Auto bi-level with pressure relief during exhalation as a rescue therapy for optimally treated obstructive sleep apnoea patients with poor compliance to continuous positive airways pressure therapy—a pilot study

Background  

Continuous positive airways pressure (CPAP) is the accepted therapy for obstructive sleep apnoea (OSA), but compliance is variable. We hypothesised that an auto bi-level device with pressure relief during exhalation (auto bi-level) would treat OSA as well as CPAP and that transitioning non-compliant CPAP patients without modifiable causes of poor compliance to this device would improve compliance and clinical outcomes.     

Pathogenesis of central and complex sleep apnoea

Central sleep apnoea (CSA) – the temporary absence or diminution of ventilatory effort during sleep – is seen in a variety of forms including periodic breathing in infancy and healthy adults at altitude and Cheyne–Stokes respiration in heart failure. In most circumstances, the cyclic absence of effort is paradoxically a consequence of hypersensitive ventilatory chemoreflex responses to oppose changes in airflow, that is elevated loop gain, leading to overshoot/undershoot ventilatory oscillations. Considerable evidence illustrates overlap between CSA and obstructive sleep apnoea (OSA), including elevated loop gain in patients with OSA and the presence of pharyngeal narrowing during central apnoeas. Indeed, treatment of OSA, whether via continuous positive airway pressure (CPAP), tracheostomy or oral appliances, can reveal CSA, an occurrence referred to as complex sleep apnoea. Factors influencing loop gain include increased chemosensitivity (increased controller gain), reduced damping of blood gas levels (increased plant gain) and increased lung to chemoreceptor circulatory delay. Sleep–wake transitions and pharyngeal dilator muscle responses effectively raise the controller gain and therefore also contribute to total loop gain and overall instability. In some circumstances, for example apnoea of infancy and central congenital hypoventilation syndrome, central apnoeas are the consequence of ventilatory depression and defective ventilatory responses, that is low loop gain. The efficacy of available treatments for CSA can be explained in terms of their effects on loop gain, for example CPAP improves lung volume (plant gain), stimulants reduce the alveolar‐inspired PCO₂ difference and supplemental oxygen lowers chemosensitivity. Understanding the magnitude of loop gain and the mechanisms contributing to instability may facilitate personalized interventions for CSA.     

Central sleep apnea and complex sleep apnea in patients with epilepsy

Purpose

We sought to examine the prevalence of central sleep apnea (CSA) and complex sleep apnea (CompSA) in patients with epilepsy and to examine their clinical profile, with respect to epilepsy type, etiology, medication use, and EEG abnormalities.

Methods

We undertook a retrospective analysis of 719 consecutive patients with epilepsy who underwent polysomnography (PSG) at our institution between 2004 and 2011. Of the 458 patients with complete data, we excluded 42 patients with congestive heart failure or left ventricular ejection fraction <40 %. Comparison of clinical and PSG variables between the three groups were conducted with Fisher exact test and analysis of variance.

Results

Out of 416 patients tested, 315 (75 %) had obstructive sleep apnea (OSA), 16 (3.7 %) had CSA, 33 (7.9 %) had CompSA. There were more males in the CSA and CompSA groups than in the OSA group (81.2, 81.8, and 59.6 %, respectively, p?=?0.04). Focal seizures were more prevalent in patients with CSA than in patients OSA or CompSA (62.5, 265, and 21.1 %, respectively, p?=?0.02).

Conclusion

About 11 % of epilepsy patients have sleep-breathing disorders with central apneas, which is not higher than that in a general population. These data should be expanded with future research investigating the role of interictal, ictal, and postictal central apneas in epileptogenesis and epilepsy.     

Oxidative stress in obstructive sleep apnoea.

