Non-sleepy obstructive sleep apnoea: to treat or not to treat?

Non-sleepy obstructive sleep apnoea (OSA) is thought to have a prevalence of around 20-25% in industrialised countries. However, the question of whether it should be routinely treated or not is controversial. This review collates the results from recent randomised controlled trials addressing OSA and examines whether treating the condition leads to improvements in quality of life and reduced cardiometabolic dysfunction, comorbidities generally attributed to untreated obstructive sleep apnoea/hypopnoea syndrome

Sleep-disordered breathing-do we have to change gears in heart failure?

The majority of patients with heart failure have sleep-disordered breathing (SDB)-with central (rather than obstructive) sleep apnoea becoming the predominant form in those with more severe disease. Cyclical apnoeas and hypopnoeas are associated with sleep disturbance, hypoxaemia, haemodynamic changes, and sympathetic activation. Such patients have a worse prognosis than those without SDB. Mask-based therapies of positive airway pressure targeted at SDB can improve measures of sleep quality and partially normalise the sleep and respiratory physiology, but recent randomised trials of cardiovascular outcomes in central sleep apnoea have been neutral or suggested the possibility of harm, likely from increased sudden death. Further randomised outcome studies (with cardiovascular mortality and hospitalisation endpoints) are required to determine whether mask-based treatment for SDB is appropriate for patients with chronic systolic heart failure and obstructive sleep apnoea, for those with heart failure with preserved ejection fraction, and for those with decompensated heart failure. New therapies for sleep apnoea-such as implantable phrenic nerve stimulators-also require robust assessment. No longer can the surrogate endpoints of improvement in respiratory and sleep metrics be taken as adequate therapeutic outcome measures in patients with heart failure and sleep apnoea

Relationship between critical pressure and volume exhaled during negative pressure in awake subjects with sleep-disordered breathing.

Background: Critical pressure (Pcrit) is considered a reliable parameter to evaluate the mechanical properties of the passive upper airway (UA) and is signifi cantly increased in patients with obstructive sleep apnea-hypopnea (OSAH) compared with normal subjects. The volume exhaled in the fi rst 0.5 s after application at the mouth of 5 cm H 2 O negative pressure at the onset of expiration (V,NEP 0.5 ) during wakefulness has been used as a marker of UA collapsibility. The aim of this study was to investigate if there is a signifi cant relationship between V,NEP 0.5 and Pcrit in normal subjects, snorers, and patients with OSAH. Methods: Thirty men, 10 with OSAH (aged 64 6 9.1 years, BMI 32 6 4.9 kg/m 2 , apnea-hypopnea index [AHI] 43.8 6 24, neck circumference 46.6 6 3.7 cm), 10 snorers (aged 68 6 11 years, BMI 26.6 6 4.6 kg/m 2 , AHI 3.5 6 0.8, snoring time 30% of sleep time, neck circumference 42.2 6 3.9 cm), and 10 controls (aged 67 6 12 years, BMI 25.4 6 2.2 kg/m 2 , AHI 1.9 6 1.2, neck circumference 41.2 6 2.2 cm) underwent V,NEP 0.5 measurement in supine position while awake and Pcrit measurement during sleep. Correlation between V,NEP 0.5 and Pcrit was performed in all subjects. Results: Controls had V,NEP 0.5 of 456 6 82 mL and Pcrit of 2 1.38 6 0.6 cm H 2 O, snorers had V,NEP 0.5 of 321 6 33 mL and Pcrit 2 0.55 6 0.3 cm H 2 O, and patients with OSAH showed V,NEP 0.5 of 295 6 67 mL and Pcrit of 0.99 6 1 cm H 2 O ( P , .001 vs normal subjects). A strong correlation was found between V,NEP 0.5 and Pcrit ( r 2 5 0.61, P , .0001). Conclusions: In males with neck circumference . 37 cm, V,NEP 0.5 during wakefulness strongly refl ects Pcrit in a wide range of values. Our fi ndings suggest that V,NEP 0.5 can be used as valuable substitute for Pcrit to assess UA collapsibility for clinical and research purposes in these subjects

Phenotyping-based treatment improves obstructive sleep apnea symptoms and severity: a pilot study

Background: Obstructive sleep apnea is a common disorder characterized by multiple pathogenetic roots. Continuous positive airway pressure (CPAP) is almost always prescribed as the first-line treatment to all patients regardless of the heterogeneous pathophysiology, because it mechanically splints the airways open and reduces the collapsibility of the upper airway. Despite its high efficacy, CPAP is burdened by poor adherence and compliance rates. In this pilot study, we treated OSA patients with composite approaches different than CPAP, tailoring the therapeutic choice on OSA phenotypic traits. Methods: We used the CPAP dial down technique to assess phenotypic traits in eight OSA patients with BMI<35. According to these traits, patients received personalized therapies for 2-week period, after which we ran a second polygraphy to compare apnea-hypopnea index (AHI) before and after therapy. Results: Two weeks of combined behavioral and pharmacological therapy induced a significant reduction in mean AHI, which dropped from 26 ± 15 at baseline to 9 ± 7 post-treatment (p = 0.01). Furthermore, there was a significant reduction in mean ODI (p = 0.03) and subjective sleepiness (p = 0.01) documented by Epworth Sleepiness Scale (ESS) from baseline to post-treatment recordings. Conclusions: Treating OSA patients with a personalized combination of pharmacological and behavioral therapies according to phenotypic traits leads to a significant improvement in AHI, ODI, and subjective sleepiness

Lung air trapping lowers respiratory arousal threshold and contributes to sleep apnea pathogenesis in COPD patients with overlap syndrome

Study objectives: Overlap syndrome occurs when obstructive sleep apnea (OSA) and chronic obstructive pulmonary disorder (COPD) coexist in the same patient. Although several studies highlighted the importance of clinical phenotyping in OSA, the trait contribution to OSA pathogenesis in overlap syndrome has not been investigated. With this pilot study, we aimed to measure OSA determinants and their relationship with functional respiratory parameters in a sample of patients with overlap syndrome. In particular, we hypothesize that patients with COPD have in the low arousal threshold a major contributor for the development of OSA. Methods: Ten consecutive non-hypercapnic COPD patients (body mass index<35 kg/m2) suffering from overlap syndrome with no other relevant comorbidities underwent a phenotyping polysomnography. Traits were measured with CPAP dial-downs. Results: Arousal threshold was found to be inversely associated to functional measures of lung air trapping and static hyperinflation. Particularly, correlations with residual volume (r2 = 0.49, p = 0.024) and residual volume to total lung capacity ratio (r2 = 0.48, p = 0.026) were evident. Only 20% of patients showed a high upper airway passive collapsibility as single pathological trait. In contrast, among those patients with multiple altered traits (6 out of 10), all had an elevated loop gain and 4 (∼65%) a low arousal threshold. Conclusions: High loop gain and particularly low arousal threshold seem important contributors to OSA pathogenesis and severity in patients with COPD. Recognizing in COPD patients these features as key traits may open avenues for personalized medicine in the field of overlap syndrome