On the Relation between Mains-Side Current THD and DC Link Voltage Loop Gain in Grid-Connected Unity Power Factor Operating Converters

<p>It is well-known that attainable DC link voltage loop bandwidth in grid-connected converters operating with unity power factor is limited due to trade-off with AC-side current total harmonic distortion (THD). The letter reveals that THD requirement directly imposes the value of voltage loop gain magnitude at double-grid frequency; therefore the dynamic performance may be improved without deteriorating the grid-side current quality by modifying the controller structure such that the loop gain magnitude at double-grid frequency and the crossover frequency are decoupled. Experimental results validate the revealed findings.</p>

On the Relation between Mains-Side Current THD and DC Link Voltage Loop Gain in Grid-Connected Unity Power Factor Operating Converters

<p>It is well-known that attainable DC link voltage loop bandwidth in grid-connected converters operating with unity power factor is limited due to trade-off with AC-side current total harmonic distortion (THD). The letter reveals that THD requirement directly imposes the value of voltage loop gain magnitude at double-grid frequency; therefore the dynamic performance may be improved without deteriorating the grid-side current quality by modifying the controller structure such that the loop gain magnitude at double-grid frequency and the crossover frequency are decoupled. Experimental results validate the revealed findings.</p>

Pathophysiology of Obstructive Sleep Apnea in Aging Women

The following review is designed to explore the pathophysiology of sleep apnea in aging women. The review initially introduces four endotypes (i.e., a more collapsible airway, upper airway muscle responsiveness, arousal threshold, and loop gain) that may have a role in the initiation of obstructive sleep apnea. Thereafter, sex differences in the prevalence of sleep apnea are considered along with differences in the prevalence that exist between younger and older women. Following this discussion, we consider how each endotype might contribute to the increase in prevalence of sleep apnea in aging women. Lastly, we address how modifications in one form of respiratory plasticity, long-term facilitation, that might serve to mitigate apneic events in younger women may be modified in aging women with obstructive sleep apnea. Overall, the published literature indicates that the prevalence of sleep apnea is increased in aging women. This increase is linked primarily to a more collapsible airway and possibly to reduced responsiveness of upper airway muscle activity. In contrast, modifications in loop gain or the arousal threshold do not appear to have a role in the increased prevalence of sleep apnea in aging women. Moreover, we suggest that mitigation of long-term facilitation could contribute to the increased prevalence of sleep apnea in aging women.

P019 Obstructive sleep apnoea endotypes in people with multiple sclerosis

Purpose Obstructive sleep apnoea (OSA) is common in people with multiple sclerosis (MS) despite a lack of typical risk factors for OSA in people with MS such as obesity and male predominance. Therefore, underlying factors other than sex and obesity may be particularly important in the pathogenesis of OSA in people with MS. Thus, the primary aim of this study was to determine the relative contributions of OSA endotypes in people with MS and compare this to matched controls with OSA only. Methods Eleven people with MS and OSA (MS-OSA group) (apnoea-hypopnoea index [AHI]&gt;5events/h) and eleven controls matched for OSA severity, age and sex without MS (OSA group) were studied. Participants underwent a detailed overnight polysomnography with an epiglottic pressure catheter and genioglossus intramuscular electrodes to allow for quantification of pathophysiological contributors to OSA. This included the respiratory arousal threshold, genioglossus muscle responsiveness, respiratory loop gain and upper airway collapsibility. Results Measures of the four primary OSA endotypes were not different between the MS-OSA and OSA groups (e.g. NREM respiratory arousal threshold -27±15 vs. -23±8 cmH2O respectively, p=0.24). Within group analysis indicated higher loop gain in non-obese MS-OSA participants compared to obese MS-OSA participants (0.53±0.11 vs. 0.37±0.11, p=0.04). Conclusions Overall, OSA endotypes are similar between MS-OSA participants and matched OSA controls. However, within the MS-OSA group, non-obese participants have higher loop gain (unstable respiratory control) compared to obese participants. Thus, unstable respiratory control may play an important role in OSA pathogenesis in many people with MS.

