Obstructive sleep apnoea and its therapy influence high-density lipoprotein cholesterol serum levels.

Recent studies suggest an association of obstructive sleep apnoea (OSA) with cardiovascular risk factors, such as dyslipidaemia. The present study analyses the effects of OSA and its therapy on serum lipid concentrations in 470 OSA patients in a single centre study. Multivariate regression showed a significant association between the apnoea-hypopnoea index and high-density lipoprotein cholesterol (HDL-C) serum levels (n = 366), independent of age, sex, body mass index, diabetes and lipid lowering medication. There were no independent associations with total cholesterol, triglyceride and low-density lipoprotein cholesterol serum levels. During follow-up (6 months) with effective bilevel or continuous positive airway pressure therapy in 127 patients (lipoproteins: n = 86) without change in their lipid lowering therapy, the mean HDL-C serum level increased significantly by 5.8% from 46.9+/-15.8 to 49.6+/-15.3 mg x dL(-1) (mean+/-SD). An independent relationship was found between the change of apnoea-hypopnoea index and the change of high-density lipoprotein cholesterol or triglycerides, respectively. All patients with abnormal serum lipid/lipoprotein levels improved significantly under bilevel or continuous positive airway pressure therapy. This study demonstrates an influence of obstructive sleep apnoea and its therapy on high-density lipoprotein cholesterol levels.

Influence of treatment on leptin levels in patients with obstructive sleep apnoea.

Obstructive sleep apnoea syndrome (OSAS) is a common disorder in obesity. Leptin, an adipocyte-derived signalling factor, plays an important role in metabolic control. There is growing evidence that leptin regulation is altered in OSAS. Therefore, the aim of this study was to test the hypothesis that effective treatment will influence leptin levels in OSAS patients. Serum leptin levels were determined in 86 consecutive patients (aged 57.5 +/- 11.0 yrs) with polysomnographically verified OSAS. In addition, leptin levels were reassessed and treatment efficacy was evaluated by polysomnography after 6 months of therapy. Patients were treated with continuous or bilevel positive airway pressure, a mandibular advancement device or conservatively, depending on the clinical symptoms. Mean serum leptin levels did not change with treatment in the whole study group (7.3 +/- 5.0 versus 7.5 +/- 4.8 ng.mL-1), however, leptin levels decreased in effectively treated patients (8.5 +/- 5.0 versus 7.4 +/- 5.1 ng.mL-1) while they increased in ineffectively treated patients (5.0 +/- 4.0 versus 7.7 +/- 4.1 ng.mL-1). Furthermore, not only was there a significant and independent correlation between the change in leptin levels with treatment and the change in body mass index, but also with the change in apnoea/hypopnoea index. Effective treatment of sleep-disordered breathing may have significant effects on leptin levels in obstructive sleep apnoea syndrome patients. Changes in leptin levels are related to changes in apnoea/hypopnoea index in obstructive sleep apnoea syndrome patients.

MRI of the pharynx and treatment efficacy of a mandibular advancement device in obstructive sleep apnoea syndrome.

In obstructive sleep apnoea syndrome (OSAS), prosthetic mandibular advancement devices (MAD) seem to be a promising treatment alternative to conventional continuous positive airway pressure therapy. Unfortunately, while they are effective in some patients, they are ineffective in others or may even worsen OSAS. At present, it is not known whether predictors can be defined which allow for estimation of the potential effect of oral appliances on the severity of OSAS. Clinical and polysomnographical efficacy of a MAD was evaluated in 15 patients with OSAS. In addition, ultrafast magnetic resonance imaging (MRI) of the pharynx was performed in 13 of these patients at rest during transnasal shallow respiration and during performance of the Muller manoeuvre, both with and without the MAD, and the site of closure was determined. The MAD reduced the mean apnoea/hypopnoea index (AHI) from 19.8+/-14.5 to 7.2+/-7.4 x h(-1). Seven subjects (53.8%) had at least a 50% reduction in AHI to a value <10 x h(-1) with the MAD, whereas the MAD was ineffective in six patients. Five of the seven treatment responders had no significant pharyngeal obstruction during the manoeuvre with the device, while all of them had pharyngeal obstruction when not equipped with the device. Four of the six patients with treatment failure had a single velopharyngeal obstruction and two a combined obstruction of the velo- and glossopharynx during the Muller manoeuvre while wearing the device. The results of this study suggest that airway patency during the Muller manoeuvre while wearing a mandibular advancement device may be predictive of the success of obstructive sleep apnoea syndrome treatment with a mandibular advancement device.