AIMS: Any sustained elevation of oxidative stress in patients with obstructive sleep apnoea (OSA) might help explain their increased risk for cardiovascular diseases. We tested the hypothesis that measures of oxidative stress are increased in otherwise healthy subjects with OSA when compared to closely matched OSA-free control subjects. METHODS AND RESULTS: Plasma indices of oxidative stress and lipid peroxidation [thiobarbituric acid-reactive substances (TBARS), oxidized LDL (oxLDL), isoprostanes] were measured in 41 moderate-severe OSA males without other diseases and in 35 matched controls first before sleep, then after 4 h of untreated OSA, and again in the morning after 4 h of effective treatment with continuous positive airway pressure (CPAP). Plasma levels of oxLDL, TBARS, and isoprostanes in OSA patients (n=34, 26, 17, respectively) were comparable to the controls (n=28, 27, 15 for the three markers, respectively). Neither untreated OSA nor CPAP treatment nor normal sleep affected levels of any of the three measures of oxidative stress. There was no association between the severity of sleep apnoea and any measure of oxidative stress. CONCLUSION: Otherwise healthy OSA patients, without any other co-morbidities, do not manifest evidence for higher oxidative stress and lipid peroxidation. Thus, oxidative stress and lipid peroxidation do not appear to be key mediators of increased cardiovascular disease in OSA patients.     

Association between continuous positive airway pressure and changes in serum leptin in patients with obstructive sleep apnoea: a meta-analysis

Purpose

The role of leptin in the development of obstructive sleep apnoea (OSA) has been identified. However, the effects of OSA treatment using continuous positive airway pressure (CPAP) on serum leptin levels remain controversial. To address this issue, a meta-analysis was conducted to evaluate the effects of CPAP therapy on serum leptin levels in OSA.

Methods

A comprehensive literature search was performed to identify studies that focused on the effects of CPAP therapy (treatment duration, ≥4 weeks) on the serum leptin levels of OSA patients. Standardised mean difference (SMD) was used to analyse the summary estimates for CPAP therapy.

Results

Fifteen studies involving 427 patients were included in the meta-analysis. Results indicate that the overall SMD of the leptin levels before and after CPAP therapy was 0.137 (95 % confidence interval (CI) 0.002 to 0.272); test for overall effect z?=?1.99 (P?=?0.046). Sources of heterogeneity were not found by subgroup and meta-regression analyses. Subgroup analyses showed that differences in OSA severity, baseline body mass index, compliance, CPAP duration and leptin assay did not affect the effectiveness of CPAP therapy.

Conclusions

The evidence for the use of CPAP therapy on decrease of leptin levels in OSA patients is low, and stronger evidence is needed.     

The significance and outcome of continuous positive airway pressure-related central sleep apnea during split-night sleep studies

OBJECTIVE: To determine whether central sleep apnea (CSA) occurring during continuous positive airway pressure (CPAP) titration in patients with obstructive sleep apnea (OSA) reflects subclinical congestive heart failure (CHF), and whether these events will improve with CPAP therapy. DESIGN: Cross-sectional analysis of patients with suspected sleep-related breathing disorders referred for split-night polysomnography PATIENTS AND METHODS: Forty-two OSA patients with and without CPAP-related CSA were analyzed. All CSA patients (n = 21) and control subjects (n = 21) underwent echocardiography, pulmonary function testing, and arterial blood gas (ABG) analysis. Repeat polysomnography with CPAP was performed 2 to 3 months after adequate CPAP therapy in CSA group patients. RESULTS: Demographic, Epworth sleepiness scale, pulmonary function test, ABG, and baseline diagnostic polysomnography findings were similar in both groups. There was no difference in the prevalence of subclinical left ventricular systolic dysfunction in the CSA group vs the control group. CSA patients had decreased sleep efficiency (SE), increased sleep stage 1 percentage, sleep stages shift, wake time after sleep onset (WASO), and total arousals compared to control subjects. Twelve of 14 patients (92%) in the CSA group demonstrated complete or near-complete resolution of CSA events on follow-up polysomnography and showed improvement in SE, WASO, and total arousals compared to their baseline study. CONCLUSIONS: CSA events occurring during CPAP titration are transient and self-limited. They may be precipitated by the sleep fragmentation associated with initial CPAP titration and are not associated with an increased prevalence of occult CHF compared to OSA patients without CPAP-related CSA.     