O013 The pathogenesis of obstructive sleep apnea in individuals with comorbid insomnia and obstructive sleep apnoea (COMISA)

Obstructive sleep apnea (OSA) and Insomnia are prevalent sleep disorders which are highly comorbid. This frequent co-occurrence suggests a shared etiology may exist. OSA is caused by the interaction of four pathophysiological traits: a highly collapsible upper airway, elevated loop gain, a low arousal threshold, and poor muscle compensation. No study has ascertained whether these traits are influenced by insomnia. We aimed to quantify the four traits which contribute to OSA in individuals diagnosed with comorbid insomnia and OSA (COMISA). We non-invasively determined these traits in 52 COMISA patients (Age: 56±14 years) with mild-to-severe OSA (AHI=21.2±10.63 events/h) using polysomnography. Our results indicated that 83% of COMISA patients had a low arousal threshold and only 2% of patients exhibited a highly collapsible airway using previously defined thresholds. Multiple linear regression revealed the arousal threshold (b=0.24, 95%CI[0.11, 0.37], β=0.47, p&lt;0.001) and loop gain (b=23.6, 95%CI[7.02, 40.18], β=0.33, p&lt;0.01) were the strongest predictors of OSA severity in our sample. There was no significant relationship between the arousal threshold and insomnia severity measured by the insomnia severity index (ISI). Further work is being performed to compare these findings with a matched sample of OSA only participants. Our preliminary findings demonstrate OSA in COMISA is characterized by a mildly collapsible airway/low arousal threshold phenotype and is largely driven by non-anatomical factors including a low arousal threshold and high loop gain. OSA treatments which are effective in patients with mild anatomical compromise and raise the arousal threshold may provide therapeutic benefit in COMISA patients.

P099 Physiological phenotypes of obstructive sleep apnoea (OSA) in Pacific Islanders and equally obese Caucasians

Background Pacific islanders (PI) have a high prevalence of severe OSA, attributed to obesity. Ethnic differences in mechanisms contributing to OSA have been reported. We compared physiological polysomnography characteristics in obese PI and Caucasian (C) patients with OSA. Methods Retrospective polysomnography (PSG) studies from a tertiary hospital sleep laboratory were identified for PI and age, gender and BMI matched C patients (BMI&gt;30 kgm²). All PSGs were rescored by a single scorer, and pharyngeal collapsibility (Vpassive), upper airway muscle compensation (Vcomp), arousal threshold (AT), [all expressed as percentage of steady-state breathing (Veupnea)], and loop gain (LG) were determined non-invasively via established/validated techniques. Progress to date 14 PI [8 female] and 29 C [15 female] were identified. There were no differences in age [52.2±17.0 PI; 52.5±13.3 C years], BMI [46.9±7.7 PI; 48.2±10.1 C kgm²] or AHI (35.6 [17.9–77.5] PI; 41.2 [20.9–83.6] C events/hour) (mean±SD or median[IQR]; all p&gt;0.4; paired t-test or Wilcoxon signed rank). There were no significant differences in Vpassive (88.8 [88.4–97.1] PI; 91.8 [44.4–95.8]C %Veupnea; p=0.38), Vcomp (1.2 [-12.0–9.2] PI; 5.8 [-1.9–9.6] C %Veupnea; p=0.30), AT (131.4 [110.5–140.8] PI; 126.1 [110.4–180.7] C %Veupnea; p=0.67) or LG (0.6±0.1 PI; 0.7±0.3 C; p=0.23). Intended outcome and impact In a small cohort of PI and age, gender and BMI matched C with OSA, upper airway obstructive event frequency was the same and there were no differences in physiological phenotypes, suggesting similar mechanisms contribute to OSA severity in both groups. Confirmation of these findings in a larger cohort is ongoing.

