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Original Research: SLEEP MEDICINE |

Outcomes of Home-Based Diagnosis and Treatment of Obstructive Sleep Apnea FREE TO VIEW

Robert P. Skomro, MD, FCCP; John Gjevre, MD, FCCP; John Reid, MD, FCCP; Brian McNab, MD, FCCP; Sunita Ghosh, PhD; Maryla Stiles, DVM; Ruzica Jokic, MD; Heather Ward, MD, FCCP; David Cotton, MD, FCCP
Author and Funding Information

From the Department of Medicine (Drs Skomro, Gjevre, Reid, Stiles, Ward, and Cotton), and the Department of Community Health and Epidemiology (Dr Ghosh), The University of Saskatchewan, Saskatoon, SK; the Department of Medicine (Dr McNab), University of Alberta, Edmonton, AB; and the Department of Psychiatry (Dr Jokic), Queens University, Kingston, ON, Canada.

Correspondence to: Robert P. Skomro, MD, FCCP, Room 563 Ellis Hall, Division of Respiratory Critical Care and Sleep Medicine, Royal University Hospital, Saskatoon, SK, S7N 0W8, Canada; e-mail: r.skomro@usask.ca


For editorial comment see page 245

Funding/Support: The financial support for this study was provided by the Kelsey Trail Health Region, the Lung Association of Saskatchewan, and Saskatoon Health Region.

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (http://www.chestpubs.org/site/misc/reprints.xhtml).


© 2010 American College of Chest Physicians


Chest. 2010;138(2):257-263. doi:10.1378/chest.09-0577
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Background:  Home diagnosis and therapy for obstructive sleep apnea (OSA) may improve access to testing and continuous positive airway pressure (CPAP) treatment. We compared subjective sleepiness, sleep quality, quality of life, BP, and CPAP adherence after 4 weeks of CPAP therapy in subjects in whom OSA was diagnosed and treated at home and in those evaluated in the sleep laboratory.

Methods:  A randomized trial was performed consisting of home-based level 3 testing followed by 1 week of auto-CPAP and fixed-pressure CPAP based on the 95% pressure derived from the auto-CPAP device, and in-laboratory polysomnography (PSG) (using mostly split-night protocol) with CPAP titration; 102 subjects were randomized (age, 47.4 ± 11.4 years; 63 men; BMI, 32.3 ± 6.3 kg/m2; Epworth Sleepiness Scale [ESS]: 12.5 ± 4.3). The outcome measures were daytime sleepiness (ESS), sleep quality (Pittsburgh Sleep Quality Index [PSQI]), quality of life (Calgary Sleep Apnea Quality of Life Index [SAQLI], 36-Item Short-Form Health Survey [SF-36], BP, and CPAP adherence after 4 weeks.

Results:  After 4 weeks of CPAP therapy, there were no significant differences in ESS (PSG 6.4 ± 3.8 vs home monitoring [HM] 6.5 ± 3.8, P = .71), PSQI (PSG 5.4 ± 3.1 vs HM 6.2 ± 3.4, P = .30), SAQLI (PSG 4.5 ± 1.1 vs HM 4.6 ± 1.1, P = .85), SF-36 vitality (PSG 62.2 ± 23.3 vs HM 64.1 ± 18.4, P = .79), SF-36 HM (PSG 84.0 ± 10.4 vs HM 81.3 ± 14.9, P = .39), and BP (PSG 129/84 ± 11/0 vs HM 125/81 ± 13/9, P = .121). There was no difference in CPAP adherence (PSG 5.6 ± 1.7 h/night vs HM 5.4 ± 1.0 h/night, P = .49).

Conclusions:  Compared with the home-based protocol, diagnosis and treatment of OSA in the sleep laboratory does not lead to superior 4-week outcomes in sleepiness scores, sleep quality, quality of life, BP, and CPAP adherence.