Leptin and ghrelin levels in patients with obstructive sleep apnoea: effect of CPAP treatment.

Serum leptin and ghrelin levels were investigated in patients with obstructive sleep apnoea (OSA) syndrome before and during continuous positive airways pressure (CPAP) treatment and compared with body mass index (BMI)-matched controls without OSA. Male patients (n=30) with OSA (apnoea/hypopnoea index=58+/-16, BMI=32.6+/-5.3 kg x m(-2)) underwent CPAP treatment. Fasting leptin and ghrelin were measured at baseline and 2 days, and in the case of leptin 2 months after initiation of treatment. Baseline plasma ghrelin levels were significantly higher in OSA patients than in controls. After 2 days of CPAP treatment, plasma ghrelin decreased in almost all OSA patients (n=9) to levels that were only slightly higher than those of controls (n=9). Leptin levels did not change significantly from baseline after 2 days of CPAP treatment, but were higher than in the control group. After 8 weeks, leptin levels decreased significantly, although the BMI of the patients showed no change. The decrease in leptin levels was more pronounced in patients with a BMI <30 kg x m(-2). These data indicate that the elevated leptin and ghrelin levels are not determined by obesity alone, since they rapidly decreased during continuous positive airways pressure therapy.     

Effective sleep apnoea treatment improves cardiac function in patients with chronic heart failure

Background

Sleep disordered breathing (SDB) is highly prevalent in patients with chronic heart failure (CHF) and is associated with adverse effects on cardiac geometry and function. Continuous positive airway pressure (CPAP) has been proved an effective treatment modality for obstructive sleep apnoea (OSA), whereas adaptive servoventilation (ASV) is more effective in patients with central sleep apnoea (CSA). The impact of selection of therapy and effective apnoea alleviation on cardiac performance and reverse left ventricular remodelling (r-LVR) has not yet been evaluated.

Methods

Eighty five patients with stable CHF were screened for SDB and underwent polysomnography and treatment according to the type of SDB. Clinical evaluation and a comprehensive echocardiographic study was performed before initiation of therapy and after six months of effective treatment (ventilator use > 5 h/day with AHI < 5 events/h).

Results

Seventeen compliant patients under effective treatment were included in the analysis (8 OSA under Autoset CPAP and 9 CSA under ASV). In both groups, a significant improvement in all measured, conventional and TDI LV systolic indexes was recorded, including LVEF (32% ± 6% vs. 27% ± 6%, p < 0.001). A decrease in LV end-systolic volume (189 ± 94 ml vs. 211 ± 88 ml, p = 0.015, difference > 10%) was indicative of r-LVR. Furthermore, RV systolic parameters were also increased (TAPSE, p < 0.001; systolic TDI wave from lateral tricuspid annular aspect, p = 0.001), whereas right heart dimensions and areas were diminished, indicating better pulmonary haemodynamics. Moreover, a significant improvement in patients' clinical status, as evaluated by New York Heart Association Class was also documented at the end of six months follow-up.

Conclusions

Effective alleviation of SDB in CHF patients is associated with significant improvements in LV and RV systolic function and r-LVR. Longitudinal studies are needed to evaluate effects on morbidity and mortality.     

Predicting uptake of continuous positive airway pressure (CPAP) therapy in obstructive sleep apnoea (OSA): a belief-based theoretical approach

Purpose

Obstructive sleep apnoea (OSA) is a common disorder, for which continuous positive airway pressure (CPAP) therapy is a standard treatment. Despite its well-established efficacy, many patients choose not to initiate CPAP treatment. The present study investigated the degree to which biological measures (e.g. Apnoea–Hypopnoea Index [AHI]), symptom experiences (e.g. fatigue) and illness representations (e.g. perceived consequences) predict the decision of individuals newly diagnosed with OSA to undergo a trial of CPAP therapy.

