QT dispersion in childhood obstructive sleep apnoea syndrome

The difference between maximal and minimal QT interval and corrected QT interval defined as QT dispersion and corrected QT dispersion may represent arrhythmogenic risks. This study sought to evaluate QT dispersion and corrected QT dispersion in childhood obstructive sleep apnoea syndrome. Forty-four children (34 male) with obstructive sleep apnoea syndrome, aged 6.2 plus or minus 3.5 years along with 38 healthy children (25 male), 6.6 plus or minus 2.1 years underwent electrocardiography to measure QT and RR intervals. Means QT dispersion and corrected QT dispersion were significantly higher in obstructive sleep apnoea syndrome than controls, 52 plus or minus 27 compared to 40 plus or minus 14 milliseconds (p equal to 0.014), and 71 plus or minus 29 compared to 57 plus or minus 19 milliseconds (p equal to 0.010), respectively. Interestingly, QT dispersion and corrected QT dispersion in obstructive sleep apnoea syndrome with obesity, 57 plus or minus 30 and 73 plus or minus 31 milliseconds, were significantly higher than in control, 40 plus or minus 14 and 57 plus or minus 19 milliseconds (p equal to 0.009 and 0.043, respectively). However, QT dispersion and corrected QT dispersion in obstructive sleep apnoea syndrome without obesity, 43 plus or minus 20 and 68 plus or minus 26 milliseconds, were not significantly different. In conclusion, QT dispersion and corrected QT dispersion were significantly increased only in childhood obstructive sleep apnoea syndrome with obesity. Obesity may be the factor affecting the increased QT dispersion and corrected QT dispersion.     

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.     

Corrected QT dispersion and cardiac sympathetic function in patients with obstructive sleep apnea-hypopnea syndrome

STUDY OBJECTIVES: Hypoxemia increases corrected QT dispersion (QTcD), which is the difference between the maximum and minimum QT intervals and is a strong risk factor for cardiovascular mortality. The aim of this study was to investigate the QTcD in patients with obstructive sleep apnea-hypopnea syndrome (OSAHS), and the relationship between the QTcD and (123)I-metaiodobenzylguanidine (MIBG) cardiac imaging, which reflects cardiac sympathetic activity. SETTING: A university hospital. PATIENTS: Forty-eight OSAHS patients without cardiac diseases (mean [+/- SD] age, 45.9 +/- 10.8 years; apnea-hypopnea index [AHI] 51.9 +/- 18.5 events per hour) who underwent polysomnography before treatment and on the first night of nasal continuous positive airway pressure (nCPAP) treatment. METHODS: Before and after nCPAP treatment was started, we measured the QTcD with computer software, before, during, and after sleep, as well as the washout rate of the MIBG administered for cardiac imaging. As a control, QTcD was also measured in the morning from 26 healthy subjects. RESULTS: Before treatment, the mean QTcD during sleep (65.0 +/- 14.6 ms) was greater than that before sleep (57.0 +/- 13.5 ms; p < 0.0001). Meanwhile, after 1 night of nCPAP therapy, the QTcD during sleep (50.6 +/- 11.4 ms) decreased from that before treatment (p < 0.0001) and was smaller than the QTcD before sleep (56.2 +/- 13.3 ms; p = 0.003). Before treatment, the QTcD during sleep correlated with the AHI (r = 0.38; p = 0.009) and the percentage of time that SaO(2) was < 90% (SaO(2) < 90% time) [r = 0.34; p = 0.018]. The QTcD did not correlate with the body mass index or the washout rate of MIBG. However, the washout rate of MIBG correlated with the AHI and the SaO(2) < 90% time. CONCLUSIONS: Nocturnal QTcD is increased in OSAHS patients but is decreased by nCPAP therapy independently of cardiac sympathetic function.     

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.     