Trial registration:  clinicaltrials.gov; Identifier: NCT00139022

Figures in this Article

Obstructive sleep apnea (OSA) is a common condition resulting from intermittent narrowing or obstruction of the upper airway during sleep resulting in poor sleep quality, daytime somnolence, decreased quality of life, and risk of cardiovascular disease and motor vehicle crashes. Current guidelines recommend overnight polysomnography (PSG) for the diagnosis of OSA, but access to PSG in many countries is limited.1-4 Home-based diagnosis and therapy for OSA may provide an alternative to in-laboratory PSG and improve access to OSA diagnosis, but the evidence supporting this strategy is very limited and the practice is not supported by current guidelines.5,6

The objective of this investigation was to compare a home-based diagnostic and therapeutic strategy for OSA with the current standard of practice, in-laboratory PSG. We hypothesized that the outcomes of in-laboratory diagnosis and treatment of OSA would be superior to home-based diagnosis and treatment.

Subjects

Adult outpatients with suspected OSA referred to the participating sleep medicine physicians (R. P. S., J. R., B. M.) at a tertiary outpatient sleep disorders clinic were eligible to take part in the study. The inclusion criteria were: age > 18 years, symptoms of OSA (at least two of the following: excessive daytime somnolence (Epworth Sleepiness Scale [ESS] > 10), witnessed apneas, snoring), and residence within a 1-h drive from the study center. Exclusion criteria were: respiratory or heart failure, clinical features of another sleep disorder, safety-sensitive occupation, use of hypnotics, upper airway surgery, CPAP or oxygen therapy, pregnancy, and inability to provide informed consent. The study was approved by the University of Saskatchewan Biomedical Ethics Review Board. All subjects provided a written informed consent prior to enrollment in the protocol. The study was registered at clinicaltrials.gov, No. NCT00139022.

Baseline Assessment

All subjects underwent a history and physical examination, including the measurement of arterial BP and height and weight, from which BMI was calculated. Arterial BP was measured during wakefulness according to recent Canadian guidelines.7 All subjects underwent baseline assessment with the ESS, Calgary Sleep Apnea Quality of Life Index (SAQLI), 36-Item Short Form Health Survey8 (SF-36), and Pittsburgh Sleep Quality Index9 (PSQI).

Protocol

Subjects were randomized to either the home arm or the in-laboratory PSG arm in blocks of four by drawing one of four tokens with a study arm assigned to them. Subjects in the home monitoring (HM) arm underwent 1 night of level three testing with Embletta (Embla; Denver, CO) followed by 1 week of auto-CPAP therapy (Auto-Set; ResMed Corp; San Diego, CA) and 3 weeks of fixed-pressure CPAP based on the 95% pressure (P95) derived from the auto-CPAP device. After completion of home testing and before application of auto-CPAP, these subjects underwent an in-laboratory overnight PSG. CPAP was applied during the PSG if the apnea-hypopnea index (AHI) was ≥ 15. If the AHI was > 5 but < 15, the subjects had a repeat in-laboratory PSG with CPAP titration. The investigators and the subjects in this arm were blinded to the results of the PSG and the results of the in-laboratory CPAP titration.

Subjects in the PSG arm underwent supervised overnight PSG in the sleep laboratory followed by 1 night of HM. CPAP titration was performed either during the split-night PSG (if AHI was > 15) or during a second in-laboratory PSG (if the AHI was > 5, but < 15). CPAP titration was performed manually by a PSG technician to abolish apneas and hypopneas. Investigators and subjects in the PSG arm were blinded to the results of HM. Figures 1 and 2 provide the details of the study protocol and the order in which tests were completed.

