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• W2150058101 abstract "Free AccessCPAPPredictors of Response to a Nasal Expiratory Resistor Device and Its Potential Mechanisms of Action for Treatment of Obstructive Sleep Apnea Amit V. Patel, M.D., Dennis Hwang, M.D., Maria J. Masdeu, M.D., Guo-Ming Chen, David M. Rapoport, M.D., Indu Ayappa, Ph.D. Amit V. Patel, M.D. Division of Pulmonary, Critical Care and Sleep Medicine, NYU School of Medicine, New York, NY Search for more papers by this author , Dennis Hwang, M.D. Division of Pulmonary, Critical Care and Sleep Medicine, NYU School of Medicine, New York, NY Search for more papers by this author , Maria J. Masdeu, M.D. Pulmonary Department, Corporacio Park Tauli, Universitat Autonoma Barcelona, Sabadell, Spain Search for more papers by this author , Guo-Ming Chen Division of Pulmonary, Critical Care and Sleep Medicine, NYU School of Medicine, New York, NY Search for more papers by this author , David M. Rapoport, M.D. Division of Pulmonary, Critical Care and Sleep Medicine, NYU School of Medicine, New York, NY Search for more papers by this author , Indu Ayappa, Ph.D. Address correspondence to: Indu Ayappa, Ph.D., Division of Pulmonary, Critical Care and Sleep Medicine, NYU School of Medicine, 462 First Avenue, Room 7N-3, New York, NY 10016; (212) 263-8437(212) 263-7445 E-mail Address: [email protected] Division of Pulmonary, Critical Care and Sleep Medicine, NYU School of Medicine, New York, NY Search for more papers by this author Published Online:February 15, 2011https://doi.org/10.5664/jcsm.28036Cited by:36SectionsAbstractPDF ShareShare onFacebookTwitterLinkedInRedditEmail ToolsAdd to favoritesDownload CitationsTrack Citations AboutABSTRACTStudy Objective:A one-way nasal resistor has recently been shown to reduce sleep disordered breathing (SDB) in a subset of patients with Obstructive Sleep Apnea Hypopnea Syndrome (OSAHS). The purpose of this study was to examine characteristics predictive of therapeutic response to the device and provide pilot data as to its potential mechanisms of action.Patients, Interventions, and Measurements:20 subjects (15M/5F, age 54 ± 12 years, BMI 33.5 ± 5.6 kg/m2) with OSAHS underwent 3 nocturnal polysomnograms (NPSG) including diagnostic, therapeutic (with a Provent® nasal valve device), and CPAP. Additional measurements included intranasal pressures and PCO2, closing pressures (Pcrit), and awake lung volumes in different body positions.Results:In 19/20 patients who slept with the device, RDI was significantly reduced with the nasal valve device compared to the diagnostic NPSG (27 ± 29/h vs 49 ± 28/h), with 50% of patients having an acceptable therapeutic response. Among demographic, lung volume, or diagnostic NPSG measures or markers of collapsibility, no significant predictors of therapeutic response were found. There was a suggestion that patients with position-dependent SDB (supine RDI > lateral RDI) were more likely to have an acceptable therapeutic response to the device. Successful elimination of SDB was associated with generation and maintenance of an elevated end expiratory pressure. No single definitive mechanism of action was elucidated.Conclusions:The present study shows that the nasal valve device can alter SDB across the full spectrum of SDB severity. There was a suggestion that subjects with positional or milder SDB in the lateral position were those most likely to respond.Citation:Patel AV; Hwang D; Masdeu MJ; Chen GM; Rapoport DM; Ayappa I. Predictors of response to a nasal expiratory resistor device and its potential mechanisms of action for treatment of obstructive sleep apnea. J Clin Sleep Med 2011;7(1):13-22.INTRODUCTIONProvent® Sleep Apnea Therapy (Ventus Medical, Belmont, CA) is a novel and easy to use device based on a nasal valve that produces expiratory resistance. This device has recently become available for treatment of obstructive sleep apnea/hypopnea syndrome (OSAHS). In 2 recent studies evaluating the effectiveness of the nasal valve device, half of the subjects with known OSAHS of varying severity demonstrated an 80% reduction in the Apnea Hypopnea Index (AHI) while using the device.1,2 As the effect of the device on AHI was independent of the severity of the sleep disordered breathing (SDB), obesity, and other demographic