摘要目的 分析炎性因子水平与急性下壁心肌梗死有无前壁导联ST段压低之间的相关性及其临床意义.方法 选取北京安贞医院2007年5月至2012年9月急诊危重症中心因急性下壁ST段抬高性心肌梗死入院的患者360例,所有患者均急诊行PCI治疗,并观察罪犯血管以外冠脉病变的情况.所有患者根据有无前壁导联ST压低分为对照组180例和前壁ST段压低组180例.所有患者均于入院即刻取静脉血8ml,分离血浆,通过生物化学和ELISA方法检测血浆超敏C反应蛋白(Hs-CRP)、纤维蛋白原(Fib)、白细胞介素6(IL-6)、肿瘤坏死因子(TNF-α)、丙二醛(MDA)、过氧化物岐化酶(SOD)的变化,并分析血浆炎性因子水平与有无前壁ST段压低急性下壁心肌梗死相关性.结果 与对照组比较,前壁导联ST段压低患者双支病变、3支病变的比例更高(P＜0.01);血浆Hs-CRP、Fib、IL-6、TNF-α水平升高更显著(P＜0.01),脂质过氧化产物MDA含量更高(P＜0.01),抗氧化物质SOD含量更低(P＜0.01).结论 血浆炎症因子及脂质过氧化程度可在一定程度上反映冠脉病变的程度,对疾病的严重程度具有一定的预测价值.

abstractsObjective To investigate the level of Hs-CRP,Fib,IL-6,TNF-α,MDA,SOD,and analyse the correlation between the level of plasma inflammatory cytokines and clinical significance in patients with anterior ST-segment depression.Methods We choosed 360 patients with inferior ST Segment elavation acute myocardial infarction from May 2007 to Sep 2012 in rescue Center of Anzhen Hospital,in Anzhen Hospital,and all the patients received percutaneous coronary intervention treatment and the vascular lesions besides culprit vessel were observed.All the patients were divided into two groups:control group(n =180) and anterior ST-segment depression group (n =180).8ml venous blood was obtained from all the patients,and then plasma were separated.The level of plasma Hs-CRP,Fib,IL-6,TNF-αt,MDA,SOD were investigated by Biochemistry and ELISA.And the relativity between the level of plasma inflammatory cytokines and anterior ST-segment depression in patients with inferior acute myocardial infarction was analysed.Results The proportion of double vessel coronary disease,three coronary artery lesion is higher in anterior ST-segment depression group compared with control group(P ＜ 0.01).Compared with control group,the level of Hs-CRP,Fib,IL-6,TNF-α,MDA,SOD of anterior ST-segment depression group are inclined signifancantly(P ＜ 0.01).Conclusion The level of plasma inflammatory cytokines and the degree of lipid peroxidation can reflect the severity of coronary artery disease and may have certain value in predicting the severity of disease.