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While public awareness of sleep related disorders is growing, sleep apnea syndrome (SAS) remains a public health and economic challenge. Over the last two decades, extensive controlled epidemiologic research has clarified the incidence, risk factors including the obesity epidemic, and global prevalence of obstructive sleep apnea (OSA), as well as establishing a growing body of literature linking OSA with cardiovascular morbidity, mortality, metabolic dysregulation, and neurocognitive impairment. The US Institute of Medicine Committee on Sleep Medicine estimates that 50-70 million US adults have sleep or wakefulness disorders. Furthermore, the American Academy of Sleep Medicine (AASM) estimates that more than 29 million US adults suffer from moderate to severe OSA, with an estimated 80% of those individuals living unaware and undiagnosed, contributing to more than $149.6 billion in healthcare and other costs in 2015. Although various devices have been used to measure physiological signals, detect apneic events, and help treat sleep apnea, significant opportunities remain to improve the quality, efficiency, and affordability of sleep apnea care. As our understanding of respiratory and neurophysiological signals and sleep apnea physiological mechanisms continues to grow, and our ability to detect and process biomedical signals improves, novel diagnostic and treatment modalities emerge., Objective: This article reviews the current engineering approaches for the detection and treatment of sleep apnea., Approach: It discusses signal acquisition and processing, highlights the current nonsurgical and nonpharmacological treatments, and discusses potential new therapeutic approaches., Main Results: This work has led to an array of validated signal and sensor modalities for acquiring, storing and viewing sleep data; a broad class of computational and signal processing approaches to detect and classify SAS disease patterns; and a set of distinctive therapeutic technologies whose use cases span the continuum of disease severity., Significance: This review provides a current perspective of the classes of tools at hand, along with a sense of their relative strengths and areas for further improvement.

Unstable periodic breathing with intermittent ventilatory overshoots and undershoots commonly occurs in chronic heart failure, in hypoxia, with chronic opioid use and in certain types of obstructive sleep apnea. Sleep promotes breathing instability because it unmasks a highly sensitive dependence of the respiratory control system on chemoreceptor input, because transient cortical arousals promote ventilatory overshoots and also because upper airway dilator muscle tonicity is reduced and airway collapsibility enhanced. We will present data in support of the premise that carotid chemoreceptors are essential in the pathogenesis of apnea and periodicity; however it is the hyperadditive influence of peripheral chemoreceptor sensory input on central chemosensitivity that accounts for apnea and periodic breathing. This chemoreceptor interdependence also provides a significant portion of the normal drive to breathe in normoxia (i.e. eupnea) and in acute hypoxia. Finally, we discuss the effects of preventing transient hypocapnia (via selective increases in FICO(2)) on centrally mediated types of periodic breathing and even some varieties of cyclical obstructive sleep apnea.

Obstructive sleep apnea (OSA) is highly prevalent in patients with asthma. Asthma, dose-dependently to its duration, promotes incident OSA, suggesting that asthma plays a role in OSA pathogenesis. We hypothesized that asthma-related inflammation alters breathing control mechanisms, specifically the carotid chemoreflex. Accordingly, we measured hypoxic ventilatory responses (HVR) in awake, unrestrained, ovalbumin (OVA)-sensitized Brown Norway rats and compared them with responses in sham-sensitized (SALINE) controls. To differentiate the role of allergic inflammation from bronchoconstriction, we repeated hypoxic ventilatory response (HVR) after administration of formoterol, a long-acting bronchodilator. Blood and bronchoalveolar lavage (BAL) fluid were collected for quantification of inflammatory cytokines. The rise in ventilatory equivalent for O2 evoked by acute exposure to hypoxia was augmented following sensitization by OVA, whereas it remained stable after SALINE. This augmentation was driven by increased breathing frequency with no change in tidal volume. Tachypneic hyperventilation in normoxia was also observed with OVA. Neither the increased HVR nor excessive normoxic ventilation was affected by formoterol, suggesting that they were not secondary to lung mechanical constraints. Higher levels of inflammatory cytokines were observed in BAL fluid and serum of OVA versus SALINE. In OVA, serum interleukin-5 levels significantly correlated with change from baseline in ventilatory responses to severe hypoxia (F I O 2 , 0.09). These observations are consistent with inflammation-induced enhancement of carotid chemoreflex function, i.e., increased controller gain, and they suggest a possible role for asthma-related allergic inflammation in the ventilatory instability known to promote upper airway collapse and sleep apnea in humans. NEW & NOTEWORTHY: Asthma is a risk factor for obstructive sleep apnea (OSA); however, the mechanisms are incompletely understood. In a rat model of allergic inflammation associated with asthma, we found that ventilation in normoxia and ventilatory responses to hypoxia were markedly enhanced and related with systemic inflammation. These alterations indicating carotid chemoreflex sensitization, known to promote ventilatory instability during sleep in humans, may contribute to the increased OSA risk in asthma. [ABSTRACT FROM AUTHOR]

