Cephalometric assessment of craniofacial morphology in Chinese patients with obstructive sleep apnoea

OBJECTIVE: To compare the differences in craniofacial morphology in Chinese patients with and without obstructive sleep apnoea (OSA). METHOD: We performed lateral cephalometric radiographs on 94 consecutive patients (77 males) referred with snoring or other symptoms suggestive of OSA for polysomnography (PSG). Significant OSA was defined as an apneoa-hypopnoea index (AHI) > or = 10/h of sleep on overnight PSG. The cephalometric data were compared between those with and without significant OSA. RESULTS: (mean +/- SD) There were 69 (56 males) with significant OSA with mean age 53 +/- 12 years, body mass index (BMI) 28.6 +/- 5.0 kg/m2, AHI 36.5 +/- 20.6/h, and minimum SaO2 76 +/- 14%. There were 25 controls (21 males) without significant OSA with similar age and BMI. The mandibular plane to hyoid bone distance (MPH) and the perpendicular distance from hyoid bone to the line connecting C3 vertebra and retrognathion (HHI) were significantly longer in the OSA patients. The angle measurement from sella to nasion to point A (SNA) was smaller in the OSA group. MPH distance was the only independent variable for significant OSA with an odds ratio of 3.47 (95% CI 1.39-8.66). Abnormalities of the MPH and SNA were more marked in the OSA patients with BMI > or = 30 kg/m2. CONCLUSIONS: Significant differences in craniofacial morphology are noted between OSA patients and non-apnoeic controls. An inferiorly positioned hyoid bone and a retropositioned maxilla may predispose obese patients to more severe OSA.     

Cephalometric analysis in obese and nonobese patients with obstructive sleep apnea syndrome

STUDY OBJECTIVES: The aims of this study were to comprehensively evaluate the cephalometric features of patients with obstructive sleep apnea syndrome (OSAS), and to elucidate the relationship between cephalometric variables and severity of the apnea-hypopnea index (AHI). PATIENTS: The study population consisted of 62 male patients with OSAS, classified into 33 obese patients (body mass index [BMI] >or= 27) and 29 nonobese patients (BMI < 27), and 13 male simple snorers (AHI < 5 events per hour). METHOD: and measurements: Diagnostic polysomnography and measurements of 22 cephalometric variables were carried out for all patients and simple snorers. RESULTS: Patients with OSAS in both subgroups showed several significant cephalometric features compared with simple snorers: (1) inferiorly positioned hyoid bone, (2) enlarged soft palate, and (3) reduced upper airway width at soft palate. More extensive and severe soft-tissue enlargements including anteriorly positioned hyoid bone and a longer tongue were found in the obese patients. In the nonobese patients, the anteroposterior distances of the bony nasopharynx and oropharynx were significantly smaller than those of simple snorers and obese patients. Stepwise regression analysis showed that anterior displacement of the hyoid bone and retroposition of the mandible were the dominant overall determinants for AHI in patients with OSAS, and that narrowing of the bony oropharynx and inferior displacement of the hyoid bone were dominant determinants for AHI in nonobese patients. A significant regression model for AHI using cephalometric variables could not be obtained for the obese patients, but the BMI proved to be the most significant determinant. CONCLUSION: Characteristics of the craniofacial bony structure such as narrowing of the nasopharynx and oropharynx and enlargement of the soft tissue in the upper airway may be important risk factors for the development of OSAS in nonobese patients. In obese patients, the deposition of adipose tissue in the upper airway may aggravate the severity of OSAS.     

Increased central adiposity in morbidly obese patients with obstructive sleep apnoea

Background: With the growing epidemic of obesity, few data are available regarding adipose distribution and the severity of sleep apnoea. Our aim was to measure precisely adipose distribution with dual‐energy X‐ray absorptiometry (DXA) in a morbidly obese population with and without obstructive sleep apnoea (OSA). Methods: Morbidly obese female subjects without a history of OSA underwent overnight polysomnography and DXA analysis. Subject demographics, DXA variables, serum laboratory markers and physical exam characteristics were compared between individuals with and without OSA. Results: For the study population (n= 26), mean body mass index (BMI) was 45.9 ± 7.8 kg/m²; mean age was 47.5 ± 10.2 years and all were female. The central adiposity ratio (CAR) was higher in individuals with OSA (apnoea–hypopnoea index > 5) than those without OSA (1.1 ± 0.05 vs 1.0 ± 0.04; P= 0.004). No difference was observed in Epworth Sleepiness Scale scores, body mass index (BMI) or neck circumference between groups. Conclusions: OSA is associated with increased central adipose deposition in patients with a BMI of >40 kg/m². These data may be helpful in designing future studies regarding the pathophysiology of OSA, and potential treatment options.     

