急性心肌梗死患者黏附分子及相关因素的研究

The study of plasma adhesive molecule and related factors in patients with acute myocardial infarction

目的 :探讨急性心肌梗死 ( AMI)患者发病早期至 1周内血清可溶性细胞间黏附分子 1 ( s ICAM1 )、可溶性血管细胞黏附分子 1 ( s VCAM 1 )、D 二聚体 ( D D)、血小板第 4因子 ( PF4 )的动态变化及其相互关系。方法 :测定 4 0例 AMI患者发病 2 4小时和 1周时的血清 s ICAM 1、s VCAM 1、D D、PF4并与健康对照组 3 0例比较。结果 :AMI患者于发病 2 4小时及 1周时 s ICAM 1、s VCAM 1、D D、PF4〔发病 2 4小时分别( 42 0 .97± 1 2 8.83 )μg/L ,( 51 .4 4± 1 4.83 )μg/L ,( 3 57.93± 1 47.0 9)μg/L和 ( 6.1 0± 1 .54 ) mg/L ;发病 1周时分别为 ( 40 4 .96± 1 1 5.2 2 ) μg/L,( 48.0 1± 1 7.2 4 ) μg/L,( 3 81 .1 2± 1 63 .0 0 ) μg/L和 ( 6.3 3± 2 .1 9) mg/L〕均明显高于对照组〔分别为 ( 1 80 .70± 3 2 .0 7)μg/L,( 1 3 .3 1± 1 2 .81 )μg/L ,( 84 .0 0± 2 6.99)μg/L和 ( 3 .0 7± 1 .3 4) mg/L ,P均 <0 .0 1〕。AMI组于发病 2 4小时及 1周时 s ICAM 1与 s VCAM 1均具有正相关性 ( P均 <0 .0 1 ) ,PF4与 s ICAM 1、s VCAM 1、D D间亦具有正相关性 ( P均 <0 .0 1 ) ,而 D D与 s ICAM 1、s VCAM 1间均无相关性 ( P均 >0 .0 5)。结论 :AMI从发病早期至 1周内 s ICAM 1、s VCAM

Objective:To investigate the dynamic changs and the relationship between the soluble intercellular adhesion molecule1(sICAM1),soluble intercellular vascular cell adhesion molecule1 (sVCAM1),Ddimer(DD),and platelet factor 4(PF4) in patients with acute myocardial infarction.Methods:Fourty patients with acute myocardial infarction (AMI) were included in the study and 30 healthy volunteers were taken as control.Serum sICAM1,sVCAM1,DD and PF4 were measured 24 hours and one week after the onset of AMI.Results:The levels of sICAM1,sVCAM1,DD and PF4 were significantly higher in AMI group within 24 hours and one week after admisson (all P <0.01) than those in control.The levels of sICAM1 ,sVCAM1,DD were decreased in the AMI group after reperfusion.The level of sVCAM1 was positively correlated to sVCAM1 in 24 hours and one week in AMI group ( P <0.01).The level of PF4 was positively correlated to sICAM1,sVCAM1,DD(all P <0.01).The level of DD was not correlated to sICAM1 and sVCAM1.Conclusions:sICAM1 and sVCAM1 increased progressively from the onset of AMI to one week after AMI in the patients.This indicate the participation of inflammation to the cardiac cellular damage which could be prevented or lightened by the early use of antiadhesion molecular antibody and drugs.