O001 Reboxetine reduces obstructive sleep apnea severity: a randomized trial

Introduction Noradrenergic and muscarinic processes are crucial for pharyngeal muscle control during sleep. Selective norepinephrine reuptake inhibitors (SNRIs) such as reboxetine combined with an antimuscarinic reduce obstructive sleep apnea (OSA) severity. The effects of reboxetine alone on OSA severity are unknown. Methods Double-blind, placebo-controlled, three-way crossover trial in 16 people with OSA. Each participant completed three overnight polysomnograms (~1-week washout). Single doses of reboxetine 4mg, placebo, or reboxetine+oxybutynin 5mg were administered before sleep (randomized order). The primary outcome was apnea-hypopnea index (AHI). Secondary outcomes included other polysomnography parameters, next day sleepiness and alertness. Endotyping analysis was performed to determine the medications’ effects on OSA pathophysiological mechanisms. Results Reboxetine reduced the AHI by 5.4 [95% CI -10.4 to -0.3] events/h, P=0.03 (men: -24±27%; women: -0.7±32%). The addition of oxybutynin did not further reduce AHI. Reboxetine alone and reboxetine+oxybutynin reduced overnight hypoxemia versus placebo (e.g. 4% oxygen desaturation index 10.4±12.8 vs. 10.6±12.8 vs. 15.7±14.7 events/h, P=0.02). Mechanistically, reboxetine and reboxetine+oxybutynin improved pharyngeal collapsibility and respiratory control stability. Men had higher baseline loop gain. Larger reductions in AHI with reboxetine occurred in those with high loop gain. Neither drug intervention changed next day sleepiness or alertness. Discussion A single 4mg dose of reboxetine modestly reduces OSA severity without further improvement with the addition of an antimuscarinic. Reboxetine increases breathing stability via improvements in pharyngeal collapsibility and respiratory control. These findings provide new insight into the role of SNRIs on upper airway stability during sleep and have important implications for pharmacotherapy development for OSA.

O027 The combination of mandibular advancement devices (MAD) and supplemental oxygen dramatically improves OSA severity: preliminary results from the MADOX trial

Introduction Patients with obstructive sleep apnoea (OSA) considered ‘non-responders’ to mandibular advancement device (MAD) therapy, typically have a high loop gain contributing to their OSA physiology. While MAD does not improve loop gain, other treatments such as supplemental oxygen can have a strong effect on this pathogenic trait. Therefore, we conducted a randomised controlled trial (RCT) to determine whether the administration of supplemental oxygen in combination with a MAD, was associated with greater improvements in OSA severity compared to MAD therapy alone. Methods Patients recently diagnosed with OSA underwent an initial screening sleep study to confirm the presence of moderate-severe OSA (Apnoea-hypopnoea index [AHI]&gt;20events/hr). Eligible patients were then enrolled in a randomised single-blind cross-over trial involving 4 sleep studies with the following treatments; MAD, oxygen (4L/min), MAD+oxygen and room-air/sham (control). The primary outcome was the reduction in AHI (%baseline). Results Of the 57 participants screened, 35 met the eligibility criteria (Baseline/Screening AHI = 52±22 events/hr). Compared to the sham night, all treatments significantly reduced the AHI; a 35% [CI: 18–48] was seen with oxygen (p&lt;0.0002), a 53% [CI: 40–64] was seen with MAD (p&lt;0.0001) and a 67% [CI: 56–76] was seen with MAD+oxygen (p&lt;0.0001). Importantly, the combination of MAD+oxygen was associated with a significant reduction in AHI relative to MAD alone (15% [CI:4–24] p=0.01). Discussion In a population with moderate-severe OSA, preliminary analyses from this trial suggests that the addition of supplemental oxygen in combination with MAD therapy provided greater reductions in OSA severity than either treatment alone.