Skip to main content

Main menu

  • Home
  • Current issue
  • Past issues
  • Authors/reviewers
    • Instructions for authors
    • Submit a manuscript
    • COVID-19 submission information
    • Institutional open access agreements
    • Peer reviewer login
  • Alerts
  • Subscriptions
  • ERS Publications
    • European Respiratory Journal
    • ERJ Open Research
    • European Respiratory Review
    • Breathe
    • ERS Books
    • ERS publications home

User menu

  • Log in
  • Subscribe
  • Contact Us
  • My Cart

Search

  • Advanced search
  • ERS Publications
    • European Respiratory Journal
    • ERJ Open Research
    • European Respiratory Review
    • Breathe
    • ERS Books
    • ERS publications home

Login

European Respiratory Society

Advanced Search

  • Home
  • Current issue
  • Past issues
  • Authors/reviewers
    • Instructions for authors
    • Submit a manuscript
    • COVID-19 submission information
    • Institutional open access agreements
    • Peer reviewer login
  • Alerts
  • Subscriptions

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

Nejat Altintas, Renata L. Riha
European Respiratory Review 2019 28: 190031; DOI: 10.1183/16000617.0031-2019
Nejat Altintas
1Pulmonary and Sleep Medicine, Namik Kemal University, Tekirdag, Turkey
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
Renata L. Riha
2Dept of Sleep Medicine, Royal Infirmary of Edinburgh, Edinburgh, UK
3Centre for Clinical Brain Sciences, University of Edinburgh, Edinburgh, UK
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
  • For correspondence: rlriha@hotmail.com
  • Article
  • Figures & Data
  • Info & Metrics
  • PDF
Loading

Abstract

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.

Abstract

Non-sleepy obstructive sleep apnoea: to treat or not to treat? http://bit.ly/2GaB7xp

Introduction

Success in treating any illness is predicated on the extent to which pain, suffering and the risk of future disability can be swiftly and effectively abolished. The prevention of illness is a more complex matter, but its success is more likely if the preventive strategies employed are simple and the evidence for them clear, e.g. when a patient is prescribed pills for hypertension to reduce the risk of stroke.

The same cannot be said for the treatment of obstructive sleep apnoea/hypopnoea syndrome (OSAHS). With daytime sleepiness as the major hallmark of the disorder, treatment to reduce the apnoeas and hypopnoeas occurring during sleep is neither simple nor straightforward. Treatment is highly dependent on self-management and most frequently comprises nightly use of either continuous positive airway pressure (CPAP) or a mandibular repositioning device.

Long-term adherence to CPAP is one of the greatest stumbling blocks in the treatment of OSAHS, with rates ranging from 40% to 60% [1–3]. This rate relates to cohorts of patients who have self-selected by their attendance at sleep disorder clinics. The evidence for successful prevention of long-term complications of untreated OSAHS, which are considered to comprise metabolic dysregulation, hypertension, driving risk and cognitive decline, even in those who are highly symptomatic, is currently moderate at best and afflicted by bias as well as problems with statistical modelling, the population examined and standardised definitions [4, 5].

The evidence for successful treatment of asymptomatic obstructive sleep apnoea (OSA) is also not strong [6]. This article aims to synthesise our current understanding of what comprises OSA, as well as the short- and long-term trials that have assessed the effects of treatment on any associated comorbidities.

Definitions of sleep disordered breathing

OSAHS is the commonest form of sleep disordered breathing within industrialised communities, affecting at least 2–7% of the middle-aged population [7, 8]. OSAHS is defined as the occurrence of disordered breathing during sleep, characterised by objective measures of recurrent apnoeas and hypopnoeas, resulting in symptoms of daytime sleepiness and possible cognitive impairment.

The current “gold standard” for treating moderate-to-severe OSAHS is CPAP, which comprises mechanical splinting of the airways using compressed air delivered through a nasal or full-face mask worn during sleep. [7].

The objective metric of OSA is the apnoea–hypopnoea index (AHI), which has been subject to a variety of definitions over the decades [8]. The third edition of the International Classification of Sleep Disorders (ICSD-3) [9], for instance, encompasses a very broad definition of OSAHS, defining it as: 1) an AHI >5 events·h–1 of sleep with one or more symptoms (e.g. sleepiness, fatigue, insomnia, snoring) or an associated medical or psychiatric disorder (e.g. hypertension, coronary artery disease, atrial fibrillation); or 2) an AHI >15 events·h–1 of sleep without symptoms or associated conditions. The implication of these definitions is that OSA should be treated, since the daytime symptoms are being driven entirely and exclusively by the disturbed breathing during sleep. Currently, however, there is little evidence to support this argument, since definitions of OSAHS are derived from two components rated separately and very differently, namely severity of AHI and daytime sleepiness [8]. Indiscriminate application of the ICSD-3 criteria to data from large community-based cohorts results in 50–70% of the population being defined as having OSAHS [10]. This is clearly not the case.

When polysomnography (PSG) is used to diagnose sleep apnoea, OSAHS is defined as mild (AHI 5–15 events·h–1 ), moderate (AHI 15–30 events·h–1) or severe (AHI >30 events·h–1) [11]. This does not account for age- or sex-related changes in sleep disordered breathing and there are few population-specific, normative data available [7, 8].

