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精神分裂症及代谢综合征患者HRV变化 被引量:3

Changes of adipocytokines and heart rate variability in Schizophrenia combined with positive risk ofmetabolic syndrome patients
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摘要 目的本文拟探讨精神分裂症合并代谢综合征阳性风险患者高敏C-反应蛋白(Hs-CRP)、肿瘤坏死因子-α(TNF-α)、心肌纤维化和长时程心率变异性(HRV)的变化。方法研究对象45例正常对照组(A组),45例精神分裂症患者作为B组,45例精神分裂症合并代谢综合征阳性风险患者作为C组。酶联免疫法检测TNF-α和Hs-CRP水平,超声心肌声学密度定量技术检测心肌纤维化,行24h动态心电图检查,检测HRV时域指标。结果精神分裂症合并代谢综合征阳性风险患者HRV时域分析较对照组下降(p<0.05)。声学密度指标CAI较对照组明显增高(p<0.05),而CVIB明显降低(p>0.05)。TNF-α和Hs-CRP水平较对照组升高(p<0.05)。结论精神分裂症合并代谢综合征阳性风险患者受高糖、高血压和肥胖等因素的作用,导致TNF-α和Hs-CRP水平升高,心室肌纤维化,组织结构发生改变,分布于心脏组织的自主神经紊乱,HRV降低。 Objective To discuss changes of adipocytokines, myocardial fibrosis and heart rate variability in schizophrenia combined with positive risk of metabolic syndrome patients. Methods Study on 45 cases the control group as A group, 45 cases schizophrenia patients as B group, 45 cases schizophrenia combinedwith positive risk of metabolism syndrome patients as C group, tumor necrosis factor α (TNF-α) and High sensitive CRP (Hs-CRP) levels were detected by Enzyme linked immunosorbent assay, myocardial fibrosis was determinated with myocardial acoustic densitometry, and time domain of heart rate variability index were detected with 24 hours of dynamic electrocardiogram. Results HRV analysis in time domain is decreased in C group than in A group (p〈0.05). and the acoustic density index of CAI were significantly increased (p〈0.05), and CVIB decreased significantly (p〉0.05). TNF-α and Hs-CRP levels were higher in C group than in A group (p〈0.05). Conclusions High glucose, hypertension , obesity and other factors lead to the increasing of TNF-α and Hs-CRP levels, ventricular muscle fibrosis, organizational structure changes, autonomic dysfunction in cardiac tissue, decreasing of HRV in schizophrenia combined with positive risk of metabolic syndrome patients.
出处 《临床心电学杂志》 2014年第3期201-204,共4页 Journal of Clinical Electrocardiology
关键词 精神分裂症 代谢综合征 心率变异性 高敏C-反应蛋白 肿瘤坏死因子-Α Schizophrenia metabolic syndrome heart rate variability high sensitivity C- reactive protein tumor necrosis factor α
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