Figure Jump LinkFigure 1. Study flow chart. CPAP = continuous positive airway pressure; OSA = obstructive sleep apnea; PSG = polysomnography.Grahic Jump Location
Figure Jump LinkFigure 2. Study protocol. HM = home monitoring; P95 = Auto-CPAP-derived 95% pressure. See Figures 1 legend for expansion of the other abbreviations.Grahic Jump Location
HM

HM was performed using Embletta. All subjects had an educational session with a technician (20-30 min) and were instructed to apply the monitoring channels at home. The following channels were monitored: airflow (nasal pressure), respiratory effort (thoracic and abdominal), oxygen saturation, heart rate, and body position. The study was thought to have acceptable quality if there were at least 4 hours of adequate recording of oxygen saturation, airflow, and respiratory effort. Home studies with < 4 h of recording were repeated.

All studies were scored manually by a technician and reviewed by a sleep medicine physician blinded to the results of the PSGs. Apnea was defined as > 80% decrease in airflow for at least 10 s. A hypopnea was defined as a decrease in airflow of at least 30% accompanied by a 3% oxygen desaturation. The respiratory disturbance index (RDI) was defined as the sum of the apneas and hypopneas divided by the recording time.

Subjects completed one night of a sleep log, estimating their sleep time and reporting any difficulties with the use of the device. Home study was considered positive for OSA if the RDI was > 5. All subjects with an RDI > 5 were offered auto-CPAP therapy for 1 week followed by fixed-pressure CPAP based on the auto-CPAP P95. Those with an RDI < 5 were withdrawn from the study and were followed by the referring physician.

PSG

Subjects assigned to the in-laboratory arm underwent an overnight PSG in the sleep laboratory as per routine clinical care. Overnight PSG was performed using the Sandman PSG diagnostic system (Embla) and was supervised by an experienced sleep laboratory technologist. The monitoring consisted of EEG (C1-A2, C3-A2, O2-A1, O4-A1), right and left electrooculography, chin electromyograph, airflow (nasal pressure; Braebon Medical; Kanata, ON, Canada), respiratory effort (piezoelectric), oxygen saturation, body position, anterior tibialis electromyograph, heart rate, and ECG. Obstructive apnea was defined as a decrease in airflow of at least 80% for 10 s or more accompanied by respiratory effort. Obstructive hypopnea was defined as a decrease in airflow of at least 30% associated with 3% oxygen desaturation or an arousal and accompanied by respiratory effort. An experienced sleep laboratory technician blinded to the study arm scored all studies according to standard criteria.10 A split-night PSG with CPAP titration was performed if there was evidence of at least moderate OSA (AHI ≥ 15) during the diagnostic portion of the study; a repeat PSG with CPAP titration was performed if the AHI was ≥ 5, but < 15. The PSG study was acceptable if there were at least 2 h of sleep time during the diagnostic portion and 2 h during CPAP titration. An AHI > 5 was considered diagnostic for OSA. All subjects with an AHI > 5 were offered CPAP therapy at the pressure obtained in the sleep laboratory. All CPAP units were provided by the Government of Saskatchewan (Saskatchewan Aids to Independent Living) free of charge. Subjects were required to purchase CPAP masks and humidifiers from one of the local home-care companies. After completion of both the level 3 home study and PSG, subjects were asked to rate their preference for the type of study using a 100-mm visual analog scale, where a number below 50 indicated a preference for the level 3 study.

Outcome Measures

After initiating CPAP therapy, all subjects were evaluated at week 1 with ESS and CPAP compliance, and at week 4 with ESS, SAQLI, SF-36, PSQI, arterial BP, and CPAP compliance. The primary outcome of the study was daytime somnolence (ESS) at 4 weeks. Secondary outcomes included quality of life (SF-36 and SAQLI), subjective sleep quality (PSQI), arterial BP, CPAP compliance at 4 weeks, and subjects’ preference for the type of diagnostic method. Outcome measures were compared between the two study groups at baseline and then again at 4 weeks. Outcome measures were also compared within each study group at baseline and 4 weeks.

