The Effect of Hypopnea Scoring on the Arousal Threshold in Patients with Obstructive Sleep Apnea.
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ABSTRACT:
SUBMITTER: Thomson LDJ
PROVIDER: S-EPMC7924649 | biostudies-literature | 2020 Nov
REPOSITORIES: biostudies-literature
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The Effect of Hypopnea Scoring on the Arousal Threshold in Patients with Obstructive Sleep Apnea.
Thomson Luke D J LDJ Landry Shane A SA Singleton Rebecca R Wong Ai-Ming AM Joosten Simon A SA Beatty Caroline J CJ Eckert Danny J DJ Malhotra Atul A Hamilton Garun S GS Edwards Bradley A BA
American journal of respiratory and critical care medicine 20201101 9
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Project description:Study objectivesIt has been hypothesized that arousals after apnea and hypopnea events in patients with obstructive sleep apnea are triggered when neural respiratory drive exceeds a certain level, but this hypothesis is based on esophageal pressure data, which are dependent on flow and lung volume. We aimed to determine whether a fixed threshold of respiratory drive is responsible for arousal at the termination of apnea and hypopnea using a flow independent technique (esophageal diaphragm electromyography, EMGdi) in patients with obstructive sleep apnea.SettingSleep center of state Key Laboratory of Respiratory Disease.PatientsSeventeen subjects (two women, mean age 53 ± 11 years) with obstructive sleep apnea/hypopnea syndrome were studied.MethodsWe recorded esophageal pressure and EMGdi simultaneously during overnight full polysomnography in all the subjects.Measurements and resultsA total of 709 hypopnea events and 986 apnea events were analyzed. There was wide variation in both esophageal pressure and EMGdi at the end of both apnea and hypopnea events within a subject and stage 2 sleep. The EMGdi at the end of events that terminated with arousal was similar to those which terminated without arousal for both hypopnea events (27.6% ± 13.9%max vs 29.9% ± 15.9%max, P = ns) and apnea events (22.9% ± 11.5%max vs 22.1% ± 12.6%max, P = ns). The Pes at the end of respiratory events terminated with arousal was also similar to those terminated without arousal. There was a small but significant difference in EMGdi at the end of respiratory events between hypopnea and apnea (25.3% ± 14.2%max vs 21.7% ± 13.2%max, P < 0.05].ConclusionsOur data do not support the concept that there is threshold of neural respiratory drive that is responsible for arousal in patients with obstructive sleep apnea.
| S-EPMC4434561 | biostudies-literature
Project description:Precision medicine for obstructive sleep apnea (OSA) requires noninvasive estimates of each patient's pathophysiological "traits." Here, we provide the first automated technique to quantify the respiratory arousal threshold-defined as the level of ventilatory drive triggering arousal from sleep-using diagnostic polysomnographic signals in patients with OSA. Ventilatory drive preceding clinically scored arousals was estimated from polysomnographic studies by fitting a respiratory control model (Terrill et al.) to the pattern of ventilation during spontaneous respiratory events. Conceptually, the magnitude of the airflow signal immediately after arousal onset reveals information on the underlying ventilatory drive that triggered the arousal. Polysomnographic arousal threshold measures were compared with gold standard values taken from esophageal pressure and intraoesophageal diaphragm electromyography recorded simultaneously (N = 29). Comparisons were also made to arousal threshold measures using continuous positive airway pressure (CPAP) dial-downs (N = 28). The validity of using (linearized) nasal pressure rather than pneumotachograph ventilation was also assessed (N = 11). Polysomnographic arousal threshold values were correlated with those measured using esophageal pressure and diaphragm EMG (R = 0.79, p < .0001; R = 0.73, p = .0001), as well as CPAP manipulation (R = 0.73, p < .0001). Arousal threshold estimates were similar using nasal pressure and pneumotachograph ventilation (R = 0.96, p < .0001). The arousal threshold in patients with OSA can be estimated using polysomnographic signals and may enable more personalized therapeutic interventions for patients with a low arousal threshold.