According to ICSD-3 [9], excessive daytime sleepiness (EDS) is defined as the inability to stay awake and alert during the major waking episodes of the day, resulting in periods of irrepressible need for sleep or unintended lapses into drowsiness or sleep. Pathological sleepiness has been found to occur in 7–13% of the general population in large surveys and in 20–25% of a primary care population [8, 12]. Men and women appear to be equally affected [13]. One review estimated that 42% of all sleepiness was likely to be secondary to a medical or psychiatric disorder rather than a sleep disorder per se [13]. However, up to 25–50% of OSAHS patients do not report subjective tiredness or sleepiness [14].

Quantifying EDS is difficult. The most commonly used scale worldwide is the Epworth sleepiness scale [15], which has numerous limitations and the subjective nature of which has not been shown to correlate with objective measures of sleepiness [16]. An ESS score of ≥11 out of 24 is considered to indicate EDS in populations with and without OSA [8]. Objective measures to quantify sleepiness, though available, are not readily applicable to everyday clinical practice and most are utilised in the assessment of ability to drive [8].

Thus, definitions of OSAHS and OSA are dependent on the technical acquisition of electrophysiological signals, fluctuating scoring definitions and somewhat arbitrary definitions of sleepiness.

Epidemiology of OSA

The prevalence of OSA in adults worldwide is currently estimated to be 938 million people, nearly 10 times greater than previous estimates [17].

The most frequently cited paper on the topic showed that 24% of men (n=325) and 9% of women (n=250) had an AHI of >5 events·h–1 of sleep [18]. However, when sleepiness was factored in as causally related to the AHI, the prevalence fell to 4% in men and 2% in women. Several population prevalence studies since then have been analysed with the resultant mean (range) prevalence of OSA found to be 27.3% (9–86%) and 22.5% (3.7–63.7%) in men and women, respectively, and the mean prevalence of OSAHS to be 6% (3–18%) and 4% (1–17%) in men and women, respectively [19]. Thus, OSA without self-reported sleepiness is almost three times as common in men and women as OSAHS. The big question remains: is OSA detrimental to health?

Is there a non-sleepy OSA phenotype?

With the prevalence of non-sleepy OSA being so high within the community, numerous studies have been undertaken over the last two decades to determine why some people with OSA develop diurnal symptoms related to nocturnal sleep disordered breathing and others do not. Additionally, sleepiness has been associated with higher levels of cardiovascular and metabolic comorbidity and many trials have attempted to ascertain whether CPAP treatment leads to improved outcomes, apart from improving quality of life primarily by reducing EDS [5, 20, 21]. Attempts at phenotyping OSA/OSAHS patients using presenting complaints have suggested other associations with comorbidities e.g. insomnia was more likely to herald cardiovascular abnormalities in European patients with OSA [22].

Table 1 summarises non-randomised clinical studies undertaken in an attempt to distinguish sleepy from non-sleepy OSA. Overall, the studies are heterogeneous and not directly comparable, due to technological variations and different definitions utilised. Although AHI has been shown to increase with age, the prevalence of OSAHS has not [8]. Despite differences among the studies, patients with OSAHS were more likely to have a higher body mass index, to be older and to have greater metabolic dysfunction than those with OSA without EDS [36, 37]. Whether OSA carries the same prognosis and symptom burden long term as the lack of any sleep disordered breathing and lack of sleepiness has never been formally studied. Natural history studies of sleep disordered breathing, as typified by the first paper to publish such observations in 2005 [38], suggest that in those with “mild” OSA and snoring, there is no significantly increased risk of mortality and morbidity compared to “normal” controls.

View this table:
  • View inline
  • View popup
TABLE 1

Studies examining sleepy and non-sleepy obstructive sleep apnoea patients with respect to demographic, sleep and comorbidity variables

Treating OSA

CPAP therapy has a long history of generally poor adherence, which has been attributed to numerous factors, ranging from severity of the AHI, perceived benefit, personality of the patient, interface issues and type of machine [39, 40].

The seminal paper by Weaver et al. [41] examining the minimum duration per night of CPAP usage in 149 patients with severe OSAHS found that 4 h·night−1 led to a reduction in self-reported sleepiness, 6 h·night−1 led to improvement in objective sleepiness and 7.5 h·night−1 led to improvement in functional status. In terms of optimal adherence to CPAP for improving cardiovascular symptoms, the evidence is less clear. A meta-analysis conducted in 2007 of 12 trials (572 patients) suggested that there was a mean reduction in blood pressure for every 1 h of increased use of CPAP per night [42]. However, further studies, including a meta-analysis published in 2012, suggested that sleepy patients benefitted most from CPAP when self-reported sleepiness (using the ESS) fell [43].

Lastly, even with adequate compliance, many patients with a moderate-to-severe AHI will still complain of post-CPAP sleepiness [44, 45]. This can also give rise to a reduction in long-term adherence and has been the subject of numerous studies and troubleshooting guidelines [46]. The previous duration and severity of OSA and its impact on physiological functions may not be entirely reversible [47–49], or the sleepiness may be due to other factors, physical or psychological, which have not been simultaneously addressed.

More than 40 randomised controlled trials investigating the effects of CPAP on blood pressure in OSAHS have demonstrated a modest reduction in blood pressure, especially in those patients with resistant hypertension [50]. Other randomised controlled trials have shown that CPAP use in OSAHS can improve surrogate markers of cardiovascular and metabolic health, e.g. endothelial function, insulin sensitivity and cardiac function [51, 52]. However, the evidence has not been as consistent for OSA without sleepiness.