Statistical Analysis

The sample size was calculated using the formula given by Diggle et al.11 To detect the smallest meaningful difference in SD units for type 1, error rate α = 0.05, power (1-β) = 0.9, and the required sample size was 29 patients in each group. Frequency was identified for gender, the only categorical variable. Mean and SD were calculated for continuous variables, and median values and ranges were identified for nonnormally distributed variables. χ2 testing was used for gender. Unpaired t tests were used to compare means for normally distributed characteristics and outcome variables of the two study groups. The Mann Whitney U test was used to compare nonnormally distributed outcome variables. Sleepiness, PSQI scores, arterial BP, and SF-36, quality of life, and SAQLI scores were compared between the two study groups for baseline and week 4 data. The t test was not appropriate because of repeated measurement on the same subject because we were interested in comparing the scores at baseline and week 4. Hence, the generalized estimating equation proposed by Zeger and Liang12 was used to compare the two study groups. The generalized estimating equation method accounts for the within-subject correlation resulting from repeated measurement on the same subject. Paired t tests were used to compare the outcome variables at baseline and at 4-week variables separately within each study group. All statistical analysis was performed using SPSS software, version 15 (SPSS Inc; Chicago, IL). A P value of .05 was considered significant.

The study flow chart is presented in Figure 1. Two hundred and seventy consecutive adult patients referred to the outpatient sleep disorders clinic at the University of Saskatchewan, Saskatoon, Canada, with suspected OSA were screened. One hundred and two met the inclusion criteria and were randomized (age, 47.4 ± 11.4 years; 63 men; BMI, 32.3 ± 6.3 kg/m2; ESS, 12.5 ± 4.3; systolic BP, 131.0 ± 16 mm Hg; diastolic BP, 85 ± 9 mm Hg). There was no difference in age, sex distribution, BMI, and ESS between the included and excluded subjects. After sleep testing, 89 subjects who had received a diagnosis of OSA were prescribed CPAP therapy, but 10 of those patients rejected CPAP (Fig 1). The majority (79/103, 77% of the entire study group; 43/51, 84% of the PSG group) of PSGs were split-night studies. Those patients who had a full-night PSG had a mean AHI of 13.7 ± 11.9, while those who had a split-night PSG had a mean AHI of 31.5 ± 23.0. The study groups were equal at baseline with regard to outcomes of interest, but the subjects in the PSG group were more obese and had more severe OSA (Table 1, Fig 2). Table 1 includes AHI scores derived from PSG (AHI PSG) and HM (AHI HM). The proportion of subjects with an AHI > 30 was significantly higher in the PSG group (Fig 2). There was no difference between the groups in ESS (PSG group 9.2 ± 4.3 vs HM group 9.4 ± 4.4; P value was not significant) and CPAP compliance at 1 week (PSG group 5.5 ± 2.0 h vs HM group 5.9 ± 1.4 h, P = .31).

Table Graphic Jump Location
Table 1 —Baseline Characteristics of Subjects With Obstructive Sleep Apnea

AHI = apnea-hypopnea index; CPAP = continuous positive airway pressure; DBP = diastolic BP: ESS = Epworth Sleepiness Scale; GH = general health; HM = home monitoring; MCS = Mental Component Summary; MH = mental health; N/A = not available; ODI = oxygen saturation index; OSA = obstructive sleep apnea; P95 = 95% pressure; PCS = Physical Component Summary; PF = physical functioning; PSG = polysomnography; PSQI = Pittsburgh Sleep Quality Index; RE = role emotional; RP = role physical; SAQLI = Calgary Sleep Apnea Quality of Life Index; SBP = systolic BP; SF = social functioning; SF-36 = 36-Item Short Form Health Survey; VT = vitality.

a 

Comparison of auto-CPAP-derived P95 and PSG-derived CPAP pressure.

Figure Jump LinkFigure 3. OSA severity. AHI = apnea-hypopnea index. See Figures 1 and 2 legends for expansion of other abbreviations.Grahic Jump Location

The 4-week outcomes are presented in Tables 2 and 3. There was a significant improvement in ESS, PSQI, and systolic and diastolic BP in both groups after four weeks of CPAP therapy. Significant improvements in both groups were also observed in the Vitality and Mental Health subscales of SF-36 as well as the composite Mental Component Summary score. There was a significant improvement in SAQLI in the HM arm only.