Introduction: Accumulating clinical evidence links Obstructive Sleep Apnea (OSA) with worse outcomes of asthma, but impact on airway function remains sparsely studied. We tested effects of Chronic Intermittent Hypoxia (CIH) – a hallmark of OSA – on airway hyperresponsiveness (AHR), in a rat model of chronic allergen-induced inflammation. Methods: Brown Norway rats were exposed to six weeks of CIH or normoxia (NORM) concurrent with weekly house dust mites (HDM) or saline (SAL) challenges. At endpoint, we assessed responses to seven Methacholine (Mch) doses (0, 4, 8, 16, 32, 64, 128 mg/mL) on a FlexiVent system (Scireq). Maximal (or plateau) responses (reactivity) for total respiratory system Resistance (Rrs) and Elastance (Ers), Newtonian airway resistance (RN, a measure of central airways function) and tissue damping (G, a measure of distal airways function) were plotted. Results: HDM/CIH–treated animals demonstrated the highest reactivity to Mch in Rrs and Ers compared to all other groups (HDM/NORM, SAL/CIH and SAL/NORM p < 0.05 for all comparisons, for doses 5–7 for Rrs, and for doses 4–7 for Ers). The enhanced Rrs response was due to an increase in G (doses 4–7, p < 0.05 for comparisons to all other groups), whereas RN was not affected by CIH. Conclusions: In rats chronically challenged with HDM, concurrent CIH exposure induces AHR primarily in the distal airways, which affects the respiratory system frequency-dependent elastic properties. [ABSTRACT FROM AUTHOR]

Obstructive sleep apnea (OSA) and asthma are highly prevalent chronic respiratory disorders. Beyond their frequent coexistence arising from their high prevalence and shared risk factors, these disorders feature a reciprocal interaction whereby each disease impacts the severity of the other. Emerging evidence implicates airway and systemic inflammation, neuroimmune interactions, and effects of asthma-controlling medications (corticosteroids) as factors that predispose patients with asthma to OSA. Conversely, undiagnosed or inadequately treated OSA adversely affects asthma control, partly via effects of intermittent hypoxia on airway inflammation and tissue remodeling. In this article, we review multiple lines of recently published evidence supporting this interaction. We provide a set of recommendations for clinicians involved in the care of adults with asthma, and identify critical gaps in our knowledge about this overlap. [ABSTRACT FROM AUTHOR]

Obstructive sleep apnea (OSA) is more common in patients with asthma, and inhaled corticosteroids may contribute to OSA pathogenesis in these patients. This study tested the effects of orally inhaled fluticasone propionate (FP) on extrinsic tongue muscles. Unanesthetized rats were treated with FP or placebo for 28 days. On day 29, tongue retrusive and protrusive functions were tested via hypoglossal nerve stimulation under a state of anesthesia, followed by genioglossus (GG), styloglossus (SG) and hyoglossus (HG) muscle extraction, after euthanasia, for histology [myosin heavy chain (MHC) fibers and laminin content reflecting extracellular matrix (ECM)]. On protrusive testing, FP increased percent maximum tetanic force at 40 Hz (P = 0.03 vs. placebo) and endurance index (P = 0.029 vs. placebo). On retrusive testing, FP increased maximum twitch (P = 0.026 vs. placebo) and tetanic forces (P = 0.02 vs. placebo) with no effect on endurance index. On histology, FP increased GG crosssectional area of MHC type IIa (P = 0.036 vs. placebo) and tended to increase type IIb (P = 0.057 vs. placebo) fibers and HG MHC IIx fibers (P = 0.065). The FP group had significantly increased lamininstained areas, of greatest magnitude in the HG muscle. FP affects tongue protrusive and retrusive functions differently, concurrent with a shift in MHC fibers and increased ECM accumulation. These differential alterations may destabilize the tongue's "muscle hydrostat" during sleep and promote collapse. [ABSTRACT FROM AUTHOR]

