Cardiac troponin T (TnT) is a regulatory contractile protein whose detection in the circulation has been shown to be a specific and sensitive marker for ischemic myocardial cell injury both in adult and pediatric populations. We measured serum cardiac TnT in 15 consecutive full-term neonates presenting with bradycardia and electrocardiographic features of transient myocardial ischemia. Their median TnT concentrations (0.5 µg/l, range 0.01–0.37) were statistically comparable to our laboratory reference values for healthy term newborns (median 0.17 µg/l, range 0.01–0.42) (p = NS), but significantly higher with respect to our reference limits for healthy adults (median 0.01 µg/l, range 0.01–0.1) (p < 0.05). Our data demonstrate high TnT levels in neonates during the first days of life with respect to adults and similar TnT concentrations in term infants with and without TMI.

The aim of our study was to evaluate the clinical relevance of serum troponin I (TnI) as a marker of ischemic myocardial injury by using an automated fluoroenzymometric assay. The reference range for serum TnI was established by measuring serum TnI concentrations in blood from 75 healthy donors. The concentration was then compared with serum creatine kinase (CK) activity, CK-MB mass, and myoglobin concentrations in 20 patients with myocardial infarction diagnosed according to the WHO criteria, 20 patients with chest pain of nonischemic origin, 9 patients with unstable angina, 11 with stable angina, 11 patients with chronic muscular diseases, 6 patients with muscular trauma without chest contusion, and 13 patients with chronic renal disease. We found that: (a) 99% of the blood donors had TnI concentrations &lt;0.26 microgram/L (detection limit of the assay in our study); (b) TnI values in acute myocardial infarction (AMI) patients 4 h after onset of chest pain showed a sensitivity of 0.769 and a specificity of 1.0 at a decisional concentration for AMI of 1 microgram/L, even in the presence of severe skeletal muscle injuries or renal diseases; (c) the increase in TnI concentrations after infarction (interquartile range 3.25-6 h) and the peak occurred later (interquartile range 11.5-24 h) than the rise found in myoglobin and CK-MB, but the increase persisted much longer (&gt;96 h); (d) receiver-operating characteristic curve analysis showed the high diagnostic accuracy of TnI in diagnosing AMI even in patients in whom traditional biochemical markers are adversely influenced by underlying clinical situations.

In preterm infants with RDS the occurrence of PDA and indomethacin treatment are not associated with ischemic cardiac damage as detected by cTnT measurements.

We evaluated different diagnostic strategies for the early diagnosis of acute myocardial infarction, combining sensitivity and specificity of different markers evaluated singly and using combination testing in parallel and serial modes. Myoglobin, cardiac troponin I (TnI), creatine kinase (CK), and CK-MB mass were tested in blood samples from 26 patients with acute myocardial infarction collected at admission (T0; mean = 3.3 hours from the onset of chest pain) and 3 and 6 hours later. The comparison group was made up of 70 patients with renal failure, skeletal muscle diseases, stable angina, unstable angina, and chest pain of nonischemic origin. Single tests showed different sensitivities in relation to the different release kinetics; myoglobin was the most sensitive (69% at T0) although less specific (46%), and TnI showed the highest specificity (90%) and a sensitivity of 54%. Combination testing in a parallel mode using myoglobin and TnI or CK-MB had the same sensitivity and specificity as myoglobin tested singly. The best combination in a serial mode is myoglobin and TnI (at T0 sensitivity, 54%; specificity, 98%), as confirmed by the analysis of the positive predictive value, the negative predictive value, and the accuracy evaluated as a function of different disease prevalences.

Summary: 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 = 220 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 = 197-234 U/l) without significant differences between groups and without a correlation between Carboxypeptidase N and creatine kinase 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 MB 2 /MB! normalization. Worthy of note is the finding that in two acute myocardial infarction patients presenting MB 2 /MBj 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.