Methods

Four hundred forty-nine individuals (316 males) newly diagnosed with OSA. Epworth sleepiness scale (ESS), Fatigue Severity Scale, Depression Anxiety Stress Scale and Illness Perception Questionnaire-Revised (IPQ-R) were administered at time of sleep study. These, patient demographics and sleep study variables were used to determine factors predicting patient decision to proceed with a trial of CPAP.

Results

The participants were most likely to attribute their OSA to unchangeable and psychological factors. For those with moderate OSA (AHI, 15 to 30) IPQ-R illness consequence was predictive of decision to initiate CPAP (p = 0.002). For severe OSA (AHI >30) age, ESS and IPQ illness causal beliefs were predictive of decision to initiate CPAP (p < 0.001).

Conclusions

Illness beliefs are important determinants of the choice of recently diagnosed OSA patients whether or not to undertake a trial of CPAP therapy. Concerns about illness consequences were important in those with moderate OSA. In severe OSA, sleepiness symptoms are more prominent and a more significant determinant of CPAP uptake along with age and causal beliefs.     

Plasma B-type natriuretic peptide level is associated with left ventricular hypertrophy among obstructive sleep apnoea patients

OBJECTIVES: To examine whether increased plasma levels of B-type natriuretic peptide (BNP) are associated with cardiac structural and functional abnormalities in obstructive sleep apnoea (OSA) patients, taking into consideration the confounding effect of obesity. MEASUREMENTS: In a cross-sectional study, polysomnography, echocardiography and the measurement of the serum levels of BNP were performed in 235 consecutive subjects (age 52 +/- 14 years) visiting our sleep clinic. Left ventricular hypertrophy (LVH) [left ventricular mass index (LVMI) > or = 125 g/m in men, and > or = 110 g/m in women] and cardiac diastolic function (E/A ratio) were determined by echocardiography. RESULTS: The LVMI, prevalence rate of LVH and body mass index (BMI) were higher, and the E/A ratio lower in the subjects with severe OSA (apnoea-hypopnoea index > or = 30/h, n = 146, LVH 80%) than in those with mild to moderate OSA (n = 89, LVH 35%; P < 0.01), although plasma BNP levels were similar in the two groups. Although the log-transformed plasma BNP level showed a negative correlation with BMI, the results of binary logistic regression analysis demonstrated that the quintile value of BNP was an independent significant variable for the identification of LVH (adjusted odds ratio in quintile 5 = 4.01, 95% confidence interval 1.18-13.70, P < 0.01), even after adjusting for obesity and other risk factors. CONCLUSION: An increased likelihood of cardiac structural and functional abnormalities was observed with increasing severity of OSA. Increased plasma levels of BNP do seem to reflect an increased likelihood of LVH in patients with severe OSA.     

Plasma homocysteine in obstructive sleep apnoea.

AIMS: Whether increased homocysteine is one mechanism linking obstructive sleep apnoea (OSA) to cardiovascular abnormalities is unclear. We hypothesised that plasma homocysteine would be higher in OSA patients than in control subjects, would increase further during sleep, and decrease after treatment with continuous positive airway pressure (CPAP). METHODS AND RESULTS: For study A, homocysteine was measured in 22 OSA patients and 20 controls first before sleep, then after 5 h of untreated OSA, and then in the morning after CPAP treatment. Homocysteine was similar in the OSA and control subjects at all three time points, and declined overnight in both groups (P=0.0017, P=0.036, respectively). To further assess this diurnal variation, we studied plasma homocysteine under a full-night protocol in 10 OSA patients and 12 controls (study B). Homocysteine was measured before sleep, in the morning after sleep, and at noon. Results in both OSA and control groups showed an overnight decline in homocysteine which was reversed by noon (repeated measures ANOVA: OSA, P=0.04; controls, P=0.02). Study C showed that disturbed sleep did not affect homocysteine levels in normal subjects. CONCLUSION: There is a significant diurnal variation in plasma homocysteine, so that homocysteine is lower in the morning after waking. Neither OSA nor disturbed sleep elicit acute or chronic changes in homocysteine.     