Craniofacial abnormalities in Japanese patients with severe obstructive sleep apnoea syndrome

Objective: To clarify that factors besides obesity play an important role in the development of obstructive sleep apnoea syndrome (OSAS) in Japanese patients, we compared craniofacial structures in patients with severe OSAS with those of normal controls.
Methodology: The craniofacial structures of 60 Japanese patients with severe OSAS and 30 normal controls were evaluated using standard cephalometric analysis. Patients were stratified according to body mass index (BMI): non-obese, BMI < 25; moderately obese, BMI = 25–30, severely obese, BMI > 30.
Results: The SNA (sella to nasion to subspinale angle) was significantly smaller in the patient groups than in the controls. The SNB (sella to nasion to supramentale angle) and NSBa (cranial base flexure) were significantly smaller in the non-obese and moderately obese patients than in controls. The MP-H (distance from the mandibular plane to the hyoid bone) and the PNS-P (distance from the posterior nasal spine to the tip of the soft palate) were significantly longer in the patient groups than in the controls. The PNS-P was significantly longer in the severely obese patients than in the non-obese patients.
Conclusions: Japanese patients with severe OSAS have enlargement of the soft tissues and palate as well as craniofacial bony structural abnormalities. This is particularly apparent in non-obese patients.     

Low sleep quality and daytime sleepiness in obese patients without obstructive sleep apnoea syndrome

OBJECTIVES: To evaluate sleep quality, sleep-related symptoms, and degree of excessive daytime sleepiness (EDS) in severe obesity, independently of obstructive sleep apnoea syndrome (OSAS). DESIGN: A cross-sectional study. SETTING: Primary-care setting. SUBJECTS, MAIN OUTCOME MEASURES: Anthropometric parameters, respiratory function data and sleep related symptoms were evaluated in 78 severely obese patients (aged 16-75 years) without OSAS and in 40 healthy sex- and age-matched normal weight subjects, who underwent a full-night polysomnography. RESULTS: Obese patients and control subjects had similar sleep latency and rapid eye movement (REM) latency, but they showed lower percentage of REM (P < 0.01) and sleep efficiency (P < 0.05) than controls. All sleep-related symptoms (observed or reported apnoea, awakenings, choking and unrefreshing sleep) were significantly more frequent in obese patients than in control subjects. Loud snoring was present in 46.7% of the obese patients and in 8.1% of the control individuals (P < 0.01). Excess daytime sleepiness was reported by 34.7% of the obese patients and by 2.7% of the normal weight subjects (P < 0.01). The Epworth Sleepiness Scale (ESS) was higher in the obese group than in the control group (P < 0.01), whereas arousals were not different between the two groups. CONCLUSIONS: This study clearly shows that severe obesity, even in the absence of OSAS, is associated with sleep-related disorders and EDS. All these alterations may be partly responsible for a lower quality of life, a higher prevalence of medical complications, an increased risk of occupational injury, and both social and family problems characterizing obese patients, independently of the presence of OSAS.     

Platelet function in patients with obstructive sleep apnoea syndrome.

