High Respiratory Arousal Threshold as a Potential Pathophysiological Biomarker of Excessive Daytime Sleepiness in Obstructive Sleep Apnoea

Obstructive sleep apnoea (OSA) is caused by impaired pharyngeal anatomy of varying severity, and in most cases, accompanying contributions from one or more non-anatomical mechanisms or “endotypes” . Non-anatomical endotypes include poor pharyngeal dilator muscle function, oversensitivity of the respiratory control system (high loop gain) and waking up too easily to minor airway narrowing episodes (low respiratory arousal threshold). In a recent publication in Respirology, Wang and colleagues applied the “phenotyping using polysomnography (PUP)” algorithm to estimate the four key OSA endotypes from overnight diagnostic study data in > 500 people with an apnoea/hypopnea index (AHI) > 5 events per hour/sleep. Consistent with gold standard quantification of OSA endotypes combined with machine learning analytical approaches in a smaller sample that indicate different combinations OSA endotypes contribute to OSA severity as defined by the AHI, and recent related findings, Wang and colleagues also found that OSA endotypes contribute to OSA severity. These data provide further support for the importance of OSA endotypes in driving OSA pathophysiology.