Zaninotto M, Altinier S, Lachin M, Plebani M
Servizio di Medicina di Laboratorio, Azienda Ospedaliera di Padova, Italy.
Eur J Clin Chem Clin Biochem. 1997 Apr;35(4):291-5. doi: 10.1515/cclm.1997.35.4.291.
The aims of our study were to evaluate the plasma carboxypeptidase N activity in normal subjects and in patients with acute myocardial infarction and to delineate its relationship with creatine kinase-MB isoforms in monitoring of acute myocardial infarction, carboxypeptidase N being the major determinant of creatine kinase isoform conversion in plasma. The study was carried out in 34 healthy subjects and 19 patients with acute myocardial infarction diagnosed according to the World Health Organization (WHO) criteria in which the blood samples were collected immediately upon admission to the coronary care unit (median time 3.5 hours), every 4 to 6 hours for 24 hours, and every 12 hours until the third day post admission. Carboxypeptidase N activity, total creatine kinase, creatine kinase-MB mass concentration and creatine kinase-MB isoforms were determined in each sample from acute myocardial infarction patients, whereas only carboxypeptidase N and total creatine kinase activities were assayed in samples from healthy subjects. The results showed a high variability in carboxypeptidase N values among healthy subjects (median = 200 U/l; interquartile range = 190-247 U/l) and in the first available samples from acute myocardial infarction patients (median = 213 U/l; interquartile range = 234 U/l) without significant differences between groups and without a correlation between carboxypeptidase N and creatine activities either in healthy subjects or in acute myocardial infarction patients; in the latter group, however, a significant correlation (p < 0.01) with creatine kinase-MB calculated on all samples, was observed. In acute myocardial infarction patients carboxypeptidase N showed time-related variations, reaching the highest levels about 48 h after onset of chest pain. A statistically significant difference in carboxypeptidase N values (p = 0.0001) was found before and after creatine kinase-MB peak values as well as before and after MB2/MB1 normalization. Worthy of note is the finding that in two acute myocardial infarction patients presenting MB2/MB1 ratios lower than the cutoff value (1.5) throughout the period of observation, the baseline values for carboxypeptidase N were higher than in other patients studied. Our results suggest that the increase of carboxypeptidase N activity after infarction could be induced by an increase in endogenous substrate concentrations, in particular creatine kinase-MB released from damaged myocardium. Furthermore, high baseline levels of carboxypeptidase N will reduce the diagnosis efficiency of creatine kinase-MB isoforms in the diagnosis of acute myocardial infarction.
我们研究的目的是评估正常受试者和急性心肌梗死患者的血浆羧肽酶N活性,并在急性心肌梗死监测中描绘其与肌酸激酶-MB同工酶的关系,羧肽酶N是血浆中肌酸激酶同工酶转化的主要决定因素。该研究在34名健康受试者和19名根据世界卫生组织(WHO)标准诊断为急性心肌梗死的患者中进行,血液样本在进入冠心病监护病房时立即采集(中位时间3.5小时),24小时内每4至6小时采集一次,入院后第三天前每12小时采集一次。测定急性心肌梗死患者每个样本中的羧肽酶N活性、总肌酸激酶、肌酸激酶-MB质量浓度和肌酸激酶-MB同工酶,而健康受试者样本中仅测定羧肽酶N和总肌酸激酶活性。结果显示,健康受试者中羧肽酶N值存在高度变异性(中位数=200 U/l;四分位间距=190-247 U/l),急性心肌梗死患者的首个可用样本中也存在高度变异性(中位数=213 U/l;四分位间距=234 U/l),两组之间无显著差异,健康受试者或急性心肌梗死患者中羧肽酶N与肌酸活性之间也无相关性;然而,在后者组中,观察到与所有样本计算的肌酸激酶-MB有显著相关性(p<0.01)。在急性心肌梗死患者中,羧肽酶N显示出与时间相关的变化,在胸痛发作后约48小时达到最高水平。在肌酸激酶-MB峰值前后以及MB2/MB1标准化前后,羧肽酶N值存在统计学显著差异(p=0.0001)。值得注意的是,在两名急性心肌梗死患者中,在整个观察期内MB2/MB1比值均低于临界值(1.5),其羧肽酶N的基线值高于其他研究患者。我们的结果表明,梗死后羧肽酶N活性的增加可能是由内源性底物浓度增加引起的,特别是受损心肌释放的肌酸激酶-MB。此外,羧肽酶N的高基线水平将降低肌酸激酶-MB同工酶在急性心肌梗死诊断中的诊断效率。