© 2006 American Thoracic Society
Understanding Cardiac Troponin T in the Newborn PeriodFrom the Authors:In response to Dr. Clark's letter about our recent article (1), we agree that although some work has been done, we lack reference values for cardiac troponin T (cTnT) in the healthy newborn infant (2–5). In our study, although a certain number of infants had undetectable values of cTnT, those values were not sufficient to modify the median of 0.014 ng/ml. Our results were reproducible, and no reasons for differences with other studies have been found. In agreement with Dr. Clark's comment, we have also found (unpublished results) a tendency toward an increase of cTnT in the third and fourth days of postnatal life. However, these determinations were not performed systematically and thus were not included. In severely asphyxiated neonates with profound acidemia, we have consistently found increased cardiac damage markers in cord blood (creatinkinase, troponin I, and cTnT). Thus, our patients had a cord pH value of less than 7.0 (2) (room-air resuscitated, 6.96 [± 0.08]; 100% oxygen group, 6.92 [± 0.06]; unpublished data). Moreover, we found a significant correlation between time elapsed since the asphyxiating process was suspected and effective birth for various parameters indicative of fetal stress (e.g., pH, Apgar, biochemical markers). Thus, in women admitted to the obstetric ward, the time elapsed between suspicion of asphyxia and birth was always less than 30 min. However, in nonhospitalized women, the time elapsed between suspicion of asphyxia and effective delivery was significantly longer. Thus, our data indicate that mean time elapsed between suspicion of the asphyctic process and initiation of resuscitation was 94 ± 45 min. These circumstances make it difficult to interpret the evolution of cTnT values after birth. Finally, in asphyxiated infants, there was a significant elevation of cTnT after the first 48 h of life. Thus, cTnT reached plateau values at 96 h in both groups (room-air resuscitated group median: 0.055 ng/ml; pure oxygen group median: 0.068 ng/ml; unpublished data). However, determinations after 48 h of life were not systematically performed and thus not reflected in the study. Since there is no previous information in the literature relating to the determination of cTnT in asphyxiated babies being resuscitated with room air versus pure oxygen, it has not been possible to establish comparison between our results and others. However, we hypothesize that some babies enrolled in previous studies (3, 5) were resuscitated using 100% oxygen, and also received oxygen supplementation in the first days after birth. Hypoxia–reoxygenation and hyperoxemia are well-known sources of oxygen free radicals, which are especially damaging for organs such as the heart and brain with their high metabolic rates and dependence on aerobic metabolism. Our results suggest that elevation of cardiac enzymes in the first days of life secondary to asphyxia is aggravated by the oxidative stress resulting from reoxygenation with pure oxygen.
Hospital Universitario Materno-Infantil La Fe, Valencia, Spain
Universidad de Valencia, Valencia, Spain FOOTNOTES Conflict of Interest Statement: None of the authors has a financial relationship with a commercial entity that has an interest in the subject of this manuscript. REFERENCES
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