焦虑抑郁情绪对冠心病患者血清炎症因子及血管内皮功能的影响

摘要

目的:探讨焦虑抑郁情绪对冠心病患者血清炎症因子水平及血管内皮功能的影响.方法:选择60例冠心病患者,使用焦虑抑郁量表评价其心理状态,根据评分将冠心病患者分为焦虑抑郁组(30例)和非焦虑抑郁组(30例),测定受试者的血清高敏C反应蛋白、细胞间黏附分子-1和肿瘤坏死因子-α水平,并采用高分辨率超声法测定肱动脉血流介导的舒张反应(FMD).结果:焦虑抑郁组血清细胞间黏附分子-1和肿瘤坏死因子-α水平较非焦虑抑郁组显著升高(P均<0.05),焦虑抑郁组的肱动脉血流介导的舒张反应较非焦虑抑郁组降低(P<0.05),差异均有统计学意义.采用多元线性回归分析发现,在调整了体重指数、收缩压、年龄、性别、吸烟史、糖尿病史、心率、低密度脂蛋白胆固醇等混杂因素的影响之后,细胞间黏附分子-1和肱动脉血流介导的舒张反应与四种不同量表得分均呈独立正相关(P<0.05),肿瘤坏死因子-α与汉密尔顿焦虑量表、汉密尔顿抑郁量表、焦虑自评量表得分呈独立正相关(P均<0.05),但肿瘤坏死因子-α与抑郁自评量表得分、高敏C反应蛋白与四种不同量表得分无明显相关性(P>0.05).结论:焦虑抑郁情绪可能加重冠心病患者体内的炎症反应及内皮功能损害.%Objective: To study the effect of anxiety and depression on senm inflammatory factor level and bbod vessel endothelial func tion in patients with coronary artery diseas( CAD).Methods:W e selected60 CAD patients and evaluated theirmental condition with four anxiety depression scales( SAS, SDS, HAMA and HAMD). According to evaluation results, the patients were divided into2 groups; Anxiety" depression group and Non Anxiety" depression group, n = 30 in each group The senm levels of inflammation factors of high sensitivity C-reactive proteir( Hs-CRF) ,intracellular adhesive molecule 4 ( 1CAM4 ) and tumor necrosis factopa( TNFa) were assessed, the high resolution ultrasound was used to detect the flow mediated dilatation^ EMD) in brachial artery h both groupsResults: The serum levels of EAM4 and TNF-a were significantly higher and the EMD was significantly lower in Anxiety" depression group than that h Non Anxiety" depression group, P <0. 05 respectively Multiple linear regressbn analysis indicated that with the adjusted EM systolic blood pressure, age, gender, heart rate and LDL-C, the history of snokhg and diabetes, JCAM-1 and FMD had independent positive correlatbn with tour evaluation scale scores, P < 0.05 respectively TNF-a had an independent positive correlation with HAMA, HAMD, and SAS scale scores, P<0. 05 respectively, TNF-a was not related to SDS scale score Hs-CRP was not related to four scale scores, P>0. 05 respectivelyConchsion Anxiety and depression may prompt inflammatory response and aggravate the endothelial dysfunction in CAD patients.