All patients were monitored with a nocturnal PSG that was performed with multichannel monitoring that included neurophysiological electrodes (electroencephalography electrodes), chest wall motion, abdominal motion, arterial oxygen saturation, and electrocardiography electrodes (Grass-Telefactor Cephalo, An Astro-med Inc. Product Group, 2005, USA). Oronasal airflow was measured using a thermistor. The oxyhemoglobin saturation was monitored with a finger pulse oximeter with a sampling rate of 1 Hz. The body position was measured by a position sensor attached to the anterior chest wall. Signals recorded in the sleep period were manually analyzed (25). Apneas were scored when the airflow decreased by at least 90% from baseline for at least 10 s and were classified as central, mixed, or obstructive depending on the occurrence of thoracoabdominal movements (25). Hypopneas were scored when airflow decreased by at least 30% for ≥10 s and was associated with an oxygen saturation (SaO2) fall of ≥3%. AHI was calculated as the average number of apneas and hypopneas per hour of recording in the sleep period. An AHI of ≥5 was used to diagnose OSA (26). SaO2 during the sleep period was automatically analyzed, and after the manual elimination of possible artifacts, mean SaO2 and lowest nocturnal SaO2 values were detected. According to their overall AHIs OSA patients were grouped as mild (5–14.9/h) and moderate to severe (>15/h) (25).
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