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We previously showed in heart failure (HF) patients that obstructive respiratory events during sleep and generation of negative intrathoracic pressure during Mueller manoeuvres, mimicking obstructive apneas, acutely reduced stroke volume (SV). We also showed that treating obstructive sleep apnea (OSA) with continuous positive airway pressure (CPAP) increased left ventricular ejection fraction over a 1-month period. We therefore hypothesized that, in HF patients, those with OSA would have greater overnight declines in SV and cardiac output (CO) than in those without sleep apnea, and that therapy of OSA using CPAP would prevent these declines.We examined overnight percent change in SV and CO in 32 HF patients with and 28 without OSA using digital photoplethysmography. Among patients with OSA, we also examined changes in SV and CO during a CPAP titration study.During the baseline polysomnogram SV and CO decreased more overnight in those with OSA than in those without sleep apnea (-12.6 ± 7.7% vs -3.2 ± 6.8%; P0.001 and -16.2 ± 9.9% vs -3.7 ± 8.3%; P0.001, respectively). Overnight changes in SV and CO correlated inversely with total apnea-hypopnea index (r = -0.551; P0.001 and r = -0.522; P0.001, respectively). In 21 patients with OSA, CPAP reduced the total apnea-hypopnea index from 37.7 ± 21.4 to 15.0 ± 16.0 (P0.001) in association with attenuation of the overnight reduction of SV (from -14.0 ± 7.9% to -3.4 ± 9.8%; P = 0.002) and CO (from -17.2 ± 9.0% to -9.7 ± 10.7%; P = 0.042).In patients with HF, coexisting OSA causes overnight declines in SV and CO that are prevented through reversal of OSA by CPAP.

Periodic leg movements during sleep (PLMs) are a disorder characterized by regularly recurring movements of the legs during sleep. Although PLMs are common in patients with heart failure (HF), their clinical significance is unknown. The aim of this study was to determine whether, in patients with HF, PLMs are associated with increased mortality risk. In a prospective cohort study, 218 consecutive patients with systolic HF newly referred to an HF clinic from 1997 to 2004 who underwent overnight polysomnography, regardless of symptoms or signs of sleep disorders, were enrolled. The frequency of PLMs per hour of sleep was quantified as the PLM index (PLMI). Patients were classified as either normal (PLMI

Background Previous studies reported high prevalences of obstructive and central sleep apnea (OSA and CSA, respectively) in patients with heart failure (HF). However, these preceded widespread use of β-blockers and spironolactone that might have reduced their prevalences. We therefore determined, in patients with HF, prevalences and predictors of OSA and CSA and the influence of changes in HF therapy on prevalences. Methods and Results A total of 218 HF patients with left ventricular ejection fraction (LVEF) ≤45% underwent sleep studies between 1997 and 2004 and were classified as having moderate to severe sleep apnea (apnea-hypopnea index ≥15hours of sleep, either OSA or CSA), or mild to no sleep apnea. The prevalence of moderate to severe OSA was 26% and of CSA was 21%. Predictors of OSA were older age, male sex, and greater body mass index, and of CSA were older age, male sex, atrial fibrillation, hypocapnia, and diuretic use. Between 1997 and 2004, the prevalences of OSA and CSA did not change significantly ( P trend =.460, P trend =.211, respectively) despite increased use of β-blockers and spironolactone ( P trend P trend P trend =.005). Conclusions OSA and CSA remain common in patients with HF, despite increases in β-blocker and spironolactone use.

