Clinical predictors of sleep apnoea in heart failure outpatients.

BACKGROUND: Sleep-disordered breathing (SDB) is common in heart failure patients. Many of them still remain undiagnosed. The aim of this study was to detect clinical predictors of sleep apnoea which may help to identify patients with SDB at a heart failure clinic. METHODS: We performed an in-home sleep study on 115 consecutive patients from our heart failure clinic. Clinical characteristics, blood samples, daytime sleepiness and quality of life were registered. RESULTS: Among 115 patients, 52% had moderate to severe SDB. Body Mass Index (BMI) ≥ 30 kg/m² was the only independent predictor of moderate to severe SDB [Odds ratio (OR) = 3.62, 95% Confidence interval (CI) 1.40-9.36, p = 0.008]. Quality of life and level of sleepiness were not significantly associated with SDB. Patients with mild to moderate chronic obstructive pulmonary disease (COPD) were unlikely to have SDB compared with patients without COPD (OR = 0.10, 95% CI 0.02-0.43, p = 0.002). Hypertension was a predictor of having obstructive sleep apnoea (OR = 2.78, 95% CI 1.15-6.75, p = 0.02), while haemoglobin ≥ 15 g/dl was associated with central sleep apnoea (OR = 6.71, 95% CI 1.96-22.99, p = 0.002). CONCLUSION: BMI ≥ 30 kg/m(2) is associated with moderate to severe SDB, both obstructive and central sleep apnoea. Thus, BMI may be used as one of the selection criteria for referral of heart failure patients to a sleep specialist.

Prevalence, risk factors, and type of sleep apnea in patients with paroxysmal atrial fibrillation.

BACKGROUND: Recent studies have suggested an association between sleep apnea (SA) and atrial fibrillation (AF). We aimed to study the prevalence, characteristics, risk factors and type of sleep apnea (SA) in ablation candidates with paroxysmal AF. METHODS/RESULTS: We prospectively studied 579 patients with paroxysmal AF, including 157 women (27.1%) and 422 men (72.9%). Mean age was 59.9 ± 9.6 years and mean body mass index (BMI) 28.5 ± 4.5 kg/m2. SA was diagnosed using polygraphy for two nights at home. The Epworth Sleepiness Scale (ESS), STOP-Bang Questionnaire, and Berlin Questionnaire (BQ) assessed the degree of SA symptoms. A total of 479 (82.7%) patients had an apnea-hypopnea index (AHI) ≥ 5, whereas moderate-severe SA (AHI ≥ 15) was diagnosed in 244 patients (42.1%). The type of SA was predominantly obstructive, with a median AHI of 12.1 (6.7-20.6) (range 0.4-85.8). The median central apnea index was 0.3 (0.1-0.7). AHI increased with age, BMI, waist and neck circumference, body and visceral fat. Using the Atrial Fibrillation Severity Scale and the SF-36, patients with more severe SA had a higher AF burden, severity and symptom score and a lower Physical-Component Summary score. Age, male gender, BMI, duration of AF, and habitual snoring were independent risk factors in multivariate analysis (AHI ≥ 15). We found no association between ESS and AHI (R2 = 0.003, p = 0.367). CONCLUSIONS: In our AF population, SA was highly prevalent and predominantly obstructive. The high prevalence of SA detected in this study may indicate that SA is under-recognized in patients with AF. None of the screening questionnaires predicted SA reliably.

Nocturnal polysomnography with and without continuous pharyngeal and esophageal pressure measurements.

PSG with simultaneous pharyngeal and esophageal pressure measurements of the upper airway may interfere with sleep architecture and cause a bias. The aim of this study was to evaluate the degree of disturbance to sleep caused by inclusion of pressure measurements of the airway, and whether this would reduce the validity of the PSG. Thirty-two consecutive patients referred for PSG for possible obstructive sleep apnea syndrome (OSAS) were included. For pressure recordings, a 6-F silicone tube, 1.9 mm in diameter, containing six pressure transducers, was introduced through one nostril into the pharynx and esophagus. Each patient had two nocturnal PSGs, one of which included airway pressure measurements. There were no statistically significant differences between PSGs performed with and without simultaneous pressure recordings for the following sleep quality parameters: total sleep time, number of sleep-stage shifts, sleep efficiency, arousal during sleep (= intrasleep wakefulness), percent REM sleep, and number of microarousals. We did not find any statistically significant differences for respiratory parameters such as type, duration, and index of different respiratory events and snoring. However, there was a slight tendency for reduced sleep quality and oxygen saturation when pressure measurements were included. The only significant change seen was in the duration of non-REM sleep with oxygen saturation below 90%. The multisensor airway pressure probe demonstrated that proximal obstructions were more common than distal obstructions, and obstruction in one or two segments was far more frequent than obstruction in more than two.