Table Graphic Jump Location
Table 2 —Sleepiness and PSQI Scores, Arterial BP, and Quality of Life Scores at 4 Weeks (Mean ± SD) for PSG and HM Arms

Numbers in parentheses represent a range. See Table 1 for expansion of abbreviations.

a 

Comparison of β estimate of arm 1 (PSG) with arm 2 (HM).

b 

Independent t tests were used to compare the two arms.

Table Graphic Jump Location
Table 3 —Outcome Variables at Baseline and After 4 Weeks of CPAP (Mean and SD)

See Table 1 for expansion of abbreviations.

After four weeks of CPAP therapy, there was no difference between the study groups in ESS, PSQI, SAQLI, and SF-36 scores, arterial BP, or CPAP compliance (PSG group 5.6 ± 1.7 h/night vs HM group 5.4 ± 1.0 h/night; P = .49) (Table 2). When compliance is defined as the percentage of patients who used CPAP at least 4 h/night at least 70% of the time, there was no difference between the groups (PSG group 89% vs HM group 88%, P = .86). The auto-CPAP-derived P95 was significantly higher than the fixed-CPAP pressure established in the sleep laboratory in the HM arm. Seventy-six percent of subjects preferred level 3 testing to PSG. The HM had to be repeated in 17 patients (16.6%) because of technical factors.

Our study results indicate that in-laboratory diagnosis and therapy for OSA, using primarily a split-night PSG, does not lead to superior 4-week outcomes (subjective somnolence, arterial BP, sleep quality, and quality of life) when compared with home-based diagnosis and treatment. Patients suspected to have OSA who were randomized to diagnosis and therapy at home had similar improvements in subjective sleepiness, quality of life scores, and arterial BP after 4 weeks of CPAP therapy. Furthermore, there was no difference in CPAP adherence between both groups at 4 weeks. There were significant differences in CPAP pressures (P95- and PSG-derived) in the HM arm. It is possible that higher CPAP pressure based on P95 resulted in additional suppression of sleep-disordered breathing that may not have been detected during split-night PSG; it is also possible that CPAP pressure derived from auto-CPAP P95, which targets flow limitation, may have led to “overtreatment” of OSA. Alternative explanations include night-to-night variability in severity of sleep-disordered breathing, use of alcohol or hypnotic agents at home, or different body position. It is reassuring, however, that there was no difference in CPAP adherence or other outcomes between the study groups at 4 weeks, suggesting that an increase in CPAP pressure of 1.3 cm H2O does not lead to suboptimal CPAP adherence or worse sleep quality.

Despite a high level of interest in home-based diagnosis of OSA, there is a paucity of data on outcomes of this approach. Current guidelines support limited use of portable monitoring for the diagnosis of OSA in patients with a high pretest probability of moderate to severe OSA.6,13,14 There is, however, little literature on outcomes of this approach and applicability of home-based strategies. Mulgrew et al5 found that patients with a high pretest probability of OSA who were treated at home had similar AHI, SAQLI, and ESS scores after 3 months of CPAP therapy. Our study confirms and extends these findings by evaluating both generic and disease-specific quality of life, sleep quality, and arterial blood pressure. It is, however, different from the study by Mulgrew and colleagues5 in several important aspects: enrollment of subjects with milder OSA, use of a lower cutoff (RDI > 5) for home diagnosis of OSA, use of a different HM technology, and use of both HM and PSG at the time of referral. In addition, our sample included 38% of all consecutive patients referred to our sleep medicine clinics, whereas Mulgrew and colleagues5 recruited a smaller subset (81/2,216, or 3.6%) of their potentially eligible subjects. Our results are also in agreement with a recent review of home diagnosis of OSA15 and extend those reported by Berry et al,16 who demonstrated that CPAP adherence, improvement in sleepiness, and Functional Outcomes of Sleep Questionnaire score were similar in the HM pathway and the PSG group. Our study extends these findings by demonstrating similar improvements in arterial blood pressure, sleep quality, and quality of life measures.