The cause of increased pharyngeal collapsibility in patients with obstructive sleep apnea is incompletely understood. In awake healthy subjects, we showed that fluid displacement from the legs into the neck induced by lower body positive pressure reduces upper airway size and increases its collapsibility. Prolonged sitting leads to dependent fluid accumulation in the legs.To test the hypotheses that the apnea-hypopnea index (AHI) during sleep will be related to the amount of fluid spontaneously displaced from the legs overnight, and that this will, in turn, be related to the time spent sitting the previous day.In 23 nonobese healthy men referred for sleep studies for suspected obstructive sleep apnea, we assessed the changes in leg fluid volume and in neck circumference from the beginning to the end of the night, and the time spent sitting during the previous day.The overnight change in leg fluid volume correlated strongly with the AHI (r = -0.773, P0.001), the change in neck circumference (r = -0.792, P0.001), and the time spent sitting (r = -0.588, P = 0.003). Multivariate analysis showed that the only significant independent correlates of the AHI were the overnight changes in leg fluid volume and neck circumference, which together explained 68% of the variability in the AHI among subjects.These novel findings suggest that overnight rostral fluid displacement from the legs, related to prolonged sitting, may play a previously unrecognized role in the pathogenesis of obstructive sleep apnea in nonobese men that is independent of body weight.

To determine whether the influence of sleep apnoea (SA) on the risk of death differs in patients with ischaemic and in those with non-ischaemic heart failure (HF).Prospective observational study.Consecutive patients with HF with left ventricular ejection fractionor =45% newly referred to the HF clinic between 1 September 1997 and 1 December 2004.Patients underwent sleep studies and were divided into those with moderate to severe SA (apnoea-hypopnoea indexor =15/h of sleep) and those with mild to no SA (apnoea-hypopnoea index15/h of sleep). They were followed up for a mean of 32 months to determine all-cause mortality rate.Of 193 patients, 34 (18%) died. In the ischaemic group, mortality risk adjusted for confounding factors was significantly higher in those with SA than in those without it (18.9 vs 4.6 deaths/100 patient-years, hazards ratio (HR) = 3.03, 95% CI 1.04 to 8.84, p = 0.043). In contrast, in the non-ischaemic HF group, there was no difference in adjusted mortality risk between those with, and those without, SA (3.9 vs 4.0 deaths/100 patient-years, p = 0.929).In patients with HF, the presence of SA is independently associated with an increased risk of death in those with ischaemic, but not in those with non-ischaemic, aetiology. These findings suggest that patients with ischaemic cardiomyopathy are more susceptible to the adverse haemodynamic, autonomic and inflammatory consequences of SA than are those with non-ischaemic cardiomyopathy.

SLEEP STRUCTURE IS INVARIABLY DISRUPTED BY AROUSALS FROM SLEEP IN PATIENTS WITH SLEEP APNEA.1,2 IN OBSTRUCTIVE SLEEP APNEA (OSA), arousals from sleep that typically terminate apneas, trigger activation of the pharyngeal dilator muscles and facilitate resumption of airflow. Indeed, several studies report that 75% to 80% of obstructive events are terminated by arousals.3,4 Accordingly, in OSA, arousals are considered to be an important defense mechanism for reestablishing airway patency, thus preventing asphyxia. On the other hand, this protective mechanism inevitably disrupts sleep. When OSA is alleviated by continuous positive airway pressure (CPAP), the frequency of arousals is immediately reduced in association with consolidation of sleep and an increase in the proportion of both slow wave and REM sleep.5–8 One can therefore conclude that OSA causes arousal from sleep, and that this, in turn, reduces the amounts of slow wave and REM sleep. In patients with heart failure (HF) and coexisting Cheyne-Stokes respiration with central sleep apnea (CSA), arousals often follow central apneas and hypopneas.2,9,10 However, in contrast to OSA, these arousals often occur several breaths after apnea termination, suggesting that in such cases, they are not an important defense mechanism that contribute to resumption of airflow. Arousals, whether occurring during the apnea-hyperpnea cycle or not, provoke abrupt increases in ventilation and decreases in PCO2. If PCO2 falls below the threshold for apnea, central apnea ensues.11,12 Among patients with CSA, either with or without HF, abrupt increases in ventilation, and falls in PCO2, mainly provoked by arousals, precede more than 90% of episodes of Cheyne-Stokes respiration and repetitive central apneas.11,12 Moreover, in previous studies, it has been shown that CPAP only partially suppresses CSA such that the frequency of apneas and hypopneas/h of sleep (apnea-hypopnea index or AHI) only falls by approximately 30% to 70% in patients with HF.13–21 Perhaps this was because it did not eliminate one stimulus to the Cheyne-Stokes respiratory cycle: arousal-mediated hyperpneas. Therefore, arousals may contribute to causation of CSA. If arousals are mainly a consequence of CSA in patients with HF, they should diminish if CSA is attenuated by treatment. If, on the other hand, arousals are a cause of, or are incidental to CSA, then suppression of CSA in HF patients may have little or no effect on arousal frequency or sleep structure. There is controversy on this point: some articles reported that CPAP and other interventions that suppress CSA either reduced arousal frequency or increased the amounts of slow wave and REM sleep,13–15 whereas others did not.16–21 However, all of these studies were small (n ≤ 24), or of short duration (1 day to 1 month), and simply reported arousal frequency and sleep structure, but without discussing the significance of whether or not they improved. Our objective, therefore, was to determine in a much larger, longer-term randomized trial, whether attenuation of CSA by CPAP in patients with HF reduces the frequency of arousals from sleep or improves sleep structure. To this end, we analyzed the arousal frequency and sleep structure at baseline and follow-up of patients enrolled in a randomized clinical trial of CPAP to treat CSA in patients with HF (Canadian Continuous Positive Airway Pressure for Patients with Central Sleep Apnea and Heart Failure trial [CANPAP]).

