CARBOXYPEPTIDASE-N AND CREATINE-KINASE-MB ISOFORMS IN ACUTE-MYOCARDIAL-INFARCTION

The aims of our study were to evaluate the plasma carboxypeptidase N a ctivity in normal subjects and in patients with acute myocardial infar ction and to delineate its relationship with creatine kinase-MB isofor ms in monitoring of acute myocardial infarction, carboxypeptidase N be ing the major determinant of creatine kinase isoform conversion in pla sma. The study was carried out in 34 healthy subjects and 19 patients with acute myocardial infarction diagnosed according to the World Heal th Organization (WHO) criteria in which the blood samples were collect ed 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 t he third day post admission. Carboxypeptidase N activity, total creati ne kinase, creatine kinase-MB mass concentration and creatine kinase-M B isoforms were determined in each sample from acute myocardial infarc tion patients, whereas only carboxypeptidase N and total creatine kina se activities were assayed in samples from healthy subjects. The resul ts showed a :high variability in carboxypeptidase N values among healt hy subjects (median = 220 U/l; interquartile range = 190-247 U/l) and in the first available samples from acute myocardial infarction patien ts (median = 213 U/l; interquartile range = 197-234 U/l) without signi ficant differences between groups and without a correlation between ca rboxypeptidase N and creatine kinase activities either in healthy subj ects 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 infarctio n patients carboxypeptidase N showed time-related variations, reaching the highest levels about 48 h after onset of chest pain. A statistica lly significant difference in carboxypeptidase N values (p = 0.0001) w as found before and after creatine kinase-MB peak values as well as be fore and after MB2/MB1 normalization. Worthy of note is the finding th at in mio acute myocardial infarction patients presenting MB2/MB1 rati os lower than the cutoff value (1.5) throughout the period of observat ion, the baseline values for carboxypeptidase N were higher than in ot her patients studied. Our results suggest that the increase of carboxy peptidase 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 creatin e kinase-MB isoforms in the diagnosis of acute myocardial infarction.