Atrial overdrive pacing compared to CPAP in patients with obstructive sleep apnoea syndrome.

AIMS: Obstructive sleep apnoea (OSA) is associated with oxygen desaturation, blood pressure increase, and neurohumoral activation, resulting in possible detrimental effects on the cardiovascular system. Continuous positive airway pressure (CPAP) is the therapy of choice for OSA. In a recent study, nocturnal atrial overdrive pacing (pacing) reduced the severity of sleep apnoea in pacemaker patients. We compared the effects of CPAP with those of pacing in patients with OSA but without pacemaker indication or clinical signs of heart failure. METHODS AND RESULTS: Ten patients with OSA on CPAP therapy were studied for three nights by polysomnography. During the nights that followed a night without any treatment (baseline), the patients were treated with CPAP or pacing in a random order. Pacing was performed with a temporary pacing lead. The pacing frequency was 15 b.p.m. higher than the baseline heart rate. The apnoea-hypopnoea index was 41.0 h(-1) (12.0-66.6) at baseline and was significantly lower during CPAP [2.2 h(-1) (0.3-12.4)] compared with pacing [39.1 h(-1) (8.2-78.5)]. Furthermore, duration and quality of sleep were significantly improved during CPAP when compared with pacing. CONCLUSION: Nocturnal atrial overdrive pacing is no alternative therapeutic strategy to CPAP for the treatment of OSA in patients without clinical signs of heart failure and without conventional indication for anti-bradycardia pacing.     

Nocturnal pulse rate and symptomatic response in patients with obstructive sleep apnoea treated with continuous positive airway pressure for one year

Background

Obstructive sleep apnoea (OSA) is the most common form of sleep-disordered breathing and a known risk factor for cardiovascular disease. We hypothesised that in patients with OSA the characteristics of nocturnal pulse rate (PR) are associated with changes in blood pressure and daytime sleepiness, following commencement of continuous positive airway pressure (CPAP) therapy.

Methods

Pulse oximetry data, demographics, daytime sleepiness and blood pressure were recorded at baseline and at one year follow up. Patients with OSA were grouped according to positive and negative changes in the PR (ΔPR) response during the first night of pulse oximetry before commencement of CPAP.

Results

A total of 115 patients (58 with OSA and 57 matched subjects without OSA) were identified and included in the analysis. The scale of improvement in daytime sleepiness could be predicted by a negative or positive ΔPR, as recorded in the initial screening pulse oximetry [ΔESS –5.8 (5.1) vs. –0.8 (7.2) points, P<0.05]. A negative correlation was observed between mean nocturnal PR and changes in systolic blood pressure (SBP) after one year of CPAP treatment (r=–0.42, P<0.05).

Conclusions

Mean nocturnal PR prior to CPAP initiation was associated with changes in SBP at one year follow up. A descending nocturnal PR in patients with OSA, prior to CPAP initiation, might help to identify a symptomatic response from long term CPAP treatment.     

Pulse wave analysis in a pilot randomised controlled trial of auto-adjusting and continuous positive airway pressure for obstructive sleep apnoea

Purpose  

Non-invasive measurements of arterial stiffness including the augmentation index (AIx) and central blood pressure (BP) have been used to assess the cardiovascular health of patients with obstructive sleep apnoea (OSA), a well-established independent risk factor of cardiovascular disease. Continuous positive airway pressure (CPAP) can significantly reduce the AIx, but no studies have analysed the effect of auto-adjusting PAP (APAP) or studied morbidly obese patients with severe OSA at higher risk of cardiovascular disease. In this randomised, single-blinded crossover pilot trial, we aimed to compare the efficacy of CPAP with APAP (ResMed S8 Autoset II) in improving peripheral BP, central BP and the AIx, using SphygmoCor technology.     