Background: Fluid accumulation in the neck during recumbency might narrow the upper airway (UA) and thereby contribute to its collapse in patients with obstructive sleep apnoea (OSA). It is hypothesised that acute fluid shifts from the legs to the upper body in healthy subjects would increase neck circumference and reduce the cross-sectional area of the UA (UA-XSA). Methods: In 27 healthy non-obese subjects of mean (SE) age 39 (3) years and body mass index 23.2 (0.6) kg/m2 studied while supine, leg fluid volume was measured using bioelectrical impedance, neck circumference using a mercury strain gauge and mean UA-XSA between the velum and the glottis using acoustic pharyngometry at end expiration. Measurements were made at baseline after which subjects were randomly assigned to a 5 min time control period or to a 5 min application of lower body positive pressure (LBPP) at 40 mm Hg by anti-shock trousers, separated by a 15 min washout period. Subjects then crossed over to the opposite arm of the study. Results: Compared with control, application of LBPP significantly reduced leg fluid volume (p

Objectives We conducted a nationwide cross-sectional survey of respiratory health in adults aged 20 to 44 years during 2001 to 2002 to determine the prevalence of bronchial hyperresponsiveness (BHR) and asthma in the adult Thai population. Design Subjects were selected by a multistage stratified random sampling. The stratification was done on geographic area, age group, and sex. Subjects were interviewed with questionnaires and underwent spirometric testing. Methacholine challenge tests were performed on all subjects without contraindication to determine BHR defined as the provocative concentration of methacholine producing a 20% fall in FEV1 ≤ 8 mg/mL. Definite asthma was defined as BHR present with any asthma symptom within the past 12 months or demonstrated reversible airflow obstruction. Current diagnosed asthma was defined as previous physician-diagnosed asthma and any asthma symptom within the past 12 months or currently receiving asthma medication. Results The study population was from 20 provinces of five geographic regions of Thailand and included 1,882 women and 1,572 men. The prevalence of BHR was 3.31% (95% confidence interval [CI], 2.68 to 3.94). However, if subjects with positive reversibility test results were included, the prevalence increased to 3.98% (95% CI, 3.30 to 4.67). The prevalence of definite asthma was 2.91% (95% CI, 2.32 to 3.50), whereas the prevalence of current diagnosed asthma by the questionnaire interview was 2.15% (95% CI, 1.66 to 2.63). The κ index of the agreement between both definitions of asthma was 0.40, indicating poor to fair agreement. Conclusion The prevalence of BHR and asthma in the adult Thai population is relatively low as compared with western countries.