Frequency and mechanism of daytime pulmonary hypertension in patients with obstructive sleep apnoea syndrome

In order to study the frequency and the mechanisms of daytime pulmonary hypertension (PH) in obstructive sleep apnoea syndrome (OSAS) lung function tests, blood gas analysis and right-heart catheterization were performed in 46 consecutive patients. OSAS was assessed by polysomnography. 9 patients only (20%) had PH (mean pulmonary artery pressure (Ppa) greater than or equal to 20 mmHg). Patients with PH had lower daytime PaO2 (60.8 +/- 7.6 vs. 76.2 +/- 9.4 mmHg; p less than 0.001), higher daytime PaCO2 (44.8 +/- 4.2 vs. 38.0 +/- 4.0 mmHg; p less than 0.001), lower forced vital capacity (FVC) and forced expiratory volume (FEV1) (p less than 0.001), but the severity of OSAS was not different whether PH was present or not (apnoea index: 62 +/- 34 hour in the PH group vs. 65 +/- 40 hour, apnoea + hypopnoea index 102 +/- 33 hour in the PH group vs. 86 +/- 36 hour, lowest sleep SaO2: 59 +/- 21% in the PH group vs. 66 +/- 18%). There were significant correlations between Ppa and: daytime PaO2 (r = -0.61; p less than 0.001), PaCO2 (r = 0.55; p less than 0.001), FEV1 (r = -0.52; p less than 0.001) but not between Ppa and apnoea index, apnoea + hypopnoea index, lowest sleep SaO2. PH and daytime hypoxaemia were associated either with chronic airway obstruction or with severe obesity.     

Hypercapnia in obstructive sleep apnoea syndrome

BACKGROUND: The reports on the prevalence of hypercapnia in Obstructive Sleep Apnoea Syndrome (OSAS) are conflicting. We studied the prevalence of hypercapnia in a population of OSAS patients referred to a Department of Respiratory Medicine and the mechanism of the respiratory failure in OSAS associated with Obesity Hypoventilation Syndrome (OHS) or with Chronic Obstructive Pulmonary Disease (COPD) (Overlap syndrome). METHODS: We studied 219 consecutive OSAS patients during a period of 3 years. We recorded age and anthropomorphic data and performed polysomnography and pulmonary function tests. In relation to the value of PaCO(2), the patients were divided in hypercapnic (PaCO(2)>45 mmHg) patients and normocapnic patients. They were also divided into three groups in relation to the presence of "simple" or "pure" OSAS, to the presence of OSAS associated with COPD, to the presence of OSAS associated with OHS. RESULTS: Seventeen per cent of the patients were hypercapnic. They were significantly heavier, had more severe lung function test abnormalities and more severe nocturnal oxyhemoglobin desaturations than the normocapnic ones, while Forced Expiratory Volume in one second as a percentage of Forced Vital Capacity (FEV1/FVC %) and Apnoea/Hypopnoea Index (AHI) were similar. OHS patients (13%) were significantly younger and heavier, had lower PaO(2) and higher PaCO(2) than "simple" OSAS patients (77%) and Overlap patients (10%) and had more severe restrictive defect. There was no difference in terms of AHI among the three groups, but nocturnal oxyhemoglobin desaturations were more severe in OHS group. In OHS group hypercapnia was correlated to FVC% of predicted and FEV1% of predicted and to the mean nocturnal oxyhemoglobin saturation; in Overlap patients PaCO(2) was correlated to Forced Expiratory Flow rate at low Vital Capacity. CONCLUSION: Seventeen per cent of OSAS patients referred to a Department of Respiratory Medicine were hypercapnic. Hypercapnia in OHS patients correlates to the restrictive ventilatory defect whereas in Overlap patients it seems to correlate to peripheral airways obstruction. The distinction between patients with "simple" or "pure" OSAS and patients affected by OSAS associated with OHS or COPD could be important not only for clinical and prognostic implications, but also for the consequences in terms of ventilatory treatment.     

Progression of obstructive sleep apnoea syndrome in Japanese patients

Sleep and Breathing - The aggravation of obstructive sleep apnoea syndrome (OSAS) is reportedly associated with weight gain. The present study investigated the factors associated with worsening of...     