Patients with obstructive sleep apnoea syndrome (OSAS) are subject to an increased cardiovascular morbidity including myocardial infarction and stroke. Platelets play an important role in the pathogenesis and triggering of acute cardiovascular syndromes. So far, the influence of OSAS on platelet function is not fully understood. Platelet aggregability to epinephrine, collagen, arachidonic acid, and adenosine diphosphate in vitro was measured in 17 consecutive male patients (53.0+/-2.1 yrs) with polysomnographically verified OSAS and compared with that of 15 male controls (50.1+/-3.6 yrs) at 20:00 h, 24:00 h, and 06:00 h. In addition, the long-term effects of continuous positive airway pressure (CPAP) therapy on platelet aggregability was assessed after 6 months. Platelet aggregation in vitro induced by epinephrine showed a slight increase overnight in the untreated OSAS patients (NS) whereas it decreased slightly (NS) in the controls and in the treated OSAS patients. Pretherapeutic platelet aggregability was significantly lowered by CPAP therapy both at 24:00 h (64.0+/-6.5 versus 55.3+/-6.7%, p<0.05) and at 06:00 h (64.1+/-6.5 versus 45.8+/-7.6%; p=0.01). Platelet aggregability during sleep in the controls resembled that found in patients with OSAS during CPAP therapy. The results suggest that obstructive sleep apnoea syndrome contributes, at least in part, to platelet dysfunction and that long-term continuous positive airway pressure treatment may reduce platelet aggregability.     

Cardiovascular risk factors in patients with obstructive sleep apnoea syndrome.

Cardiovascular disorders are common in patients with obstructive sleep apnoea syndrome (OSAS) but there is debate as to whether OSAS is an independent risk factor for their development, since OSAS may be associated with other disorders and risk factors that predispose to cardiovascular disease. In an effort to quantify the risk of OSAS patients for cardiovascular disease arising from these other factors, the authors assessed the future risk for cardiovascular disease among a group of 114 consecutive patients with established OSAS prior to nasal continuous positive airway pressure therapy, using an established method of risk prediction employed in the Framingham studies. Patients were 100 males, aged (mean+/-SD) 52+/-9.0 yrs, and 14 females, aged 51+/-10.4 yrs, with an apnoea/hypopnoea index of 45+/-22 x h(-1). Based on either a prior diagnosis, or a mean of three resting blood pressure recordings >140 mmHg systolic and/or 90 diastolic, 68% of patients were hypertensive. Only 18% were current smokers, while 16% had either diabetes mellitus or impaired glucose tolerance, and 63% had elevated fasting cholesterol and/or triglyceride levels. The estimated 10-yr risk of a coronary heart disease (CHD) event in males was (mean+/-SEM) 13.9+/-0.9%, 95% confidence interval (95% CI) 12.1-16.0, and for a stroke was 12.3+/-1.4%; 95% CI 9.4-15.1, with a combined 10 yr risk for stroke and CHD events of 32.9+/-2.7%; 95% CI 27.8-38.5 in males aged >53 yrs. These findings indicate that obstructive sleep apnoea syndrome patients are at high risk of future cardiovascular disease from factors other than obstructive sleep apnoea syndrome, and may help explain the difficulties in identifying a potential independent risk from obstructive sleep apnoea syndrome.     

Craniofacial abnormalities in obstructive sleep apnoea: Implications for treatment

Abstract Obstructive sleep apnoea (OSA) is a common disorder, and is characterized by repetitive closure of the upper airway during sleep. Upper airway narrowing and sleep-induced loss of muscle tone are important factors in the development of OSA. Over the last decade there has been a growing recognition that craniofacial abnormalities occur commonly in OSA patients. The more commonly identified abnormalities include mandibular deficiency, an inferiorly placed hyoid bone relative to the mandibular plane, a narrowed posterior air space, a greater flexion of the cranial base, and elongation of the soft palate. It is thought that these abnormalities result. in upper airway narrowing, thereby predisposing to OSA. When the well established role of obesity in the development of OSA is taken into account, a model of OSA emerges in which the degree of craniofacial abnormalities determines the extent of obesity required to produce OSA in a given individual. The recognition of the role of craniofacial abnormalities in the development of OSA has led to a number of treatment strategies aimed at correcting or improving craniofacial structure, thereby preventing upper airway collapse during sleep. These treatments include dental appliances, and various maxillofacial surgical procedures. An improved understanding of the evolution of OSA from childhood to adulthood, in relation to facial development, may lead to a preventative strategy for this disorder.     

