TY - JOUR
T1 - Assessment of continuous positive airway pressure treatment in obstructive sleep apnea syndrome using 24-hour urinary catecholamines
AU - Sukegawa, Mayo
AU - Noda, Akiko
AU - Sugiura, Tatsuki
AU - Nakata, Seiichi
AU - Yoshizaki, Shigehito
AU - Soga, Taro
AU - Yasuda, Yoshinari
AU - Iwayama, Norihisa
AU - Nakai, Shigeru
AU - Koike, Yasuo
PY - 2005/11
Y1 - 2005/11
N2 - Background: Obstructive sleep apnea syndrome (OSAS) is related to diurnal sympathetic hyperactivity and increased blood pressure, both factors that are likely to lead to the development of cardiovascular disease. Hypothesis: The study investigated whether 24-h urinary catecholamines would reflect the effect of obstructive sleep apnea on autonomic activity. Methods: Standard polysomnography was performed in 17 patients with OSAS (age 53.7 ± 13.5 years, mean ± standard deviation). The number of apnea/hypopnea episodes per hour of sleep (apnea/hypopnea index [AHI]); number of oxygen desaturation episodes per hour (desaturation index [DSI]); arousals per hour (arousal index); lowest oxygen saturation (lowest SpO2); and percentages of stages 1,2,3/4, and rapid eye movement sleep (% stage 1, -2, and -3/4, and % REM, respectively) were measured. Overnight continuous positive airway pressure (CPAP) titration was performed the night after the baseline sleep measurements had been taken. Twenty-four-hour urinary adrenaline and noradrenaline were also examined. Results: During the CPAP treatment, both 24-h urinary adrenaline and noradrenaline were significantly lower compared with natural sleep. Continuous positive airway pressure significantly decreased the AHI, DSI, % stage 1, and arousal index and significantly increased the lowest SpO2. There were no significant differences in % stage 2, % stage 3/4, and % REM between before and during CPAP treatment. Multiple analysis of covariance tests revealed that lowest SpO2 was the most important factor for increasing 24-h urinary noradrenaline levels (F = 4.75, p = 0.048). Conclusions: One night CPAP treatment could improve autonomic dysfunction. The assessment of 24-h urinary noradrenaline would provide important information for evaluating the effect of CPAP treatment.
AB - Background: Obstructive sleep apnea syndrome (OSAS) is related to diurnal sympathetic hyperactivity and increased blood pressure, both factors that are likely to lead to the development of cardiovascular disease. Hypothesis: The study investigated whether 24-h urinary catecholamines would reflect the effect of obstructive sleep apnea on autonomic activity. Methods: Standard polysomnography was performed in 17 patients with OSAS (age 53.7 ± 13.5 years, mean ± standard deviation). The number of apnea/hypopnea episodes per hour of sleep (apnea/hypopnea index [AHI]); number of oxygen desaturation episodes per hour (desaturation index [DSI]); arousals per hour (arousal index); lowest oxygen saturation (lowest SpO2); and percentages of stages 1,2,3/4, and rapid eye movement sleep (% stage 1, -2, and -3/4, and % REM, respectively) were measured. Overnight continuous positive airway pressure (CPAP) titration was performed the night after the baseline sleep measurements had been taken. Twenty-four-hour urinary adrenaline and noradrenaline were also examined. Results: During the CPAP treatment, both 24-h urinary adrenaline and noradrenaline were significantly lower compared with natural sleep. Continuous positive airway pressure significantly decreased the AHI, DSI, % stage 1, and arousal index and significantly increased the lowest SpO2. There were no significant differences in % stage 2, % stage 3/4, and % REM between before and during CPAP treatment. Multiple analysis of covariance tests revealed that lowest SpO2 was the most important factor for increasing 24-h urinary noradrenaline levels (F = 4.75, p = 0.048). Conclusions: One night CPAP treatment could improve autonomic dysfunction. The assessment of 24-h urinary noradrenaline would provide important information for evaluating the effect of CPAP treatment.
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U2 - 10.1002/clc.4960281106
DO - 10.1002/clc.4960281106
M3 - Article
C2 - 16450795
AN - SCOPUS:27744555030
SN - 0160-9289
VL - 28
SP - 519
EP - 522
JO - Clinical Cardiology
JF - Clinical Cardiology
IS - 11
ER -