Phenotyping OSAH patients during wakefulness

Abstract

Purpose Although currently there are simplified methods to measure the pathophysiological traits that stimulate the occurrence and maintenance of obstructive sleep apnea-hypopnea (OSAH), they remain difficult to implement in routine practice. This pilot study aimed to find a simpler daytime approach to obtain a meaningful, similar pathophysiological phenotypic profile in patients with OSAH. Methods After obtaining diagnostic polygraphy from a group of consecutive patients with OSAH, we performed the dial-down CPAP technique during nocturnal polysomnography and used it as reference method. This allowed assessment of upper airway collapsibility, loop gain (LG), arousal threshold (AT), and upper airway muscle gain (UAG). We compared these results with a daytime protocol based on negative expiratory pressure (NEP) technique for evaluating upper airway collapsibility and UAG, on maximal voluntary apnea for LG, and on clinical predictors for AT. Results Of 15 patients studied, 13 patients with OSAH accurately completed the two procedures. There were strong (all r 2 > 0.75) and significant (all p < 0.001) correlations for each phenotypic trait between the measurements obtained through the reference method and those achieved during wakefulness. Conclusion It is possible to phenotype patients with OSAH from a pathophysiological point of view while they are awake. Using this approach, cutoff values corresponding to those usually adopted using the reference method can be identified to detect abnormal traits, achieving profiles similar to those obtained through the dial-down CPAP technique.

Obstructive Sleep Apnea and Adherence to Continuous Positive Airway Pressure (CPAP) Treatment: Let’s Talk about Partners!

“…It is estimated that 2 to 4% of normal-weight individuals, 3 to 28% of overweight individuals, and 40% of obese individuals suffer from this disease, with a higher prevalence in men compared to women [2,3]. A small and collapsible UA, and a lack of responsiveness in the pharyngeal muscles during sleep, are some of the key factors responsible for OSA [4,5]. Thus, structural alterations of the UA, such as adenotonsillar hypertrophy or craniofacial alterations, may induce UA collapse.…”