Tracing air flow and diagnosing hypopnoeas in normal subjects.

Hypopnoea is a type of sleep-related breathing disorder (SRBD), and the apnoea plus hypopnoea index (AHI) is usually computed to diagnose this condition. We introduce a new method to diagnose flow with internal thermistors located on the same sensors as we use to diagnose obstructive segments in patients with sleep-related breathing disorders. The aim of this study is to investigate whether internal thermistors are reliable for diagnosis of hypopnoeas. Fifteen volunteers participated in a prospective comparative study in healthy subjects without SRBD. We simultaneously measured minute ventilation by a pneumotachograph and indirectly air flow by internal thermistors in awake subjects was manually analysed from both the pneumotachograph and the internal thermistors. We found a close agreement between the different methods for percentage reduction in air flow both for the hypopnoea and the apnoea data. The mean difference between the percentage reduction in flow from normal breathing to hypopnoea measured by the pneumotachograph and the internal thermistors lying supine was 3.8% (SD 7.4). In the lateral position the corresponding figures were 1.0% and 4.6. This study in awake, normal subjects indicates that internal thermistors are as reliable as the pneumotachograph in diagnosing hypopnoeas and we believe that the reliability of this monitoring method is adequate for clinical use.

Diagnosing respiratory events and tracing air flow by internal thermistors.

We have developed a new method to measure flow in patients with sleep-related breathing disorders (SRBD). These flow sensors are modified thermistors located in the same sensors we use for pressure measurement in the upper airways to find the obstructive segments during apnoeas. The aim of this study was to test if using internal thermistors as indicator of air flow has advantages compared with the external thermistor method in detecting respiratory events. A total of 50 consecutive patients with an apnoea-hypopnoea index (AHI) of more than 15 were studied. A standard nocturnal polysomnography (PSG) with both internal and external thermistors was performed in all patients. To estimate the patients' AHI, a detailed analysis viewing all parameters except external and internal thermistors was performed. This was followed by an analysis viewing only internal thermistors signals indicating airflow in the pharynx, and finally an analysis viewing only external thermistor signals indicating air flow at the mouth and nose. Mean AHI measured by the three methods showed 49.8 (SD 23.4) by the PSG, 47.8 (SD 24.9) by internal thermistors alone, and 31.5 (SD 22.2) by external thermistors. There was no statistical difference between AHI detected by PSG and internal thermistors, but highly significant differences between PSG and external thermistors (p < 0.001). The external thermistors missed an average of almost 20 respiratory events per hour.

Internal thermistors in differentiating between oral and nasal breathing during sleep.

To select patients with sleep apnoea hypopnoea syndrome (SAHS) who will benefit from surgery, we use information from four different pressure sensors in the upper airways and oesophagus during polysomnography (PSG). These pressure sensors also have the ability to act as internal thermistors and can hence indirectly measure flow as well as pressure. This new method for measuring flow has proven to be very accurate for scoring hypopnoeas as well as apnoeas. The aim of this study was to determine whether the flow and pressure sensors located in the epipharynx, oropharynx and hypopharynx could differentiate between nasal and oral breathing. The design was a prospective cross-over study in 124 patients referred to the hospital for SAHS diagnosis. The awake patients were asked to breathe first through the nose and then through the mouth while the nose was blocked with a clip. A standard nocturnal PSG with pressure and flow measurement in the upper airways was performed in all patients. The procedure was repeated in a lateral position, and again the next morning in 32 of the patients. Reduction in flow signals from the nose was calculated, and a paired t-test was performed for statistical analysis. The difference between nasal and oral breathing was quite distinct in the flow tracings from the internal thermistors. The mean reduction in nasal flow signals when changing from nasal to oral breathing was 83.7% (SD 14.5, p < 0.0001). The same was seen in a lateral position, 82.2% (SD 16.4, p < 0.0001). Testing for changes in properties of the internal thermistors revealed no significant difference between the reduction in flow when the test started and after the patients had slept the whole night (p > 0.1). It is possible to differentiate between nasal and oral breathing using internal thermistors.