| S-EPMC5804982 | biostudies-literature
Project description:Obstructive sleep apnea (OSA) severity is markedly reduced during slow-wave sleep (SWS) even in patients with a severe disease. The reason for this improvement is uncertain but likely relates to non-anatomical factors (i.e. reduced arousability, chemosensitivity, and increased dilator muscle activity). The anticonvulsant tiagabine produces a dose-dependent increase in SWS in subjects without OSA. This study aimed to test the hypothesis that tiagabine would reduce OSA severity by raising the overall arousal threshold during sleep. After a baseline physiology night to assess patients' OSA phenotypic traits, a placebo-controlled, double-blind, crossover trial of tiagabine 12 mg administered before sleep was performed in 14 OSA patients. Under each condition, we assessed the effects on sleep and OSA severity using standard clinical polysomnography. Tiagabine increased slow-wave activity (SWA) of the electroencephalogram (1-4 Hz) compared to placebo (1.8 [0.4] vs. 2.0 [0.5] LogμV2, p = .04) but did not reduce OSA severity (apnea-hypopnea index [AHI] 41.5 [20.3] vs. 39.1 [16.5], p > .5). SWS duration (25 [20] vs. 26 [43] mins, p > .5) and arousal threshold (-26.5 [5.0] vs. -27.6 [5.1] cmH2O, p = .26) were also unchanged between nights. Tiagabine modified sleep microstructure (increase in SWA) but did not change the duration of SWS, OSA severity, or arousal threshold in this group of OSA patients. Based on these findings, tiagabine should not be considered as a therapeutic option for OSA treatment.
| S-EPMC6084757 | biostudies-literature
Project description:In order to investigate the gene expression patterns and molecular regulatory mechanisms of obstructive sleep apnea hypopnea syndrome (OSAHS), the global transcriptome expression profiles of OSAHS patients and healthy people were analyzed using transcriptome sequencing technology. Differential expression of circular RNA, microRNA, long noncoding RNA, and messenger RNA was investigated between the two groups.
2025-04-01 | GSE293433 | GEO
Project description:RationaleObstructive sleep apnea (OSA) has multiple pathophysiological causes. A low respiratory arousal threshold (ArTh) and a high loop gain (unstable ventilatory control) can contribute to recurrent respiratory events in patients with OSA. Prior studies have shown that donepezil, an acetylcholinesterase inhibitor, might improve OSA, but the mechanism is unknown.ObjectivesTo determine whether a single dose of donepezil lowers the apnea-hypopnea index by modulating the ArTh or loop gain.MethodsIn this randomized, double-blind, crossover trial, 41 subjects with OSA underwent two polysomnograms with ArTh and loop gain evaluated, during which 10 mg of donepezil or placebo was administered.Measurements and main resultsCompared with placebo, sleep efficiency (77.2 vs. 71.9%; P = 0.015) and total sleep time decreased with donepezil (372 vs. 351 min; P = 0.004). No differences were found in apnea-hypopnea index (51.8 vs. 50.0 events/h; P = 0.576) or nadir oxygen saturation as determined by pulse oximetry (80.3 vs. 81.1%; P = 0.241) between placebo and donepezil, respectively. ArTh was not significantly changed (-18.9 vs. -18.0 cm H2O; P = 0.394) with donepezil. As a whole group, loop gain (ventilatory response to a 1-cycle/min disturbance) did not change significantly (P = 0.089).ConclusionsA single dose of donepezil did not appear to affect the overall severity of OSA in this patient group, and no consistent effects on ArTh or loop gain were observed. Donepezil may have minor effects on sleep architecture. Clinical trial registered with www.clinicaltrials.gov (NCT02264353).