Sexual function in male patients with obstructive sleep apnoea

Objective: Our objective was to investigate general and functional aspects of sexuality in male patients with a confirmed diagnosis of obstructive sleep apnoea (OSA) and compare the results with normative data. Materials and Methods: We investigated 308 male patients (age 30–69) admitted to a sleep laboratory and receiving a diagnosis of OSA, using questions drawn from two self‐administered questionnaires on sexuality [Fugl‐Meyer Life satisfaction checklist (LiSat) and Brief Sexual Function Inventory (BSFI)]. Results: We found that both general (Fugl‐Meyer LiSat) and functional (BSFI) aspects of sexuality were worse in patients with (untreated) OSA when compared with normative data. Both aspects were dependent on age, obesity, social factors and concomitant medication but not on the severity of OSA as reflected by the apnoea–hypopnoea index or subjective sleepiness. Conclusion: We conclude that although sexual dysfunction is more prevalent in OSA patients than in the general population, it is a complex problem relating more to age, obesity, social factors and comorbidity than to the severity of OSA. Please cite this paper as: Petersen M, Kristensen E, Berg S, Midgren B. Sexual function in male patients with obstructive sleep apnoea. The Clinical Respiratory Journal 2010; 4: 186–191.     

Exhaled breath markers in patients with obstructive sleep apnoea

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.     

阻塞性睡眠呼吸暂停对肥胖和非肥胖的急性冠脉综合征患者临床特点的影响

目的：本研究分别在肥胖和非肥胖人群中分析比较阻塞性睡眠呼吸暂停(OSA)对急性冠脉综合征（ACS）患者临床特点的影响。 方法：2015年12月至2017年12月在北京安贞医院前瞻性连续纳入ACS患者,对符合入排标准的患者行便携式睡眠呼吸监测检查。在肥胖人群(BMI≥28 kg/m2)中根据睡眠呼吸暂停低通气指数（apnea-hypopnea index,AHI）将患者分为OSA组（AHI≥15）和非OSA组（AHI＜15）,比较两组患者的一般临床特征、实验室检查、睡眠呼吸监测等结果。在非肥胖人群(BMI＜28 kg/m2）中根据AHI将患者分为OSA组（AHI≥15）和非OSA组（AHI＜15）,比较两组的患者一般临床特征、实验室检查、睡眠呼吸监测等结果。 结果：研究共纳入837例ACS患者：肥胖患者292例,其中OSA患者199例（68%）;非肥胖患者545例,其中OSA患者233例（43%）。在非肥胖人群中,OSA组患者年龄大于非OSA组(59.74±9.85 vs. 57.66±9.7, p=0.014) , OSA组的中性粒细胞（6.06±2.78 vs. 5.52±2.71, p=0.023）、hs-CRP（8.54±10.57vs. 5.84±9.27, p=0.002）、血糖(7.05±2.66 vs. 6.54±2.29, p=0.021)、多支病变比例高于非OSA组,左心射血分数低于非OSA组（58.12±8.63vs.59.71±8.09,p=0.042）。肥胖人群中以上情况未见统计学差异。 结论：在非肥胖的ACS患者中,OSA组的炎症严重程度、血糖水平、多支病变比例高于非OSA组,左心射血分数低于非OSA组。在肥胖的ACS患者中,两组的炎症反应、血糖水平、血管病变情况等未见统计学差异。 关键词：急性冠脉综合征;阻塞性睡眠呼吸暂停;肥胖     

Impact of CPAP on asthmatic patients with obstructive sleep apnoea.

The impact of continuous positive airway pressure (CPAP) treatment on the airway responsiveness of asthmatic subjects with obstructive sleep apnoea (OSA) has scarcely been studied. A prospective study was performed comparing the changes in airway responsiveness and quality of life in stable asthmatic OSA patients, before and 6 weeks after their nocturnal CPAP treatment. A total of 20 subjects (11 males and nine females) participated in the study. With the nocturnal CPAP treatment, the apnoea/hypopnoea index dropped from 48.1 +/- 23.6 x h(-1) to 2.6 +/- 2.5 x h(-1). There were no significant changes in airway responsiveness after CPAP treatment (provocative concentration causing a 20% fall in forced expiratory volume in one second (FEV(1); PC(20) 2.5 mg x mL(-1) (1.4-4.5)) compared with baseline (PC(20) 2.2 mg x mL(-1) (1.3-3.5)). There was no significant change in FEV(1) either. However, the asthma quality of life of the subjects improved from 5.0 +/- 1.2 at baseline to 5.8 +/- 0.9 at the end of the study. In conclusion, nocturnal continuous positive airway pressure treatment did not alter airway responsiveness or forced expiratory volume in one second in subjects with stable mild-to-moderate asthma and newly diagnosed obstructive sleep apnoea. However, nocturnal continuous positive airway pressure treatment did improve asthma quality of life.     