Our study has a few important limitations. It was performed at a single tertiary sleep center in a population with a high pretest probability of OSA. Even though recruitment took place at a tertiary center, we are confident that our results apply to our general population because all patients suspected to have OSA in our region are referred to this single sleep laboratory. Nevertheless there may be differences in OSA severity and prevalence in other regions, and our results should be confirmed by a larger, multicenter, randomized clinical trial. In our study, the majority of subjects had split-night PSG, therefore our results should not be extended to outcomes of CPAP therapy derived from a full night of CPAP titration. In addition, our split-night PSG criteria were not consistent with those of the American Academy of Sleep Medicine: we allowed a lower AHI17 cutoff for initiation of CPAP titration and allowed less time (2 h) for CPAP titration. In reviewing our data, 65% of subjects had over 3 h of CPAP titration. It is possible, however, that better control of OSA (and consequently better outcomes of CPAP therapy in the PSG group) could have been accomplished by longer CPAP titration. Our study was relatively short in duration; existing evidence, however, suggests that significant improvement in somnolence occurs within the first month of CPAP therapy.18 Furthermore CPAP compliance within the first 4 weeks is predictive of long-term CPAP compliance.17 Our subjects were not blinded to the allocation arm because subjects in the HM arm would be able to detect variability in CPAP pressure. They were, however, blinded to the results of PSG (home arm) or level 3 testing (PSG arm).

The results of our study are not generalizable to populations with medical comorbidities; nevertheless, in this cohort of 270 patients only 58 were excluded for this reason. Given our strict enrollment criteria, we do not recommend that the home treatment strategy be applied to all patients suspected to have OSA, but rather to a subset with a high clinical suspicion of OSA and no contraindication to either level 3 testing or auto-CPAP use. Our findings are in agreement with a recent review of home diagnosis of OSA that cautioned against the use of level 3 and 4 monitors in patients with comorbidities.15 Finally, the cost-effectiveness of this approach has not yet been established. In our study, the failure rate of HM was 16.6%, resulting in repeated level 3 studies; this is significantly higher then the failure rate of PSG. This factor has to be taken into account when performing cost-effectiveness analysis. While we have not performed a detailed cost analysis, we estimate the costs of the home-based program to equal $400 to $450 Canadian per patient (not including physician interpretation fees and costs incurred by the patient). More research in this area is needed to justify the use of HM on economic grounds.

Study Implications

Our study has important implications for areas with limited access to PSG.19 OSA is already one of the most common chronic conditions and a significant public health problem.20 It is unlikely that access to PSG will keep pace with the rise in obesity and OSA rates; therefore, the home diagnosis and treatment approach may be useful in the treatment of a subgroup of subjects with OSA when access to PSG is limited.21,22 If confirmed by a larger, multicenter, randomized clinical trial, this approach may become a standard of care in a subset of patients with OSA. In addition to easier access, other potential advantages of this approach include less invasive testing, potentially lower cost of OSA testing, and subject convenience and preference. In this study, over 75% of subjects preferred level 3 testing over PSG, and 38% of suspected OSA cases met the inclusion criteria, potentially avoiding a PSG. These results are very similar to those of Senn et al,23 who reported that a trial of auto-CPAP had 97% specificity for the diagnosis of OSA and avoided up to 46% of PSGs. Our subject numbers would have likely been higher had we not excluded subjects outside of our health region. We have to be cautious, however, in extending our findings to other jurisdictions. The prevalence of OSA in our clinic population is high (67%), and the pretest probability of disease may be lower in other centers. Despite these limitations, we believe that selected subjects suspected to have OSA could receive a diagnosis and be treated at home using this algorithm.

Author contributions:Dr Skomro: participated in the study design, subject recruitment, data analysis, and manuscript preparation and review.

