D. Mann

Loop Gain Predicts the Response to Upper Airway Surgery in Patients With Obstructive Sleep Apnea

Study Objectives Upper airway surgery is often recommended to treat patients with obstructive sleep apnea (OSA) who cannot tolerate continuous positive airways pressure. However, the response to surgery is variable, potentially because it does not improve the nonanatomical factors (ie, loop gain [LG] and arousal threshold) causing OSA. Measuring these traits clinically might predict responses to surgery. Our primary objective was to test the value of LG and arousal threshold to predict surgical success defined as 50% reduction in apnea-hypopnea index (AHI) and AHI <10 events/hour post surgery. Methods We retrospectively analyzed data from patients who underwent upper airway surgery for OSA (n = 46). Clinical estimates of LG and arousal threshold were calculated from routine polysomnographic recordings presurgery and postsurgery (median of 124 [91-170] days follow-up). Results Surgery reduced both the AHI (39.1 ± 4.2 vs. 26.5 ± 3.6 events/hour; p < .005) and estimated arousal threshold (-14.8 [-22.9 to -10.2] vs. -9.4 [-14.5 to -6.0] cmH2O) but did not alter LG (0.45 ± 0.08 vs. 0.45 ± 0.12; p = .278). Responders to surgery had a lower baseline LG (0.38 ± 0.02 vs. 0.48 ± 0.01, p < .05) and were younger (31.0 [27.3-42.5] vs. 43.0 [33.0-55.3] years, p < .05) than nonresponders. Lower LG remained a significant predictor of surgical success after controlling for covariates (logistic regression p = .018; receiver operating characteristic area under curve = 0.80). Conclusions Our study provides proof-of-principle that upper airway surgery most effectively resolves OSA in patients with lower LG. Predicting the failure of surgical treatment, consequent to less stable ventilatory control (elevated LG), can be achieved in the clinic and may facilitate avoidance of surgical failures.

Dynamic loop gain increases upon adopting the supine body position during sleep in patients with obstructive sleep apnoea

Obstructive sleep apnoea (OSA) is typically worse in the supine versus lateral sleeping position. One potential factor driving this observation is a decrease in lung volume in the supine position which is expected by theory to increase a key OSA pathogenic factor: dynamic ventilatory control instability (i.e. loop gain). We aimed to quantify dynamic loop gain in OSA patients in the lateral and supine positions, and to explore the relationship between change in dynamic loop gain and change in lung volume with position.

Ventilatory control sensitivity in patients with obstructive sleep apnea is sleep stage dependent

Study Objectives The severity of obstructive sleep apnea (OSA) is known to vary according to sleep stage; however, the pathophysiology responsible for this robust observation is incompletely understood. The objective of the present work was to examine how ventilatory control system sensitivity (i.e. loop gain) varies during sleep in patients with OSA. Methods Loop gain was estimated using signals collected from standard diagnostic polysomnographic recordings performed in 44 patients with OSA. Loop gain measurements associated with nonrapid eye movement (NREM) stage 2 (N2), stage 3 (N3), and REM sleep were calculated and compared. The sleep period was also split into three equal duration tertiles to investigate how loop gain changes over the course of sleep. Results Loop gain was significantly lower (i.e. ventilatory control more stable) in REM (Mean ± SEM: 0.51 ± 0.04) compared with N2 sleep (0.63 ± 0.04; p = 0.001). Differences in loop gain between REM and N3 (p = 0.095), and N2 and N3 (p = 0.247) sleep were not significant. Furthermore, N2 loop gain was significantly lower in the first third (0.57 ± 0.03) of the sleep period compared with later second (0.64 ± 0.03, p = 0.012) and third (0.64 ± 0.03, p = 0.015) tertiles. REM loop gain also tended to increase across the night; however, this trend was not statistically significant [F(2, 12) = 3.49, p = 0.09]. Conclusions These data suggest that loop gain varies between REM and NREM sleep and modestly increases over the course of sleep. Lower loop gain in REM is unlikely to contribute to the worsened OSA severity typically observed in REM sleep, but may explain the reduced propensity for central sleep apnea in this sleep stage.

