Pro: can physiological risk factors for obstructive sleep apnea be determined by analysis of data obtained from routine polysomnography?

Abstract

This article is a written debate between the author(s) of this article and the author(s) of the opposing argument [1]. The following argument was prepared in response to the question without the knowledge of the contents of the opposing argument. Obstructive sleep apnea (OSA) is a highly prevalent disorder characterized by heterogeneous underlying mechanisms and heterogeneous adverse outcomes. Over the last 20 years, investigators have described how OSA is manifest as a combination of several established physiological risk factors or “endotypic traits”: greater pharyngeal collapsibility, dampened pharyngeal dilator muscle compensation, hyper-responsive ventilatory control (elevated loop gain), and a low arousal threshold (increased arousability from sleep). Evidence for important roles of each pathophysiological pathway are extensive. Profoundly improving pharyngeal collapsibility with CPAP is highly efficacious for resolving OSA, and individuals without a collapsible pharynx (critical collapsing pressure <5 cmH2O) very rarely exhibit OSA [2, 3]; thus, a level of pharyngeal mechanical vulnerability is considered a requirement for OSA. Yet measures of collapsibility alone do not accurately predict the presence/absence of OSA, that is, for the same level of collapsibility some patients exhibit severe OSA and others do not. The two leading endotypic traits responsible for modifying OSA risk are reduced muscle compensation and elevated loop gain. Notably, obese individuals without OSA typically exhibit augmented muscle responses [4], and loop gain is elevated in OSA patients with less-severe collapsibility [5]. A lower arousal threshold is considered to contribute to more severe OSA within participants in lighter non-REM and REM [6].