The objectives of the present study were to assess the level of exhaled breath markers indicating airway inflammation and oxidative stress in patients with obstructive sleep apnoea syndrome (OSAS) in comparison with non-apnoeic (obese and non-obese) subjects and investigate whether therapy with continuous positive airway pressure (CPAP) can modify them. The design was a retrospective observational study, set in Evgeneidio Hospital. Twenty-six OSAS patients and nine obese and 10 non-obese non-apnoeic subjects participated in this study. We measured nasal nitric oxide (nNO), exhaled nitric oxide (eNO), exhaled carbon monoxide (eCO) in exhaled breath, and 8-isoprostane, leukotriene B(4) (LTB(4)), nitrates, hydrogen peroxide (H(2)O(2)), and pH in exhaled breath condensate (EBC) before and after 1 month of CPAP therapy. The levels of eNO and eCO were higher in OSAS patients than in control subjects (p < 0.05). Nasal NO was higher in OSAS patients than in obese controls (p < 0.01). The level of H(2)O(2), 8-isoprostane, LTB(4), and nitrates were elevated in OSAS patients in comparison with obese subjects (p < 0.01). Conversely, pH was lower in OSAS patients than in non-apnoeic controls (p < 0.01). One month of CPAP therapy increased pH (p < 0.05) and reduced eNO (p < 0.001) and nNO (p < 0.05). Apnea/hypopnoea index was positively correlated with 8-isoprostane (r = 0.42; p < 0.05), LTB(4) (r = 0.35; p < 0.05), nitrates (r = 0.54; p < 0.001), and H(2)O(2) (r = 0.42; p < 0.05). Airway inflammation and oxidative stress are present in the airway of OSAS patients in contrast to non-apnoeic subjects. Exhaled breath markers are positively correlated with the severity of OSAS. One-month administration of CPAP improved airway inflammation and oxidative stress.

Although nasal surgery has limited efficacy in obstructive sleep apnoea (OSA) treatment, some patients experience improvement. The present study tested the hypothesis that post-surgery improvement is associated with increased nasal breathing epochs. A total of 49 OSA patients (mean apnoea/hypopnoea index (AHI) 30.1+/-16.3 events x h(-1)) with symptomatic fixed nasal obstruction due to deviated septum were randomly assigned to either septoplasty (surgery group; 27 patients) or sham surgery (placebo group; 22 patients). The breathing route was examined during overnight polysomnography. All patients in the placebo group were nonresponders, whereas in the surgery group four (14.8%) patients were responders and exhibited considerable increase in nasal breathing epochs (epochs containing more than three consecutive phasic nasal signals), and 23 patients were nonresponders, presenting a modest increase in nasal breathing epochs. The change in AHI was inversely related to the change in nasal breathing epochs, with responders exhibiting among the greatest increases in nasal breathing epochs. Baseline nasal breathing epochs were positively related to per cent change in AHI. Responders had among the lowest baseline nasal breathing epochs; a cut-off value of 62.4% of total sleep epochs best separated (100% sensitivity, 82.6% specificity) responders/nonresponders. In conclusion, nasal surgery rarely treats obstructive sleep apnoea effectively. Baseline nasal breathing epochs can predict the surgery outcome.

Although there is an association between nasal obstruction, oral breathing and obstructive sleep apnoea syndrome (OSAS), it remains unknown whether increased oral breathing occurs in patients with OSAS who are free of nasal obstruction. The present study evaluated the relationship between breathing route and OSAS in patients without nasal obstruction.The breathing route of 41 snorers (25 male; aged 26-77 yrs) with normal nasal resistance was examined during overnight polysomnography using a nasal cannula/pressure transducer and an oral thermistor.In total, 28 patients had OSAS (apnoeics) and 13 patients were simple snorers. Apnoeics had a higher percentage of oral and oro-nasal breathing epochs. Oral and oro-nasal breathing epochs were positively related with apnoea/hypopnoea index (AHI) and duration of apnoeas/hypopnoeas and inversely related to oxygen saturation. Additionally, oro-nasal breathing epochs correlated with body mass index (BMI). In multiple linear regression analysis, oral breathing epochs were independently related only to AHI (r 2 50.443), and oro-nasal breathing epochs were independently related to AHI (r 2 50.736) and BMI (r 2 50.036).In conclusion, apnoeics spent more time breathing orally and oro-nasally than simple snorers, and the apnoea/hypopnoea index is a major determinant of the time spent breathing orally and oro-nasally.