Advantages of measuring air flow in the pharynx with internal thermistors.

The measurement of air flow in patients suffering from breathing disturbances during sleep is usually accomplished by an oro-nasal thermistor located at the upper lip. The detection of hypopneas using this system may be difficult because the external thermistor may be unable to differentiate between high and low air flow rates. To improve the diagnosis of hypopneas we introduced a new method using internal thermistors contained in the same tube and using the same sensors as when recording pressures in the upper airways for localization of obstructions and measuring the respiratory work. The internal thermistors/pressure transducers (Camtip) were contained in a silicone tube that had a 1.9-mm external diameter. Standard polysomnography was performed, and internal flow and estimated volume were included in the polysomnographic setup. Ten consecutive hypopneas were studied in six patients having sleep-related breathing disorders. Preliminary results indicate that this method of monitoring air flow is more sensitive to minor changes in air flow than the external thermistor. It also simplifies the detection of hypopneas. Our findings shows that measuring air flow by internal thermistors is better than that of external devices to monitor tidal air flow. The internal sensors also facilitate the diagnosis of hypopneas in patients with sleep-related breathing disorders. Determinations of temperature changes and airway pressure in the pharynx can also be performed by the same sensors. Hence, no additional equipment is necessary for flow tracings when pressure recordings are used in the PSG setup.

Does the oral device Noiselezz prevent sleep apnoea?

Both snoring and apnoea are caused by the collapse of soft tissue in the upper airways during sleep. Increasing the cross-sectional area of the airways in these segments by moving the mandible and/or the tongue forward stabilizes the upper airways in obstructive sleep apnoea syndrome (OSAS) patients. The aim of this study was to determine the effect of Noiselezz, which is an oral appliance of the mandibular advancing type, designed for easy use. Twenty-one patients, all men (aged 50.6 +/- 10.4, body mass index 26.5 +/- 3.3) were included in the study. Polysomnography (PSG) was performed before the patients started using Noiselezz. After a period of 2 weeks accustomizing to the oral device, the patients had another PSG performed with Noiselezz inserted. We found no significant differences in total sleep time, percentage of time spent snoring, duration of rapid eye movement (REM) sleep, slow-wave sleep, inter-sleep wake and sleep efficiency, apnoea/hypopnoea index (AHI) or lowest measured oxygen saturation after apnoea (minSaO2). No significant differences were found in the localization of obstructions or intrathoracal inspiratory pressure with and without the use of the Noiselezz oral device. Three patients (14%) reported satisfaction with treatment by the oral device. All three continued to use Noiselezz as treatment. The rest of the patients (86%) either did not tolerate the device at all or tried it for a period and then requested alternative treatment (n = 12). Most patients found the oral device "Noiselezz" inconvenient to use, and our results show that the device has little or no effect on snoring and sleep apnoea.

Continuous pressure measurements in the evaluation of patients for laser assisted uvulopalatoplasty.

The aim of the present study was to evaluate the effect of laser-assisted uvulopalatoplasty (LUPP) performed under local anesthesia in an outpatient setting. No procedure included tonsillectomy. Obstruction related mainly to the velopharyngeal segment of the airway was defined in 16 consecutive patients by clinical examination, nocturnal polysomnography and pressure measurements. The mean follow-up period was 7 months, range 3-16 months. Using five pressure sensors, four separate upper airway segments could be defined. The preoperative location of obstructive segments in obstructive apneas was proximal and was identified in the velopharyngeal segments in 90% of the patients. This was the case in 92% of the patients with hypopneas. After LUPP, there were statistically significant improvements in the duration of respiratory events (P < 0.02), incidence of sleep with snoring (P < 0.001), apnea-hypopnea index (P < 0.01), microarousal index (P < 0.02) and the mean duration of non-rapid eye movement sleep with oxygen saturation < 80% (P < 0.0001). Four patients still had proximal obstructions after LUPP, but these were clinically tolerable.