Results from a meta-analysis of randomised controlled trials published in 2016 [53], examining the impact of CPAP on patients with non-sleepy OSA, found minimal overall benefit on subjective sleepiness, systolic blood pressure or cardiovascular risk. Six published studies were included [54–59], as well as a seventh study [60] which incorporated and re-analysed data from a previously published dataset [56]. In total, data from 1541 patients were reviewed. The studies were published between 2001 and 2016 from sleep medicine centres in Spain, Canada, Great Britain and Sweden. Inclusion criteria were based on an AHI of ≥15 events·h–1 of sleep, an oxygen desaturation index (ODI) of 4% from baseline >10 events·h–1 of sleep, or an ODI >7.5 events·h–1 of sleep. Lack of sleepiness was defined as an ESS score of ≤10 out of 24 in all studies. The percentage of men in these studies ranged from 76% to 91%; the mean±sd age of the patients ranged from 53.1±2.2 years to 66±8.3 years and their body mass indexes ranged from 28.5±3.6 kg·m−2 to 33.2±5.3 kg·m−2. CPAP use was recorded in four studies with average overall usage ranging from 2.65±0.73 h·night−1 to 6±1.7 h·night−1 and study duration from 4 weeks to 4.75 years. CPAP did not improve ESS score overall but it did improve the AHI/ODI significantly versus controls (p=0.026). Diastolic blood pressure in those treated with CPAP fell on average by 0.92 mmHg (95% CI −1.39 to −0.46 mmHg; p<0.001).

Of course, there are limitations to every study. This should be borne in mind when interpreting post hoc analyses. Barbe et al. [55] reported cardiovascular risk reduction in patients who used CPAP for ≥4 h·night−1, as did Peker et al. [59]. Choosing 4 h·night−1 usage as a cut-off appears arbitrary in the context of what is known about CPAP use as discussed above.

Two studies have examined whether reasonable adherence can be reached with CPAP in non-sleepy OSA. Campos-Rodriguez et al. [61] reported that after following 357 non-sleepy patients with an AHI ≥20 events·h–1 in multiple Spanish sleep centres for a median of 4 years, 230 (64.4%) had a compliance of ≥4 h·night−1. They found that a higher AHI at baseline and the presence of hypertension were associated with better adherence. In their group of patients with coronary artery disease and OSA, Luyster et al. [62] demonstrated that the probability of remaining on CPAP at 2 years was 60% in non-sleepy patients and 77% in sleepy patients. A positive experience of using CPAP initially was a strong determinant of long-term use.

These results bring to attention the difficulties in defining EDS in these groups of patients and possibly do not account for issues with bed-partners (who may reinforce CPAP use even in the non-sleepy to control noise levels), the amount and quality of effort and input that a nurse or physician contributes to encouraging a patient to continue on CPAP, and personality. In the context of a trial, the Hawthorne effect can cause bias in both control and treatment groups not present in real life.

Finally, one trial published in 2016 is worth discussing in the context of non-sleepy OSA, although the enrolment criterion of an ESS score of ≤15 out of 24 does not conform to the accepted definition of not being sleepy. This was the “CPAP for prevention of cardiovascular events in obstructive sleep apnoea trial” (SAVE trial) [63], which recruited a very large population (n=2717 total; aged 45–75 years) in order to examine the effects of CPAP on cardiovascular and cerebrovascular outcomes. The trial was designed to be multicentre, parallel-group and open-label, enrolling moderate to severe OSA patients with an ESS score of ≤15 out of 24 with cardiovascular disease or cerebrovascular disease. Follow-up was for a mean of 3.7 years only. CPAP failed to protect patients from a composite death score which included heart failure, myocardial infarction, hospitalisation for unstable angina, stroke or transient ischaemic attack, compared to controls without CPAP, despite significantly reducing daytime sleepiness and improving quality of life, mood and work capacity. However, mean duration of CPAP adherence was 3.3 h·night−1 during follow-up. A post hoc analysis [64] used latent class analysis to identify high-risk OSA clinical phenotypes. Latent class analysis identified four OSA clinical phenotypes: coronary artery disease (CAD) alone, CAD+diabetes mellitus (DM), cardiovascular disease alone and cerebrovascular disease +DM. Composite cardiovascular events were highest for the CAD+DM phenotype. The presence of diabetes in OSA patients with CAD or cardiovascular disease increased the risk of the composite outcome occurring despite treatment. However, adequate CPAP treatment (>4 h·night−1) reduced cardiovascular risk in diabetic patients with OSA, with the strongest effect being seen in patients with cerebrovascular disease. Although disappointing, the results of the SAVE trial may have been subject to a number of important biases and complications. The majority of the subjects enrolled in the study were from two distinctly different ethnic groups (62%); there was a high dropout rate (83%) and high cross-over of control group patients (57 patients) into the CPAP treatment arm. For ethical reasons, patients with EDS and severe hypoxaemia (oxyhaemoglobin saturation <80% for >10% of sleep study time) were excluded, thus limiting the sample to a potentially lower-risk group, and finally, the CPAP usage rates were low. The use of CPAP for only a short part of the night may have resulted in patients missing most of their rapid eye movement (REM) sleep on treatment. REM-linked apnoeas and hypopneas are typically lengthy and are associated with greater oxyhaemoglobin desaturations and higher sympathetic tone. REM-related OSA is specifically associated with incident or recent onset hypertension and cardiovascular disease [65–67].