Effect of continuous positive airway pressure therapy on infectious complications in patients with obstructive sleep apnea syndrome.

BACKGROUND: Nasal continuous positive airway pressure (CPAP) is a well-established, widely used and effective treatment of obstructive sleep apnea syndrome (OSAS). Unfortunately, side effects are frequent during CPAP treatment. OBJECTIVES: Little is known about the effects of CPAP on infectious complications in patients with OSAS. METHODS: We retrospectively analyzed the kinds and rate of infections of the upper airway in 246 consecutive patients (mean age, 59.7 years) with polysomnographically verified OSAS using CPAP with or without a heated humidifier and compared them with OSAS patients who received non-CPAP therapy. RESULTS: Of the 246 patients, 40 received conservative therapy and 206 CPAP treatment, 36 of them with a heated humidifier. The mean follow-up period of the study group was 165.4 +/- 92.1 weeks and did not differ between the three groups. Infectious diseases were frequent in all three groups, but patients using CPAP without humidifier suffered from upper airway infections significantly more frequently than controls (42.9 vs. 25%; p < 0.05), and more patients on CPAP therapy with humidifier than controls (22.2 vs. 2.5%; p < 0.01) reported an increased rate of upper airway infections since initiation of CPAP therapy or diagnosis of OSAS. Especially patients using a hot water bath humidifier who cleaned their devices inadequately had significantly more upper airway infections since diagnosis (57.1 vs. 20%; p < 0.05) or during the past 6 months (52.4 vs. 13.3%; p < 0.05) than patients who regularly cleaned CPAP machines, humidifiers and ventilatory circuits. CONCLUSIONS: Our results suggest that patients using CPAP therapy either with or without heated humidity seem to be at an increased risk of upper airway infections compared to conservatively treated patients.

Sleep-Disordered breathing in patients referred for angina evaluation--association with left ventricular dysfunction.

BACKGROUND: Clinical observations have linked sleep-disordered breathing to cardiovascular morbidity and mortality, and especially to coronary artery disease. HYPOTHESIS: The study was undertaken to determine the prevalence of sleep-disordered breathing in consecutive patients referred for angina evaluation, and analyzed the parameters influencing the severity of sleep-disordered breathing. METHODS: In all, 68 consecutive patients (53 men, 15 women, aged 63.4 +/- 10.0 years) referred for angina evaluation were studied. Coronary angiography, selective left ventriculography, and a polygraphic study with a validated six-channel monitoring device were performed. Full-night polysomnography was used to reevaluate patients with an apnea/hypopnea index > or = 10/h. RESULTS: Sleep-disordered breathing as defined by an apnea/hypopnea index > or = 10/h was found in 30.9% of patients; its prevalence was not increased in patients with and without coronary artery disease (26.5 vs. 42.1%). Multiple stepwise linear regression analysis revealed that the severity of sleep-disordered breathing was significantly and independently associated with left ventricular ejection fraction (r = -0.38; p = 0.002), but not with age, body mass index, gender, diabetes mellitus, hypertension, hyperuricemia, hypercholesterolemia, smoking habits, or coronary artery disease. In this group of patients, multiple logistic regression analysis could not demonstrate sleep-disordered breathing to be an independent predictor of coronary artery disease. CONCLUSIONS: Sleep-disordered breathing is common in patients referred for angina evaluation. The degree of sleep-disordered breathing is mainly determined by the extent of left ventricular dysfunction.

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.

[Effect of ACE-inhibitors on left ventricular remodeling after acute anterior or posterior myocardial infarct. Cine- magnetic resonance tomography study]. / Einfluss von ACE-Hemmern auf das Remodeling des linken Ventrikels nach akutem Vorder- oder Hinterwandinfarkt. Untersuchungen mit der Cine-Magnetresonanztomographie.