IMPORTANCE Obstructive sleep apnea (OSA) is more common among patients with asthma; whether asthma is associated with the development of OSA is unknown. OBJECTIVE To examine the prospective relationship of asthma with incident OSA. DESIGN, SETTING, AND PARTICIPANTS Population-based prospective epidemiologic study (the Wisconsin Sleep Cohort Study) beginning in 1988. Adult participants were recruited from a random sample of Wisconsin state employees to attend overnight polysomnography studies at 4-year intervals. Asthma and covariate information were assessed during polysomnography studies through March 2013. Eligible participants were identified as free of OSA (apnea-hypopnea index [AHI] of <5 events/h and not treated) by 2 baseline polysomnography studies. There were 1105 4-year follow-up intervals provided by 547 participants (52% women,- mean [SD] baseline age, 50 [8] years). EXPOSURES Questionnaire-assessed presence and duration of self-reported physician-diagnosed asthma. MAIN OUTCOMES AND MEASURES The associations of presence and duration of asthma with 4-year incidences of both OSA (AHI of >5 or positive airway pressure treatment) and OSA concomitant with habitual daytime sleepiness were estimated using repeated-measures Poisson regression, adjusting for confounders. RESULTS Twenty-two of 81 participants (27% [95% CI, 17%-37%]) with asthma experienced incident OSA over their first observed 4-year follow-up interval compared with 75 of 466 participants (16% [95% CI, 13%-19%]) without asthma. Using all 4-year intervals, participants with asthma experienced 45 cases of incident OSA during 1674-year intervals (27% [95% CI, 20%-34%]) and participants without asthma experienced 160 cases of incident OSA during 9384-year intervals (17% [95% CI, 15%-19%]); the corresponding adjusted relative risk (RR) was 1.39 (95% CI, 1.06-1.82), controlling for sex, age, baseline and change in body mass index, and other factors. Asthma was also associated with new-onset OSA with habitual sleepiness (RR, 2.72 [95% CI, 1.26-5.89], P = .045). Asthma duration was related to both incident OSA (RR, 1.07 per 5-year increment in asthma duration [95% CI, 1.02-1.13], P = .01) and incident OSA with habitual sleepiness (RR, 1.18 [95% CI, 1.07-1.31], P = .02). CONCLUSIONS AND RELEVANCE Asthma was associated with an increased risk of new-onset OSA. Studies investigating the mechanisms underlying this association and the value of periodic OSA evaluation in patients with asthma are warranted. [ABSTRACT FROM AUTHOR]

Purpose: Asthmatics have unique characteristics that may influence cardiovascular morbidity. We tested the association of lower airway caliber, obstructive sleep apnea (OSA), and other asthma-related factors, with systemic hypertension (HTN). Methods: Asthma individuals at specialty clinics completed the Sleep Apnea scale of the Sleep Disorders Questionnaire (SA-SDQ). Medical records were reviewed for diagnosed HTN, OSA and comorbidities, spirometry, and current medications. FEV% predicted was categorized as ≥80 (reference), 70-79, 60-69, and <60. SA-SDQ ≥36 for men and ≥32 for women defined high OSA risk. Results: Among 812 asthmatics (mean age ± standard deviation: 46 ± 14 years), HTN was diagnosed in 191 (24 %), OSA in 65 (8 %), and OSA or high OSA risk (combined OSA variable) in 239 (29 %). HTN was more prevalent in lower FEV% categories ( p < 0.0001), in subjects with OSA, and those with combined OSA variable (55 vs. 21 % and 46 vs. 14 %, respectively, both p < 0.0001). With adjustment for covariates, associations with HTN remained significant for some FEV% categories (70-79 % odds ratio = 1.60 [95 % CI 0.90-2.87]; 60-69 % 2.73 [1.28-5.79]; <60 % 0.96 [0.43-2.14]), and for OSA (2.20 [1.16-4.19]). The combined OSA variable in comparison with OSA alone demonstrated a stronger association with HTN (3.17 [1.99-5.04]) in a reiteration of this model. Inhaled corticosteroids (ICS) at lowest doses, in comparison to no ICS use had an independent 'protective' association with HTN (0.44 [0.22-0.90]). Conclusions: In this young population, worse lower airways obstruction and OSA were associated with HTN. In contrast, lower ICS doses attenuated likelihood for HTN. Adequate control of airway inflammation at appropriate ICS doses, and screening for OSA may reduce the burden of HTN in asthma. [ABSTRACT FROM AUTHOR]

