From Pulse to Phenotype: Sleep Apnea Endotyping for Polygraphy via Oximeter-Derived Autonomic Arousal.
case_series · Level IV
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- Record sourced from PubMed, PMID 41421575.
- Also identified by DOI 10.1016/j.chest.2025.12.005.
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Abstract
Understanding the underlying cause of OSA in the individual patient, referred to as pathophysiologic endotyping, is essential for personalized care. The current classification of these traits from routine sleep recordings relies on manually scored arousals from sleep. Automating this process could widen the applicability of endotyping. Can analyzing autonomic variability, derived from finger oximeter photoplethysmography, accurately classify sleep apnea pathophysiologic endotypes with results comparable with the established EEG-based method? Eighty-seven patients referred for suspected OSA underwent ambulatory polysomnography. Pulse wave amplitude, pulse rate, pulse propagation time, and blood oxygen saturation were extracted from photoplethysmography findings. A logistic mixed-effect model was developed to predict the presence of EEG-based arousals using these photoplethysmography-derived parameters after respiratory events. The automatically predicted photoplethysmography-based arousals then were incorporated into an established model (Phenotyping Using Polysomnography) to determine OSA endotypic traits from the airflow and photoplethysmography signal. The agreement between endotypes with photoplethysmography-based and EEG-based arousals was assessed using intraclass correlation coefficient (ICC). Photoplethysmography responses to respiratory events were more pronounced in the presence of arousal (P < .001 for all). The model using photoplethysmography metrics to predict cortical arousal demonstrated moderate performance (sensitivity, 0.71; specificity, 0.59). Endotypic traits derived by photoplethysmography-derived arousals showed strong agreement compared with the EEG-derived reference (ICC for loop gain at 1 cycle/min, 0.95 [95% CI, [0.88-0.98]; ICC for ventilation at active muscle activity, 0.96 [95% CI, 0.81-0.99]; ICC for ventilation at passive muscle activity, 0.99 [95% CI, 0.99-0.99]; ICC for ventilation at min muscle activity, 0.99 [0.99-0.99]; ICC for arousal threshold, 0.85 [95% CI, 0.48-0.96]; ICC for muscle compensation, 0.80 [95% CI, 0.60-0.91]). Using pulse wave features instead of manually scored EEG-based arousals in respiratory modelling allows for accurately determining OSA endotypes. This approach might enable physiologic endotyping in non-EEG-based sleep studies, expanding the accessibility of personalized OSA management.