factors, it has been difficult to define which patient population will respond favorably to the nasal valve device. In addition, the mechanism of action of the device still remains undefined.1,2A commentary on this article appears in this issue on page 23.The nasal valve device consists of a small valve attached externally to each nostril with adhesive tape. The valve acts as a one-way resistor, producing expiratory resistance while leaving inspiration unaffected. It differs fundamentally from the current standard pressure treatment for obstructive sleep disordered breathing, nasal continuous positive airway pressure (CPAP), in that it provides no positive pressure to the airway during inspiration. Mahadevia, et al.3 showed in 1983 that the application of expiratory positive airway pressure (EPAP) via a threshold valve reduced frequency and duration of apneas in patients with OSAHS, but other studies, as well as clinical experience, did not confirm Mahadevia's findings. In 2008, Heinzer et al.4 showed no significant change in SDB by application of EPAP of 10 cm H2O. Despite this, the recently published studies1,2with successful outcomes using the nasal valve device suggest that this type of therapy needs to be reevaluated.BRIEF SUMMARYCurrent Knowledge/Study Rationale: Current data suggest that up to 50% of patients with OSAHS may respond to nEPAP applied with a one-way nasal resistor device. The purpose of the present study was to confirm these data, identify the patient population for whom nEPAP therapy may be beneficial and the relative role of possible mechanisms of action.Study Impact: Our data confirmed that 50% of patients with OSAHS had a therapeutically acceptable response with no clear factors identified that predicted response. Establishment and maintenance of an expiratory positive pressure was closely associated with acceptable therapeutic response, suggesting a role for mechanical factors including increased tracheal traction, but upper airway effects and stimulation by retained CO2 as contributing mechanisms could not be ruled out.As pointed out in a recent editorial by White,5 there are several possible mechanisms of action for EPAP: (1) dilatation of the upper airway by the pressure generated during expiration, with carryover of this dilatation into inspiration, (2) mild hypercapnia resulting from hypoventilation induced by the expiratory resistance of nasal expiratory positive pressure (nEPAP), resulting in increased respiratory drive to the upper airway, (3) induction of lung hyperinflation by the elevated end-expiratory pressure, resulting in reduced upper airway collapsibility due to the increased tracheal traction.6,7A therapeutic effect of the nasal valve device on SDB has been demonstrated in only a subset of patients.1,2 It is therefore desirable to define patient characteristics predictive of therapeutic response. Predictive characteristics may relate to patient demographics, severity of SDB, anatomic factors determining the degree of airway collapsibility, and/or the potential mechanisms of action of the device. As the degree of airway collapsibility has been shown to be influenced by lung volume acting through tracheal traction,6,7 we were interested in both static lung volumes and positional changes in lung volume as potential predictive characteristics of the nasal valve device responsiveness.The purpose of the present study was to (1) confirm efficacy of nEPAP therapy using the nasal valve device, (2) attempt to identify the patient population for whom nEPAP therapy may be appropriate, and (3) examine the relative role of the several possible mechanisms of action of the nasal valve device.METHODS AND MATERIALSSubject SelectionTwenty subjects (15M/5F, age 54.3 ± 12.0 years, BMI 33.5 ± 5.6 kg/m2) with clinical OSAHS defined by Apnea plus Hypopnea with 4% desaturation Index (AHI4%) > 5/hr on full overnight polysomnography were recruited for the present study from subjects seen at the New York University Sleep Disorders Center. Subjects were excluded if they were unable to breathe through the nose because of significant nasal congestion/obstruction, or if they had congestive heart failure, central sleep apnea, or neuromuscular diseases associated with weakness. Patients with known alveolar hypoventilation or with elevated arterial