). Depending upon the current occupation, the tendency to fall asleep decreased in the following order: watching TV, passenger in a means of transport, reading, attending a show, attending a meeting, driving a car, and eating. This order is the same in patients and controls, irrespective of their "overall sleepiness". Thus, the circumstances of falling asleep are indicative of the severity of sleepiness.

An increased urine excretion has been reported in obstructive sleep apnea (OSA) patients, but it is not clear whether it results in an increased number of nocturnal micturitions. The present study was aimed at investigating the frequency of nocturnal micturitions in OSA patients using a standardized questionnaire prospectively given to 102 OSA patients and 86 healthy male subjects. The frequency of nocturnal micturitions was significantly greater in the OSA patients than in the healthy subjects (more than 70% of the OSA patients with an apnea+hypopnea index > 50 reported nocturnal micturitions more than twice a week versus less than 25% of the healthy subjects, p < 0.0001). The number of nocturnal micturitions was also greater in the OSA patients than in the healthy subjects. There was an effect of age on the frequency of nocturnal micturitions; however, when age-matched subsamples were considered, there was still a significant difference between OSA patients and healthy subjects. In a subgroup of 25 OSA patients reevaluated after at least 1 year of home treatment with nasal continuous positive airway pressure the reported frequency of nocturnal micturitions had significantly decreased (p < 0.001). These results suggest that investigations aimed at establishing a diagnosis of OSA should be part of the work-up of patients complaining of nocturnal pollakiuria.

In a prospective study aimed at evaluating objectively the compliance with nasal continuous positive airway pressure (CPAP) treatment, 233 obstructive sleep apnea (OSA) (apnea index, > 10 apneas/hour) patients and 36 nonapneic snorers were studied. The compliance to treatment was measured by the mean rate of use of the CPAP device, obtained from a built-in time counter. The follow-up period was 874 +/- 48 in OSA patients and 675 +/- 83 in snorers. CPAP was proposed to all OSA patients but only to those snorers who felt improved after an initial laboratory night on CPAP. Nineteen OSA patients refused CPAP. Of the 214 OSA patients who accepted CPAP, 181 are still on treatment, with a mean daily rate of use of 5.6 +/- 0.1 hours (mean +/- SEM); 22 patients stopped CPAP after a variable period of time; 10 patients died and one acromegalic patient was considered cured after hypophysectomy for a pituitary adenoma. Depending upon the definition of acceptable compliance, the compliance rate in this group was between 77% and 89%. The mean rate of use was correlated with indices of disease severity (apnea index, apnea+hypopnea index, minimal SaO2 during sleep, daytime PaO2, pulmonary artery pressure). Thirty-six nonapneic snorers accepted CPAP. In this group, 26 are still on CPAP, with a mean daily rate of use of 5.4 +/- 0.5 hours; one patient died; one underwent uvolopalatopharyngoplasty without follow-up; and eight stopped CPAP. The compliance rate in this group was between 58% and 78%. This study shows that CPAP is reasonably accepted by OSA patients as well as by nonapneic snorers.(ABSTRACT TRUNCATED AT 250 WORDS)

The term "overlap syndrome" was introduced by Flenley to describe the association of sleep apnea syndrome (SAS) with chronic obstructive pulmonary disease (COPD). Epidemiologic data on the prevalence of the overlap syndrome are not available, but the frequency of an associated COPD in SAS patients has been emphasized in almost all the studies analyzing the development of respiratory insufficiency in SAS patients. In a large series (n = 264) of unselected SAS patients who had undergone detailed pulmonary function tests, we observed an obstructive ventilatory defect (FEV1/VC < 60%) in 30 of 264 patients (11%). These patients had lower daytime PaO2 and higher PaCO2 than the other patients and they had higher resting and exercising pulmonary artery mean pressure (right heart catheterization was performed in 215 of 264 patients). We conclude that the risk of developing respiratory insufficiency and cor pulmonale is higher in overlap patients.