The question whether patients with posterior infarctions (PMI) have a comparable benefit of an ACE-inhibitor therapy to those with anterior infarction (AMI) is still open. The study was undertaken to investigate the different influence of ACE inhibitors on the remodeling of the left ventricle after AMI or PMI. 52 patients (Pt.) (17 female, 38-73 years) were randomized to receive either 25-75 mg/day captopril (C) or 5-20 mg/day fosinopril (F) beginning on day 7 after acute myocardial infarction. 28 Pt. had AMI, 24 Pt. PMI. Infarct size was determined by the creatine kinase integral method. 50 Pt. were examined by cine magnetic resonance imaging 1 and 26 weeks after infarction. We determined: left ventricular end-diastolic (LVEDVI) and end-systolic (LVESVI) volume index, ejection fraction (EF), infarction weight (IW), left ventricular muscle mass (MM), systolic wall thickening (SWT) and motility (MOT) of the vital myocardium, and clinical behavior according to the guidelines of the New York Heart Association (NYHA). The results were compared with those of a sample (V) without ACE inhibitor therapy (10 females, 21 males, 36-75 years, 19 AMI, 12 PMI). There were no significant differences between C and F. Without ACE-inhibition therapy LVEDVI increased by 28.2% in AMI, by 18.4% in PMI (p < 0.001), with ACE-inhibition by 13.7% in AMI and by 9.9% in PMI (p < 0.001). LVESVI increased in V by 40.1% in AMI, by 28.5% in PMI (p < 0.001). With ACE-inhibitor we found an increase of 11.2% in AMI and 5.3% in PMI (p < 0.001). EF decreased without ACE-inhibitor by 18.7% in AMI and by 10.2% in PMI (p < 0.001), with ACE-inhibition increased by 4.3% in AMI and PMI, respectively (n. s.). NYHA got better in all groups, by 17.4% in AMI and 20.8% in PMI without ACE-inhibitor (n.s.), by 45.5% in AMI and 31.6% in PMI with ACE-inhibitor (p < 0.001). IG increased by 15.5% in AMI and 8.8% in PMI in V (p < 0.001), by 11.2% in AMI and 5.3% in PMI with C or F (p < 0.001). MM got bigger in V by 16.6% in AMI and 12.7% in PMI (p < 0.05), with ACE-inhibitor by 11.7% in AMI and 8.0% in PMI (p < 0.05). sWD increased by 12.9% in AMI and by 6.7% in PMI in V (p < 0.01), by 37.1% in AMI and 88.0% in PMI with C or F (p < 0.001). MOT decreased by 39.6% in AMI and 14.9% in PMI without ACE-inhibition (p < 0.001) and increased by 4.3% in AMI and by 5.0% in PMI with ACE-inhibitor (n. s.). All differences between V and the ACE-inhibitor groups were significant. Even patients with PMI clearly benefit from ACE-inhibitor therapy, but less than those with AMI. Captopril and fosinopril show no different effects after myocardial infarction.

Increased sodium-proton antiporter activity in patients with obstructive sleep apnoea.

Cytosolic pH (pH(i)) and the activity of the sodium-proton antiporter (Na(+)/H(+) antiporter) were measured in lymphocytes from 22 patients with obstructive sleep apnoea and from 24 age-matched healthy subjects (Controls). The cellular Na(+)/H(+) antiporter was measured spectrophotometrically using a pH-sensitive fluorescent dye after intracellular acidification using sodium propionate. Resting pHi was similar in lymphocytes from patients with obstructive sleep apnoea and from controls (7.36 +/- 0.20, n=22; vs. 7.35 +/- 0.19, n=24; mean +/- SD). The Na(+)/H(+) antiporter activity was significantly higher in patients with obstructive sleep apnoea than in controls (11.87 +/- 3.26 x 10(-3) pH(i)/s vs. 4.38 +/- 1.40 x 10(-3) pH(i)/s; P < 0. 0001). The apparent affinity of the Na+/H+ antiporter was not significantly different between the groups (6.90 +/- 0.23 vs. 6.87 +/- 0.20). In patients with obstructive sleep apnoea the activity of the Na(+)/H(+) antiporter remained stable during the night. The activity of the Na(+)/H(+) antiporter was 13.49 +/- 4.80 x 10(-3) pH(i)/s at 20.00 and 13.26 +/- 6.13 x 10(-3) pH(i)/s at 02.00. From the present results it is concluded that an increased cellular Na(+)/H(+) antiporter activity may be a genetic marker for patients who are predisposed to obstructive sleep apnoea.