Regulation of ventilation before and after sleep in patients with obstructive sleep apnoea

The objective was to examine whether abnormal breathing during sleep may affect regulation of ventilation after awakening in patients with obstructive sleep apnoea (OSAS). In 19 patients with OSA and 12 normal subjects we examined ventilatory responses to hypoxia (HVR) and to hypercapnia (HCVR) before and after sleep (BS and AS), and compared the changes in ventilatory responses with respiratory events during sleep. In the OSA group, the values of resting ventilation were significantly smaller in AS than those in BS and end-tidal partial pressure of CO2 in arterial blood (Pco2) (PETCO2) rose significantly from BS to AS. The slopes of the HVR or HCVR did not differ between BS and AS. However, both the response lines shifted downward and minute ventilation (VE)80 (VE at arterial oxygen saturation (Sao2) of 80%) in HVR and VE60 (VE at PETCO2 of 60 mmHg) in HCVR decreased significantly from BS to AS. The percentage changes of VE80 and VE60 were significantly correlated with mean Sao2, total sleep time below Sao2 of 90% and lowest Sao2 during sleep. However, in normal subjects we observed no circadian variation in their ventilatory responses. These data support the hypothesis that repeated episodes of nocturnal hypoxia and hypercapnia may modify the regulation of ventilation after awakening in patients with OSA.     

Cephalometric calcified carotid artery atheromas in patients with obstructive sleep apnea

Background  

In the progress of atherosclerosis, the carotid artery calcifies and sometimes appears as a calcified mass on a cephalometric radiograph.     

Cephalometric findings in facioscapulohumeral muscular dystrophy patients with obstructive sleep apneas

Purposes

The purposes of the study are: (1) to establish if cephalometry and upper airway examination may provide tools for detecting facioscapulohumeral (FSHD) patients at risk for obstructive sleep apnea syndrome (OSAS); and (2) to correlate cephalometry and otorhinolaryngologic evaluation with clinical and polysomnographic features of FHSD patients with OSAS.

Methods

Patients were 13 adults affected by genetically confirmed FSHD and OSAS, 11 men, with mean age 47.1?±?12.8 years (range, 33?C72 years). All underwent clinical evaluation, Manual Muscle Test, Clinical Severity Scale for FSHD, Epworth Sleepiness Scale, polysomnography, otorhinolaryngologic evaluation, and cephalometry.

Results

Cephalometric evidence of pharyngeal narrowing [posterior airways space (PAS)?<?10 mm] was present in only one patient. The mandibular planus and hyoid (MP-H) distance ranged from 6.5 to 33.1 mm (mean, 17.5?±?7.8 mm). The mean length of soft palate (PNS-P) was 31.9?±?4.8 mm (range, 22.2 to 39.7 mm). No patient presented an ANB angle?>?7°. There was no significant correlation between cephalometric measures, clinical scores, and PSG indexes. PAS and MP-H were not related to the severity of the disease.

Conclusions

Upper airway morphological evaluation is of poor utility in the clinical assessment of FSHD patients and do not allow to predict the occurrence of sleep-related upper airway obstruction. This suggests that the pathogenesis of OSAS in FSHD is dependent on the muscular impairment, rather than to the anatomy of upper airways.     