A modified maintenance of wakefulness test was performed in 58 patients with obstructive sleep apnea (OSA) syndrome before treatment and after long-term (554 +/- 28 days) home therapy with nasal continuous positive airway pressure (CPAP). Before treatment the patients had a shorter mean sleep latency than controls (16 +/- 1 vs. 27 +/- 1 min, mean +/- SEM, P less than 0.001). After treatment, the mean sleep latency increased to 20 +/- 1 min (P less than 0.002 as compared to baseline), but was still shorter than in controls (P less than 0.001). The incomplete normalization of the mean latency contrasted with the patients' claim that they no longer felt sleepy. The improvement in daytime alertness was significantly correlated with the reduction in sleep fragmentation after CPAP treatment and with the baseline mean sleep latency. These results support the hypothesis that sleep disruption related to respiratory events plays a role in the pathogenesis of daytime sleepiness.

Previous preliminary results have shown an overnight decrease in haematocrit and red cell count after the first night of treatment with nasal continuous positive airway pressure (CPAP) in obstructive sleep apnoea (OSA) patients. The present study was designed to confirm these preliminary data, and to analyse the long-term effects of CPAP. The haematocrit and red cell count (RCC) were measured in 80 OSA patients on two consecutive mornings, after an untreated night and after a CPAP treatment night. The haematocrit and RCC significantly decreased with CPAP (from 44.0 +/- 0.5 to 42.4 +/- 0.4%, p less than 0.0001 and from 4.769 +/- 0.051 to 4.597 +/- 0.052 x 10(12) red cells.l-1, p less than 0.0001, respectively). Neither the decrease in haematocrit nor the decrease in RCC were correlated with the decrease in urine volume or flow which occurred with CPAP. Thirty five of these patients remained untreated for 45 +/- 4 days, before home treatment with CPAP was initiated. The haematocrit and RCC had returned to values close to those before initial treatment and decreased again after the first treatment night. Twenty one of the patients were re-evaluated after at least one year of home treatment with CPAP, again on two consecutive nights either with CPAP or untreated. The follow-up, post-CPAP haematocrit and RCC were slightly and nonsignificantly higher than after the baseline CPAP night, but still lower than after the baseline untreated night (p less than 0.02). After the untreated follow-up night, no significant change in haematocrit was observed.(ABSTRACT TRUNCATED AT 250 WORDS)

Variations in natural head posture (NHP) and hyoid bone (HB) positioning impart changes in the size and shape of the pharyngeal airways. In SAS, which was shown to be correlated with detrimental craniofacial anatomical conditions, control of pharyngeal permeability is lost during sleep. The aim of this study was determine if functional adaptation of NHP and HB position to these detrimental conditions could be observed, using Bonferonni probabilities, in a cephalometric comparison of 38 SAS adults in the wakeful state and a control group of 38 healthy adults. Since HB relationships with craniofacial anatomical structures vary with the positioning of the head, the cephalograms were taken according to the preliminarily tested NHP, thus making the method reproducible. In SAS craniovertical angulation was unchanged, but the head was maintained in a forward position (increased cervico-vertical angulation, P < 0.001). Maintenance of an acceptable pharyngeal permeability was associated with a more distant positioning of HB from the cervical column (P < 0.01) and from craniofacial references (P < 0.001). In spite of these facts lower pharynx opening was still reduced (P < 0.05). Soft palate and facial divergence were expectedly increased in the apneic group. All the individuals but one control could be correctly reclassified with the help of soft palate length, facial divergence, and two HB related variables. Prevention of pharyngeal collapsibility in SAS seems to be commonly associated with functional adaptation of NHP and HP position. The precise control mechanisms of this adaptation remains to be elucidated. Skeletal predispositions to SAS do probably develop already during infancy.

The effects of treatment with nasal continuous positive airway pressure (CPAP) on left ventricular ejection fraction (LVEF) were assessed in 29 patients with obstructive sleep apnea (OSA) in a prospective study using multiple gated equilibrium radionuclide angiocardiography. All patients were evaluated before CPAP treatment was initiated and were reevaluated after one year (mean +/- SE, 415 +/- 6 days), of home treatment with nasal CPAP. The mean LVEF increased from 59 +/- 1 percent to 63 +/- 1 percent (p less than 0.005). The degree of improvement in LVEF was correlated with baseline LVEF (r = 0.54; p less than 0.003), meaning that the lower the baseline value, the greater the increase with treatment. The changes were not different when subgroups of medicated and unmedicated patients were considered separately. These results show that long-term nasal CPAP treatment results in improved left ventricular function in OSA.

