Journal
AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE
Volume 194, Issue 11, Pages 1413-1422Publisher
AMER THORACIC SOC
DOI: 10.1164/rccm.201601-0099OC
Keywords
upper-airway anatomy; obstructive sleep apnea; ventilation
Categories
Funding
- National Institutes of Health [5R01HL102321-02]
- Harvard Catalyst Clinical Research Center [UL1 RR 025758-01]
- Monash Lung and Sleep Department
- National Health and Medical Research Council (NHMRC) of Australia's CJ Martin Overseas Biomedical Fellowship [1035115]
- NHMRC Centre of Research Excellence
- NeuroSleep
- NHMRC Early Career Fellowship
- R. G. Menzies award [1053201]
- American Heart Association [11POST7360012, 15SDG25890059]
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Rationale: Oral appliances (OAs) are commonly used as an alternative treatment to continuous positive airway pressure for patients with obstructive sleep apnea (OSA). However, OAs have variable success at reducing the apnea-hypopnea index (AHI), and predicting responders is challenging. Understanding this variability may lie with the recognition that OSA is a multifactorial disorder and that OAs may affect more than just upper-airway anatomy/collapsibility. Objectives: The objectives of this study were to determine how OA alters AHI and four phenotypic traits (upper-airway anatomy/collapsibility and muscle function, loop gain, and arousal threshold), and baseline predictors of which patients gain the greatest benefit from therapy. Methods: In a randomized crossover study, 14 patients with OSA attended two sleep studies with and without their OA. Under each condition, AHI and the phenotypic traits were assessed. Multiple linear regression was used to determine independent predictors of the reduction in AHI. Measurements and Main Results: OA therapy reduced the AHI (30 +/- 5 vs. 11 +/- 2 events/h; P < 0.05), which was driven by improvements in upper-airway anatomy/collapsibility under passive (1.9 +/- 0.7 vs. 4.7 +/- 0.6 L/min; P < 0.005) and active conditions (2.4 +/- 0.9 vs. 6.2 +/- 0.4 L/min; P < 0.001). No changes were seen in muscle function, loop gain, or the arousal threshold. Using multivariate analysis, baseline passive upper-airway collapsibility and loop gain were independent predictors of the reduction in AHI (r(2) = 0.70; P = 0.001). Conclusions: Our findings suggest that OA therapy improves the upper-airway collapsibility under passive and active conditions. Importantly, a greater response to therapy occurred in those patients with a mild anatomic compromise and a lower loop gain.
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