Dr Gjevre: participated in the study design, subject recruitment, data analysis, and manuscript preparation and review.

Dr Reid: participated in the study design, subject recruitment, data analysis, and manuscript preparation and review.

Dr McNab: participated in the study design, subject recruitment, data analysis, and manuscript preparation and review.

Dr Ghosh: participated in the study design, statistical analysis, and manuscript preparation and review.

Dr Stiles: participated in the study design, subject recruitment, data analysis, and manuscript preparation and review.

Dr Jokic: participated in the study design, data analysis, and manuscript review.

Dr Ward: participated in the study design, statistical analysis, and manuscript preparation and review.

Dr Cotton: participated in the study design, subject recruitment, data analysis, and manuscript preparation and review.

Financial/nonfinancial disclosures: The authors have reported to CHEST that no potential conflicts of interest exist with any companies/organizations whose products or services may be discussed in this article.

Role of sponsors: Continuous positive airway pressure (CPAP) units were provided at no cost by Saskatchewan Aids to Independent Living and auto-CPAP units were provided by ResMed. The funding sources had no involvement in study design, data collection or analysis, writing the report, or the decision to submit the paper for publication.

Other contributions: We thank the Lung Association of Saskatchewan, Saskatoon Health Region, and Kelsey Trail Heath Region for their support of this study. We wish to thank Ms L. King and Messrs J. Mink and E. Dash for technical assistance during this study.

AHI

apnea-hypopnea index

CPAP

continuous positive airway pressure

ESS

Epworth Sleepiness Scale

HM

home monitoring

OSA

obstructive sleep apnea

P95

95% pressure

PSG

polysomnography

PSQI

Pittsburgh Sleep Quality Index

RDI

respiratory disturbance index

SAQLI

Calgary Sleep Apnea Quality of Life Index

SF-36

36-Item Short-Form Health Survey

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Figures

Figure Jump LinkFigure 1. Study flow chart. CPAP = continuous positive airway pressure; OSA = obstructive sleep apnea; PSG = polysomnography.Grahic Jump Location
Figure Jump LinkFigure 2. Study protocol. HM = home monitoring; P95 = Auto-CPAP-derived 95% pressure. See Figures 1 legend for expansion of the other abbreviations.Grahic Jump Location
Figure Jump LinkFigure 3. OSA severity. AHI = apnea-hypopnea index. See Figures 1 and 2 legends for expansion of other abbreviations.Grahic Jump Location

Tables

Table Graphic Jump Location
Table 1 —Baseline Characteristics of Subjects With Obstructive Sleep Apnea

AHI = apnea-hypopnea index; CPAP = continuous positive airway pressure; DBP = diastolic BP: ESS = Epworth Sleepiness Scale; GH = general health; HM = home monitoring; MCS = Mental Component Summary; MH = mental health; N/A = not available; ODI = oxygen saturation index; OSA = obstructive sleep apnea; P95 = 95% pressure; PCS = Physical Component Summary; PF = physical functioning; PSG = polysomnography; PSQI = Pittsburgh Sleep Quality Index; RE = role emotional; RP = role physical; SAQLI = Calgary Sleep Apnea Quality of Life Index; SBP = systolic BP; SF = social functioning; SF-36 = 36-Item Short Form Health Survey; VT = vitality.

a 

Comparison of auto-CPAP-derived P95 and PSG-derived CPAP pressure.

Table Graphic Jump Location
Table 2 —Sleepiness and PSQI Scores, Arterial BP, and Quality of Life Scores at 4 Weeks (Mean ± SD) for PSG and HM Arms

Numbers in parentheses represent a range. See Table 1 for expansion of abbreviations.

a 

Comparison of β estimate of arm 1 (PSG) with arm 2 (HM).

b 

Independent t tests were used to compare the two arms.

Table Graphic Jump Location
Table 3 —Outcome Variables at Baseline and After 4 Weeks of CPAP (Mean and SD)

See Table 1 for expansion of abbreviations.

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