| S-EPMC5122481 | biostudies-literature
Project description:RationaleAlthough obstructive sleep apnea is associated with physiological perturbations that increase risk of hypertension and are proatherogenic, it is uncertain whether sleep apnea is associated with increased stroke risk in the general population.ObjectivesTo quantify the incidence of ischemic stroke with sleep apnea in a community-based sample of men and women across a wide range of sleep apnea.MethodsBaseline polysomnography was performed between 1995 and 1998 in a longitudinal cohort study. The primary exposure was the obstructive apnea-hypopnea index (OAHI) and outcome was incident ischemic stroke.Measurements and main resultsA total of 5,422 participants without a history of stroke at the baseline examination and untreated for sleep apnea were followed for a median of 8.7 years. One hundred ninety-three ischemic strokes were observed. In covariate-adjusted Cox proportional hazard models, a significant positive association between ischemic stroke and OAHI was observed in men (P value for linear trend: P = 0.016). Men in the highest OAHI quartile (>19) had an adjusted hazard ratio of 2.86 (95% confidence interval, 1.1-7.4). In the mild to moderate range (OAHI, 5-25), each one-unit increase in OAHI in men was estimated to increase stroke risk by 6% (95% confidence interval, 2-10%). In women, stroke was not significantly associated with OAHI quartiles, but increased risk was observed at an OAHI greater than 25.ConclusionsThe strong adjusted association between ischemic stroke and OAHI in community-dwelling men with mild to moderate sleep apnea suggests that this is an appropriate target for future stroke prevention trials.
| S-EPMC2913239 | biostudies-literature
Project description:ObjectivePatients with sleep apnea/hypopnea syndrome and episodes of increased systolic pressure during sleep, with and without arterial hypertension, and HT as a marker of increased cardiovascular risk, were studied in a prospective study. The objective of our study was to demonstrate that patients with increased systolic pressure during sleep who also had arterial hypertension had a higher cardiovascular risk than non-hypertensive patients.MethodsWe analyzed various biometric (muscle mass index, baseline blood pressure) and polysomnographic parameters, including AHI (apnea-hypopnea index/hour), O2 desaturation index/hour, arousal index, baseline and minimum O2 saturation and the proportion of different sleep phases, together with comorbidities and associated treatments in patients with sleep apnea/hypopnea syndrome (64 with arterial hypertension and 38 non-hypertensive patients) with episodes of increased systolic blood pressure during sleep during polysomnographic studies conducted between 2013 and 2017 and in 2020.ResultsThere were no statistically significant differences in the different parameters between study groups. Patients in both groups developed comorbidities in the follow-up period, more frequently in the hypertensive group, and required new treatments, especially the group of patients with HT.ConclusionEpisodes of increased systolic pressure during sleep suggest an increased cardiovascular risk in patients with sleep apnea syndrome and arterial hypertension in terms of associated comorbidities. However, in non-hypertensive patients, episodes of increased systolic pressure may also be associated with a higher risk of vascular comorbidities (higher than the risk associated with isolated obstructive sleep apneas).
| S-EPMC10369631 | biostudies-literature
Project description:Rationale: Patients with obstructive sleep apnea (OSA) experience respiratory events with greater frequency and severity while in the supine sleeping position. Postural preference (associated with the sleep monitoring device) and "first night effect" could explain a night-to-night variability in OSA severity. Objectives: We evaluated the variability of internight polysomnography (PSG) in a large group of OSA patients and explored factors explaining this variability. Methods: 188 patients referred for probable OSA (aged 54.9 ± 11.8 y) underwent two consecutive nights of at-home PSG. The effect of age, gender, obesity, neck circumference, sleep position and sleep parameters were considered to explain changes in respiratory parameters. Main Results: The mean apnea-hypopnea index (AHI) and oxygen desaturation index (ODI) were respectively, 36.3 ± 27.5 and 22.0 ± 22.7 in the first night, with a tendency to decrease during the second night. While in mild cases (5 ? AHI < 15) there was a significant increase in AHI related to an increase in dorsal position time during the second night, there were no changes in moderate cases (15 ? AHI < 30); and in severe cases (AHI ? 30) there was a significant decrease in both AHI and ODI during the second night independent of sleep position. Conclusion: The internight variability in AHI and ODI was related to changes in sleep structure with a contribution of indices of sleep fragmentation and dorsal position. Since the changes were greater in mild OSA cases, a second night could be routinely proposed in cases with relevant clinical uncertainty.
