急性心肌梗死患者血浆乙醛脱氢酶2活性水平的变化及意义

Changes and clinical significance of aldehyde dehydrogenase 2 level in patients with acute myocardial infarction

目的探讨急性心肌梗死(AMI)患者乙醛脱氢酶2(ALDH2)活性水平的动态变化及其与心肌梗死面积、心功能的关系和临床意义。方法采用基因芯片法分析ALDH2基因型。入选27例ALDH2基因野生型(GG型)的AMI患者作为实验组,15例ALDH2基因野生型且排除冠状动脉性心脏病的患者作为对照组。实验组患者于AMI发病后12、24和48h,对照组于入院后12、24和48h采外周静脉血,应用血液ALDH2活性比色法定量检测试剂盒测定ALDH2活性水平。应用Selvester QRS计分系统对AMI患者进行梗死面积估测。实验组根据心肌梗死面积大小分为梗死面积>15%和梗死面积≤15%两个亚组;根据Killip分级法分为Killip Ⅰ级、Killip Ⅱ级和Killip Ⅲ～Ⅳ级3个亚组。结果实验组在AMI发病后12、24和48h的ALDH2活性水平分别为(61.9±15.0)、(97.2±22.5)和(52.9±15.3)U/L,显著高于对照组入院后12、24和48h的(21.2±3.5)、(22.9±5.9)和(24.5±6.5)U/L(P值均<0.01)。实验组ALDH2活性水平呈动态变化,峰值出现在AMI后24h。小面积心肌梗死亚组在AMI发病后12、24和48h的血浆ALDH2活性水平的总和显著高于大面积心肌梗死亚组(P<0.01)。Pearson直线相关分析显示,实验组3个时间点的ALDH2活性水平的总和与心肌梗死的面积呈负相关(r=-0.484,P=0.01)。KillipⅠ级亚组3个时间点的血浆ALDH2活性水平的总和显著高于KillipⅡ级和Ⅲ～Ⅳ级亚组(P值均<0.01)。结论 ALDH2基因野生型AMI患者的血浆ALDH2活性水平有动态变化,峰值出现在AMI发病后24h。ALDH2基因野生型AMI患者的血浆ALDH2活性水平与心肌梗死面积呈负相关,即血浆ALDH2活性水平越低,心肌梗死面积越大,心功能越差,提示其可能作为分析病情及判断预后的一项重要指标,并为应用ALDH2激活剂在AMI的治疗中发挥心脏保护效应提供新的思路。

Objective To investigate the changes and clinical significance of aldehyde dehydrogenase 2 （ALDH2） level in patients with acute myocardial infarction （AMI）. Methods Forty-two subjects were enrolled in this study. The genotypes of ALDH2 were all GG genotype as determined by ALDH2 genotyping kit （gene chip）. The patients were divided into two groups according to the inclusion/exclusion criteria： trial group and control group. The trial group comprised 27 patients who were diagnosed with AMI. Levels of ALDH2 activities were determined at three different time points （12 hours, 24 hours and 48 hours after severe chest pain）. Their levels were compared with those of the control group, which comprised 15 healthy volunteers. The trial group was further divided into two subgroups according to the final infarct size： big infarct size subgroup （〉 15% ） and small infarct size subgroup （≤15%）. According to heart function, the trial group was divided into three subgroups,, Killip Ⅰ subgroup, Killip Ⅱsubgroup and Killip Ⅲ～Ⅳ subgroup. The levels of ALDH2 were compared between different groups. Final infarct size of the AMI was assessed by the QRS score system of Selvester. ALDH2 activity was measured by the method of acetaldehyde metabolism. All data were collected and analyzed with SPSS 17.0 software. Results The level of ALDH2 at three different time points in trial group （[61.9±15.0], [97.2 ± 22.5], and [52.9 ± 15.3] U/L） were significantly higher than those of the control group （[21.2 ± 3.5], [22.9±5.9], and [24.5 ±6.5] U/L, all P〈0.01）. The level of ALDH2 descended with the lapse of time, and reach the highest point 24 hours after severe chest pain in the trail group. The ALDH2 level of the small infarct size subgroup was significantly higher than that of the big infarct size subgroup （P〈0.01）. Linear correlation analysis showed that ALDH2 level was negatively correlated with infarct size （r = -0. 484, P = 0.01 ）. The levels of ALDH2 in Killip Ⅱ subgroup and Killip Ⅲ～Ⅳ subgroup were significantly lower than those of the Killip Ⅰ subgroup （both P.〈0.01）.Conclusion The activity of plasma ALDH2 changes in AMI patients （GG genotype） reached the highest level 24 hours after severe chest pain. Plasma ALDH2 activity is negatively correlated with the infarct size. The plasma ALDH2 activity is also correlated with heart function. All these results suggest that ALDH2 cari inhibit myocardial ischemic necrosis in the patients with AMI.