PCO2, elevated serum bicarbonate, or unexplained periods of sustained desaturation on polysomnogram were excluded.All subjects underwent or had recently undergone full-night diagnostic PSG for diagnosis. On 2 separate nights, therapy was applied. On one of the therapeutic nights (full-night study), patients wore the nasal valve device (Provent®, Ventus Medical, Belmont, CA). On a separate full night, patients wore CPAP which was titrated; during this night the CPAP circuit was used to also measure the critical closing pressure (Pcrit) (see below). The order of these therapeutic nights (but not the diagnostic night) was randomized. Patients also underwent daytime assessment of sitting, supine, and lateral awake lung volumes. All testing except for the diagnostic PSG was completed within 3 months, and the diagnostic PSG was always performed within one year prior to enrollment.Diagnostic Polysomnography ProcedureThe in-laboratory PSG was performed according to standard clinical guidelines and included frontal, central, and occipital electroencephalogram, electrooculogram, submental electromyogram to monitor sleep; an anterior tibialis electromyogram to monitor leg movements; a unipolar electrocardiogram for cardiac monitoring; pulse oximeter for oxygen saturation; piezoelectric strain gauges for chest and abdominal movements; and a multiposition switch for determining sleep position. A nasal cannula pressure transducer system (Protech PTAF2, Woodinville WA) was used to measure airflow, and an oral thermistor was used to detect mouth breathing.Therapeutic (Nasal Valve Device) Polysomnography ProcedureThis in-laboratory PSG was performed on a separate night and was identical to the diagnostic NPSG except for respiratory monitoring. Nasal flow was recorded with a pneumotachograph (Hans Rudolph Inc, Kansas City MO) attached to an unpressurized nasal mask placed over the nasal valve device. The static volume of the nasal mask and pneumotachograph system was < 110 cc, which was within the range reported in other studies of sleep ventilation.8 Preliminary testing in patients not wearing the nasal valve device showed that monitoring of nasal flow with this unpressurized mask produced a signal essentially identical to the signal from a nasal cannula.During this night of testing, the patients wore the nasal valve device (80 cm H2O*sec/L), which consists of 2 separate adhesive valves designed to produce nEPAP, on each nostril. These had been modified by Ventus Medical, Inc. to allow for attachment of a small catheter that gave access to the intranasal cavity behind the valve for intranasal pressure monitoring (one naris) and end-tidal CO2 (recorded from the other naris). This intranasal pressure tracing was not used to record airflow. Figure 1 shows the airflow and pressure tracings recorded during the NPSG with the nasal valve device in place, demonstrating increased pressure during expiration with no pressure during inspiration.Figure 1 15-second window showing airflow and pressure tracings recorded during the NPSG with the nasal valve device in place, demonstrating increased pressure during expiration with no pressure during inspirationDownload FigureAnalysis of Expiratory PressureFor each patient, pressure data from the intra-nasal cavity were analyzed across the night and tabulated during at least 3 periods of NREM sleep in the supine and lateral positions when there was no evidence of SDB (wherever this was possible). The intranasal pressure at end expiration was identified for each breath and averaged over 3 consecutive breaths to define each measurement. We tabulated the range of intranasal pressures throughout the whole night that was associated with absence of SDB ≥ 5 min during sleep. To address the relationship of therapy to pressure, a further analysis was performed restricting the dataset to time spent in supine stage N2 sleep. Within this restricted set, we analyzed the time spent above and below the lowest effective nEPAP pressure (LEP_N2) after LEP_N2 was defined as the lowest pressure during supine N2 sleep that was effective at eliminating SDB for at least 5 min.Analysis of End-Tidal CO2 SignalPCO2 values were obtained across the night during the awake periods of nasal breathing, as well as during ≥ 3 periods of NREM sleep in the supine and