Abstract

Autonomic dysfunction is recognized to contribute to cardiovascular consequences in obstructive sleep apnea/hypopnea syndrome (OSAHS) patients who present predominant cardiovascular sympathetic activity that persists during wakefulness. Here, we examined 1) the factors that influence sympathetic cardiac modulation in response to apneas/hypopneas; and 2) the influence of autonomic activity during apneas/hypopneas on CA. Sixteen OSAHS patients underwent in-hospital polysomnography. RR interval (RR) and RR spectral analysis using wavelet transform were used to study parasympathetic (high frequency power: HFWV) and sympathetic (low frequency power: LFWV and LFWV/HFWV ratio) activity before and after apnea/hypopnea termination. Autonomic cardiac modulations were compared according to sleep stage, apnea/hypopnea type and duration, arterial oxygen saturation, and presence of CA. At apnea/hypopnea termination, RR decreased (p<0.001) while LFWV (p = 0.001) and LFWV/HFWV ratio (p = 0.001) increased. Only RR and LFWV/HFWV ratio changes were higher when apneas/hypopneas produced CA (p = 0.030 and p = 0.035, respectively) or deep hypoxia (p = 0.023 and p = 0.046, respectively). Multivariate statistical analysis showed that elevated LFWV (p = 0.006) and LFWV/HFWV ratio (p = 0.029) during apneas/hypopneas were independently related to higher CA occurrence. Both the arousal and hypoxia processes may contribute to sympathetic cardiovascular overactivity by recurrent cardiac sympathetic modulation in response to apneas/hypopneas. Sympathetic overactivity also may play an important role in the acute central response to apneas/hypopneas, and in the sleep fragmentation.

Highlights

  • Epidemiological studies suggest that obstructive sleep apnea/ hypopnea syndrome (OSAHS) is common in the general population [1], and provide strong evidence that OSAHS is associated with significantly high cardiovascular morbidity and mortality [2]

  • Autonomic dysfunction is recognized to contribute to these cardiovascular consequences [3] in OSAHS patients who present decrease in heart rate variability (HRV) [4] and predominant cardiovascular sympathetic activity that persists during wakefulness [5]

  • Due to lack of apneas/hypopneas during SWS in some OSAHS patients, statistical analysis was performed on 7 subjects for comparison between sleep stages

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Summary

Introduction

Epidemiological studies suggest that obstructive sleep apnea/ hypopnea syndrome (OSAHS) is common in the general population [1], and provide strong evidence that OSAHS is associated with significantly high cardiovascular morbidity and mortality [2]. Sympathetic sleep fragmentation was associated with elevated nocturnal and diurnal systolic blood pressure and higher risk of systolic hypertension [6]. Studying the mechanisms that control sympathetic cardiac modulation in response to apneas/hypopneas by HRV should improve our understanding of the cardiovascular risk factor in OSAHS populations. OSAHS is characterized by repeated episodes of total (apneas) or partial (hypopneas) upper airway occlusion during sleep, resulting in exaggerated negative intrathoracic pressure and often oxygen desaturation and carbon dioxide retention [3]. Apneas/hypopneas elicit oscillations in both parasympathetic and sympathetic cardiac activities that affect RR intervals (RR), characterized by increased parasympathetic activity during apneas/hypopneas and increased sympathetic activity at apnea/hypopnea termination [8,9,10]

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