Long-term treatment with continuous positive airway pressure improves quality of life in obstructive sleep apnoea syndrome.

Continuous positive airway pressure (CPAP) is an established treatment of obstructive sleep apnoea syndrome (OSAS). While it is known that CPAP reverses the pathological breathing pattern and improves daytime sleepiness, there are no sufficient data on the long-term influence of CPAP on quality of life in patients with OSAS. Thirty-nine patients with polysomnographically verified OSAS (apnoea/hypopnoea index (AHI): (mean+/-SD) 46.8+/-21.8 events x h(-1)) were prospectively studied. All patients answered three quality of life measures (Complaint List, Nottingham Health Profile Part 1 (NHP), and Verbal Analogue-Scale "quality of life") prior to the initiation of CPAP therapy. After a mean of 9 months they were re-evaluated by polysomnography, and completed the questionnaires once again. As expected, CPAP was effective in treating the sleep-related breathing disorder. AHI decreased significantly from (mean+/-SD) 46.8+/-21.8 events x h(-1) to 3.3+/-6.3 events x h(-1), and minimum oxygen saturation increased from 77.1+/-9.3% to 89.9+/-3.4%, while body mass index did not change significantly (31.3+/-5.4 versus 30.8+/-4.8 kg x m(-2)). During long-term treatment with CPAP the Complaint List revealed a significant improvement of the extent of subjective impairment due to physical and general complaints (26.4+/-9.9 versus 20.4+/-11.1), and NHP a significant improvement of emotional reactions (19.8+/-21.7 versus 11.1+/-14.0) and energy (50.8+/-36.6 versus 32.1+/-36.7), but not of pain, physical mobility, sleep, social isolation, and quality of life as assessed by the It is concluded that long-term continuous positive airway pressure therapy is effective in improving not only pathological breathing patterns but also parameters that estimate quality of life in patients with obstructive sleep apnoea syndrome.

Is the tissue affinity of ACE inhibitors of relevance for the remodeling of the left ventricular wall following myocardial infarction? Estimations with cine magnetic resonance imaging.

BACKGROUND: Angiotensin-converting enzyme (ACE) inhibitors have been shown to be of value in the treatment of postinfarction remodeling. The question whether substances with a greater tissue affinity are associated with advantages for the acute and the chronic course is, however, still unclear. AIM: The aim of the present study was to investigate the influence of ACE inhibitors with differing tissue affinities on the remodeling of the left ventricular wall in patients recovering from myocardial infarction. METHODS: 52 patients (17 women, aged 38-73 years) suffering their first acute myocardial infarction were randomized to receive a daily dose of either 25-75 mg captopril or 10-20 mg fosinopril, beginning on the 7th postinfarction day. 28 patients had an anterior wall infarction and 24 patients an inferior wall infarction. The size of the infarct was determined using the creatine kinase integral method. 50 patients were investigated by cine magnetic resonance imaging 1 and 26 weeks after the infarction. The following parameters were determined: infarct weight and diastolic diameter of the infarcted zone, systolic wall stress, muscle mass, diastolic and systolic diameters, systolic wall thickening, and motility of the noninfarcted myocardium. RESULTS: The infarct weight increased under captopril by 5.7% (p < 0.05) and under fosinopril by 6.1% (p < 0.05). The diastolic diameter of the infarcted zone decreased by 12% under captopril (p < 0.001) and by 11% under fosinopril (p < 0.001). The systolic wall thickness increased by 12.1% (p < 0.001) and the muscle mass by 12.7% (p < 0.001) under captopril and by 15.4% (p < 0.001) and 9.6% (p < 0.01), respectively, under fosinopril. Under captopril, the diastolic diameter increased by 2.3% (p < 0.05) and the systolic diameter by 17.8% (p < 0.01) and under fosinopril by 2.8% (n.s.) and 17.5% (p < 0.001), respectively. The systolic wall thickening increased by 73.9% under captopril (p < 0.001) and by 129.4% under fosinopril (p < 0.001). The motility decreased by 13.8% (p < 0.05) under captopril and by 6.0% (n.s.) under fosinopril. For all parameters, the results seen in anterior wall infarction were appreciably poorer than those seen in inferior wall infarction. All the differences between captopril and fosinopril were not significant. CONCLUSIONS: Captopril and fosinopril show no major differences in their influence on left ventricular wall remodeling following myocardial infarction. On the basis of the present results, the tissue affinity of an ACE inhibitor does not appear to be of a significant relevance for postinfarction treatment.