Loop Gain Predicts Response to Upper Airway Surgery for Obstructive Sleep Apnoea

007 EFFECTS OF 1 MONTH OF NIGHTLY ZOPICLONE ON OBSTRUCTIVE SLEEP APNOEA SEVERITY AND MEASURES OF ALERTNESS: A RANDOMISED CONTROLLED TRIAL S. CARTER, J. CARBERRY, L. FISHER, G. CHO, C. ROLLO, D. STEVENS, A. D’ROZARIO, D. MCKENZIE, R. GRUNSTEIN AND D. ECKERT Neuroscience Research Australia, The University of New South Wales, Woolcock Institute of Medical Research, The University of Sydney, Prince of Wales Hospital, Sydney, NSW, Australia Introduction: Hypnotics have historically not been recommended in obstructive sleep apnoea (OSA) due to concerns they may worsen OSA severity via pharyngeal muscle relaxation and arousal suppression. However, recent physiology studies: 1) do not show systematic impairment in upper airway muscle activity with certain hypnotics and 2) indicate that hypnotics worsen OSA in some patients and reduce OSA severity in others depending on the patient’s arousal threshold and severity of nocturnal hypoxaemia. However, clinical trial data is lacking. Accordingly, this study aimed to determine the effects of 1 month of nightly zopiclone on OSA severity and measures of alertness in OSA patients who have low-moderate respiratory arousal thresholds and mild overnight hypoxaemia. Methods: Initially, a screening physiology night to quantify the respiratory arousal threshold (nadir epiglottic pressure just prior to arousal) and nadir arterial blood oxygen saturation (SaO2) was performed. Thirty OSA patients (apnoea/hypopnoea index [AHI] = 22.4 11.3/h) with low-moderate arousal thresholds (> 25 cm H2O) and nadir SaO2 ≥ 75% were then studied in-lab (PSG) on three occasions at baseline, night 1 and night 30. Participants received either nightly zopiclone (7.5 mg) or placebo during the 30 day study according to a double-blind, randomised, parallel design. Subjective sleepiness (ESS and KSS) and a 30 min driving simulator task (AusEd) were performed following each PSG. Results: The median reduction in AHI on night 30 from baseline was 23 [ 4.47]% during zopiclone vs. 12 [ 8.29]% during placebo (P > 0.05). Change in mean SaO2 from baseline to night 30 was not different between zopiclone and placebo ( 0.1 0.7 vs. 0.1 1.4%). Similarly, neither the change in ESS ( 1.3 2.7 vs. 0.2 2.4), KSS (0 [ 1.0, 1.5] vs. 0 [ 1.0, 1.3]), or steering deviation (7.1 [ 1.3, 40.8] vs. 9.4 [ 20.6, 34.8]) during the AusEd driving task differed from baseline to night 30 during zopiclone vs. placebo. Conclusions: A standard dose of nightly zopiclone does not worsen OSA severity, next day sleepiness or alertness during a simulated driving task in OSA patients who have low to moderate arousal thresholds and nadir overnight SaO2 ≥ 75%. These findings challenge previous assumptions that hypnotics worsen OSA. 008 BRIEF SLEEP PSYCHOEDUCATION PROGRAM IMPROVES SLEEP QUALITY AND REDUCES INSOMNIA SYMPTOMS IN NEW MOTHERS L. KEMPLER, L. SHARPE AND D. BARTLETT Woolcock Institute of Medical Research, University of Sydney, Sydney, NSW, Australia Sleep in the postpartum period is fragmented and often difficult. Infants wake frequently in the early weeks of life requiring care and attention. Increased sleep disturbance is associated with mood disorders and postnatal depression. The aim of this randomised controlled trial was to determine whether a brief sleep psychoeducation program delivered to mothers during their third trimester of pregnancy with their first baby could improve sleep and, if so, mood outcomes in the postnatal period. Method: Two hundred and fifteen mothers were randomised to receive either 2 9 1.5 h slide presentations with a set of sleep & relaxation booklets or general sleep booklets only. Participants were followed up with phone calls at 3 & 6 weeks postpartum and with questionnaires at 6 weeks, 4 months and 10 months postpartum. A Subgroup of participants wore an actiwatch for a week during their third trimester and for a week at 4 months postpartum. The primary outcome was sleep measured by sleep quality (PSQI), Insomnia, (ISI), sleepiness (ESS) and fatigue (MAF). The secondary outcome was mood measured using Edinburgh Postnatal Depression Scales (EPDS) and the depression subscale of the Depression Anxiety and Stress Scales (DASS). Results: A linear mixed model analysis was used for each factor (PSQI, ISI, ESS and MAF) at each time point (baseline, 6 week, 4 months, 10 months). Results indicated better sleep quality (mean difference 1.27; 95% CI [0.12 to 2.41] P = 0.032) and fewer insomnia symptoms (mean difference 1.55; 95% CI [1.66 to 2.93]; P = 0.028) at 4 months postpartum in the intervention group than the control group. There were no group differences in sleepiness, fatigue or mood outcomes, nor at other time-points. Conclusions: These results suggest that there is some short-term benefit of this intervention for women around 4 months postpartum. Given the low cost associated with this intervention, its inclusion in routine antenatal classes could hasten improvements in mothers’ sleep. a 2016 The Authors Journal of Sleep Research

Characterising sleeping posture by measuring torso rotation as a continuous variable

