Peter Durdik1, Anna Sujanska1,2, Stanislava Suroviakova1, Melania Evangelisti2, Peter Banovcin1, Maria Pia Villa2. 1. Comenius University in Bratislava, Jessenius Faculty of Medicine in Martin, Pediatric Department, Slovakia. 2. Neuroscience, Mental Health and Sense Organs Department, Pediatric Sleep Disease Centre, S. Andrea Hospital, "Sapienza" University of Rome, Rome, Italy.
Abstract
STUDY OBJECTIVES: In children, the effect of the common phenotype of obstructive sleep apnea (OSA) on sleep architecture is not adequately documented. The aim of this study was to evaluate sleep architecture in a pediatric population with the common phenotype of OSA. METHODS: The prospective cross-sectional study included 116 children in the age range of 3 to 8 years with suspected OSA and 51 healthy children. All children underwent standard overnight in-laboratory video polysomnography. Patients with obstructive apnea-hypopnea index ≥ 1, adenotonsillar hypertrophy, a long face, narrow palate or minor malocclusions, and no obesity were defined as a common phenotype. Polysomnographic parameters of sleep architecture and sleep clinical record were statistically analyzed according to OSA and its severity. RESULTS: In total, 94 pediatric patients (59.60% male) received the diagnosis of the common phenotype of OSA (mean age of 5.25 ± 1.39 years). A lower percentage of stage N3 sleep (27.70 ± 3.76% versus 31.02 ± 4.23%; P < .05), a greater percentage of stage N1 sleep (8.40 ± 3.98% versus 2.68 ± 3.02%, P < .01), reduced deep sleep efficiency (46.01 ± 4.98% versus 50.25 ± 3.72%; P < .05) and longer sleep latency (18.40 ± 8.48 minutes versus 9.90 ± 11.55 minutes, P < .01) were found in children with the common phenotype of OSA compared with healthy controls. No significant differences were found in total sleep time, sleep efficiency, and percentage of stage R sleep and stage N2 sleep between groups and in sleep stage distribution and cyclization. CONCLUSIONS: These findings suggest that the most common phenotype of pediatric OSA has a negative effect on the structure of sleep, but other clinical studies are needed to confirm this result.
STUDY OBJECTIVES: In children, the effect of the common phenotype of obstructive sleep apnea (OSA) on sleep architecture is not adequately documented. The aim of this study was to evaluate sleep architecture in a pediatric population with the common phenotype of OSA. METHODS: The prospective cross-sectional study included 116 children in the age range of 3 to 8 years with suspected OSA and 51 healthy children. All children underwent standard overnight in-laboratory video polysomnography. Patients with obstructive apnea-hypopnea index ≥ 1, adenotonsillar hypertrophy, a long face, narrow palate or minor malocclusions, and no obesity were defined as a common phenotype. Polysomnographic parameters of sleep architecture and sleep clinical record were statistically analyzed according to OSA and its severity. RESULTS: In total, 94 pediatric patients (59.60% male) received the diagnosis of the common phenotype of OSA (mean age of 5.25 ± 1.39 years). A lower percentage of stage N3 sleep (27.70 ± 3.76% versus 31.02 ± 4.23%; P < .05), a greater percentage of stage N1 sleep (8.40 ± 3.98% versus 2.68 ± 3.02%, P < .01), reduced deep sleep efficiency (46.01 ± 4.98% versus 50.25 ± 3.72%; P < .05) and longer sleep latency (18.40 ± 8.48 minutes versus 9.90 ± 11.55 minutes, P < .01) were found in children with the common phenotype of OSA compared with healthy controls. No significant differences were found in total sleep time, sleep efficiency, and percentage of stage R sleep and stage N2 sleep between groups and in sleep stage distribution and cyclization. CONCLUSIONS: These findings suggest that the most common phenotype of pediatric OSA has a negative effect on the structure of sleep, but other clinical studies are needed to confirm this result.
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