To assess the internal consistency, test-retest reliability, and validity of the Thai version of the Pittsburgh Sleep Quality Index (Thai-PSQI), which was recently translated using a standardized method, in Thai patients with major sleep disorders.The Thai-PSQI was developed under a standard translation protocol and administered to "bad" sleepers (i.e. patients with suspected obstructive sleep apnea [OSA], depression, or insomnia) and "good" sleepers in an academic tertiary care setting. All participants were asked to complete the same questionnaire after 2-4 weeks.A total of 138 participants consisting of 69 patients with OSA, 28 with major depression, 11 with primary insomnia, and 30 controls completed the questionnaire. The global scores of the Thai-PSQI revealed that it had excellent internal consistency (Cronbach's alpha = 0.837) and test-retest reliability (intraclass correlation coefficient = 0.89). An analysis of covariance demonstrated a significant difference in Thai-PSQI global score between good sleepers and bad sleepers (p0.001). A cut-off point of 5 out of 6 on the global score resulted in a sensitivity of 77.78% and specificity of 93.33%.The Thai-PSQI is a valid and reliable tool for screening and identifying the presence of significant sleep disturbances, and is comparable to the original English version.

Aims Patients with sleep apnoea (SA) and heart failure (HF) are less sleepy than SA patients without HF. HF and SA both increase sympathetic nervous system activity (SNA). SNA can augment alertness. We previously showed that in HF patients, the degree of daytime sleepiness was not related to the severity of SA but was inversely related to SNA. Elevated SNA is associated with increased mortality in HF. Therefore, we hypothesized that in HF patients with SA, the degree of daytime sleepiness will be inversely related to mortality. Methods and results In a prospective cohort study, 218 consecutive patients with systolic HF had overnight polysomnography. Among them, 80 subjects with SA (apnoea–hypopnoea index ≥15) were followed for a mean of 28 months to determine all‐cause mortality rate. Subjective daytime sleepiness was assessed by the Epworth Sleepiness Scale (ESS). During follow‐up, 20 patients died. The 5 year death rate in patients with ESS less than 6 (i.e. less sleepy) was significantly higher than in patients with an ESS at or above the median of 6 (i.e. sleepier) [21.3 deaths/100 patient‐years vs. 6.2 deaths/100 patient‐years, unadjusted hazard ratio (HR) 2.94, 95% confidence interval (CI) 1.20 to 7.20, P = 0.018]. After adjusting for confounding factors that included sex, history of hypertension, and mean arterial oxyhaemoglobin saturation, compared with the sleepier patients, less sleepy patients had greater risk of mortality (HR 2.56, 95% CI 1.01 to 6.47, P = 0.047). As a continuous variable, ESS scores were inversely related to mortality risk (HR 0.86, 95% CI 0.75 to 0.98, P = 0.022). Conclusions In patients with HF and SA, the degree of subjective daytime sleepiness is inversely related to the mortality risk, suggesting that among HF patients with SA, those with the least daytime sleepiness are at greater risk of death. They may therefore have greater potential for mortality benefit from therapy of SA than those with greater daytime sleepiness.

To determine the association between degree of obesity and severity of OSA in Thai childrenThe present retrospective study recruited obese children aged 3 to 15 years who had habitual snoring and underwent polysomnography (PSG) between January 2009 and June 2010. Obesity was defined as percentage of ideal weight for height (%W/H)or = 120 and was classified as mild (%W/H of 120-139), moderate (140-159), severe (160-199) and morbid (or = 200). OSA was classified as severe (AHIor = 10) and non-severe (AHI10).Of 73 obese children, the mean age was 9.92 +/- 3.42 years of which 60.3% were boys. The mean +/- SD of BMI was 28.38 +/- 5.99 kg/m2 and %W/H +/- SD was 162.63 +/- 26 26. Gender age, height, weight and BMI were not significantly different between severe and non-severe OSA groups. However, the %W/H of the severe OSA group (171.38% +/- 29.54%) was significantly greater than the non-severe group (157.19% +/- 22.68%) (p = 0.02). Severe to morbid obesity (OR 2.80, 95% CI 1.06-7.42; p = 0.038) and enlarged tonsils at least 3+ (OR 3.28, 95% CI 1.22-8.81; p = 0.018) were the risk factors for severe OSA.Severe to morbid obesity was a predicting factor for severe OSA. These results suggested that severely obese children with snoring should have early recognition for severe OSA, which is highly contributing to multiple sequalae.

