黏附分子及CD40配体与急性心肌梗死的关系

目的观察青年急性心肌梗死患者淋巴细胞的血管间黏附分子、淋巴细胞黏附分子(VCAM-1及ICAM-1)及CD40配体(CD40L)的表达,探讨其急性心肌梗死炎症免疫学发病机制。方法将年龄≤45岁,与年龄>45岁急性心肌梗死患者上述指标比较,体检正常者作为对照。用流式细胞仪检测淋巴细胞VCAM-1、ICAM-1及CD40L阳性表达率。结果≥45岁组VCAM-1、ICAM-1及CD40L明显高于正常对照组(P<0.05),但与老年心肌梗死组对比差异无显著意义(P>0.05)。≤45岁心肌梗死组中VCAM-1、ICAM-1与CD40L显著相关。结论VCAM-1、ICAM-1及CD40L的高表达是急性心肌梗死发生和发展的重要炎症免疫学机制之一。

Relationship between cell adhesion molecule, CD40L and acute myocardial infarction in young adult

Objective To observe the expression of intercellular adhesion molecule-1(ICAM-1),vascular cell adhesion molecule-1(VCAM-1) and CD40L in lymphocytes in young adults with acute myocardial infarction(AMI) and to investigate the inflammatory aspects in the pathogenesis of AMI. Methods Sixty AMI cases were divided into 2 groups: age ≤45 years old group and age>45 years old group;30 healthy adults were enrolled for control.VCAM-1,ICAM-1 and CD40L were analyzed by monofluorescence flow cytometry. Results VCAM-1,ICAM-1 and CD40L were significantly higher in young AMI patients than in controls(P<0.05),while no significant difference was found between age ≤ 45 years old group and age > 45 years old group(P>0.05).CD40L level was positively related to ICAM-1 and VCAM-1 levels. Conclusions The high expressions of VCAM-1,ICAM-1 and CD40L in lymphocyte is one of the important inflammatory pathogenic mechanisms in the genesis and development of AMI in young adults.