Discussion

Recently, a pro–con debate on whether non-sleepy, moderate to severe OSA should be treated or not has been published [6, 47].

In arguing against treating OSA indiscriminately, Vakulin et al. [6] pointed out that the cost of new technologies and the pressures on healthcare worldwide means that allocation of resources for any disease is dependent on the knowledge that the disorder causes significant ill health and that a high level of evidence exists to show that treatments offered are effective, cost-effective and safe. This is true for OSAHS, where sufficient evidence exists to offer treatment for symptom control. However, the evidence is not so convincing in those who have OSA. On the other hand, Ryan [47] argues that the term “asymptomatic” is likely to be misleading and that randomised controlled trials have demonstrated that, even in patients with an ESS score ≤10 out of 24, further improvement in quality of life can occur with treatment in addition to subtle changes in endothelial function and normalisation of nocturnal blood pressure profiles. The relatively short-term follow-up in published randomised controlled studies [54–59], which are likely to be underpowered with respect to such observations, cannot address these questions. Additionally, Ryan [47] argues that there is large interindividual variability in CPAP response that may be linked to the duration of the disease prior to diagnosis, which may have resulted in irreversible tissue damage [48, 49].

CPAP adherence has been a source of contention in the studies discussed in this review and an important variable which may influence outcomes. The literature currently advocates a threshold approach to CPAP use with data overall supporting a dose–response relationship dependent on the variable or outcome being studied [39]. However, no absolute optimal adherence levels to CPAP have ever been determined [39]. Although patients with OSA have been shown to adhere to CPAP successfully, the overall rates of use after a few years fall to around 60%, worse by at least 10% in comparison to patients with OSAHS [39].

To date, phenotyping patients with non-sleepy OSA has been somewhat elusive and is likely to be unhelpful on a practical basis when the clinician is faced with each patient as an individual with their own set of particular characteristics. In this situation, extrapolation of results from short-term trials is not likely to be helpful in making long-term treatment decisions.

Conclusion

Diurnal dysfunction secondary to intermittent hypoxaemia and recurrent sympathetic arousals during the sleep period are not universal findings in sleep apnoea. However, the evidence for a direct link between untreated OSAHS and cardiometabolic consequences is considerable, even though treatment does not always fully reverse the abnormalities. The association of these abnormalities with OSA is not strong and trials reporting positive treatment effects are of short-term duration, uncontrolled or have been undertaken in very specific population cohorts. How these data are then applied on a daily basis to other populations and patients with other clinical characteristics remains the difficulty and the dilemma. Challenges in future research include the incorporation of precise, objectively assessed definitions of sleepiness, long-term follow-up, correction for age- and sex-related norms in AHI and sleepiness and adequate study power. In the future, one way of simplifying diagnostic and treatment pathways would be to classify patients as CPAP or non-CPAP responsive, irrespective of AHI and degree of sleepiness. Since sleepiness is not always the direct result of sleep apnoea, this might form the basis for a more practical approach in our day-to-day clinical practice and help resolve some of the less soluble questions we face.

Footnotes

  • Number 7 in the Series “Sleep Disordered Breathing” Edited by Renata Riha and Maria Bonsignore

  • No. 1: Masa JF, Pépin J-L, Borel J-C, et al. Obesity hypoventilation syndrome. Eur Respir Rev 2019; 28: 180097. No. 2: Bruyneel M. Telemedicine in the diagnosis and treatment of sleep apnoea. Eur Respir Rev 2019; 28: 180093. No. 3: Ryan S, Arnaud C, Fitzpatrick SF, et al. Adipose tissue as a key player in obstructive sleep apnoea. Eur Respir Rev 2019; 28: 190006. No. 4: Cayanan EA, Bartlett DJ, Chapman JL, et al. A review of psychosocial factors and personality in the treatment of obstructive sleep apnoea. Eur Respir Rev 2019; 28: 190005. No. 5: Randerath W, Bonsignore M, Herkenrath S. Obstructive sleep apnoea in acute coronary syndrome. Eur Respir Rev 2019; 28: 180114. No. 6: Bonsignore MR, Saaresranta T, Riha RL. Sex differences in obstructive sleep apnoea. Eur Respir Rev 2019; 28: 190030.

  • Provenance: Commissioned article, peer reviewed.

  • Conflict of interest: N. Altintas has nothing to disclose.

  • Conflict of interest: R.L. Riha has nothing to disclose.

  • Received March 26, 2019.
  • Accepted July 8, 2019.
  • Copyright ©ERS 2019.
http://creativecommons.org/licenses/by-nc/4.0/

This article is open access and distributed under the terms of the Creative Commons Attribution Non-Commercial Licence 4.0.