Background— Obstructive sleep apnea (OSA) and central sleep apnea are common in patients with heart failure. We hypothesized that in such patients, severity of OSA is related to overnight rostral leg fluid displacement and increase in neck circumference, severity of central sleep apnea is related to overnight rostral fluid displacement and to sleep P co 2 , and continuous positive airway pressure alleviates OSA in association with prevention of fluid accumulation in the neck. Methods and Results— In 57 patients with heart failure (ejection fraction ≤45%), we measured change in leg fluid volume and neck circumference before and after polysomnography, and we measured transcutaneous P co 2 during polysomnography. Patients were divided into an obstructive-dominant group (≥50% of apneas and hypopneas obstructive) and a central-dominant group (>50% of events central). Patients with OSA received continuous positive airway pressure. In obstructive-dominant patients, there were inverse relationships between overnight change in leg fluid volume and both the overnight change in neck circumference ( r =−0.780, P r =−0.881, P co 2 . In central-dominant patients, the overnight reduction in leg fluid volume correlated inversely with the apnea-hypopnea index ( r =−0.919, P r =−0.568, P =0.013) and directly with transcutaneous P co 2 ( r =0.569, P =0.009). Continuous positive airway pressure alleviated OSA in association with prevention of the overnight increase in neck circumference ( P Conclusions— Our findings suggest that nocturnal rostral fluid shift is a unifying concept contributing to the pathogenesis of both OSA and central sleep apnea in patients with heart failure.

Background Experimentally induced sleep deprivation can raise blood pressure (BP) and worsen hypertension. We recently reported a significantly higher prevalence of obstructive sleep apnea (OSA) and reduced rapid eye movement (REM) sleep time in drug-resistant hypertensives compared to controlled hypertensives. The objective of this study was to test the hypothesis that short sleep duration is associated with resistant hypertension (RH) independently of OSA, which can itself disrupt and shorten sleep. Methods In a case-control study, overnight polysomnographic results of subjects with OSA and RH (n = 62) were compared to those with OSA of equal severity and either controlled hypertension (CH) (n = 49) or normotension (n = 40). Results Subjects with RH slept 33.8 min (P = 0.02) and 37.2 min (P = 0.02) less than those with CH and normotension, respectively. Consequently, sleep efficiency was reduced by 7.9% (P = 0.007) and 10.2% (P = 0.002), respectively. They also spent 9.7 min (P = 0.06) and 11.6 min (P = 0.04) less time in REM sleep compared to those with CH and normotension, respectively. Older age, greater body mass index (BMI) and greater apnea-hypopnea index (AHI) were also associated with shorter sleep time (P = 0.02, P = 0.001, and P = 0.03, respectively) and reduced sleep efficiency (P = 0.0003, P = 0.03, and P = 0.01, respectively). Conclusions Our study demonstrates that, compared to subjects with CH or normotension, those with RH have shorter total and REM sleep times and lower sleep efficiency independently of OSA. These data suggest that reduced sleep time may contribute to the severity of hypertension.