Prevalence of ventricular late potentials in patients with obstructive sleep apnea syndrome.

BACKGROUND: It is known from various cardiac disorders that the presence of ventricular late potentials (VLP) in the signal-averaged electrocardiogram (ECG) is associated with an increased risk of sudden cardiac death. HYPOTHESIS: In view of the increased cardiovascular mortality of patients with obstructive sleep apnea syndrome (OSAS), we assessed the prevalence of VLP in these patients. METHODS: In all, 118 consecutive patients with polysomnographically verified OSAS were prospectively studied; 21 snorers without evidence of a sleep-related breathing disorder served as a control group. Signal-averaged ECG and 24-h Holter ECG were performed in all patients and controls, and left ventricular function was determined by radionuclide ventriculography in the OSAS group. Furthermore, patients and controls were followed for up to 45.5 months for arrhythmic events, syncopes, or sudden cardiac death. RESULTS: An abnormal signal-averaged ECG was seen in seven patients (5.9%) and in one snorer (4.8%). Patients with and without VLP did not differ with respect to age, body mass index, left ventricular ejection fraction, or ectopic activity in the 24-h Holter ECG, but the former had significantly higher mean (standard deviation) apnea/hypopnea indices [55.4 (25.2)/h vs. 37.4 (22.6)/h; p < 0.05]. Of the 118 patients, 110 could be followed for 26.7 (7.9) months. During this period, two patients had syncopes and one patient had sudden cardiac death. The seven patients with VLP remained free of events during the follow-up period, as did the 21 snorers. CONCLUSIONS: Patients with OSAS have a low prevalence of VLP in the signal-averaged ECG, not exceeding that in normal subjects. Moreover, abnormal signal-averaged ECGs do not appear to be useful as a prognostic marker.

[Nocturnal gastroesophageal reflux as a cause of refractory chronic laryngitis--pathophysiology and management]. / Nächtlicher gastroösophagealer Reflux als Ursache der therapierefraktären chronischen Laryngitis--Mechanismen und Management.

Chronic laryngitis is a common disease with a multifactoral genesis. One of the known causal factors is gastrolaryngeal acid reflux as a consequence of gastroesophageal reflux disease (GERD). 10 to 30% of the patients do not show an adequate response to the standard treatment with proton pump inhibitors, which could not be well explained in the past. Our own observations indicate, that sleep related gastroesophageal reflux may play an important role. The special physiological conditions in sleep can impair the reflux, and an increased nocturnal breathing effort in snoring or sleep apnea induces an intensive gastrolaryngeal reflux. This paper explains the pathophysiological background and the diagnostics and differential treatment.

Use of conventional and self-adjusting nasal continuous positive airway pressure for treatment of severe obstructive sleep apnea syndrome: a comparative study.