Endothelial function in patients with obstructive sleep apnea syndrome but without hypertension

BACKGROUND: Obstructive sleep apnea syndrome (OSAS) influences endothelial function and causes hypertension. OBJECTIVES: Our aim was to evaluate the role of endothelial dysfunction in the pathogenesis of hypertension in OSAS. METHODS: Twenty-three patients with OSAS but without hypertension and 15 healthy normotensive subjects were investigated. The presence or absence of OSAS was evaluated with a sleep study. Endothelial function was investigated with brachial artery ultrasound examination. RESULTS: Baseline characteristics were equivalent between the two groups. Minimal oxygen saturation and apnea-hypopnea indexes in the OSAS and control groups were 62.9 +/- 16.5 versus 94.9 +/- 1.1% (p < 0.0001) and 53.1 +/- 20.3 versus 3.8 +/- 0.9 (p < 0.0001), respectively. There was not statistically significant difference between basal brachial artery diameters measured in the morning and in the evening in all groups. Flow-mediated dilation (FMD) values measured in the morning were lower than those measured in the evening in both OSAS patients and the control group: FMD of OSAS patients was 6.04 +/- 3.18% in the morning and 10.38 +/- 4.23% in the evening hours (p = 0.001), and FMD of control subjects was 10.9 +/- 2.6% in the morning and 13.9 +/- 2.32 in the evening hours (p = 0.002). Differences in FMD values measured both in the morning and evening hours in OSAS patients were lower compared with those in control subjects (p < 0.0001 in the morning hours and p = 0.003 in the evening hours). CONCLUSIONS: We detected a prominent diurnal deterioration in endothelial function in normotensive OSAS patients compared with healthy subjects. This deterioration may occur due to ongoing hypoxemia during the night and it may be a possible cause of hypertension and atherosclerotic cardiovascular diseases in patients with OSAS.     

肺动脉高压患者心率校正QT间期和QT离散度的研究

目的:检测肺动脉高压(pulmonary hypertension,PH)患者的心率校正的QT间期(heartrate-corrected QT interval,QTc)和QTc离散度(QTc dispersion,QTcd),并评价其与肺动脉压力的关系。方法:入选2003年12月至2008年7月因初步诊断为PH而进行右心导管术的患者。记录静息12导联心电图,手工测量QT间期并用Bazett公式进行校正。根据平均肺动脉压,将患者分为对照组,轻-中度PH组和重度PH组。结果:共入选201例患者。男性患者的QTc和QTcd在3组间差异无统计学意义。女性患者中,重度PH组的QTc比对照组高〔(436.1±39.4)msvs.(407.6±24.8)ms,P=0.037〕,重度PH组的QTcd(68.5±20.9)ms高于对照组(45.1±12.6)ms和轻-中度组(58.6±14.7)ms(P=0.002;P=0.003)。此外,女性患者的QTc和QTcd与平均肺动脉压正相关(r=0.207,P=0.03;r=0.236,P=0.012)。结论:本组资料中女性PH患者的QTc和QTcd与平均肺动脉压正相关,且在重度PH患者中显著增高,有待于进一步探讨。     

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.     

Evidence for left ventricular dysfunction in patients with obstructive sleep apnoea syndrome.

There is limited information on the development of left ventricular (LV) dysfunction in patients with obstructive sleep apnoea (OSA) in the absence of lung and cardiac comorbidity. This study aimed to investigate whether OSA patients without heart morbidity develop LV dysfunction, and to assess the effect of continuous positive airway pressure (CPAP) on LV function. Twenty-nine OSA patients and 12 control subjects were studied using technetium-99m ventriculography to estimate LV ejection fraction (LVEF), LV peak emptying rate (LVPER), time to peak emptying rate (TPER), peak filling rate (LVPFR) and time to peak filling rate (TPFR) before and after 6 months of treatment with CPAP. A significantly lower LVEF was found in OSA patients, compared to control subjects, (53+/-7 versus 61+/-6%) along with a reduced LVPER (2.82+/-0.58 versus 3.82+/-0.77 end-diastolic volumes x s(-1)). Furthermore, OSA patients had significantly lower LVPFR (2.67+/-0.71 versus 3.93+/-0.58 end-diastolic volumes x s(-1)) and delayed TPFR (0.19+/-0.04 versus 0.15+/-0.03 s) in comparison with the control group. Six-months of CPAP treatment was effective in significantly improving LVEF, LVPER, LVPFR and TPFR. In conclusion, obstructive sleep apnoea patients without any cardiovascular disease seem to develop left ventricular systolic and diastolic dysfunction, which may be reversed, either partially or completely, after 6 months of continuous positive airway pressure treatment.     