References

  1. ↵
    1. McArdle N,
    2. Devereux G,
    3. Heidarnejad H, et al.
    Long-term use of CPAP therapy for sleep apnea/hypopnea syndrome. Am J Respir Crit Care Med 1999; 159: 4 Pt. 1, 1108–1114.
    OpenUrlCrossRefPubMed
    1. Weaver TE,
    2. Grunstein RR
    . Adherence to continuous positive airway pressure therapy: the challenge to effective treatment. Proc Am Thorac Soc 2008; 5: 173–178.
    OpenUrlCrossRefPubMed
  2. ↵
    1. Rotenberg BW,
    2. Murariu D,
    3. Pang KP
    . Trends in CPAP adherence over twenty years of data collection: a flattened curve. J Otolaryngol Head Neck Surg 2016; 45: 43.
    OpenUrl
  3. ↵
    1. Antic NA,
    2. Catcheside P,
    3. Buchan C, et al.
    The effect of CPAP in normalizing daytime sleepiness, quality of life, and neurocognitive function in patients with moderate to severe OSA. Sleep 2011; 34: 111–119.
    OpenUrlPubMed
  4. ↵
    1. Patil SP,
    2. Ayappa IA,
    3. Caples SM, et al.
    Treatment of adult obstructive sleep apnea with positive airway pressure: an American Academy of Sleep Medicine clinical practice guideline. J Clin Sleep Med 2019; 15: 335–343.
    OpenUrl
  5. ↵
    1. Vakulin A,
    2. Chai-Coetzer CL,
    3. McEvoy RD
    . Con: should asymptomatic patients with moderate-to-severe OSA be treated? Breathe 2019; 15: 11–14.
    OpenUrlAbstract/FREE Full Text
  6. ↵
    1. Jennum P,
    2. Riha RL
    . Epidemiology of sleep apnoea/hypopnoea syndrome and sleep-disordered breathing. Eur Respir J 2009; 33: 907–914.
    OpenUrlAbstract/FREE Full Text
  7. ↵
    1. Riha RL
    . Diagnostic approaches to respiratory sleep disorders. J Thorac Dis 2015; 7: 1373–1384.
    OpenUrl
  8. ↵
    AASM. International classification of sleep disorders, third edition: diagnostic and coding manual. Darien, IL, American Academy of Sleep Medicine, 2014.
  9. ↵
    1. Adams R,
    2. Appleton S,
    3. Taylor A, et al.
    Are the ICSD-3 criteria for sleep apnoea syndrome too inclusive? Lancet Respir Med 2016; 4: e19–e20.
    OpenUrl
  10. ↵
    Sleep-related breathing disorders in adults: recommendations for syndrome definition and measurement techniques in clinical research. The report of an American Academy of Sleep Medicine task force. Sleep 1999; 22: 667–689.
    OpenUrlCrossRefPubMed
  11. ↵
    1. Kushida CA,
    2. Nichols DA,
    3. Simon RD, et al.
    Symptom-based prevalence of sleep disorders in an adult primary care population. Sleep Breath 2000; 4: 9–14.
    OpenUrlPubMed
  12. ↵
    1. Ohayon MM
    . From wakefulness to excessive sleepiness: what we know and still need to know. Sleep Med Rev 2008; 12: 129–141.
    OpenUrlCrossRefPubMed
  13. ↵
    1. Chervin RD
    . Sleepiness, fatigue, tiredness, and lack of energy in obstructive sleep apnea. Chest 2000; 118: 372–379.
    OpenUrlCrossRefPubMed
  14. ↵
    1. Johns MW
    . A new method for measuring daytime sleepiness: the Epworth sleepiness scale. Sleep 1991; 14: 540–545.
    OpenUrlCrossRefPubMed
  15. ↵
    1. Johns MW
    . Sensitivity and specificity of the multiple sleep latency test (MSLT), the maintenance of wakefulness test and the Epworth sleepiness scale: failure of the MSLT as a gold standard. J Sleep Res 2000; 9: 5–11.
    OpenUrlCrossRefPubMed
  16. ↵
    1. Benjafield A,
    2. Valentine K,
    3. Ayas N
    . Global prevalence of obstructive sleep apnea in adults: estimation using currently available data. Am J Respir Crit Care Med 2018; 197: A3962.
    OpenUrl
  17. ↵
    1. Young T,
    2. Palta M,
    3. Dempsey J, et al.
    The occurrence of sleep-disordered breathing among middle-aged adults. N Engl J Med 1993; 328: 1230–1235.
    OpenUrlCrossRefPubMed
  18. ↵
    1. Theorell-Haglöw J,
    2. Miller CB,
    3. Bartlett DJ, et al.
    Gender differences in obstructive sleep apnoea, insomnia and restless legs syndrome in adults – What do we know? A clinical update. Sleep Med Rev 2018; 38: 28–38.
    OpenUrl
  19. ↵
    1. McNicholas WT,
    2. Bonsignore MR
    , Management Committee of EU COST ACTION B26. Sleep apnoea as an independent risk factor for cardiovascular disease: current evidence, basic mechanisms and research priorities. Eur Respir J 2007; 29: 156–178.
    OpenUrlAbstract/FREE Full Text
  20. ↵
    1. Pataka A,
    2. Riha RL
    . Continuous positive airway pressure and cardiovascular events in patients with obstructive sleep apnea. Curr Cardiol Rep 2013; 15: 385.
    OpenUrl
  21. ↵
    1. Saaresranta T,
    2. Hedner J,
    3. Bonsignore MR, et al.
    Clinical phenotypes and comorbidity in European sleep apnoea patients. PLoS One 2016; 11: e0163439.
    OpenUrl
    1. Kapur VK,
    2. Baldwin CM,
    3. Resnick HE, et al.
    Sleepiness in patients with moderate to severe sleep-disordered breathing. Sleep 2005; 28: 472–477.
    OpenUrlPubMed
    1. Mediano O,
    2. Barcelo A,
    3. la Pena de M, et al.
    Daytime sleepiness and polysomnographic variables in sleep apnoea patients. Eur Respir J 2007; 30: 110–113.
    OpenUrlAbstract/FREE Full Text
    1. Roure N,
    2. Gomez S,
    3. Mediano O, et al.