To determine how the obstructive sleep apnea (OSA) patient's pathophysiological traits predict the success of the treatment aimed at stabilization or increase in respiratory motor outputs, we studied 26 newly diagnosed OSA patients [apnea-hypopnea index (AHI) 42 ± 5 events/h with 92% of apneas obstructive] who were treated with O2 supplementation, an isocapnic rebreathing system in which CO2 was added only during hyperpnea to prevent transient hypocapnia, and a continuous rebreathing system. We also measured each patient's controller gain below eupnea [change in minute volume/change in end-tidal PcO2 (ΔVe/ΔPetCO2)], CO2 reserve (eupnea-apnea threshold PetCO2), and plant gain (ΔPetCO2/ΔVe), as well as passive upper airway closing pressure (Pcrit). With isocapnic rebreathing, 14/26 reduced their AHI to 31 ± 6% of control (P < 0.01) (responder); 12/26 did not show significant change (nonresponder). The responders vs. nonresponders had a greater controller gain (6.5 ± 1.7 vs. 2.1 ± 0.2 l·min(-1)·mmHg(-1), P < 0.01) and a smaller CO2 reserve (1.9 ± 0.3 vs. 4.3 ± 0.4 mmHg, P < 0.01) with no differences in Pcrit (-0.1 ± 1.2 vs. 0.2 ± 0.9 cmH2O, P > 0.05). Hypercapnic rebreathing (+4.2 ± 1 mmHg PetCO2) reduced AHI to 15 ± 4% of control (P < 0.001) in 17/21 subjects with a wide range of CO2 reserve. Hyperoxia (SaO2 ~95-98%) reduced AHI to 36 ± 11% of control in 7/19 OSA patients tested. We concluded that stabilizing central respiratory motor output via prevention of transient hypocapnia prevents most OSA in selected patients with a high chemosensitivity and a collapsible upper airway, whereas increasing respiratory motor output via moderate hypercapnia eliminates OSA in most patients with a wider range of chemosensitivity and CO2 reserve. Reducing chemosensitivity via hyperoxia had a limited and unpredictable effect on OSA. [ABSTRACT FROM AUTHOR]

Obstructive lung diseases ( OLD) such as asthma and chronic obstructive pulmonary disease ( COPD) are very prevalent conditions. Disease phenotypes (e.g. chronic bronchitis, emphysema, etc.) often overlap, and significant confusion exists about their optimal nosologic characterization. Obstructive sleep apnoea ( OSA) is also a common condition that features bidirectional interactions with OLD. OSA appears to be more commonly seen in patients with OLD, perhaps as a result of shared risk factors, for example obesity, smoking, increased airway resistance, local and systemic inflammation, anti-inflammatory therapy. Conversely, OSA is associated with worse clinical outcomes in patients with OLD, and continuous positive airway pressure therapy has potential beneficial effects on this vicious pathophysiological interaction. Possible shared mechanistic links include increased parasympathetic tone, hypoxaemia-related reflex bronchoconstriction/vasoconstriction, irritation of upper airway neural receptors, altered nocturnal neurohormonal secretion, pro-inflammatory mediators, within and inter-breath interactions between upper and lower airways, lung volume-airway dependence, etc. While the term overlap syndrome has been defined as the comorbid association of COPD and OSA, the interaction between asthma and OSA has not been integrated yet nosologically; in this review, the latter will be called alternative overlap syndrome. In an effort to bolster further investigations in this area, an integrated, lumping nomenclature for OSA in the setting of OLD is proposed here- OLDOSA (obstructive lung disease and obstructive sleep apnoea) syndrome. [ABSTRACT FROM AUTHOR]

Background/Objectives. Asthma in older individuals is poorly understood. We aimed to characterize the older asthma phenotype and test its associationwithobstructive sleep apnea (OSA). Design. Cross-sectional. Setting. Pulmonary and Asthma/Allergy clinics. Participants. 659 asthma subjects aged 18-59 years (younger) and 154 aged 60-75 (older). Measurements. Sleep Apnea scale of Sleep Disorders Questionnaire (SA-SDQ), asthma severity step (1-4, severe if step 3 or 4), established OSA diagnosis, continuous positive airway pressure (CPAP) use, and comorbidities. Results. Older versus younger had worse control, as assessed by asthma step, lung function, and inhaled corticosteroid use. Among older subjects, after controlling for known asthma aggravators, OSA diagnosis was the only factor robustly associated with severe asthma: on average, OSA was associated with nearly 7 times greater likelihood of severe asthma in an older individual (OR = 6.67). This relationship was of greatermagnitude than in younger subjects (OR = 2.16). CPAP use attenuated the likelihood of severe asthma in older subjects by 91% (P = 0.005), much more than in the younger asthmatics. Conclusion. Diagnosed OSA increases the risk for worse asthma control in older patients, while CPAP therapy may have greater impact on asthma outcomes. Unrecognized OSA may be a reason for poor asthma control, particularly among older patients. [ABSTRACT FROM AUTHOR]