007 EFFECTS OF 1 MONTH OF NIGHTLY ZOPICLONE ON OBSTRUCTIVE SLEEP APNOEA SEVERITY AND MEASURES OF ALERTNESS: A RANDOMISED CONTROLLED TRIAL S. CARTER, J. CARBERRY, L. FISHER, G. CHO, C. ROLLO, D. STEVENS, A. D’ROZARIO, D. MCKENZIE, R. GRUNSTEIN AND D. ECKERT Neuroscience Research Australia, The University of New South Wales, Woolcock Institute of Medical Research, The University of Sydney, Prince of Wales Hospital, Sydney, NSW, Australia Introduction: Hypnotics have historically not been recommended in obstructive sleep apnoea (OSA) due to concerns they may worsen OSA severity via pharyngeal muscle relaxation and arousal suppression. However, recent physiology studies: 1) do not show systematic impairment in upper airway muscle activity with certain hypnotics and 2) indicate that hypnotics worsen OSA in some patients and reduce OSA severity in others depending on the patient’s arousal threshold and severity of nocturnal hypoxaemia. However, clinical trial data is lacking. Accordingly, this study aimed to determine the effects of 1 month of nightly zopiclone on OSA severity and measures of alertness in OSA patients who have low-moderate respiratory arousal thresholds and mild overnight hypoxaemia. Methods: Initially, a screening physiology night to quantify the respiratory arousal threshold (nadir epiglottic pressure just prior to arousal) and nadir arterial blood oxygen saturation (SaO2) was performed. Thirty OSA patients (apnoea/hypopnoea index [AHI] = 22.4 11.3/h) with low-moderate arousal thresholds (> 25 cm H2O) and nadir SaO2 ≥ 75% were then studied in-lab (PSG) on three occasions at baseline, night 1 and night 30. Participants received either nightly zopiclone (7.5 mg) or placebo during the 30 day study according to a double-blind, randomised, parallel design. Subjective sleepiness (ESS and KSS) and a 30 min driving simulator task (AusEd) were performed following each PSG. Results: The median reduction in AHI on night 30 from baseline was 23 [ 4.47]% during zopiclone vs. 12 [ 8.29]% during placebo (P > 0.05). Change in mean SaO2 from baseline to night 30 was not different between zopiclone and placebo ( 0.1 0.7 vs. 0.1 1.4%). Similarly, neither the change in ESS ( 1.3 2.7 vs. 0.2 2.4), KSS (0 [ 1.0, 1.5] vs. 0 [ 1.0, 1.3]), or steering deviation (7.1 [ 1.3, 40.8] vs. 9.4 [ 20.6, 34.8]) during the AusEd driving task differed from baseline to night 30 during zopiclone vs. placebo. Conclusions: A standard dose of nightly zopiclone does not worsen OSA severity, next day sleepiness or alertness during a simulated driving task in OSA patients who have low to moderate arousal thresholds and nadir overnight SaO2 ≥ 75%. These findings challenge previous assumptions that hypnotics worsen OSA. 008 BRIEF SLEEP PSYCHOEDUCATION PROGRAM IMPROVES SLEEP QUALITY AND REDUCES INSOMNIA SYMPTOMS IN NEW MOTHERS L. KEMPLER, L. SHARPE AND D. BARTLETT Woolcock Institute of Medical Research, University of Sydney, Sydney, NSW, Australia Sleep in the postpartum period is fragmented and often difficult. Infants wake frequently in the early weeks of life requiring care and attention. Increased sleep disturbance is associated with mood disorders and postnatal depression. The aim of this randomised controlled trial was to determine whether a brief sleep psychoeducation program delivered to mothers during their third trimester of pregnancy with their first baby could improve sleep and, if so, mood outcomes in the postnatal period. Method: Two hundred and fifteen mothers were randomised to receive either 2 9 1.5 h slide presentations with a set of sleep & relaxation booklets or general sleep booklets only. Participants were followed up with phone calls at 3 & 6 weeks postpartum and with questionnaires at 6 weeks, 4 months and 10 months postpartum. A Subgroup of participants wore an actiwatch for a week during their third trimester and for a week at 4 months postpartum. The primary outcome was sleep measured by sleep quality (PSQI), Insomnia, (ISI), sleepiness (ESS) and fatigue (MAF). The secondary outcome was mood measured using Edinburgh Postnatal Depression Scales (EPDS) and the depression subscale of the Depression Anxiety and Stress Scales (DASS). Results: A linear mixed model analysis was used for each factor (PSQI, ISI, ESS and MAF) at each time point (baseline, 6 week, 4 months, 10 months). Results indicated better sleep quality (mean difference 1.27; 95% CI [0.12 to 2.41] P = 0.032) and fewer insomnia symptoms (mean difference 1.55; 95% CI [1.66 to 2.93]; P = 0.028) at 4 months postpartum in the intervention group than the control group. There were no group differences in sleepiness, fatigue or mood outcomes, nor at other time-points. Conclusions: These results suggest that there is some short-term benefit of this intervention for women around 4 months postpartum. Given the low cost associated with this intervention, its inclusion in routine antenatal classes could hasten improvements in mothers’ sleep. a 2016 The Authors Journal of Sleep Research