Adverse effects of nicotine and interleukin-1beta on autoresuscitation after apnea in piglets: implications for sudden infant death syndrome.

OBJECTIVES: Maternal cigarette smoking is established as a major dose-dependent risk factor for sudden infant death syndrome (SIDS). Both prenatal and postnatal exposures to constituents of tobacco smoke are associated with SIDS, but no mechanism of death attributable to nicotine has been found. Breastfeeding gives a substantial increase in absorbed nicotine compared with only environmental tobacco smoke when the mother smokes, because the milk:plasma concentration ratio of nicotine is 2.9 in smoking mothers. Furthermore, many SIDS victims have a slight infection and a triggered immune system before their death, thus experiencing a release of cytokines like interleukin-1beta (IL-1beta) that may depress respiration. Because apneas in infancy are associated with SIDS, we have tested the hypothesis that postnatal exposure to tobacco constituents and infections might adversely affect an infant's ability to cope with an apneic episode. This is performed by investigating the acute effects of nicotine and IL-1beta on apnea by laryngeal reflex stimulation and on the subsequent autoresuscitation. DESIGN: Thirty 1-week-old piglets (+/-1 day) were sedated with azaperone. A tracheal and an arterial catheter were inserted during a short halothane anesthesia. The piglets were allowed a 30-minute stabilization period before baseline values were recorded and they were randomized to 4 pretreatment groups (avoiding siblings in the same group): 1) immediate infusion of 10 pmol IL-1beta intravenously/kg (IL-1beta group; n = 8); 2) slow infusion of 5 microg nicotine intravenously/kg 5 minutes later (NIC group; n = 8); 3) both IL-1beta and NIC combined (NIC + IL-1beta group; n = 6); or 4) placebo by infusion of 1 ml .9% NaCl (CTR group; n = 8). Fifteen minutes later, apnea was induced by insufflation of .1 ml of acidified saline (pH = 2) in the subglottic space 5 times with 5-minute intervals, and variables of respiration, heart rate, blood pressure, and blood gases were recorded. RESULTS: Stimulation of the laryngeal chemoreflex by insufflation of acidified saline in the subglottic space produced apneas, primarily of central origin. This was followed by a decrease in heart rate, a fall in blood pressure, swallowing, occasional coughs, and finally autoresuscitation with gasping followed by rapid increase in heart rate, rise in blood pressure, and (in the CTR group) an increase of respiratory rate. Piglets pretreated with nicotine had more spontaneous apneas, and repeated spontaneous apneas caused an inability to perform a compensatory increase of the respiratory rate after induced apnea. This resulted in a lower SaO(2) than did CTR at 2 minutes after apnea (data shown as median [interquartile range]: 91% [91-94] vs 97% [94-98]). The pretreatment with IL-1beta caused prolonged apneas in piglets and an inability to hyperventilate causing a postapneic respiratory rate similar to the NIC. When nicotine and IL-1beta were combined, additive adverse effects on respiratory control and autoresuscitation compared with CTR were observed: NIC + IL-1beta had significantly more spontaneous apneas the last 5 minutes before induction of apnea (2 [.3-3] vs 0 [0-0]). Apneas were prolonged (46 seconds [39-51] vs 26 seconds [22-31]) and followed by far more spontaneous apneas the following 5 minutes (6.6 [4.0-7.9] vs.5 [.2- .9]). Instead of normal hyperventilation after apnea, a dramatic decrease in respiratory rate was seen (at 20 seconds: -45% [-28 to -53] vs +29% [+24-+50], and at 60 seconds: -27% [-23 to -32] vs +3% [-2-+6), leading to SaO(2) below 90% 3 minutes after end of apnea: 89% (87-93) versus 97% (95-98). These prolonged adverse effects on ventilation were reflected in lowered PaO(2), elevated PaCO(2) and lowered pH 2 minutes, and even 5 minutes, after induction of apnea. CONCLUSIONS: Nicotine interferes with normal autoresuscitation after apnea when given in doses within the range of what the child of a smoking mother could receive through environmental t