Event-related potentials (ERPs) were recorded in 47 patients with obstructive sleep apnea (OSA) syndrome prior to and after 6 weeks of treatment with continuous positive airway pressure (CPAP). Compared with a control group, the OSA patients showed ERP abnormalities: lengthened P3 latencies and decreased N2-P3 amplitudes. After 6 weeks of CPAP treatment, there was a highly significant improvement in the abnormal ERPs: the P3 and N2 latencies were shortened, but remained longer than in controls, and the N2-P3 and N1-P2 amplitudes were increased. No correlations could be established with various sleep variables. ERPs may be used as an electrophysiological marker of brain dysfunction; treatment of OSA with CPAP is probably responsible for functional brain modifications. On the other hand, possible relationships between the ERP abnormalities and the neuropsychological disorders observed in OSA remain to be established.

1. Given the unexplained frequent association between systemic hypertension and obstructive sleep apnoea (OSA), the secretion of prostanoids during sleep was investigated (more specifically, the ratio of prostacyclin (PGI2) to thromboxane A2 (TxA2), since they have marked opposite effects on vascular tone). Prostacyclin has vasodilating effects, whereas thromboxane results in vasoconstriction. 2. In 11 OSA drug-free male patients (age 53 +/- 2 years, mean +/- s.e.m.; apnoea index 55 +/- 15 apnoeas/hour of sleep; body mass index 31 +/- 2 kg/m2), we measured the urinary excretion during sleep of 6-keto-PGF1-alpha and of thromboxane TxB2 (the stable metabolites of prostacyclin PGI2 and of thromboxane A2 respectively). This was done on two consecutive nights; one untreated, the other with nasal continuous positive airway pressure (CPAP) treatment. The results were compared with those of nine normal unobese male subjects. 3. The urinary ratio of 6-keto-PGF1-alpha to TxB2 was significantly (P less than 0.001) lower in the untreated OSA patients (1.7 +/- 0.2) than in the controls (3.1 +/- 0.3). It significantly increased with CPAP treatment to 2.3 +/- 0.2, P less than 0.02, which was no longer different from the controls. 4. These results suggest that OSA is associated with an abnormal release of prostanoids during sleep resulting in a decrease of the prostacyclin to thromboxane ratio which potentially has a vasoconstricting effect. The relationship between these changes and the systemic hypertension often observed in OSA patients remains to be established.

To assess the effect of obstructive sleep apnea treatment on plasma renin activity (PRA) and plasma aldosterone seven male patients were studied under two conditions: untreated and treated with nasal continuous positive airways pressure (CPAP). PRA and plasma aldosterone were measured at 10-min intervals for both nights. CPAP treatment diminished the urinary and Na+ excretion, whereas plasma volume increased. The mean levels of PRA and aldosterone were significantly enhanced by the treatment, increasing respectively from 1.5 +/- 0.3 to 3.0 +/- 0.7 ngAI ml-1.hr-1 (p less than 0.05) and from 8.0 +/- 1.0 to 12.0 +/- 1.7 ng.100 ml-1 (p less than 0.05). PRA curves reflected the overall sleep structure as similarly described in normal subjects. The apnea-induced sleep disturbance led to flat PRA profiles and the restoration of a normal sleep pattern by treatment restored the PRA oscillations related to the sleep cycles and consequently restored aldosterone oscillations. The mean amplitude of these oscillations increased respectively from 1.0 +/- 0.1 to 1.8 +/- 0.4 ngAI ml-1.hr-1 and from 5.4 +/- 1.2 to 10.9 +/- 1.9 ng.100 ml-1. These results suggest that CPAP treatment modifies the nocturnal patterns of PRA and aldosterone by increasing their mean levels and their oscillation amplitude. This indicates increased secretion, which contributes to the normalization of urine and Na output.