    Daytime sleepiness and polysomnography in obstructive sleep apnea patients. Sleep Med 2008; 9: 727–731.
    OpenUrlCrossRefPubMed
    1. Oksenberg A,
    2. Arons E,
    3. Nasser K, et al.
    Severe obstructive sleep apnea: sleepy versus nonsleepy patients. Laryngoscope 2010; 120: 643–648.
    OpenUrlPubMed
    1. Taranto Montemurro L,
    2. Floras JS,
    3. Picton P, et al.
    Relationship of heart rate variability to sleepiness in patients with obstructive sleep apnea with and without heart failure. J Clin Sleep Med 2014; 10: 271–276.
    OpenUrlPubMed
    1. Bravo M,
    2. de LP,
    3. Serpero LD, et al.
    Inflammatory proteins in patients with obstructive sleep apnea with and without daytime sleepiness. Sleep Breath 2007; 11: 177–185.
    OpenUrlCrossRefPubMed
    1. Koutsourelakis I,
    2. Perraki E,
    3. Bonakis A, et al.
    Determinants of subjective sleepiness in suspected obstructive sleep apnoea. J Sleep Res 2008; 17: 437–443.
    OpenUrlCrossRefPubMed
    1. Uysal A,
    2. Liendo C,
    3. McCarty DE, et al.
    Nocturnal hypoxemia biomarker predicts sleepiness in patients with severe obstructive sleep apnea. Sleep Breath 2014; 18: 77–84.
    OpenUrl
    1. Sun Y,
    2. Ning Y,
    3. Huang L, et al.
    Polysomnographic characteristics of daytime sleepiness in obstructive sleep apnea syndrome. Sleep Breath 2012; 16: 375–381.
    OpenUrlPubMed
    1. Seneviratne U,
    2. Puvanendran K
    . Excessive daytime sleepiness in obstructive sleep apnea: prevalence, severity, and predictors. Sleep Med 2004; 5: 339–343.
    OpenUrlCrossRefPubMed
    1. Wang Q,
    2. Zhang C,
    3. Jia P, et al.
    The association between the phenotype of excessive daytime sleepiness and blood pressure in patients with obstructive sleep apnea-hypopnea syndrome. Int J Med Sci 2014; 11: 713–720.
    OpenUrl
    1. Barcelo A,
    2. Barbe F,
    3. la Pena de M, et al.
    Insulin resistance and daytime sleepiness in patients with sleep apnoea. Thorax 2008; 63: 946–950.
    OpenUrlAbstract/FREE Full Text
    1. Nena E,
    2. Steiropoulos P,
    3. Papanas N, et al.
    Sleepiness as a marker of glucose deregulation in obstructive sleep apnea. Sleep Breath 2012; 16: 181–186.
    OpenUrlCrossRefPubMed
  22. ↵
    1. Huang J-F,
    2. Chen L-D,
    3. Lin Q-C, et al.
    The relationship between excessive daytime sleepiness and metabolic syndrome in severe obstructive sleep apnea syndrome. Clin Respir J 2016; 10: 714–721.
    OpenUrl
  23. ↵
    1. Chowdhuri S,
    2. Patel P,
    3. Badr MS
    . Apnea in older adults. Sleep Med Clin 2018; 13: 21–37.
    OpenUrl
  24. ↵
    1. Marin JM,
    2. Carrizo SJ,
    3. Vicente E, et al.
    Long-term cardiovascular outcomes in men with obstructive sleep apnoea-hypopnoea with or without treatment with continuous positive airway pressure: an observational study. Lancet 2005; 365: 1046–1053.
    OpenUrlCrossRefPubMed
  25. ↵
    1. Bakker JP,
    2. Weaver TE,
    3. Parthasarathy S, et al.
    Adherence to CPAP: what should we be aiming for, and how can we get there? Chest 2019; 155: 1272–1287.
    OpenUrl
  26. ↵
    1. Maschauer EL,
    2. Fairley DM,
    3. Riha RL
    . Does personality play a role in continuous positive airway pressure compliance? Breathe 2017; 13: 32–43.
    OpenUrlAbstract/FREE Full Text
  27. ↵
    1. Weaver TE,
    2. Maislin G,
    3. Dinges DF, et al.
    Relationship between hours of CPAP use and achieving normal levels of sleepiness and daily functioning. Sleep 2007; 30: 711–719.
    OpenUrlPubMed
  28. ↵
    1. Haentjens P,
    2. Van Meerhaeghe A,
    3. Moscariello A, et al.
    The impact of continuous positive airway pressure on blood pressure in patients with obstructive sleep apnea syndrome: evidence from a meta-analysis of placebo-controlled randomized trials. Arch Intern Med 2007; 167: 757–764.
    OpenUrlCrossRefPubMed
  29. ↵
    1. Montesi SB,
    2. Edwards BA,
    3. Malhotra A, et al.
    The effect of continuous positive airway pressure treatment on blood pressure: a systematic review and meta-analysis of randomized controlled trials. J Clin Sleep Med 2012; 8: 587–596.
    OpenUrlPubMed
  30. ↵
    1. Stradling JR,
    2. Smith D,
    3. Crosby J
    . Post-CPAP sleepiness – a specific syndrome? J Sleep Res 2007; 16: 436–438.
    OpenUrlCrossRefPubMed
  31. ↵
    1. Leclerc G,
    2. Lacasse Y,
    3. Page D, et al.
    Do obstructive sleep apnea syndrome patients underestimate their daytime symptoms before continuous positive airway pressure treatment? Can Respir J 2014; 21: 216–220.
    OpenUrl
  32. ↵
    1. Santamaria J,
    2. Iranzo A,
    3. Ma Montserrat J, et al.
    Persistent sleepiness in CPAP treated obstructive sleep apnea patients: evaluation and treatment. Sleep Med Rev 2007; 11: 195–207.
    OpenUrlCrossRefPubMed
  33. ↵
    1. Ryan S
    . Pro: should asymptomatic patients with moderate-to-severe OSA be treated? Breathe 2019; 15: 7–10.
    OpenUrlAbstract/FREE Full Text
  34. ↵
    1. Iftikhar IH,
    2. Hoyos CM,
    3. Phillips CL, et al.