Dysfunctional breathing treated with continuous positive airway pressure in newly diagnosed obstructive sleep apnoea: a prospective cohort study

A prospective cohort study investigating patients with obstructive sleep apnoea (OSA) was conducted to determine the prevalence of dysfunctional breathing and if continuous positive airway pressure (CPAP) therapy improves associated symptoms. Almost half of newly diagnosed patients with OSA had dysfunctional breathing and CPAP was not an effective treatment. Dysfunctional breathing is common in patients with OSA.     

Continuous positive airway pressure in heart failure patients with obstructive sleep apnoea

Background: The aim of the study was to study the effect of 6 months of continuous positive airway pressure (CPAP) in community heart failure (HF) patients with obstructive sleep apnoea (OSA). Methods: Clinically stable outpatients with HF and OSA (left ventricular ejection fraction (LVEF) <45%, apnoea/hypopnoea index >15/h, n = 19) treated with CPAP and a control group (LVEF <45%, apnoea/hypopnoea index <10/h, n = 7) were compared at baseline and at 6 months by Minnesota heart failure score, Epworth sleepiness score, shuttle walk distance, brain natriuretic peptide, urinary catecholamines and echocardiographic indices using paired t‐test, McNemar’s tests and effect sizes. Results: In HF patients with OSA, CPAP improved LVEF (35.9 ± 6.1% to 40.6 ± 8.0%, P = 0.015), decreased LV end‐systolic volume (152 ± 74 to 135 ± 62 cm³, P = 0.03), systolic blood pressure (P = 0.04) and sleepiness (Epworth sleepiness score 8.8 ± 4.8 to 6.3 ± 3.2, P = 0.01), whereas walk distance, catecholamines, brain natriuretic peptide levels and symptoms were unchanged. These outcomes did not change in the HF control group. Conclusion: In community HF patients with OSA, CPAP therapy over 6 months improved LVEF, systolic blood pressure and sleepiness, but not sympathetic activation, brain natriuretic peptide or exercise levels. Acceptance was relatively low, potentially limiting therapeutic effectiveness.     

Associated factors for sleep apnea in heart failure

Objective

Genesis of sleep apnoea syndrome (SAS) in chronic heart failure (CHF) is not well known. The aim of our study was to find associated factors to SAS in heart failure (HF) and to look for differences between central sleep apnea (CSA) and obstructive sleep apnea (OSA).

Patients and methods

We realised a cross-sectional and retrospective study. Thirty patients with stable heart failure under medical optimal therapy were included. Polygraphy, echocardiography and cardiopulmonary exercise were systematically performed.

Results

Men were predominant (80%) in the group. Mean age, left ventricular ejection fraction (LVEF) were respectively 64.1 ± 13.8 years and 40 ± 9.8%. SAS was present in 60% of patients (33.3% were classified as central sleep apnoea [CSA] and 26.7% as obstructive sleep apnoea [OSA]). Body mass index, blood pressure and left ventricular pressures estimated by the E/Ea ratio were significantly higher in the group with SAS (P < 0.05) compared to the non SAS group. New York Heart Association class was significantly higher (P = 0.04) and the predicted peak VO₂ was significantly lower in CSA patients compared to OSA patients.

Conclusion

High left ventricular pressures estimated by the E/Ea are significantly associated with SAS in heart failure. CSA patients tend to have a worse functional state than OSA patients.     

Reverse atrial electrical remodelling induced by continuous positive airway pressure in patients with severe obstructive sleep apnoea

Background

Obstructive sleep apnoea (OSA) is associated with cardiovascular morbidity and mortality, including atrial arrhythmias. Continuous positive airway pressure (CPAP) is the gold standard treatment for OSA; its impact on atrial electrical remodelling has not been fully investigated. Signal-averaged p-wave (SAPW) duration is an accepted marker for atrial electrical remodelling.

Objective

The objective of this study is to determine whether CPAP induces reverse atrial electrical remodelling in patients with severe OSA.