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Summary Although daytime sleepiness is commonly associated with obstructive sleep apnoea (OSA), the relationship between OSA severity and subjective sleepiness has been documented elusive. This study aimed to identify clinical and polysomnographic determinants of subjective sleepiness among patients suspected of having OSA. A sleep clinic‐based sample of 915 patients was interviewed with a structured questionnaire and underwent diagnostic overnight polysomnography. Subjective sleepiness was quantified by Epworth Sleepiness Scale (ESS). Excessive daytime sleepiness (defined as ESS score > 10) was present in 38.8% of patients. In multiple linear regression analysis, respiratory disturbance index [RDI; used to define (whenever RDI was >5) and quantify OSA], depression and diabetes were the most important determinants of ESS score accounting for 17%, 11% and 6% of its variability respectively. Chronic obstructive pulmonary disease (COPD), stroke, heart disease, alcohol use and body mass index were less important determinants of ESS score explaining 1–3% of its variability. In conclusion, OSA should not be considered the sole potential cause of increased subjective sleepiness in patients suspected of having OSA. Primarily depression and diabetes, but also COPD, stroke, heart disease, alcohol use and increased body mass index may contribute to increased subjective sleepiness.

Nasal continuous positive airway pressure (CPAP) can cause undesirable nasal symptoms, such as congestion to obstructive sleep apnoea (OSA) patients, whose symptoms can be attenuated by the addition of heated humidification. However, neither the nature of nasal symptoms nor the effect of heated humidification on nasal pathophysiology and pathology are convincingly known.20 patients with OSA on nasal CPAP who exhibited symptomatic nasal obstruction were randomised to receive either 3 weeks of CPAP treatment with heated humidification or 3 weeks of CPAP treatment with sham-heated humidification, followed by 3 weeks of the opposite treatment, respectively. Nasal symptom score, nasal resistance, nasal lavage interleukin-6, interleukin-12 and tumour necrosis factor-a and nasal mucosa histopathology were assessed at baseline and after each treatment arm.Heated humidification in comparison with sham-heated humidification was associated with decrease in nasal symptomatology, resistance and lavage cytokines, and attenuation of inflammatory cell infiltration and fibrosis of the nasal mucosa.In conclusion, nasal obstruction of OSA patients on CPAP treatment is inflammatory in origin and the addition of heated humidification decreases nasal resistance and mucosal inflammation.

Some patients with obstructive sleep apnoea syndrome (OSAS; respiratory distress index (RDI) of .5 events?h -1 ) experience residual excessive daytime subjective sleepiness (Epworth Sleepiness Scale (ESS) score of .10), despite adequate use of continuous positive airway pressure (CPAP) therapy. The aim of the present study was to identify clinical and polysomnographic predictors of this sleepiness.Clinical and polysomnographic variables and ESS score were evaluated in 208 OSAS patients with an ESS score of .10 before (initial assessment) and after o6 months of adequate (o4 h?day -1 ) CPAP use. Following CPAP treatment, 114 (55%) patients showed an abnormal ESS score (.10; CPAP nonresponders), whereas 94 (45%) showed a normal ESS score (,11; CPAP responders). Of the CPAP responders, none had a history of depression, whereas the converse was true for 38.8% of CPAP nonresponders. In addition, multivariate logistic regression analysis revealed that the independent predictors of residual excessive daytime sleepiness following CPAP therapy were a history of diabetes and heart disease, and a higher ESS score and lower RDI on initial assessment.In conclusion, predictors of residual excessive sleepiness in adequately CPAP-treated OSAS were a history of depression, diabetes and heart disease, and a higher ESS score and lower RDI on initial assessment.

Background: Patients who suffer from obstructive sleep apnea (OSA) have a decreased exercise capacity and abnormal autonomic nervous function. However, the kinetics of early oxygen (O 2 ) and heart rate recovery (HRR) have not been described. Materials and Methods:We evaluated 21 men with moderate to severe OSA (mean age: 48 ± 11 yrs, mean apnea-hypopnea index [AHI]: 55 ± 13) and without known heart disease and 10 healthy men matched for age and body mass index (BMI; controls). Men with OSA underwent overnight polysomnography, and both groups underwent symptom-limited incremental cardiopulmonary exercise testing (CPET). We recorded the CPET parameters including peak O 2 uptake (VO 2 p), kinetics of early O 2 recovery by the first degree slope of VO 2 during the first minute (VO 2 /t slope), the time required for a 50% decline of VO 2 p during recovery (T 1/2 ), and early heart rate recovery (HRR = HR at maximal exercise − HR at 1 min of recovery), as well as the chronotropic reserve to exercise ([CR] = [peak HR − resting HR/220 − age − resting HR] × 100). Patients with OSA had a lower VO 2 p (28.7 ± 4.0 vs 34.7 ± 6.2 mL/kg/min), VO 2 /t slope (1.04 ± 0.3 vs 1.4 ± 0.17 mL/kg/min 2 ), and T 1/2 (74 ± 10 vs 56 ± 6 sec) compared to controls (all P < 0.001). In addition, both HRR and CR were lower in the OSA group (22.0 ± 7.0 vs 31.0 ± 6.0 bpm,P:0.003, and 79.0% ± 15% vs 99.0% ± 13.0%, P:0.01, respectively). Conclusions: Patients with OSA demonstrate reduced exercise capacity, delayed oxygen kinetics, and reduced HRR. These data point to abnormal oxygen delivery and/or oxidative function of the peripheral muscles and impaired autonomic nervous activity in OSA patients.