Simon A Joosten1,2,3,4, Michael Tan1,4, Ai-Ming Wong1,2, Shane A Landry5,6, Paul Leong1,2, Scott A Sands7,8, Caroline Beatty5,6, Luke Thomson5,6, Jeremy Stonehouse1, Anthony Turton1, Garun S Hamilton1,2,3, Bradley A Edwards5,6. 1. Monash Lung and Sleep, Monash Medical Centre, Clayton, Victoria, Australia. 2. School of Clinical Sciences, Monash University, Melbourne, Victoria, Australia. 3. Monash Partners-Epworth, Melbourne, Victoria, Australia. 4. Contributed equally. 5. Department of Physiology, School of Biomedical Sciences and Biomedical Discovery Institute, Monash University, Melbourne, Victoria, Australia. 6. Turner Institute for Brain and Mental Health, Monash University, Melbourne, Victoria, Australia. 7. Division of Sleep and Circadian Disorders, Departments of Medicine and Neurology, Brigham & Women's Hospital & Harvard Medical School, Boston, Massachusetts. 8. The Alfred and Monash University, Melbourne, Victoria, Australia.
Abstract
STUDY OBJECTIVES: We aimed to determine whether patients diagnosed with obstructive sleep apnea (OSA) who fail to respond to upper airway surgery may be successfully treated with supplemental oxygen and whether we could identify baseline physiologic endotypes (ie, collapsibility, loop gain, arousal threshold, and muscle compensation) that predict response to oxygen therapy. METHODS: We conducted a single night, randomized double-blinded cross over trial in which patients with OSA who failed to respond to upper airway surgery were treated on separate nights with oxygen therapy (4 L/min) or placebo (medical air). Effect of oxygen/air on OSA on key polysomnography outcomes were assessed: apnea-hypopnea index (AHI), AHI without desaturation (ie, flow-based AHI), arousal index, and morning blood pressure. OSA endotypes were estimated from the polysomnography signals to determine whether baseline OSA physiology could be used to predict response to oxygen therapy. RESULTS: There was a statistically significant reduction in AHI and flow-based AHI on oxygen vs placebo (flow-based AHI: 42.4 ± 21.5 vs 30.5 ± 17.1 events/h, P = .008). Arousal index was also reduced on oxygen vs placebo (41.1 ± 19.5 vs 33.0 ± 15.3 events/h, P = .006). There was no significant difference in morning blood pressure between oxygen and placebo. Although 7 of 20 individuals experienced a 50% reduction or greater in flow-based AHI on oxygen (responders), there was no difference in the baseline OSA endotypes (or clinical characteristics) between responders and nonresponders. CONCLUSIONS: Our findings demonstrate that a proportion of patients who fail to respond to upper airway surgery for OSA respond acutely to treatment with supplemental oxygen. CLINICAL TRIAL REGISTRATION: Registry: Australian New Zealand Clinical Trials Registry; Name: Oxygen therapy for treating patients with residual obstructive sleep apnea following upper airway surgery; URL: https://www.anzctr.org.au/Trial/Registration/TrialReview.aspx?id=373566; Identifier: ACTRN12617001361392.
STUDY OBJECTIVES: We aimed to determine whether patients diagnosed with obstructive sleep apnea (OSA) who fail to respond to upper airway surgery may be successfully treated with supplemental oxygen and whether we could identify baseline physiologic endotypes (ie, collapsibility, loop gain, arousal threshold, and muscle compensation) that predict response to oxygen therapy. METHODS: We conducted a single night, randomized double-blinded cross over trial in which patients with OSA who failed to respond to upper airway surgery were treated on separate nights with oxygen therapy (4 L/min) or placebo (medical air). Effect of oxygen/air on OSA on key polysomnography outcomes were assessed: apnea-hypopnea index (AHI), AHI without desaturation (ie, flow-based AHI), arousal index, and morning blood pressure. OSA endotypes were estimated from the polysomnography signals to determine whether baseline OSA physiology could be used to predict response to oxygen therapy. RESULTS: There was a statistically significant reduction in AHI and flow-based AHI on oxygen vs placebo (flow-based AHI: 42.4 ± 21.5 vs 30.5 ± 17.1 events/h, P = .008). Arousal index was also reduced on oxygen vs placebo (41.1 ± 19.5 vs 33.0 ± 15.3 events/h, P = .006). There was no significant difference in morning blood pressure between oxygen and placebo. Although 7 of 20 individuals experienced a 50% reduction or greater in flow-based AHI on oxygen (responders), there was no difference in the baseline OSA endotypes (or clinical characteristics) between responders and nonresponders. CONCLUSIONS: Our findings demonstrate that a proportion of patients who fail to respond to upper airway surgery for OSA respond acutely to treatment with supplemental oxygen. CLINICAL TRIAL REGISTRATION: Registry: Australian New Zealand Clinical Trials Registry; Name: Oxygen therapy for treating patients with residual obstructive sleep apnea following upper airway surgery; URL: https://www.anzctr.org.au/Trial/Registration/TrialReview.aspx?id=373566; Identifier: ACTRN12617001361392.
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