非糖尿病性慢性肾病患者的心率变异性受损-迷走神经控制和每日波动的显著破坏

Hisaki Makimoto , Katsuhito Fujiu , Kohei Shimizu , Tina Lin , Eisuke Amiya , Kazuo Asada , Toshiya Kojima , Masao Daimon , Christian Meyer , Issei Komuro
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引用次数: 2

摘要

背景:慢性肾脏疾病(CKD)患者的昼夜节律自主波动尚未完全阐明。本研究的目的是比较CKD患者和非CKD患者之间使用心率变异性的自主神经波动。方法研究人群包括101例连续的非糖尿病性CKD患者(3-5期,54例男性,70±10岁)和129例年龄和性别匹配的非CKD对照组(65例男性,68±10岁),他们接受24小时动态心电图监测。连续正窦NN间隔不同的比例;采用50 ms (pNN50)和高频分量(HF)作为迷走神经参数。低频与高频比值(LF/HF比值)作为交感神经-迷走神经平衡参数进行评估。为了评估CKD和其他合并症对自主神经变异的直接影响,我们将24小时随机分为夜间(晚上10点至上午8点)和白天(上午8点至晚上10点)进行回归分析。结果CKD患者的高血压、高尿酸血症和低血红蛋白患病率高于对照组(P <0.05)。两组夜间均出现pNN50和HF增高。然而,这些夜间高潮在CKD中被显著抑制(P <0.05),反映迷走神经活动受损。回归分析显示夜间迷走神经参数降低与CKD之间存在独立关系(P <0.05), LF/HF比值与CKD无关(P >0.05),但低Hb (P <0.05)。结论非糖尿病性CKD患者的昼夜自主神经,特别是迷走神经波动受到损害,与年龄和合并症无关。需要进一步的研究来评估这种损害与CKD患者预后之间的关系。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Impaired heart rate variability in patients with non-diabetic chronic kidney disease — Prominent disruption of vagal control and daily fluctuation

Background

The circadian autonomic fluctuation in chronic kidney disease (CKD) patients has not yet been fully elucidated. The aim of this study was to compare the autonomic fluctuation using heart rate variability between patients with and without CKD.

Methods

The study population consisted of consecutive 101 non-diabetic CKD patients (Stages 3–5, 54 males, 70 ± 10 years) and 129 age- and sex-matched controls without CKD (65 males, 68 ± 10 years) who underwent 24-hour Holter monitoring. The proportion of successive normal sinus NN intervals that differ > 50 ms (pNN50) and the high-frequency component (HF) were adopted as vagal parameters. The low- to high-frequency ratio (LF/HF ratio) was evaluated as a sympatho-vagal balance parameter. To evaluate the direct contribution of CKD and other comorbidities to the autonomic variation, the regression analysis was performed after we arbitrarily divided 24 h into night-time (10 PM–8 AM) and day-time (8 AM–10 PM).

Results

The CKD patients had higher prevalence of hypertension, hyperuricemia, and low hemoglobin as compared to controls (P < 0.05). Both groups showed surges of pNN50 and HF nocturnally. However, these nocturnal surges were significantly suppressed in CKD (P < 0.05), reflecting the impaired vagal activity. Regression analysis demonstrated an independent relation between the nocturnal reduction of vagal parameters and CKD (P < 0.05), and also revealed that the LF/HF ratio was not related to CKD (P > 0.05), but to low Hb (P < 0.05).

Conclusion

The circadian autonomic, particularly vagal, fluctuations were impaired in non-diabetic CKD patients independently from aging and comorbidities. Further research is required to assess the association between this impairment and prognosis of CKD patients.

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