Background Obstructive sleep apnea (OSA) increases the risk for mild hypertension, but its relationship to refractory hypertension (RHT) has not been systematically examined. We previously reported a high prevalence of OSA in patients with RHT, but did not have a control group with which to compare. Rapid eye movement (REM) sleep deprivation can raise blood pressure in animals. However, a potential relationship of OSA and REM sleep time with RHT has not been examined. Objective To determine whether, compared with patients with well controlled hypertension, those with RHT have a higher prevalence of OSA (apnea-hypopnea index > or = 10 per hour of sleep) and shorter REM sleep time. Methods We compared the prevalence of OSA and sleep structure in 42 patients with RHT with 22 patients with controlled hypertension, matched for age, sex and BMI. Results Compared with the controlled hypertension group, the RHT group had a significantly higher prevalence of OSA (81 versus 55%, P = 0.03) and less REM sleep time (47.0 +/- 4.5 versus 63.2 +/- 4.9 min, P = 0.02). Multivariate analysis revealed significantly increased odds of having RHT associated with OSA independent of other risk factors (adjusted odds ratio, 3.994; 95% confidence interval, 1.191-13.388). Reduced REM sleep time was also independently associated with the presence of RHT (adjusted odds ratio, 1.025; 95% confidence interval, 1.002-1.049). Conclusion OSA and reduced REM sleep time are associated with increased odds of having RHT and, therefore, may play roles in its pathogenesis.

To compare the clinical features, anthropometric indices, and polysomnographic data between different body mass index (BMI) subgroups of obstructive sleep apnea (OSA) patients.The authors reviewed the data from OSA patients in Siriraj Sleep Clinic from April 2005 to September 2006. Objective measurement for sleepiness (Epworth Sleepiness Scale, ESS), anthropometric measurements [body mass index (BMI), neck circumference, thyromental distance, Mallampati S score, and occlusion pattern] and polysomnographic recordings [apnea/hypopnea index (AHI) during REM and NREM periods, respiratory arousal index, periodic leg movement index, minimal oxygen saturation, total sleep time with oxygen saturation90%, and desaturation index] were collected. The patients were stratified into the non-obese group and obese group if their BMI was27 oror =27 kg/m2 respectively.Of the total 158 patients, 71 were non-obese and 87 were obese, no difference in mean age and sex was observed, but more patients with hypertension and coronary artery disease were noted in the obese group. Mean ESS was not different between the 2 groups. In anthropometric measurements, the obese group had statistically significant large neck circumference (41.6 +/- 3.5 cm vs. 37.0 +/- 2.9 cm, p0.001), but the nonobese group had a shorter thyromental distance (56.4 +/- 11.7 mm vs. 61.4 +/- 11.2 mm, p=0.006), with no significant difference in Mallampatis score and occlusion pattern. In polysomnographic data, the obese group had statistical significantly more severity of various indices except for AHI during the REM period and the periodic limb movement index.Non-obese obstructive sleep apnea patients have more bony structural change than the obese ones as demonstrated by shorter thyromental distance. But degree of abnormalities during sleep was less severe in nearly all aspects.

Fluid shift from the legs to the neck induced by LBPP (lower-body positive pressure) increases UA (upper airway) collapsibility in healthy men. Rostral fluid displacement during recumbency may therefore contribute to the pathogenesis of OSA (obstructive sleep apnoea). There is a higher prevalence of OSA in men than in women. We therefore hypothesized that UA collapsibility increases more in men in response to rostral fluid displacement than in women. UA collapsibility was assessed in healthy, non-obese men and women while awake by determining UA Pcrit (critical closing pressure) during application of different suction pressures to the UA. Subjects were randomized to 5 min control or LBPP arms after which they crossed-over into the other arm following a 30 min washout. LBPP was applied by inflating anti-shock trousers wrapped around both legs to 40 mmHg. Pcrit, leg fluid volume and neck circumference were measured at baseline and after 5 min of both control and LBPP periods. LBPP caused a decrease in leg fluid volume and an increase in neck circumference that did not differ between men and women. However, compared with the control period, LBPP induced a much greater increase in Pcrit in men than in women (7.2±1.8 compared with 2.0±1.5 cmH2O, P=0.035). We conclude that rostral fluid displacement by LBPP increases UA collapsibility more in healthy, non-obese men than in women. This may be one mechanism contributing to the higher prevalence of OSA in men than in women.