Left ventricular hypertrophy independent of hypertension in patients with obstructive sleep apnoea

To evaluate cardiac structure and function as well as blood pressure in the obstructive sleep apnoea syndrome (OSAS), we investigated 61 male patients and 61 male controls with M-mode and two-dimensional echocardiography. All patients had a history of habitual snoring and a diagnosed light to severe OSAS by previous investigations of nocturnal oxygen saturation status. No subject in the control group had a history of OSAS or hypertension. Body weight was higher in the OSAS patients than in the controls (P less than 0.001). Fifty per cent (31 out of 61) of the OSAS patients had systemic hypertension; 17 of these 31 were on pharmacological antihypertensive treatment. Neither the systolic nor the diastolic blood pressures were found to correlate to the severity of the OSAS (desaturation index). The heart rate was higher at rest in the OSAS patients with or without systemic hypertension compared to the controls with or without a blood pressure level above 165/95 mmHg (P less than 0.05 and P less than 0.01, respectively). Left ventricular (LV) internal dimensions as assessed by echocardiography did not differ between the two groups, while the interventricular septum and the LV posterior wall were thicker in the OSAS group. Thus, the LV mass and the LV mass index were significantly higher among the OSAS patients (P less than 0.001 and P less than 0.001). The LV mass index was approximately 15% higher among the 30 normotensive OSAS patients with no history of cardiac disease compared with the normotensive controls (P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)     

Neurocognitive impairment in Chinese patients with obstructive sleep apnoea hypopnoea syndrome

Background and objective: Sleep‐disordered breathing is known to be associated with impairment in cognitive function. The aim of this study was to characterize neurocognitive impairment in a cohort of Chinese patients with varying severities of obstructive sleep apnoea hypopnoea syndrome (OSAHS), and to develop a sensitive instrument for routine screening of cognitive impairment. Methods: Eligible patients (n = 394) were categorized into a primary snoring group, and mild, moderate and severe OSAHS groups, based on assessment of AHI. The Montreal Cognitive Assessment (MoCA) and the Mini‐Mental State Examination (MMSE) questionnaires were administered to assess cognitive function, and the correlations between questionnaire scores and clinical and polysomnographic parameters were further evaluated by stepwise multivariate regression. Results: MoCA scores decreased progressively across the spectrum from primary snoring to severe OSAHS. Importantly, mild neurocognitive impairment as defined by a MoCA score <26 was more common in the moderate (38.6%) and severe (41.4%) OSAHS groups than in the mild OSAHS (25.0%) and primary snoring (15.2%) groups. In contrast, MMSE scores were largely normal and comparable among all four groups. Evaluation of MoCA subdomains further revealed selective reduction in memory/delayed recall, visuospatial and executive function, and attention span in the severe OSAHS group compared with the other groups. Stepwise multivariate regression analysis demonstrated that MoCA scores correlated significantly with lowest oxygen saturation (L‐SaO₂) and years of education. Conclusions: Neurocognitive impairment is common in patients with OSAHS. The MoCA is a brief and sensitive tool for the assessment of cognitive impairment in OSAHS patients, whose performance on the MMSE is in the normal range.     

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.     