1. Patients with obstructive sleep apnoea have increased diuresis during sleep, which decreases with nasal continuous positive airway pressure treatment. These changes have been attributed to an increased release of atrial natriuretic peptide in obstructive sleep apnoea, and its decrease with continuous positive airway pressure treatment. 2. In order to clarify the change in plasma atrial natriuretic peptide level and to investigate the underlying mechanisms, blood samples were taken at 10 min intervals from nine patients with obstructive sleep apnoea during two nights when the patients were either untreated or treated with continuous positive airway pressure. Polysomnographic monitoring, including transcutaneous oximetry, and measurement of oesophageal pressure were performed simultaneously. Plasma arginine vasopressin was also measured. 3. The plasma level of arginine vasopressin did not change. The level of atrial natriuretic peptide was high and exhibited secretion bursts in six out of the nine patients; it drastically decreased with continuous positive airway pressure treatment. 4. Across the patients, the mean plasma levels of atrial natriuretic peptide was correlated with the degree of hypoxaemia and the degree of oesophageal pressure swings during the sleep apnoeas. 5. Within the patients, cross-correlation studies suggested that the atrial natriuretic peptide secretory bursts were related either to the oesophageal pressure swings or to the apnoea-related hypoxaemia. 6. We conclude that release of atrial natriuretic peptide decreases with continuous positive airway pressure treatment in those patients with obstructive sleep apnoea who have increased release of atrial natriuretic peptide before treatment.(ABSTRACT TRUNCATED AT 250 WORDS)

This report describes the polysomnographic findings and the respiratory alterations during sleep in a 20-year-old patient with the Prader-Willi syndrome. Nocturnal recordings and a variant of the multiple sleep latency test showed excessive daytime sleepiness, sleep onset rapid eye movement episodes, snoring and sleep apnea. Treatment with nasal continuous positive airway pressure normalized the respiratory pattern and the sleep structure, except for rapid eye movement sleep onset. Whereas upper airway obstruction and obesity may explain the respiratory disorders, as shown by their resolution with continuous positive airway pressure treatment, hypothalamic dysfunction could play a role in the disruption of the normal nonrapid eye movement/rapid eye movement sleep periodicity.

In order to study the frequency and the mechanisms of daytime pulmonary hypertension (PH) in obstructive sleep apnoea syndrome (OSAS) lung function tests, blood gas analysis and right-heart catheterization were performed in 46 consecutive patients. OSAS was assessed by polysomnography. 9 patients only (20%) had PH (mean pulmonary artery pressure (Ppa) greater than or equal to 20 mmHg). Patients with PH had lower daytime PaO2 (60.8 +/- 7.6 vs. 76.2 +/- 9.4 mmHg; p less than 0.001), higher daytime PaCO2 (44.8 +/- 4.2 vs. 38.0 +/- 4.0 mmHg; p less than 0.001), lower forced vital capacity (FVC) and forced expiratory volume (FEV1) (p less than 0.001), but the severity of OSAS was not different whether PH was present or not (apnoea index: 62 +/- 34 hour in the PH group vs. 65 +/- 40 hour, apnoea + hypopnoea index 102 +/- 33 hour in the PH group vs. 86 +/- 36 hour, lowest sleep SaO2: 59 +/- 21% in the PH group vs. 66 +/- 18%). There were significant correlations between Ppa and: daytime PaO2 (r = -0.61; p less than 0.001), PaCO2 (r = 0.55; p less than 0.001), FEV1 (r = -0.52; p less than 0.001) but not between Ppa and apnoea index, apnoea + hypopnoea index, lowest sleep SaO2. PH and daytime hypoxaemia were associated either with chronic airway obstruction or with severe obesity.

Because sleep apnoea syndrome is often associated with arterial hypertension, it has been suggested that sleep apnoea might be responsible for hypertension. This hypothesis is mainly based on epidemiological studies showing a statistically significant association between snoring and arterial hypertension; this association remains true even after data correction to take into account the increased frequency of snoring with age and overweight. However, this statistical link is no evidence of a cause-effect relationship, and the mechanism through which sleep apnoea syndrome could produce arterial hypertension remains unknown. Yet treatment of sleep apnoea syndrome seems to improve arterial hypertension, and this alone would justify a search for sleep apnoea syndrome in all patients presenting with arterial hypertension.