Objective. Obstructive sleep apnea (OSA) worsens nocturnal asthma, but its potential impact on daytime asthma remains largely unassessed. We investigated whether the sleep disorder is associated with daytime, in addition to nighttime, asthma symptoms. Methods. Asthma patients at tertiary-care centers completed the Sleep Apnea scale of the Sleep Disorders Questionnaire (SA-SDQ), and an asthma control questionnaire. SA-SDQ scores ≥36 for males and ≥32 for females defined high OSA risk. Medical records were reviewed for established diagnosis of OSA and continuous positive airway pressure (CPAP) use. Results. Among 752 asthma patients, high OSA risk was associated similarly with persistent daytime and nighttime asthma symptoms ( p < .0001 for each). A diagnosis of OSA was robustly associated with persistent daytime ( p < .0001) in addition to nighttime ( p = .0008) asthma symptoms. In regression models that included obesity and other known asthma aggravators, high OSA risk retained associations with persistent daytime (odds ratio [OR] = 1.96 [95% confidence interval [CI] = 1.31-2.94]) and nighttime (1.97 [1.32-2.94]) asthma symptoms. Diagnosed OSA retained an association with persistent daytime (2.08 [1.13-3.82]) but not with nighttime (1.48 [0.82-2.69]) asthma symptoms. CPAP use was associated with lower likelihood of persistent daytime symptoms (0.46 [0.23-0.94]). Conclusions. Questionnaire-defined OSA risk and historical diagnosis were each associated with persistent daytime asthma symptoms, to an extent that matched or exceeded associations with nighttime asthma symptoms. Unrecognized OSA may be a reason for persistent asthma symptoms during the day as well as the night. [ABSTRACT FROM AUTHOR]

The article presents information on a study which evaluated the relationship between obstructive sleep apnea (OSA) risk and asthma control in adults. Validations were done using Sleep Apnea Scale of the Sleep Disorders Questionnaire and Asthma Control Questionnaire. A discussion on the research findings is offered. In conclusion, high OSA risk is highly related with not-well-controlled asthma independent of known asthma aggravators and regardless of the ACQ version used.

The article discusses the study which aims to evaluate the risk of snoring and obstructive sleep apnea (OSA) in patients with asthma. The study surveyed clinics with the Sleep Apnea scale of the Sleep Asthma Questionnaire regarding the frequency of asthma symptoms for men and women with OSA. The study found that OSA symptoms in patients with asthma helped to explain the increased presence of the symptom in asthma specifically to female with asthma morbidity.

Background and Purpose: Patients with asthma often complain of daytime sleepiness, which is usually attributed to a direct effect of asthma on nocturnal sleep quality. We investigated this and other potential explanations for daytime sleepiness among asthmatics.Patients and Methods: One hundred fifteen adult asthmatics were assessed for perceived daytime sleepiness (one question item), subjective sleepiness (Epworth Sleepiness Scale score, ESS), obstructive sleep apnea risk (Sleep Apnea scale score within Sleep Disorders Questionnaire, SA-SDQ), asthma severity step, relevant comorbid conditions, and current asthma medications.Results: Among all subjects, 55% perceived excessive daytime sleepiness and 47% had ESS>10. Most subjects reported snoring (n=99, or 86%) and many snored habitually (n=44, 38%). The ESS correlated with SA-SDQ (P<0.0001), male gender (P=0.01), and asthma severity step (P=0.04). In a multiple regression model, the ESS was independently associated with SA-SDQ (P=0.0003) and male gender (P=0.02), but not with asthma severity step (P=0.51). There were no correlations between ESS and age, body mass index (BMI), forced expiratory volume in one second as percent of predicted value (FEV(1)%), comorbidities, or medication used to treat asthma.Conclusions: Sleepiness is common in asthmatics and may reflect occult obstructive sleep apnea more often than effects of asthma itself, other comorbid conditions, or asthma medications. [ABSTRACT FROM AUTHOR]