| S-EPMC6630080 | biostudies-literature
Project description:A low arousal threshold (LAT) is a pathophysiological trait of obstructive sleep apnea (OSA) that may be associated with brainstem ascending reticular activating system-cortical functional connectivity changes. We evaluated resting-state connectivity between the brainstem nuclei and 105 cortical/subcortical regions in OSA patients with or without a LAT and healthy controls. Twenty-five patients with moderate to severe OSA with an apnea-hypopnea index between 20 and 40/hr (15 with and 10 without a LAT) and 15 age- and sex-matched controls were evaluated. Participants underwent functional magnetic resonance imaging after overnight polysomnography. Three brainstem nuclei-the locus coeruleus (LC), laterodorsal tegmental nucleus (LDTg), and ventral tegmental area (VTA)-associated with OSA in our previous study were used as seeds. Functional connectivity values of the two brainstem nuclei (LC and LDTg) significantly differed among the three groups. The connectivity of the LC with the precuneus was stronger in OSA patients than in controls regardless of the concomitant LAT. The connectivity between the LDTg and the posterior cingulate cortex was also stronger in OSA patients regardless of the LAT. Moreover, OSA patients without a LAT showed stronger LDTg-posterior cingulate cortex connectivity than those with a LAT (post hoc p = 0.013), and this connectivity strength was negatively correlated with the minimum oxygen saturation in OSA patients (r = - 0.463, p = 0.023). The LAT in OSA patients was associated with altered LDTg-posterior cingulate cortex connectivity. This result may suggested that cholinergic activity may play a role in the LAT in OSA patients.
| S-EPMC11315983 | biostudies-literature
Project description:BackgroundPatients with obstructive sleep apnea/hypopnea syndrome (OSAHS), even those generally compliant with CPAP therapy, often intermittently discontinue CPAP.Study objectiveExamine the impact of CPAP withdrawal on sleep, sleep disordered breathing (SDB), and daytime function in subjects with varying severity of OSAHS.Patients and interventionsForty-two subjects (26M/16 F) with OSAHS (AHI4% = 45.2 ± 35.5/h pretreatment) on CPAP for 4 months were evaluated on the second night of CPAP withdrawal. Sleep architecture, SDB indices, and subjective/objective daytime function were assessed pretreatment, on CPAP therapy, and after CPAP withdrawal. Comparisons were made between pretreatment and CPAP withdrawal for the entire group, and for subgroups of mild/moderate (AHI4% < 30/h, n = 22) and severe (AHI4% > 30/h, n = 20) SDB.ResultsOverall, and for mild/moderate subjects, SDB indices returned to pretreatment values on CPAP withdrawal but with fewer apneas and more hypopneas/RERAs. For severe SDB, the event frequency (AI, AHI4%, and RDI) was lower and O2 desaturation was improved on CPAP withdrawal. Across SDB severity, sleep architecture showed lower %REM (15.6% vs 12.9%, P = 0.009) on the CPAP withdrawal compared to pretreatment. Stanford Sleepiness Score, MSLT, and PVT measures were not significantly different between pretreatment and CPAP withdrawal.ConclusionsOver a wide range of SDB severity CPAP withdrawal results in recurrence of SDB, albeit with less severe O2 desaturation. Subjective/objective daytime function returned to pretreatment levels. Sleep architecture changes on CPAP withdrawal (acute SDB) may reflect reduced sleep pressure compared to pretreatment chronic SDB. Our data suggest detrimental effects of even brief withdrawal of CPAP in subjects with both mild and severe OSAHS.CitationYoung LR; Taxin ZH; Norman RG; Walsleben JA; Rapoport DM; Ayappa I. Response to CPAP withdrawal in patients with mild versus severe obstructive sleep apnea/hypopnea syndrome. SLEEP 2013;36(3):405-412.
| S-EPMC3571747 | biostudies-literature