急性心肌梗死患者血清类胰蛋白酶水平与吸烟的关系

发布时间：2018-04-12 15:46

本文选题：急性心肌梗死 + 冠状动脉粥样硬化性心脏病　；参考：《浙江大学》2015年博士论文

【摘要】：冠状动脉粥样硬化斑块的破裂及继发血栓形成是急性心肌梗死的主要发病机制。多种炎症细胞参与动脉粥样硬化的发生与发展过程。近年来研究发现,血管壁肥大细胞可被多种动脉粥样硬化危险因子激活,引起脱颗粒反应,释放颗粒内的一系列炎症因子,介导冠状动脉内局部慢性炎症的发生。肥大细胞的激活是引起动脉粥样硬化斑块破裂的重要因素之一,急性心肌梗死患者中斑块破裂口可见肥大细胞聚集及活化。吸烟是冠状动脉粥样硬化性心脏病及心肌梗死的传统危险因素之一,然而吸烟与血管壁肥大细胞激活的相关性尚未见报道。肥大细胞在免疫球蛋白Ig E、氧化的低密度脂蛋白胆固醇(oxLDL)、烟草中的尼古丁等的作用下可被激活,释放出一系列介质和蛋白酶,其中类胰蛋白酶是肥大细胞特有的一种中性丝氨酸蛋白酶,研究表明检测其浓度可反映肥大细胞激活的水平。目的本研究拟通过检测急性心肌梗死患者中血清类胰蛋白酶水平,反应肥大细胞的激活程度,研究其与吸烟史的相关性,从而探讨急性心肌梗死患者中,吸烟与肥大细胞激活的关系及其在冠脉粥样硬化发生及斑块破裂过程中所起的作用。方法本研究纳入2013.01.01-2014.10.01期间在浙江大学附属第二医院心血管内科因胸闷、胸痛、胸前区不适、心功能不全(心超示LVEF50%)、心肌酶谱水平异常升高或心电图ST-T异常改变而住院进行冠状动脉造影的患者共2785人。其中诊断急性心肌梗死(194人),急性ST段抬高心肌梗死(59人),非ST段抬高心肌梗死(135人)。另入选经冠状动脉造影排除冠状动脉粥样硬化性心脏病(冠脉无明显狭窄或狭窄50%)的患者201名。纳入的375名患者按出院诊断分为急性心肌梗死患者(n=183)及非冠心病患者(n=192)。患者行冠状动脉造影前留取空腹(禁食8小时)外周肘静脉血标本患者血清类胰蛋白酶水平测定采用武汉优尔生公司类胰蛋白酶(TPS)检测试剂盒(酶联免疫吸附试验法),根据标准曲线测算血清样本中类胰蛋白酶水平。数据分析采用SPSS16.0版本,ELISA结果以平均值士标准误表示,满足正态分布的定序性数据采用独立样本t检验进行两两比较,和One-way ANOVA进行多组间的比较分析,LSD法进行多组样本的两两分析；Fisher精确检验及Pearson卡方检验用于分析两组和多组分类数据；非参数Kruskal-WallisH检验用于分析不满足正态分布的数据。多元线性回归用于进行两组定序数据间的相关性研究,P0.05为显著。结果急性心肌梗死患者血清中类胰蛋白酶水平显著高于非冠心病患者(6.324±0.26vs.0.33±0.04,p0.05),而非ST段抬高型急性心肌梗死和ST段抬高型急性心肌梗死患者的血清类胰蛋白酶水平无显著差异。血清类胰蛋白酶水平是急性心肌梗死的独立危险因素。急性心肌梗死患者的吸烟量显著高于非冠心病患者,且吸烟量与发生急性心肌梗死的不同类型相关。不吸烟与吸烟患者血清类胰蛋白酶水平(2.56±0.24vs.3.95±0.34,p0.05)存在显著差异。血清类胰蛋白酶水平与吸烟量呈独立相关(β=0.183,p=0.000)。结论急性心肌梗死患者中吸烟者血清类胰蛋白酶水平与不吸烟者未见显著差异,而在全部入组人群中类胰蛋白酶水平有差异,这可能由于吸烟与急性心肌梗死的强相关性导致。未来需进一步采纳更大样本量的研究以尽可能减少基线水平差异所导致的影响。
[Abstract]:In recent years , it has been found that vascular wall mast cells can be activated by various atherosclerosis risk factors to induce degranulation reaction , release a series of inflammatory factors in the particles , mediate local chronic inflammation in the coronary artery . The activation of mast cells is one of the important factors causing the rupture of atherosclerotic plaques .

Purpose

The relationship between smoking and mast cell activation in patients with acute myocardial infarction and its role in coronary atherosclerosis and plaque rupture were investigated by detecting the serum tryptase levels in patients with acute myocardial infarction , and investigating the correlation between smoking and mast cell activation in patients with acute myocardial infarction .

One hundred and twenty - two patients with acute myocardial infarction ( 194 ) , acute ST - segment elevation myocardial infarction ( 59 ) and non - ST - segment elevation myocardial infarction ( n = 192 ) were enrolled .
Fisher ' s exact test and Pearson chi - square test were used to analyze two groups of data ;
The non - parametric Kruskal - WallisH test was used to analyze the data that did not meet the normal distribution . Multiple linear regression was used to study the correlation between two groups of sequencing data , P0.05 was significant .

Results

Serum tryptase levels were significantly higher in patients with acute myocardial infarction than those in non - coronary heart disease ( 6.324 卤 0.26 vs . 0.33 卤 0.04 , p < 0.05 ) . The levels of serum tryptase were significantly higher in patients with acute myocardial infarction than those in patients with acute myocardial infarction . There was a significant difference in serum tryptase levels in patients with acute myocardial infarction ( 2.56 卤 0.24 vs . 3.95 卤 0.34 , p < 0.05 ) . There was an independent correlation between serum tryptase levels and smoking amount ( 尾 = 0.183 , p = 0.000 ) .

Conclusion

The serum tryptase levels of smokers in patients with acute myocardial infarction were not significantly different from those of non - smokers , and there was a difference in tryptase levels in all enrolled population , which could result from a strong correlation between smoking and acute myocardial infarction . A larger sample size study was needed to minimize the effects of baseline level differences .

【学位授予单位】：浙江大学
【学位级别】：博士
【学位授予年份】：2015
【分类号】：R542.22

【共引文献】