Objective <p>Nocturnal blood pressure (BP) surge is a characteristic phenomenon in patients with obstructive sleep apnea (OSA) associated with sympathetic nerve overactivity. This study aimed to explore the relationship between the sleep-breathing events induced nocturnal BP surge and sympathetic nerve activity.</p> Methods <p>A total of 85 patients with moderate-to-serve OSA and 44 controls were included in the study between April 2022 and October 2023 based on the inclusion and exclusion criteria. Full-night BP and heart rate variability (HRV) were monitored continuously and synchronized with polysomnography (PSG). The average of nocturnal BPs was taken as the asleep BP and the average of the highest BPs induced by all sleep-breathing events as the asleep peak BP. Nocturnal short-term BP variability (BPV) was calculated as follows: event-related systolic BP elevation (ΔSBP) as the gap between the peak and the lowest value of post-apneic SBP, BP index as the number of ΔSBP ≥ 12&#xa0;mm Hg within 30&#xa0;s/h, and the percentage of BP fluctuation induced by sleep-breathing events (PBPF) as the ratio of BP index and apnea-hypopnea index. Patients with OSA were divided into two subgroups (high– and low–BP surge groups) according to the median PBPF. The sympathetic nerve activity was reflected by plasma norepinephrine (NE) level and HRV. The PSG and BP parameters were compared among three groups, and the correlation between nocturnal short-term BPV and sympathetic nerve activity was analyzed.</p> Results <p>Patients with OSA were fatter and suffered from dyslipidemia and sympathetic nerve overactivity compared to controls. The high–BP surge group displayed higher sympathetic nerve activity and more severe hypoxia compared with the low–BP surge group. The Pearson correlation analysis showed a positive correlation of the higher nocturnal short-term BPV with increased sympathetic nerve activity (all <i>P</i> &lt; 0.05). After excluding confounding factors, such as age, body mass index, and smoking history, the multiple linear regression revealed a positive correlation of the LF/HF (ratio of low-frequency to high-frequency power, indicating the activity of sympathetic nerve activity) with the BP index (<i>β</i> = 7.337, <i>P</i> &lt; 0.001), ΔSBP (<i>β</i> = 2.797, <i>P</i> &lt; 0.001), and PBPF (<i>β</i> = 9.036, <i>P</i> &lt; 0.001). The plasma NE level also had a positive correlation with the BP index (<i>β</i> = 3.939, <i>P</i> = 0.022) and PBPF (<i>β</i> = 8.752, <i>P</i> &lt; 0.001).</p> Conclusion <p>The sleep-breathing events induced nocturnal BP surge was positively correlated with sympathetic nerve activity in patients with moderate-to-serve OSA.</p>

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Relationship between sleep-breathing events induced nocturnal blood pressure surge and sympathetic nervous activity in patients with obstructive sleep apnea

  • Bo Sun,
  • Zhengqing Mu,
  • Yujiao Wan,
  • Jiani Shen,
  • Yujie Yuan,
  • Xiaochen Xie,
  • Zili Meng,
  • Qiyun Ma,
  • Jing Xu

摘要

Objective

Nocturnal blood pressure (BP) surge is a characteristic phenomenon in patients with obstructive sleep apnea (OSA) associated with sympathetic nerve overactivity. This study aimed to explore the relationship between the sleep-breathing events induced nocturnal BP surge and sympathetic nerve activity.

Methods

A total of 85 patients with moderate-to-serve OSA and 44 controls were included in the study between April 2022 and October 2023 based on the inclusion and exclusion criteria. Full-night BP and heart rate variability (HRV) were monitored continuously and synchronized with polysomnography (PSG). The average of nocturnal BPs was taken as the asleep BP and the average of the highest BPs induced by all sleep-breathing events as the asleep peak BP. Nocturnal short-term BP variability (BPV) was calculated as follows: event-related systolic BP elevation (ΔSBP) as the gap between the peak and the lowest value of post-apneic SBP, BP index as the number of ΔSBP ≥ 12 mm Hg within 30 s/h, and the percentage of BP fluctuation induced by sleep-breathing events (PBPF) as the ratio of BP index and apnea-hypopnea index. Patients with OSA were divided into two subgroups (high– and low–BP surge groups) according to the median PBPF. The sympathetic nerve activity was reflected by plasma norepinephrine (NE) level and HRV. The PSG and BP parameters were compared among three groups, and the correlation between nocturnal short-term BPV and sympathetic nerve activity was analyzed.

Results

Patients with OSA were fatter and suffered from dyslipidemia and sympathetic nerve overactivity compared to controls. The high–BP surge group displayed higher sympathetic nerve activity and more severe hypoxia compared with the low–BP surge group. The Pearson correlation analysis showed a positive correlation of the higher nocturnal short-term BPV with increased sympathetic nerve activity (all P < 0.05). After excluding confounding factors, such as age, body mass index, and smoking history, the multiple linear regression revealed a positive correlation of the LF/HF (ratio of low-frequency to high-frequency power, indicating the activity of sympathetic nerve activity) with the BP index (β = 7.337, P < 0.001), ΔSBP (β = 2.797, P < 0.001), and PBPF (β = 9.036, P < 0.001). The plasma NE level also had a positive correlation with the BP index (β = 3.939, P = 0.022) and PBPF (β = 8.752, P < 0.001).

Conclusion

The sleep-breathing events induced nocturnal BP surge was positively correlated with sympathetic nerve activity in patients with moderate-to-serve OSA.