    Meta-analyses of the association of sleep apnea with insulin resistance, and the effects of CPAP on HOMA-IR, adiponectin, and visceral adipose fat. J Clin Sleep Med 2015; 11: 475–485.
    OpenUrlPubMed
  35. ↵
    1. Yang D,
    2. Liu Z,
    3. Yang H, et al.
    Effects of continuous positive airway pressure on glycemic control and insulin resistance in patients with obstructive sleep apnea: a meta-analysis. Sleep Breath 2013; 17: 33–38.
    OpenUrl
  36. ↵
    1. Iftikhar IH,
    2. Valentine CW,
    3. Bittencourt LR, et al.
    Effects of continuous positive airway pressure on blood pressure in patients with resistant hypertension and obstructive sleep apnea: a meta-analysis. J Hypertens 2014; 32: 2341–2350.
    OpenUrlCrossRefPubMed
  37. ↵
    1. Iftikhar IH,
    2. Khan MF,
    3. Das A, et al.
    Meta-analysis: continuous positive airway pressure improves insulin resistance in patients with sleep apnea without diabetes. Ann Am Thorac Soc 2013; 10: 115–120.
    OpenUrlCrossRefPubMed
  38. ↵
    1. Schwarz EI,
    2. Puhan MA,
    3. Schlatzer C, et al.
    Effect of CPAP therapy on endothelial function in obstructive sleep apnoea: a systematic review and meta-analysis. Respirology 2015; 20: 889–895.
    OpenUrl
  39. ↵
    1. Zhang D,
    2. Luo J,
    3. Qiao Y, et al.
    Continuous positive airway pressure therapy in non-sleepy patients with obstructive sleep apnea: results of a meta-analysis. J Thorac Dis 2016; 8: 2738–2747.
    OpenUrl
  40. ↵
    1. Robinson GV,
    2. Smith DM,
    3. Langford BA, et al.
    Continuous positive airway pressure does not reduce blood pressure in nonsleepy hypertensive OSA patients. Eur Respir J 2006; 27: 1229–1235.
    OpenUrlAbstract/FREE Full Text
  41. ↵
    1. Barbé F,
    2. Duran-Cantolla J,
    3. Sanchez-de-la-Torre M, et al.
    Effect of continuous positive airway pressure on the incidence of hypertension and cardiovascular events in nonsleepy patients with obstructive sleep apnea: a randomized controlled trial. JAMA 2012; 307: 2161–2168.
    OpenUrlCrossRefPubMed
  42. ↵
    1. Craig SE,
    2. Kohler M,
    3. Nicoll D, et al.
    Continuous positive airway pressure improves sleepiness but not calculated vascular risk in patients with minimally symptomatic obstructive sleep apnoea: the MOSAIC randomised controlled trial. Thorax 2012; 67: 1090–1096.
    OpenUrlAbstract/FREE Full Text
    1. Kasiakogias A,
    2. Tsioufis C,
    3. Thomopoulos C, et al.
    Effects of continuous positive airway pressure on blood pressure in hypertensive patients with obstructive sleep apnea: a 3-year follow-up. J Hypertens 2013; 31: 352–360.
    OpenUrlCrossRefPubMed
    1. Barbé F,
    2. Mayoralas LR,
    3. Duran J, et al.
    Treatment with continuous positive airway pressure is not effective in patients with sleep apnea but no daytime sleepiness. a randomized, controlled trial. Ann Intern Med 2001; 134: 1015–1023.
    OpenUrlCrossRefPubMed
  43. ↵
    1. Peker Y,
    2. Glantz H,
    3. Eulenburg C, et al.
    Effect of positive airway pressure on cardiovascular outcomes in coronary artery disease patients with non-sleepy obstructive sleep apnea: the RICCADSA randomized controlled trial. Am J Respir Crit Care Med 2016; 194: 613–620.
    OpenUrlPubMed
  44. ↵
    1. Turnbull CD,
    2. Craig SE,
    3. Kohler M, et al.
    Cardiovascular event rates in the MOSAIC trial: 2-year follow-up data. Thorax 2014; 69: 950.
    OpenUrlAbstract/FREE Full Text
  45. ↵
    1. Campos-Rodriguez F,
    2. Martinez-Alonso M,
    3. Sanchez-de-la-Torre M, et al.
    Long-term adherence to continuous positive airway pressure therapy in non-sleepy sleep apnea patients. Sleep Med 2016; 17: 1–6.
    OpenUrl
  46. ↵
    1. Luyster FS,
    2. Strollo PJ Jr.,
    3. Thunström E, et al.
    Long-term use of continuous positive airway pressure therapy in coronary artery disease patients with nonsleepy obstructive sleep apnea. Clin Cardiol 2017; 40: 1297–1302.
    OpenUrl
  47. ↵
    1. McEvoy RD,
    2. Antic NA,
    3. Heeley E, et al.
    CPAP for prevention of cardiovascular events in obstructive sleep apnea. N Engl J Med 2016; 375: 919–931.
    OpenUrlCrossRefPubMed
  48. ↵
    1. Quan W,
    2. Zheng D,
    3. McEvoy RD, et al.
    High risk characteristics for recurrent cardiovascular events among patients with obstructive sleep apnoea in the SAVE study. E-ClinicalMedicine 2018; 2–3: 59–65.
    OpenUrl
  49. ↵
    1. Mokhlesi B,
    2. Finn LA,
    3. Hagen EW, et al.
    Obstructive sleep apnea during REM sleep and hypertension: results of the Wisconsin Sleep Cohort. Am J Respir Crit Care Med 2014; 190: 1158–1167.
    OpenUrlCrossRefPubMed
    1. Appleton SL,
    2. Vakulin A,
    3. Martin SA, et al.
    Hypertension is associated with undiagnosed OSA during rapid eye movement sleep. Chest 2016; 150: 495–505.
    OpenUrl
  50. ↵
    1. Mokhlesi B,
    2. Varga AW
    . Obstructive sleep apnea and cardiovascular disease. REM sleep matters!. Am J Respir Crit Care Med 2018; 197: 554–556.
    OpenUrl
PreviousNext
Back to top
View this article with LENS
Vol 28 Issue 154 Table of Contents
European Respiratory Review: 28 (154)
  • Table of Contents
  • Index by author
Email