lateral positions during both effective and ineffective intranasal pressures. The values of intranasal end tidal CO2 as reported are the average of values obtained from 3 consecutive breaths.Diagnostic and Therapeutic (nEPAP) PSG scoring:For the PSG data, sleep, arousals and periodic legs movements were scored by American Academy of Sleep Medicine (AASM) standards.9 Respiratory events were scored manually as follows: Apneas were identified when the airflow amplitude on the nasal cannula was < 10% of baseline and no flow occurred on the oral thermistor. Hypopneas 4% were identified when airflow amplitude was reduced by 30% from baseline and the event was followed by 4% O2 desaturation. AHI4% was defined as the sum of apneas and hypopneas4% divided by total sleep time. In order to identify subtle obstructive events, we also performed a calculation of the respiratory disturbance index (RDI) which included both the AHI and additional events when airflow amplitude was < 50% but without 4% oxygen desaturation or, alternatively, whenever a discernable change occurred in the airflow amplitude (50%-80% of baseline) and the event was followed by 4% O2 desaturation within 30 sec or an EEG arousal within 5 sec, as suggested by recent criteria of the AASM.9Passive Pcrit ProcedureThe in-laboratory PSG on nasal CPAP was performed as per standard clinical guidelines. Flow was recorded via a pneumotachograph (Hans Rudolph Inc, Kansas City, MO) attached between the nasal mask and CPAP tubing. Measurements were performed during stage N2 sleep in the supine position and with the head elevated on one pillow. Two modified CPAP machines (Fisher and Paykel SleepStyle 2000, Auckland, New Zealand) were used to deliver pressures from +20 cm H2O to −20 cm H2O. Pressure at the mask (Pn) was measured continuously. CPAP was titrated manually during the first hour of the study to a level which eliminated all sleep disordered breathing events, including obstructive apneas, hypopneas, and runs of flow limitation. The optimal pressure was defined as the pressure at which flow limitation disappeared and was used as the “holding pressure” for subsequent passive Pcrit maneuvers. For each measurement, Pn was abruptly decreased from the holding pressure to a predetermined pressure for 6 breaths before being returned back to holding pressure. Measurements were separated by ≥ 1 min before repeating a pressure drop. The maximum flow (VImax) for the last 3 breaths (#4-6) during the pressure drop was assessed and used in determining the passive Pcrit. During successive maneuvers Pn was progressively lowered until an apnea was produced (VImax = zero). The Pn where the VImax went to zero from a positive flow was termed the passive critical pressure (Pcrit). The Pcrit was reassessed for reproducibility on ≥ 2 occasions in supine N2 sleep in each patient. In the 4 cases where zero flow (apnea) could not be reached without producing an arousal, the Pcrit was extrapolated as per the criteria described by Patil et al.10 If an EEG arousal or awakening occurred during a pressure drop, then that measurement was not included in the analysis. At least 2 minutes of stable stage N2 sleep was required prior to proceeding with further measuremenLung VolumesStandard spirometry and body plethysmography (Sensormedics, Yorba Linda, CA) were performed during the daytime in the sitting position to determine Forced Expiratory Volume in 1 second (FEV1), Forced Vital Capacity (FVC), Functional Residual Capacity (FRC), Expiratory Reserve Volume (ERV), and Total Lung capacity (TLC) in each subject. Lung volumes were measured within 8 weeks of the PSG study with nEPAP. At the same setting, and while awake, FRC was determined by Nitrogen (N2) washout in the sitting position. Lung volume data was excluded if either the patient's FEV1/FVC ratio on spirometry was < 70%, or if the difference between N2 washout and plethysmography lung volumes was > 750 cc. N2 washout FRC measurements were repeated in the supine and right-lateral positions in random order.Statistical AnalysisMeasures of sleep disordered breathing between baseline and on the nasal valve were compared using paired t-tests.For purposes of evaluating potential predictors of therapeutic response to the nasal valve device in a given patient, we compared anthropomorphic