Influence of movement arousal on circardian rhythm of blood pressure in obstructive sleep apnea syndrome

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ObjectiveTo investigate the hypothesis that repeated arousals at the termination of apnea/hypopnea in obstructive sleep apnea syndrome (OSAS) are related to abnormal circadian rhythm of blood pressure (BP).Design and methods We performed polysomnography (PSG) with pulse oximetry in 26 middle-aged patients with OSAS aged 42–58 years (mean age 51.8 years). The intensity of arousal on PSG was graded into two levels: grade 1 (EEG arousal, EA), an abrupt shift in EEG frequency, and grade 2 (movement arousal, MA), EEG arousal with an increase in electromyogram activity lasting at least 3 s. The number of apnea/hypopneas per hour (apnea/hypopnea index, AHI), and length of time during which nocturnal oxygen saturation decreased below 90% (oxygen desaturation time, ODT) were also evaluated. Percentage EA and %MA were assessed by the ratio of the number of apneas and hypopneas with EA or MA to the number of apneas and hypopneas in total. The 24 h systolic blood pressure (SBP) and diastolic blood pressure (DBP) were measured noninvasively. Multiple regression analysis was performed among AHI, ODT, %EA and %MA or among age, body mass index and %MA.ResultsThe %MA was the most significant factor contributing to the elevated 24 h SBP (r = 0.46, P <0.05); oxygen desaturation (r = 0.44, P <0.05) was the next most important contributing factor. The level and pattern of 24 h BP differed significantly between the patients with %MA 85% and %MA <85% (mean 24 h SBP: 147 ± 16.8 versus 125 ± 19.6 mmHg, P <0.01; mean 24 h DBP: 97.5 ± 14.3 versus 85.6 ± 14.6 mmHg, P <0.01), and also differed between those with severe OSAS, i.e. ODT >130 min, and mild to moderate OSAS, i.e. ODT <130 min, (mean 24 h SBP: 149 ± 15.8 versus 132 ± 20.6 mmHg, P <0.01; mean 24 h DBP: 100 ± 14.1 versus 87.4 ± 14.0 mmHg, P <0.01).ConclusionOur findings suggest that MA and oxygen desaturation in OSAS make an important contribution to abnormal circadian rhythm of BP. We conclude that repeated end-apneic arousal and/or hypoxic asphyxia and the subsequent sleep fragmentation may contibute to nocturnal and diurnal elevation of BP.

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