Cardiovascular Consequences of Repetitive Arousals over the Entire Sleep Duration

Objectives. To explore the cardiovascular effects of nightlong repetitive arousals (RA). Methods. Twenty healthy subjects participated in two consecutive sleep studies. The first one was free of intervention and the second study involved repetitive arousals induced by acoustical stimuli. Blood pressure, heart rate variability (HRV), arterial stiffness index (ASI), and serum markers including nitric oxide (NO), endothelin-1 (ET-1), C-reactive protein (CRP), interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), and vascular endothelial growth factor (VEGF) were studied. Results. RA led to overnight elevation in diastolic blood pressure (DBP) but not in systolic blood pressure (SBP). Regarding HRV, overnight increase in low frequency power (LF) and low frequency to high frequency ratio (LHR) and decrease in high frequency power (HF) were evident. The relative overnight differences in HF and LHR correlated with the amount of rapid-eye movement (REM) sleep. RA did not cause detectable change in either ASI or serum markers of interest. Conclusions. Nightlong RA alters the sympathovagal modulation significantly and this effect seems to be associated with the amount of REM sleep. Exposure to RA also causes an elevation in postsleep DBP. Disturbance to autonomic nervous system (ANS) may precede endothelial dysfunction and increased arterial stiffness as cardiovascular consequences of RA.

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