Patients with either heart failure or obstructive sleep apnea have a reduced baroreflex sensitivity for heart rate, a sign of poor prognosis. We previously demonstrated that nocturnal application of continuous positive airway pressure to heart failure patients with obstructive sleep apnea increased baroreflex sensitivity acutely, but it is not known whether these effects persist into wakefulness.To determine whether treating obstructive sleep apnea in heart failure patients with continuous positive airway pressure improves baroreflex sensitivity during wakefulness.Spontaneous baroreflex sensitivity was assessed during wakefulness in 33 heart failure patients (left ventricular ejection fractionor = 45%) with obstructive sleep apnea (apnea-hypopnea indexor = 20). Subsequently, baroreflex sensitivity was reassessed 1 month after patients were randomly allocated to nocturnal continuous positive airway pressure treatment or no treatment (control).Compared with the 14 control patients, the 19 continuous positive airway pressure-treated patients experienced a greater increase in baroreflex sensitivity [median, (25%, 75%)] [from 5.4 (2.2, 8.3) to 7.9 (4.4, 9.4) ms/mmHg; P = 0.01] and left ventricular ejection fraction (P0.001). In addition, daytime systolic blood pressure and heart rate decreased more in the continuous positive airway pressure group (from 122 +/- 15 to 113 +/- 12 mmHg; P = 0.02, and from 66 +/- 8 to 62 +/- 8 bpm; P0.001, respectively) than in the control group.Treatment of coexisting obstructive sleep apnea by continuous positive airway pressure in heart failure patients improves baroreflex sensitivity during wakefulness in addition to improving left ventricular ejection fraction and lowering blood pressure and heart rate. These data indicate that the improved autonomic regulation of heart rate in heart failure patients treated for obstructive sleep apnea during sleep persists into wakefulness.

Fluid displacement into nuchal and peripharyngeal soft tissues while recumbent may contribute to narrowing and increased airflow resistance of the pharynx (Rph), and predispose to pharyngeal collapse in patients at risk for obstructive sleep apnea.To determine whether displacement of fluid from the lower body to the neck will increase both neck circumference and Rph in healthy subjects.In 11 healthy, nonobese subjects, studied while awake and supine, leg fluid volume, neck circumference, and Rph were measured at baseline. Subjects were then randomized to a control period or to application of lower body positive pressure (LBPP) of 40 mm Hg via antishock trousers to displace fluid from the legs, after which they crossed over to the other arm. Baseline measurements were repeated at 1 and 5 min during the control and LBPP periods.Compared with the control period, application of LBPP caused a significant reduction in leg fluid volume (p0.001) and a significant increase in neck circumference (p = 0.004). Rph remained stable during the control period, but increased significantly from baseline after 1 and 5 min of LBPP (from 0.43 +/- 0.10 to 0.60 +/- 0.11 cm H(2)O/L/s, p = 0.034, and to 0.87 +/- 0.19 cm H(2)O/L/s, p0.001, compared with baseline, respectively).Fluid displacement from the legs by LBPP increases neck circumference and Rph in healthy subjects. These findings suggest the hypothesis that fluid displacement to the upper body during recumbency may predispose to pharyngeal obstruction during sleep, especially in fluid overload states, such as heart and renal failure.

ObjectivesThis study sought to determine, in patients with heart failure (HF), whether untreated moderate to severe obstructive sleep apnea (OSA) is associated with a higher mortality rate than in patients with mild to no sleep apnea (M-NSA).BackgroundObstructive sleep apnea is common in patients with HF and exposes the heart and circulation to adverse mechanical and autonomic effects. However, its effect on mortality rates of patients with HF has not been reported.MethodsIn a prospective study involving 164 HF patients with left ventricular ejection fractions (LVEFs) ≤45%, we performed polysomnography and compared death rates between those with M-NSA (apnea-hypopnea index [AHI]