STUDY OBJECTIVES: To compare conventional and self-adjusting nasal continuous positive airway pressure (nCPAP) therapy in patients with severe obstructive sleep apnea syndrome with respect to suppression of respiratory disturbances, quality of sleep, mean mask pressure, and patient compliance. DESIGN: Cohort study of consecutive patients with obstructive sleep apnea syndrome, single-blinded. SETTING: Clinical sleep laboratory in Germany. PATIENTS: Fifty patients (44 men, 6 women who ranged in age from 35 to 71 years) with polysomnographically confirmed severe obstructive sleep apnea syndrome (respiratory disturbance index [RDI], >20/h). MEASUREMENTS AND INTERVENTIONS: After baseline polysomnography, patients were randomly treated with nCPAP either in conventional (group 1) or in automatically adjusting (group 2) mode. Three to 6 months after adjustment, all patients underwent polysomnography again. They also were examined with a portable monitoring device and received a questionnaire on subjective well-being and device evaluation. RESULTS: Anthropometric and respiratory data were comparable in both groups; body mass index had not changed significantly in the follow-up. RDI dropped by 91.5% (from 38.3+/- 13.9/h to 3.6+/-4.4/h) in conventional and by 93.6% (from 35.5+/-9.6/h to 2.4+/-1.6/h) in self-adjusting mode (statistically not significant [NS]). Sleep efficiency decreased by 4.0% in conventional and increased by 2.0% in self-adjusting mode (NS). In both groups, normal sleep structure was largely restored. Mean mask pressure was 8.1+/-2.5 cm H2O in group 1 and 6.5+/-1.7 cm H2O in group 2 (p<0.01). Patient compliance in terms of nights per week of mask appliance was better in the self-adjusting mode (5.7+/-0.7 to 6.5+/-0.4; p<0.01). CONCLUSION: Self-adjusting nCPAP demonstrates the same reliability in suppression of respiratory disturbances as fixed-mask pressure therapy. Sleep quality is slightly superior, patient compliance is highly significantly better.

Pulmonary hypertension in patients with obstructive sleep apnea syndrome.

BACKGROUND: Obstructive sleep apnea syndrome (OSAS) is associated with an increased cardiovascular morbidity, including pulmonary hypertension. Little is known about factors influencing the degree of pulmonary hypertension and left ventricular dysfunction in patients with OSAS, especially in the absence of concomitant lung disease. METHODS: Right heart catheterization, arterial blood gas analysis, and pulmonary function tests were performed in 92 consecutive patients (81 men and 11 women; mean +/- SD age, 53.1 +/- 11.0 years) with polysomnographically verified OSAS, in whom clinically significant lung disease was excluded. RESULTS: Eighteen patients (20%) had mild pulmonary hypertension; 8 (44%) of them also had increased pulmonary capillary wedge pressures (Ppew). Left ventricular dysfunction was associated with arterial hypertension. Only Ppcw (r = 0.51; P < .001) and the percentage of time during sleep spent with an oxygen saturation below 90% (as an indicator of the severity of OSAS) (r = 0.34; P = .003) were significantly and independently associated with pulmonary artery pressure. CONCLUSIONS: Obstructive sleep apnea syndrome can cause mild pulmonary hypertension, even in the absence of pulmonary disease. In these patients, pulmonary hypertension is of the postcapillary type, or-in patients with normal left ventricular function-strongly related to the severity of OSAS. Our findings indicate that OSAS may constitute an important, and independent, risk factor for pulmonary hypertension.

Right ventricular dysfunction in patients with obstructive sleep apnoea syndrome.

There is conclusive evidence that obstructive sleep apnoea syndrome (OSAS) influences right heart haemodynamics and can also induce pulmonary hypertension. It is not known, however, whether right ventricular dysfunction can occur in patients with OSAS in the absence of lung disease. We studied 107 patients (94 males, 13 females, mean age 55 +/- 11 yrs) with polysomnographically verified OSAS in whom clinically significant lung disease was excluded. Right ventricular ejection fraction (RVEF) was determined by radionuclide ventriculography. In addition, pulmonary function tests, arterial blood gas analysis and right heart catheterization were performed. RVEF was impaired in 19 patients (18%). Eighteen (95%) had signs or symptoms consistent with mild right ventricular failure. Patients with or without impaired RVEF did not differ with respect to body mass index, age or lung function. Stepwise multiple logistic regression analysis revealed that RVEF was significantly associated with the apnoea/hypopnoea index (r = -0.68; p = 0.0009) and the extent of nocturnal oxyhaemoglobin saturation (r = 0.42; p = 0.035), but not with age, body mass index, blood gas analysis, gender, lung function, pulmonary artery pressure and left ventricular ejection fraction. We conclude that in patients with otherwise unexplained right ventricular failure, obstructive sleep apnoea syndrome may underlie the right ventricular dysfunction.