and sleep variables between subjects with both > 50% reduction in RDI and RDI < 20/h on therapy with those that met neither condition. The value of RDI = 20/h was chosen based on previous data showing that this is the upper limit of normal in asymptomatic individuals.11The protocol was approved by the IRB of the NYU School of Medicine; all patients provided informed consent.RESULTSDuring the diagnostic NPSG (n = 20), mean AHI4% was 34 ± 30/h overall, and mean RDI (AHI4% plus RERAs) was 49 ± 28/h. RDI supine was 58 ± 31/h, and RDI lateral was 39 ± 30/h. Table 1 shows the individual patient data from the diagnostic night and the response to the nasal valve device on the night that it was used. One patient was unable to sleep with the device in place and is excluded from Table 1. In the 19 subjects who tolerated the use of the nasal valve device during sleep, the overall mean AHI4% was lowered to 19.9 ± 26/h (p < 0.05), and RDI was lowered to 27 ± 29/h (p < 0.0001). However, there was wide variability between patients in the therapeutic efficacy: in 10 patients we considered the reduction in RDI therapeutically acceptable because it met usual clinical criteria with both > 50% reduction in RDI from the diagnostic studies and an absolute RDI < 20/h, which is the upper limit of normal we use for respiratory scoring in our laboratory. In these 10 patients, the mean AHI4% was reduced from 26.5 ± 26 events/h on the diagnostic study to 6 ± 6 events/h while using the nasal EPAP device. From the group of patients who did not meet both criteria for therapeutically acceptable response (RDI < 20/h and > 50% reduction), we identified 4 additional patients as “partial responders”—those having a substantial drop (> 40%) in RDI. The remaining 5 patients were labeled “non-responders.” In the therapeutically acceptable responders, the reduction in RDI was not caused by a decrease in the time spent in the supine position (percent time spent supine 71% ± 22% on the diagnostic study and 76% ± 25% on the study using the nasal valve device); furthermore, in all 3 therapeutic response groups, the RDI supine showed the same therapeutic pattern of improvement as the overall RDI (Table 1). In the therapeutically acceptable response group, 3 of the 10 subjects had persistent severe SDB during REM sleep. One patient did not have REM sleep while on the nasal valve device, but had a baseline REM RDI of only 6/h on the diagnostic night. The remaining 6 subjects all had significant improvement in REM as well as overall sleep. There was no significant change in weight between the time of the diagnostic NPSG and NPSG with the nasal valve device in the responders (−0.2 ± 1.4 kg), the non-responders (1 ± 2.4 kg), or overall (−0.75 ± 0.3 kg).Table 1 Measures of SDB overall, in supine position, and REM sleep at baseline and on the nasal valve deviceTable 1 Measures of SDB overall, in supine position, and REM sleep at baseline and on the nasal valve deviceDespite their improvement in SDB events, the 10 patients with therapeutically acceptable results did not show statistically significant improvement in their sleep variables with the nasal valve device compared to the diagnostic sleep study. However, in these patients a trend towards improvement was seen for all sleep variables: sleep efficiency (diagnostic: 72% ± 14% vs therapeutic: 78% ± 14%), percent time N1 (diagnostic: 26 ± 13 vs therapeutic: 23 ± 8), percent time REM (diagnostic:11 ± 5 vs therapeutic: 13 ± 5), percent delta sleep (diagnostic: 8 ± 11 vs therapeutic: 11 ± 8 ) or arousal index (diagnostic: 32 ± 15.1/h vs therapeutic: 25 ± 12/h). Of note, all patients were either on their first night of using the nasal valve device or had only used it for < 3 nights prior to their NPSG with the device.Predictors of Therapeutic Response to the Nasal Valve DeviceExamination of potential predictors of therapeutic response showed that the group with a therapeutically acceptable response and the group with no response did not differ with respect to age, BMI, baseline SDB severity based on RDI, passive Pcrit, or prescribed CPAP level. Table 2 summarizes data grouped by class of therapeutic response to the nasal valve device and shows that therapeutic response could also not be predicted by intranasal pressure required to eliminate SDB, CO2 levels (awake or asleep with the valves in place), or ratio of REM to NREM RDI at baseline. However, there was a trend for the ratio of supine to lateral RDI at baseline to be higher in the group with therapeutically acceptable response compared to non-responders (2.8 ± 2.3 vs 1.2 ± 0.2), though this did not reach statistical significance. The lateral RDI at baseline (25.6 ± 19.4/h vs 59.8 ± 43.9/h, P = NS) and the ratio of apneas to hypopneas in the lateral position at baseline (0.25 vs 1.3, P = NS) also tended to be lower in the responders, again suggesting that positional variability of RDI may be predictive of the response to nEPAP (Figure 2).Table 2 Potential predictors of therapeutic responseTable 2 Potential predictors of therapeutic response*No effective pressure generated.&Therapeutic CPAP value obtain on prior full night CPAP titration.#Range of effective end expiratory pressures measured intranasallyFigure 2 When comparing the group with therapeutically acceptable response to the non-responders, the lateral RDI at baseline tended to be lower (6 ± 19.4/h vs 59.8 ± 43.9/h, p = NS), while the ratio of supine to lateral RDI at baseline tended to be higher (2.8 ± 2.3 vs 1.2 ± 0.2), suggesting that positional variability of RDI may be predictive of the response to NEPAPDownload FigureAs expected, with the device in place there was a change in the pattern of flow during expiration: (1) there was elimination of the pause at end-expiration that is usually seen during normal spontaneous breathing; (2) there was a prolongation of the expiratory phase when compared to breathing during sleep without the device in place.Relationship of awake lung volumes to therapeutic response of the nasal valve deviceFigure 3 shows awake lung volumes (FRC) obtained without the device; data shown are the FRC in the sitting, supine, and lateral positions. In Figure 3, subjects are grouped by response to the nasal valve device (therapeutic, partial, and no response). Sitting FRC values ranged from 46% to 107% predicted but did not differ between groups. FRC dropped by 18%-23% from sitting to supine and increased by 12%-16% from supine to lateral position, but there were no differences between the groups.Figure 3 Awake lung volumes (FRC) obtained without nEPAP; data shown are the FRC in sitting supine and lateral positionsIn this figure subjects are grouped by response to the nasal valve device (therapeutic, partial, and no response).Download FigureEnd-Expiratory Pressure and Therapeutic ResponseFifteen of the 19 subjects who tolerated the nasal valve device had periods ≥ 5 min during which SDB was abolished and during which there was consolidated sleep, allowing us to evaluate the relationship of end-expiratory pressure and therapeutic response. Within each patient, end-expiratory pressure varied widely (as much as from 5–23 cm H2O) across the night, particularly in different positions and sleep stages. However, as the pressure at each moment was set by the patient/valve interaction and not titratable, it was not possible to test whether there was a single consistent minimal pressure needed for therapy.Table 3 shows the data during N2 supine sleep only. During those times when the pressure achieved was above LEP_N2 (the lowest pressure shown to be at least transiently effective), RDI fell to near zero; during those times when pressure achieved was below LEP_N2, the RDI remained elevated. This suggests, but does not prove, that this pressure would have been effective throughout all supine N2 sleep had it been constrained. Furthermore, the patients with therapeutically acceptable response spent a greater proportion of sleep above LEP_N2 compared to the partial responders (72.7% ± 21% vs 43.8% ± 16%, respectively). One subject demonstrated an LEP_N2 of zero during some periods of the night despite obvious SDB during other portions of the night when no intranasal pressure was generated during N2 sleep in the supine position. We suspect that this is similar to what is seen during diagnostic studies in patients with OSAHS where there are periods seen without SDB.Table 3 RDI during periods above and below the LEP during supine N2 sleep in therapeutically acceptable and partial respondersTable 3 RDI during periods above and below the LEP during supine N2 sleep in therapeutically