Skeletal muscle changes in patients with obstructive sleep apnoea syndrome

Previous studies have shown that chronic hypoxia leads to changes in skeletal muscle structure (fibre size and type) and activities of several bioenergetic enzymes. Whether this occurs also in conditions characterised by intermittent hypoxia, such as the obstructive sleep apnoea syndrome (OSAS), is unknown. To explore this possibility, we obtained a needle biopsy of the quadriceps femoris in 12 consecutive stable outpatients with severe OSAS (52 +/- 9 year, apnoea-hypopnoea index 70 +/- 14 h(-1)) (x +/- SD) and in six healthy volunteers (49 +/- 8 year), where we quantified fibre type, size and protein content, as well as phosphofructo-kinase (PFK) and cytochrome oxidase (CytOx) activities. We found that fibre-type distribution was similar in patients and controls. In contrast, the diameter of type II fibres (74 +/- 10 microm vs. 56 +/- 11 microm, P < 0.05) and protein content (100 +/- 14 vs. 88 +/- 8 microg/mg) was higher in patients with OSAS. Likewise, we observed upregulation of CytOx (0.93 +/- 0.38 vs. 0.40 +/- 0.22 microkat/mg protein, P < 0.01) and PFK activities (5.35 +/- 4.8 vs. 1.3 +/- 1.3 microkat/ mg protein, P < 0.05) in patients with OSAS. These results show that, paralleling which occurs in conditions characterised by continuous hypoxia, patients with OSAS (and intermittent hypoxia) also show structural and bioenergetic changes in their skeletal muscle.     

NT-proBNP is not elevated in patients with obstructive sleep apnoea

BACKGROUND: N-terminal pro-brain natriuretic peptide (NT-ProBNP) has emerged as an important marker of cardiac stress and may reflect the severity of underlying cardiac dysfunction, which is thought to be associated with obstructive sleep apnoea syndrome (OSAS). METHODS: This study evaluated the plasma concentration of NT-ProBNP in 60 consecutive patients (median age 55.7 years, median body mass index (BMI) 31.8) who were referred to a sleep laboratory with a suspicion of OSAS. Each subject underwent measurement of morning NT-ProBNP plasma levels, polysomnography and echocardiography. Patients were treated with nasal continuous or bilevel positive airway pressure ventilation (nCPAP/BIPAP) or without mechanical respiratory support, depending on clinical symptoms and results of polysomnography. Three months after treatment of OSAS 28 of the patients were reassessed for re-evaluation of NT-ProBNP and polysomnography. RESULTS: Low or high levels of NT-proBNP were not associated with AHI and other sleep related indices (p>0.3). There was no correlation between NT-proBNP and AHI or other sleep related indices. In multiple regression analysis, NT-proBNP was significantly correlated with left ventricular ejection fraction, creatinine clearance and the presence of systemic arterial hypertension but not with AHI. CONCLUSIONS: Our results show by a robust multiple regression analysis, that NT-pro BNP is not associated with OSAS and NT-pro BNP cannot be used as a sensitive marker for underlying cardiovascular abnormalities in patients with OSAS.     

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.     

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.     

The cost-effectiveness of nCPAP treatment in patients with moderate-to-severe obstructive sleep apnoea.

The demand for diagnostic and therapeutic services for obstructive sleep apnoea syndrome (OSAS) showed marked growth during the 1990s. This paper analyses the long-term cost-effectiveness of nasal continuous positive airway pressure (nCPAP) treatment in comparison to conventional null treatment. A Markov model was used to represent the natural history of OSAS based upon published evidence. Utility values came from a survey of OSAS patients. Data on health costs were collected from hospitals in the Basque Country, Spain. The incremental cost-effectiveness ratio of nCPAP treatment is <6,000 Euros per quality-adjusted life year. On disaggregated analysis, nCPAP treatment accounts for 86% of incremental costs; 84% of incremental effectiveness is attributable to improved quality of life. Treatment of obstructive sleep apnoea syndrome with nasal continuous positive airway pressure has a cost-effectiveness that is in line with that of other commonly funded treatments such as antihypertensive drugs. The key clinical benefit of nasal continuous positive airway pressure treatment is improvement in the quality of life of patients with obstructive sleep apnoea syndrome. This benefit is also precisely the one for which the evidence base is strongest. The remaining uncertainties concerning the impact of nasal continuous positive airway pressure on long-term mortality have only a relatively small impact on the economics of treatment.