Methods

Consecutive patients attending the Sleep Disorder Clinic at Kingston General Hospital underwent full polysomnography. OSA-negative controls and severe OSA were defined as apnoea–hypopnea index (AHI)?<?5 events/hour and AHI?≥?30 events/hour, respectively. SAPW duration was determined at baseline and after 4–6 weeks of CPAP in severe OSA patients or without intervention controls.

Results

Nineteen severe OSA patients and 10 controls were included in the analysis. Mean AHI and minimum oxygen saturation were 41.4?±?10.1 events/hour and 80.5?±?6.5 % in severe OSA patients and 2.8?±?1.2 events/hour and 91.4?±?2.1 % in controls. At baseline, severe OSA patients had a greater SAPW duration than controls (131.9?±?10.4 vs 122.8?±?10.5 ms; p?=?0.02). After CPAP, there was a significant reduction of SAPW duration in severe OSA patients (131.9?±?10.4 to 126.2?±?8.8 ms; p?<?0.001), while SAPW duration did not change after 4–6 weeks in controls.

Conclusion

CPAP induced reverse atrial electrical remodelling in patients with severe OSA as represented by a significant reduction in SAPW duration.     

The role of the expiratory phase in obstructive sleep apnoea.

The role of the expiratory phase in obstructive sleep apnoea (OSA) is not well known. The aim of our study was to verify the contribution of expiratory narrowing to apnoea in a group of OSA patients by evaluating the effects of short-term treatment with continuous positive airway pressure (CPAP), intermittent positive pressure ventilation (IPPV) and bi-level positive airway pressure (BIPAP). We studied a selected group of 10 OSA patients whose therapeutic pressure level of CPAP was at least 10 cm H2O. During CPAP therapy the mean apnoea/hypopnoea index (AHI) and oxyhaemoglobin desaturation index (ODI) decreased from 64.8 to 6.3 (P < 0.001) and from 58.5 to 6.1 (P < 0.001), respectively and mean nadir SAO2 increased from 62.0 to 91.6 (P < 0.001). None of the patients reached optimal setting (elimination of snoring, reduction of apnoeas and non-apnoeic desaturation events at least to 15 or less per hour of sleep and maintenance of oxygen saturation approximately 90%) during IPPV and two patients did not tolerate final IPAP pressure levels. When a critical level of EPAP (BIPAP) was applied in the same night to these patients, optimal setting was reached in all subjects. During BIPAP, mean AHI decreased from 64.8 to 7.4 (P < 0.001); ODI decreased from 58.5 to 7.6 (P < 0.001) and nadir SAO2 increased from 62.0 to 91.2 (P < 0.001). Our study confirms the essential role of a critical level of EPAP in successful ventilatory treatment in OSA, thereby indicating, in agreement with few previous studies, the critical role of end of expiratory occlusion in OSA pathogenesis.     

Resistant hypertension, obstructive sleep apnoea and aldosterone

Obstructive sleep apnoea (OSA) and hypertension commonly coexist. Observational studies indicate that untreated OSA is strongly associated with an increased risk of prevalent hypertension, whereas prospective studies of normotensive cohorts suggest that OSA may increase the risk of incident hypertension. Randomized evaluations of continuous positive airway pressure (CPAP) indicate an overall modest effect on blood pressure (BP). Determining why OSA is so strongly linked to having hypertension in cross-sectional studies, but yet CPAP therapy has limited BP benefit needs further exploration. The CPAP studies do, however, indicate a wide variation in the BP effects of CPAP, with some patients manifesting a large antihypertensive benefit such that a meaningful BP effect can be anticipated in some individuals. OSA is particularly common in patients with resistant hypertension (RHTN). The reason for this high prevalence of OSA is not fully explained, but data suggest that it may be related to the high occurrence of hyperaldosteronism in patients with RHTN. In patients with RHTN, it has been shown that aldosterone levels correlate with severity of OSA and that blockade of aldosterone reduces the severity of OSA. Overall, these findings are consistent with aldosterone excess contributing to worsening of underlying OSA. We hypothesize that aldosterone excess worsens OSA by promoting accumulation of fluid within the neck, which then contributes to increased upper airway resistance.