Resistant hypertension, obstructive sleep apnoea and aldosterone

Obstructive sleep apnoea (OSA) and hypertension commonly coexist. Observational studies indicate that untreated OSA is strongly associated with an increased risk of prevalent hypertension, whereas prospective studies of normotensive cohorts suggest that OSA may increase the risk of incident hypertension. Randomized evaluations of continuous positive airway pressure (CPAP) indicate an overall modest effect on blood pressure (BP). Determining why OSA is so strongly linked to having hypertension in cross-sectional studies, but yet CPAP therapy has limited BP benefit needs further exploration. The CPAP studies do, however, indicate a wide variation in the BP effects of CPAP, with some patients manifesting a large antihypertensive benefit such that a meaningful BP effect can be anticipated in some individuals. OSA is particularly common in patients with resistant hypertension (RHTN). The reason for this high prevalence of OSA is not fully explained, but data suggest that it may be related to the high occurrence of hyperaldosteronism in patients with RHTN. In patients with RHTN, it has been shown that aldosterone levels correlate with severity of OSA and that blockade of aldosterone reduces the severity of OSA. Overall, these findings are consistent with aldosterone excess contributing to worsening of underlying OSA. We hypothesize that aldosterone excess worsens OSA by promoting accumulation of fluid within the neck, which then contributes to increased upper airway resistance.     

Differences in abdominal and neck circumferences in patients with and without obstructive sleep apnoea.

We have recently shown that patients with sleep apnoea have thicker necks than non-apnoeic snoring controls. However, it was not clear whether this difference simply reflects the fact that apnoeic patients are more obese than the non-apnoeic ones, or whether it represents a preferential distribution of fat over the neck region compared to the abnormal region. We therefore measured the neck and abdominal circumferences in a large group of 670 patients suspected of having sleep apnoea, all of whom had full nocturnal polysomnography, including measurement of snoring. We divided these patients into apnoeic and non-apnoeic groups based on the apnoea/hypopnoea index (AHI) of 10. Apnoeic patients had significantly higher body mass index (BMI), neck, and abdominal circumferences than non-apnoeic controls. We then matched apnoeic and non-apnoeic patients exactly, one-for-one for BMI and age; this procedure left us with 156 patients in each group. Abdominal circumferences were similar, but the neck circumference was significantly higher in apnoeic patients (41.2 +/- 3.5 cm vs 39.1 +/- 3.7 cm, p less than 0.0001). Multiple stepwise linear regression analysis revealed that neck circumference and BMI correlated significantly with apnoea (multiple R2 = 0.27, p less than 0.001) and snoring (multiple R2 = 0.19, p less than 0.001). We conclude that obese patients with sleep apnoea have fatter necks than equally obese non-apnoeic snorers, and that the neck circumference could be a significant determinant of apnoea and snoring.     

Atrial overdrive pacing compared to CPAP in patients with obstructive sleep apnoea syndrome.

AIMS: Obstructive sleep apnoea (OSA) is associated with oxygen desaturation, blood pressure increase, and neurohumoral activation, resulting in possible detrimental effects on the cardiovascular system. Continuous positive airway pressure (CPAP) is the therapy of choice for OSA. In a recent study, nocturnal atrial overdrive pacing (pacing) reduced the severity of sleep apnoea in pacemaker patients. We compared the effects of CPAP with those of pacing in patients with OSA but without pacemaker indication or clinical signs of heart failure. METHODS AND RESULTS: Ten patients with OSA on CPAP therapy were studied for three nights by polysomnography. During the nights that followed a night without any treatment (baseline), the patients were treated with CPAP or pacing in a random order. Pacing was performed with a temporary pacing lead. The pacing frequency was 15 b.p.m. higher than the baseline heart rate. The apnoea-hypopnoea index was 41.0 h(-1) (12.0-66.6) at baseline and was significantly lower during CPAP [2.2 h(-1) (0.3-12.4)] compared with pacing [39.1 h(-1) (8.2-78.5)]. Furthermore, duration and quality of sleep were significantly improved during CPAP when compared with pacing. CONCLUSION: Nocturnal atrial overdrive pacing is no alternative therapeutic strategy to CPAP for the treatment of OSA in patients without clinical signs of heart failure and without conventional indication for anti-bradycardia pacing.