Mani Ali R, Montagnese Sara, Jackson Clive D, Jenkins Christopher W, Head Ian M, Stephens Robert C, Moore Kevin P, Morgan Marsha Y
Centre for Hepatology, Royal Free Campus, University College London Medical School, London, UK.
Am J Physiol Gastrointest Liver Physiol. 2009 Feb;296(2):G330-8. doi: 10.1152/ajpgi.90488.2008. Epub 2008 Nov 20.
Heart rate variability (HRV) is reduced in several clinical settings associated with either systemic inflammation or neuropsychiatric impairment. The possibility that the changes in HRV observed in patients with neuropsychiatric impairment might relate to the overproduction of inflammatory cytokines does not seem to have been considered in the studies undertaken to date. HRV is decreased in patients with liver cirrhosis but its relationship to the impairment of neuropsychiatric performance, commonly observed in these patients, is unknown. The aim of this study was to investigate the relationship between HRV, hepatic encephalopathy, and production of inflammatory cytokines in patients with cirrhosis. Eighty patients with cirrhosis [53 men, 27 women; mean (+/-1SD) age 54 +/- 10 yr], classified as neuropsychiatrically unimpaired or as having minimal or overt hepatic encephalopathy, and 11 healthy subjects were studied. HRV was assessed by applying Poincaré plot analysis to the R-R interval series on a 5-min ECG. Inflammatory cytokines (TNF-alpha, IL-6, IL-10, and IL-12) were measured in a subgroup of patients. Long-term R-R variability was significantly decreased in the patients with cirrhosis, in parallel with the degree of neuropsychiatric impairment (P < 0.01) and independently of the degree of hepatic dysfunction (P = 0.011). The relative risk of death increased by 7.7% for every 1-ms drop in this variable. Plasma levels of IL-6 significantly correlated with indexes of both HRV and neuropsychiatric performance. The changes observed in HRV and in neuropsychiatric status in patients with cirrhosis are significantly correlated, most likely reflecting a common pathogenic mechanism mediated by inflammatory cytokines.
在与全身炎症或神经精神障碍相关的多种临床情况下，心率变异性（HRV）会降低。迄今为止所进行的研究似乎尚未考虑到神经精神障碍患者中观察到的HRV变化可能与炎性细胞因子过度产生有关这一可能性。肝硬化患者的HRV降低，但其与这些患者中常见的神经精神功能损害之间的关系尚不清楚。本研究的目的是调查肝硬化患者中HRV、肝性脑病和炎性细胞因子产生之间的关系。研究了80例肝硬化患者[53例男性，27例女性；平均（±1标准差）年龄54±10岁]，这些患者被分类为神经精神未受损或患有轻微或明显的肝性脑病，以及11名健康受试者。通过对5分钟心电图上的R-R间期系列应用庞加莱图分析来评估HRV。在一部分患者中测量了炎性细胞因子（TNF-α、IL-6、IL-10和IL-12）。肝硬化患者的长期R-R变异性显著降低，与神经精神损害程度平行（P<0.01），且与肝功能障碍程度无关（P=0.011）。该变量每下降1毫秒，死亡相对风险增加7.7%。IL-6的血浆水平与HRV和神经精神功能指标均显著相关。肝硬化患者中观察到的HRV和神经精神状态变化显著相关，很可能反映了由炎性细胞因子介导的共同致病机制。
