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Caution is required when interpreting neonatal cardiac troponin concentrations.
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David C. Gaze, Cardiac Research Scientist , Paul O. Collinson
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david.gaze{at}stgeorges.nhs.uk David C. Gaze, et al.
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The letter by AraÚjo et al (1) regarding the plasma concentration of cardiac troponin I (cTnI) in apparently healthy neonates raises some interesting issues. Recent reports in the literature have suggested using cTnI as a marker in myocardial damage in neonates (2-3), however, the data is confusing and controversial. During development, a fetal isoform of cardiac troponin T (cTnT) is transiently expressed in skeletal muscle (4) but is down-regulated in adult skeletal muscle tissue (5). Such isoforms are not detected by the Elecsys M7 and M11.7 antibody pair used in the Roche Diagnostics cTnT assay (6). The dominant form of troponin I however, appears as slow muscle skeletal TnI (sTnI). This is down regulated with concurrent up regulation of cTnI expression during the first nine months of life (7-8). Therefore cTnI is not a suitable candidate biomarker of cardiomyocyte damage in the neonatal period (9-10). The findings presented by AraÚjo and colleagues pose some challenges to these findings. Their data suggest that the neonatal cTnI is cleared quickly as the cTnI concentrations were significantly lower in infants 48 hours or older than those younger than 48 hours. Circulating maternal cTnI is detectable in mothers who suffer myocardial ischemia during post partum hemorrhage (11), although the incidence of post partum maternal cardiac ischaemia is a rare complication of pregnancy (12). Interestingly, maternal cTnI concentrations are not affected by either vaginal or caesarean modes of delivery (13). Also published in same issue of Clinical Chemistry, Masuzaki and colleagues (14) demonstrate an increase in maternal DNA in umbilical cord blood following labor, adding further evidence of a heterogeneous cellular matrix in situ in the only patent link between the mother and neonate. Furthermore, cTnT is also detectable in apparently healthy neonates, and variations in concentrations are associated with need for respiratory and inotropic support. Healthy neonates (n=113) had a median (interquartile range) cTnT of 0.025 (0.010-0.062) microgram per liter, which was significantly lower than sick infants (n=49), whose median cTnT was 0.159 (0.075-0.308) microgram per liter, p=<0.001 (15). The findings of elevated cTnT and cTnI in neonates in the absence of overt cardiac disease may represent circulating fetal troponin, maternal troponin or probably a mixture of both. Further studies are required to assess the prognostic value of a raised serum troponin in neonates. David C Gaze* Cardiac Research Scientist Paul O Collinson Consultant Chemical Pathologist *Addressee for Correspondence Chemical Pathology, St George’s healthcare NHS Trust, London, SW17 0RE, United Kingdom Tel +44 (0)20 8725 5878 Fax +44(0)20 8682 0744 Email david.gaze@stgeorges.nhs.uk References 1. AraÚjo K, da Silva J, Sanudo A, Kopelman B. Plasma concentrations of cardiac troponin I in Newborn Infants. Clin Chem 2004;50:1717-1718 2. McAuliffe F, Mears K, Fleming S, Grimes H, Morrison JJ. Fetal Cardiac Troponin I in Relation to Intrapartum Events and Umbilical Artery pH. Am J Perinatol 2004;21(3):147-52 3. Turker G, Babaoglu K, Gokalp AS, Sarper N, Zengin E, Arisoy AE. Cord Blood Cardiac Troponin I as an Early Predictor of Short-Term Outcome in Perinatal Hypoxia. Biol Neonate 2004;86:131-137 4. Sutherland CJ, Esser KA, Elsom VL, Gordon ML, Hardeman EC. Identification of a program of contractile protein gene expression initiated upon skeletal muscle differentiation. Dev Dynam 1993;196:25-36 5. Anderson PAW, Malouf NN, Oakeley AE, Pagani ED, Allen PD. Troponin T isoform expression in humans: a comparison among normal and failing adult heart, fetal heart, and adult and fetal skeletal muscle. Circ Res 1991;69:1226-1233 6. Ricchuiti V, Voss EM, Ney A, Odland M, Anderson PAW, Apple FS. Cardiac troponin T isoforms expressed in renal diseased skeletal muscle will not cause false-positive results by the second generation cardiac troponin T assay by Boehringer Mannheim. Clin Chem 1998;44:1919-1924 7. Collinson PO, Boa FG, Gaze DC. Measurement of cardiac troponin. Ann Clin Biochem 2001;38:423-449 8. Sasse S, Brand NJ, Kyprianou P, Dhoot GK, Wade R, Arai M et al, Troponin I gene expression during human cardiac development and in end stage heart failure. Circ Res 2003;72:932-38 9. Higgins JP and Higgins JA: Elevation of cardiac troponin I indicates more than myocardial ischemia. Clin Invest Med 2003;26:133-47 10. Gaze DC, Collinson PO: Cardiac troponin I should be interpreted with caution in paediatric neonatal patients [Letter]. Biol Neonate 2004;87:19 11. Karpati PCJ, Rossignol M, Pirot M, Cholley B, Vicaut E, Henry P, Kevorkian JP, Schurando P, Peynet J, Jacob M, Payen D, Mebazaa A: High incidence of myocardial ischemia during post partum hemorrhage Anesthesiology 2004;100:30-6 12. Hankins GDV, Wendel GD Jr, Leveno KJ, Stoneham J. Myocardial infarction during pregnancy: a review. Obstet Gynecol 1985;65:139-46 13. Koscica KL, Bebbington M, Bernstein PS: Are maternal serum troponin I levels affected by vaginal or caesarean delivery? Am J Perinatol 2004;21:31-34 14. Masuzaki H, Miura K, Yoshiura S, Mapendano CK, Nakayama D, Yoshimura D, Niikawa N, Ishimaru T: Labor increases maternal DNA concentration in cord blood. Clin Chem 2004;50:1709-1711 15. Clark SJ, Newland P, Yoxall CW, Subhedar NV: Concentrations of cardiac troponin T in neonates with and without respiratory distress. Arch Dis Child Fetal Neonatal Ed 2004;89:F348-F352 |
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