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)

No abstract

"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 daytime 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-tomoderate, 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,O 2 ), ≤7.3 kPa (55 mmHg) conventional O 2 therapy (nocturnal + diurnal) is required. Eur Respir J., 1996, 9, 787-794

The frequency of daytime pulmonary hypertension (PH) in patients with obstructive sleep apnea syndrome (OSAS) has not been well established and its mechanisms are still under debate. We have thus performed right heart catheterization, in addition to standard spirography and arterial blood gas measurements, in a series of 46 consecutive patients in whom OSAS was firmly diagnosed by whole-night polysomnography. Only 9 of the 46 patients (20%) had PH defined by a mean resting pulmonary arterial pressure (Ppa) greater than or equal to 20 mm Hg. Among the patients without resting PH, 14 had exercising PH (defined by a Ppa greater than 30 mm Hg during 40-watt, steady-state exercise). Patients with resting PH differed from the others by a lower daytime PaO2 (60.8 +/- 7.6 versus 76.2 +/- 9.4 mm Hg; p less than 0.001), a higher daytime PaCO2 (44.6 +/- 4.2 versus 38.0 +/- 4.0 mm Hg; p less than 0.001), and lower VC and FEV1 (p less than 0.001). There was no difference between the 2 groups with regard to apnea index (62 +/- 34 versus 65 +/- 40) or the lowest sleep SaO2 (59 +/- 21 versus 66 +/- 18%) or the time spent in apnea. For the group as a whole, there was a good correlation between Ppa and daytime PaO2 (r = -0.61; p less than 0.001), PaCO2 (r = 0.55; p less than 0.001), and FEV1 (r = -0.52; p less than 0.001), but there was no significant correlation between Ppa and the apnea index, the lowest sleep SaO2, or the time spent in apnea.(ABSTRACT TRUNCATED AT 250 WORDS)

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 $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. Eur Respir J 1999; 13: 1091±1096.