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   <subfield code="a">Effect of patent ductus arteriosus and indomethacin treatment on serum cardiac troponin T levels in preterm infants with respiratory distress syndrome</subfield>
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   <subfield code="c">[D. Trevisanuto, M. Zaninotto, M. Lachin, S. Altinier, M. Plebani, P. Ferrarese, V. Zanardo]</subfield>
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   <subfield code="a">Cardiac troponin T (cTnT) represents a sensitive and specific marker of ischemic myocardial damage in adult and neonatal populations. The aim of this study was to detect the potential ischemic effect of persistent patent ductus arteriosus (PDA) and indomethacin treatment on the coronary vascular bed by measuring cTnT concentrations. cTnT levels were measured in 23 preterm infants (&lt;32 weeks of gestational age) with respiratory distress syndrome (RDS), 11 with PDA and 12 without, at 2, 4, and 7 days after birth. cTnT concentrations (mean ± SEM) significantly decreased (P &lt; 0.05) from the 2nd (0.63 ± 0.09 μg/l) and the 4th (0.77 ± 0.13 μg/l) to the 7th postnatal day (0.28 ± 0.04 μg/l). At day 2 after birth, cTnT levels in preterm infants with RDS were significantly higher (P &lt; 0.05) than our reference values for healthy preterm neonates (0.63 ± 0.09 μg/l vs 0.18 ± 0.04 μg/l). No differences were found between RDS infants with and without PDA at 2 (0.65 ± 0.13 vs 0.61 ± 0.14 μg/l), 4 (0.71 ± 0.21 vs 0.87 ± 0.16 μg/l), and 7 (0.26 ± 0.05 vs 0.29 ± 0.07 μg/l) days of life. In infants with PDA, cTnT levels did not differ before the first dose of indomethacin was given (0.65 ± 0.14 μg/l) or 2 h (0.65 ± 0.15 μg/l) and 48 h (0.71 ± 0.21 μg/l) afterwards. Conclusion In preterm infants with RDS the occurrence of PDA and indomethacin treatment are not associated with ischemic cardiac damage as detected by cTnT measurements.</subfield>
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   <subfield code="a">Springer-Verlag Berlin Heidelberg, 2000</subfield>
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   <subfield code="a">Key words Indomethacin</subfield>
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   <subfield code="u">Department of Pediatrics, University of Padova, Via Giustiniani 3, 35128 Padova, Italy e-mail: trevo@child.pedi.unipd.it Tel.: +39-049-8213545/46; Fax: +39-049-8213502, IT</subfield>
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