RATIONALE: Increased variability in ventilation may contribute to the pathogenesis of obstructive sleep apnea (OSA) by promoting ventilatory instability, fluctuations of neuromuscular output to the upper airway, and pharyngeal collapsibility. We assessed the association of a measure of ventilatory variability measured at the wake-sleep transition with OSA and associated covariates. METHODS: Four hundred eighty-five participants in the Cleveland Family Study underwent overnight polysomnography with independent derivation of the ventilatory variability index (VVI) and the apnea-hypopnea index (AHI). The VVI was calculated from the variability in the power spectrum of the abdominal inductance signal over a 2-min period beginning at sleep onset. RESULTS: The VVI was strongly correlated with the AHI (r=0.43; p<0.001). After adjusting for age, body mass index, sex, and race, the VVI remained significantly associated with AHI (p<0.001). The adjusted odds ratio for OSA (AHI, >or=15) with each half SD increase in VVI was 1.41 (range, 1.25 to 1.59). In a subgroup analysis of obese snorers, to limit analyses to those with a presumed anatomic predisposition for apnea, VVI remained associated with an elevated AHI. CONCLUSIONS: Increased ventilatory variability may be a useful phenotype in characterizing OSA.
RATIONALE: Increased variability in ventilation may contribute to the pathogenesis of obstructive sleep apnea (OSA) by promoting ventilatory instability, fluctuations of neuromuscular output to the upper airway, and pharyngeal collapsibility. We assessed the association of a measure of ventilatory variability measured at the wake-sleep transition with OSA and associated covariates. METHODS: Four hundred eighty-five participants in the Cleveland Family Study underwent overnight polysomnography with independent derivation of the ventilatory variability index (VVI) and the apnea-hypopnea index (AHI). The VVI was calculated from the variability in the power spectrum of the abdominal inductance signal over a 2-min period beginning at sleep onset. RESULTS: The VVI was strongly correlated with the AHI (r=0.43; p<0.001). After adjusting for age, body mass index, sex, and race, the VVI remained significantly associated with AHI (p<0.001). The adjusted odds ratio for OSA (AHI, >or=15) with each half SD increase in VVI was 1.41 (range, 1.25 to 1.59). In a subgroup analysis of obese snorers, to limit analyses to those with a presumed anatomic predisposition for apnea, VVI remained associated with an elevated AHI. CONCLUSIONS: Increased ventilatory variability may be a useful phenotype in characterizing OSA.
Authors: K Kump; C Whalen; P V Tishler; I Browner; V Ferrette; K P Strohl; C Rosenberg; S Redline Journal: Am J Respir Crit Care Med Date: 1994-09 Impact factor: 21.405
Authors: Frank J Jacono; Catherine A Mayer; Yee-Hsee Hsieh; Christopher G Wilson; Thomas E Dick Journal: Respir Physiol Neurobiol Date: 2011-05-06 Impact factor: 1.931