acceptable and partial responders*LEP_N2 = the lowest pressure during supine N2 sleep that was effective at eliminating SDB for at least 5 minBased on the above analysis suggesting that within each patient a lowest effective pressure existed for each condition (e.g., position and sleep state), we obtained the one value (LEP_overall) that would have been effective over all positions and sleep states in that patient. Since this represents an algorithm similar to that used in titration of CPAP, we examined the relationship for each patient of the LEP_overall and the separately titrated clinically prescribed CPAP. Figure 4 demonstrates that there was a trend towards higher CPAP in patients with higher LEP_overall, but this did not reach statistical significance. (r = 0.49, p = 0.07).Figure 4 Lowest effective expiratory pressure (LEP) which was sufficient in ameliorating SDB throughout the entire night against therapeutic CPAPEach point represents data from one subject.Download FigureFailure to Generate/Maintain Therapeutic PressurePeriods during which there was therapeutic failure of the nasal valve device (recurrence of SDB) were closely related to (i) the inability to build up end-expiratory pressure as breathing shifted from mouth to nose (at sleep onset), or (ii) loss of previously established therapeutic pressure, which generally related to onset of a mouth leak and occurred predominantly after transient arousals. Examples of these patterns are shown in Figures 5 and 6.Figure 5 Two-min periods during sleep with the nasal valve device in one patientFigure 5A shows maintenance of 17 cm H2O of end-expiratory pressure without evidence of sleep disordered breathing. Figure 5B shows evidence of sleep disordered breathing events during a period of lower end expiratory pressures.Download FigureFigure 6 Repeat episodes of mouth breathing (arrowhead▲) resulting in immediate loss of intranasal pressure (arrow↓)Mouth closure results in reestablishment of therapeutic intranasal pressures.Download FigureOf the 19 patients who tolerated the nasal valve device, 4 had no periods where SDB was abolished (therapeutic non-responders). In 1 of these 4 patients, the intranasal pressure remained near 0 cm H2O during the entire study, presumably due to persistent mouth breathing. In the other 3 patients, the maximal nasal pressures achieved were 4, 7, and 13 cm H2O, but did not result in reduction of SDB.In a fifth patient with overall non-therapeutic response to the nasal valve device, we noted only transient benefit, despite what appeared to be an “effective” pressure of 8 cm H2O. In this patient, pressure rose intermittently to a much higher value than the apparently effective pressure of 8 cm H2O (up to 20 cm H2O), and many arousals occurred that were not typical of obstructive respiratory events (see Figure 7). It is possible that these events may have been due to high intranasal pressures causing arousal; and this is supported by the observation that the expiratory pressure was highest just prior to the arousal.Figure 7 Period of regular arousals which appear to be related to rapid increases in intranasal pressure (up to 22 cm H2O) without evidence of sleep disordered breathingPatient with therapeutic nEPAP pressure of 8 cm H2O elsewhere during the study.Download FigureDISCUSSIONThis study shows that use of the nasal valve device produced improvement in SDB in 75% of patients with OSAHS across wide range of SDB severity, with 50% of patients reaching a clinically significant reduction in RDI. While this confirms previous small studies showing that in some patients the device is effective, we could not demonstrate associations between therapeutic success/failure of the nasal valve device and demographics, baseline severity of SDB, pattern of SDB related to sleep stage (e.g., REM dependence), therapeutic CPAP level, passive Pcrit, or awake lung volumes. Thus these appear NOT to be the predictors that will help select patients for therapy with this device. Our data do, however, suggest that" @default.
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• W2150058101 title "Predictors of Response to a Nasal Expiratory Resistor Device and Its Potential Mechanisms of Action for Treatment of Obstructive Sleep Apnea" @default.
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