Thank you for your interest in spreading the word on European Respiratory Society .

NOTE: We only request your email address so that the person you are recommending the page to knows that you wanted them to see it, and that it is not junk mail. We do not capture any email address.

Enter multiple addresses on separate lines or separate them with commas.
Non-sleepy obstructive sleep apnoea: to treat or not to treat?
(Your Name) has sent you a message from European Respiratory Society
(Your Name) thought you would like to see the European Respiratory Society web site.
CAPTCHA
This question is for testing whether or not you are a human visitor and to prevent automated spam submissions.
Print
Citation Tools
Non-sleepy obstructive sleep apnoea: to treat or not to treat?
Nejat Altintas, Renata L. Riha
European Respiratory Review Dec 2019, 28 (154) 190031; DOI: 10.1183/16000617.0031-2019

Citation Manager Formats

  • BibTeX
  • Bookends
  • EasyBib
  • EndNote (tagged)
  • EndNote 8 (xml)
  • Medlars
  • Mendeley
  • Papers
  • RefWorks Tagged
  • Ref Manager
  • RIS
  • Zotero

Share
Non-sleepy obstructive sleep apnoea: to treat or not to treat?
Nejat Altintas, Renata L. Riha
European Respiratory Review Dec 2019, 28 (154) 190031; DOI: 10.1183/16000617.0031-2019
Reddit logo Technorati logo Twitter logo Connotea logo Facebook logo Mendeley logo
Full Text (PDF)

Jump To

  • Article
    • Abstract
    • Abstract
    • Introduction
    • Discussion
    • Footnotes
    • References
  • Figures & Data
  • Info & Metrics
  • PDF

Subjects

  • Sleep medicine
  • Tweet Widget
  • Facebook Like
  • Google Plus One

More in this TOC Section

Series

  • New trends in pulmonary hypertension
  • Diagnostic workup of childhood interstitial lung disease
  • The world of rare interstitial lung diseases
Show more Series

Sleep disordered breathing

  • Sex differences in OSA
  • OSA in acute coronary syndrome
Show more Sleep disordered breathing

Related Articles

Navigate

  • Home
  • Current issue
  • Archive

About the ERR

  • Journal information
  • Editorial board
  • Press
  • Permissions and reprints
  • Advertising
  • Sponsorship

The European Respiratory Society

  • Society home
  • myERS
  • Privacy policy
  • Accessibility

ERS publications

  • European Respiratory Journal
  • ERJ Open Research
  • European Respiratory Review
  • Breathe
  • ERS books online
  • ERS Bookshop

Help

  • Feedback

For authors

  • Instructions for authors
  • Publication ethics and malpractice
  • Submit a manuscript

For readers

  • Alerts
  • Subjects
  • RSS

Subscriptions

  • Accessing the ERS publications

Contact us

European Respiratory Society
442 Glossop Road
Sheffield S10 2PX
United Kingdom
Tel: +44 114 2672860
Email: journals@ersnet.org

ISSN

Print ISSN: 0905-9180
Online ISSN: 1600-0617

Copyright © 2023 by the European Respiratory Society