Zolpidem and Eszopiclone Pre-medication for PSG: Effects on Staging, Titration, and Adherence.

Introduction: The non-benzodiazepine sedative hypnotic (NBSH) eszopiclone improves polysomnography (PSG) quality and continuous positive airway pressure (CPAP) adherence. It is unclear whether zolpidem has the same effect and neither NBSH has been studied in populations with milder forms of obstructive sleep apnea. Materials and Methods: We performed a retrospective analysis on patients undergoing level I PSG at our institution. Patients are pre-medicated with NBSHs at the discretion of the sleep physician. We compared PSG/CPAP titration quality and subsequent CPAP adherence for patients receiving NBSHs or no pre-study medication. We adjusted for obstructive sleep apnea pre-test probability (PTP), arousal threshold, and other factors showing differences at baseline. Results: Data on 560 patients were analyzed. Mean age and body mass index were 42.2 ± 10.1 and 28.8 ± 4.5, respectively. Median apnea hypopnea index was 12.9 (6.4-25.3), 100 (18.0%) patients had normal studies, 97 (17.3%) were split, and 457 (81.6%) had a respiratory low-arousal threshold. After adjusting for differences at baseline, neither NBSH was associated with sleep efficiency, wake after sleep onset, or total sleep time on PSG. After adjustment, patients receiving eszopiclone had a higher apnea hypopnea index at the final CPAP pressure (ß = 14.2; 95% confidence intervals (CI) 7.2-21.2; p < 0.001) and were more likely to have an unacceptable titration (odds ratio (OR) = 6.6; 95% CI 2.0-21.0; p = 0.002). When only split-night studies were examined, there were no differences in any adherence variables across or between categories. Conclusions: In a population with predominantly mild obstructive sleep apnea, NBSHs did not improve PSG or CPAP titration quality and did not increase CPAP adherence. There was no difference in effect between eszopiclone and zolpidem.

Using the STOPBANG questionnaire and other pre-test probability tools to predict OSA in younger, thinner patients referred to a sleep medicine clinic.

BACKGROUND: The STOPBANG questionnaire is used to predict the presence of obstructive sleep apnea (OSA). We sought to assess the performance of the STOPBANG questionnaire in younger, thinner patients referred to a sleep medicine clinic. METHODS: We applied the STOPBANG questionnaire to patients referred for level I polysomnography (PSG) at our sleep center. We calculated likelihood ratios and area under the receiver operator characteristic (AUROC) curve and performed sensitivity analyses. RESULTS: We performed our analysis on 338 patients referred for PSG. Only 17.2% (n = 58) were above age 50 years, and 30.5 and 6.8% had a BMI above 30 and 35 years, respectively. The mean apnea-hypopnea index (AHI) was 12.9 ± 16.4 and 63.9% had an AHI ≥5. The STOPBANG (threshold ≥3) identified 83.1% of patients as high risk for an AHI ≥5, and sensitivity, specificity, positive (PPV), and negative predictive values (NPV) were 83.8, 18.0, 64.4, and 38.0%, respectively. Positive and negative likelihood ratios were poor at 1.02-1.11 and 0.55-0.90, respectively, across AHI thresholds (AHI ≥5, AHI ≥15 and AHI ≥30), and AUROCs were 0.52 (AHI ≥5) and 0.56 (AHI ≥15). Sensitivity analyses adjusting for insomnia, combat deployment, traumatic brain injury, post-traumatic stress disorder, clinically significant OSA (ESS >10 and/or co-morbid disease), and obesity did not significantly alter STOPBANG performance. CONCLUSIONS: In a younger, thinner population with predominantly mild-to-moderate OSA, the STOPBANG Score does not accurately predict the presence of obstructive sleep apnea.

A mobile, web-based system can improve positive airway pressure adherence.

SleepMapper is a mobile, web-based system that allows patients to self-monitor their positive airway pressure therapy, and provides feedback and education in real time. In addition to the usual, comprehensive support provided at our clinic, we gave the SleepMapper to 30 patients initiating positive airway pressure. They were compared with patients initiating positive airway pressure at our clinic without SleepMapper (controls) to determine whether SleepMapper affected adherence. A total of 61 patients had polysomnographic and adherence data analysed, 30 were given SleepMapper and 31 received our standard of care. The two groups were well matched at baseline to include no significant differences in age, apnea-hypopnea index, percentage receiving split-night polysomnographs and starting pressures. Patients in the control group received significantly more non-benzodiazepine sedative hypnotics the night of their polysomnography and during positive airway pressure initiation. At 11 weeks, patients in the SleepMapper group had a greater percentage of nights with any use (78.0 ± 22.0 versus 55.5 ± 24.0%; P < 0.001) and >4 h positive airway pressure use (78.0 ± 22.0 versus 55.5 ± 24.0%; P = 0.02). There was a trend toward more patients in the SleepMapper group achieving >4 h of use for at least 70% of nights [9/30 (30%) versus 3/31 (9.7%); P = 0.06]. In multivariate linear regression, the SleepMapper remained significantly associated with percentage of nights >4 h positive airway pressure use (ß coefficient = 0.18; P = 0.02). Added to our usual, comprehensive programme to maximize positive airway pressure adherence in new users, the SleepMapper was independently associated with an 18% increase in nights >4 h of use.

Eszopiclone and Zolpidem Do Not Affect the Prevalence of the Low Arousal Threshold Phenotype.

STUDY OBJECTIVES: We sought to determine whether non benzodiazepine sedative hypnotics (NBSH) reduce the occurrence of the low arousal threshold (LAT) phenotype. METHODS: Consecutive patients with suspected obstructive sleep apnea (OSA) referred for polysomnography (PSG) had demographic and PSG data abstracted. LAT was estimated using PSG criteria. After adjusting for pretest probability (PTP) for OSA, we calculated the effect that premedication with NBSHs has on LAT prevalence. RESULTS: Five hundred seventy-nine patients with a mean age and body mass index of 42.2 ± 10.1 y and 28.9 ± 4.5 kg/m2, respectively, had data available for analysis. Most patients (444, or 80.9%) had a LAT, and administering a NBSH (zolpidem or eszopiclone) on the same night as the PSG did not change LAT prevalence (NBSH: 339 (83.3%) versus no drug: 100 (80.6%); p = 0.50). Adjusting for PTP, neither administration of eszopiclone (odds ratio 0.80 (95% confidence interval: 0.33-2.0); 0.69) nor zolpidem (odds ratio 1.65 (95% confidence interval: 0.8-3.5); p = 0.19) reduced the odds that a patient had a LAT. NBSHs did not change the mean SpO2 nadir, percentage hypopneas, or apnea-hypopnea index. There was no association between zolpidem or eszopiclone dosing and SpO2 nadir (zolpidem: ß = -0.69, p = 0.80; eszopiclone: ß = -1.53, p = 0.68), percentage hypopneas (zolpidem: ß = 2.2, p = 0.43; eszopiclone ß = -6.2, p = 0.46), or apnea-hypopnea index (zolpidem: ß = 3.1, p = 0.22; eszopiclone: ß = 2.6, p = 0.39). CONCLUSIONS: The LAT is common in our population and NBSH premedication does not alter its occurrence. Further studies are needed to determine how the LAT can be optimally managed to improve OSA treatment.