4 separate studies found a correlation between increased cTnT and signs of myocardial damage in infants with perinatal asphyxia [8, 9]. More recently El-Khuﬀash et al. developed a predic- tive model using echocardiographic data, cTnT, B-type natruretic peptide, and a PDA scoring system in 60 infants with less than 32 weeks and less than 1500 g, who were fol- lowed until two years of age. They concluded that the use of biochemical markers and the PDA scoring system may pro- vide a better approach to the management of PDA in the ﬁrst 48 hours of life, with improved intact long term survival [10]. Our study was conducted with the aim of characterizing the behavior of the cTnT in the very-low-birth-weight newborn. We conducted prospective measurements of cTnT using third-generation assay method, for all newborns admitted to a neonatal NICU, for eighteen months, in a series of nonselected patients and observed increased values in 40% of the infants, according to our deﬁnition. We recorded clinical events and perinatal morbidity in this group, looking for associations with the cTnT levels. Measurements were made between 24 and 48 hours of life, based on adult data after a myocardial injury. The value of 0.1 ng/mL for a cutoﬀ was chosen according to the studies conducted in adults by Alpert et al., Ohman et al., and Costa et al. in newborns [4, 7, 8]. We found an association of increased cTnT values with low birth weight and gestational age and a positive association with several variables related to illness severity (Table 3). Similar to our study, Clark et al. studied a total of 162 newborns (113 healthy and 49 sick) and observed more elevated values of cTnT in sick preterm. A multiple regression analysis demonstrated that the rise of cTnT was associated to the need of respiratory support and to the use of inotropic drugs [3]. Szymankiewicz et al. studied 39 asphyxiated newborn versus 44 nonasphyxiated newborns and tried to relate the cTnT to echocardiographic ﬁndings of myocardial damage. The cTnT was measured within 12 and 24 hours of life. The asphyxiated infants had higher levels of cTnT (0.141 versus 0.087 ng/mL) than the nonasphyxiated infants (P < 0.01) [11]. In our study, two variables related to asphyxia showed a positive association with cTnT: the need for intubation in the delivery room and the mean Apgar scores of 1st and 5th minute. Our ﬁndings are similar to many other studies that suggested a positive association of cTnT and asphyxia in the neonatal period [2, 3, 8–10]. We performed a logistic regression analysis adjusting for neonatal morbidities and severity scores. The best model showed that an abnormal maternal doppler and the use of diuretics had a protective eﬀect, while low gestational age, the persistence of ductus arteriosus, and the use of dopamine were associated with a positive cTnT. The frequency of maternal arterial hypertension and changes in the Doppler ﬂuxometry was high in this popula- tion (42% and 47%). These are the most common maternal risk factors for elective interruption of pregnancy. Abnormal Doppler ﬂuxometry, when conjugated with intrauterine International Journal of Pediatrics growth retardation, is associated to adverse neonatal out- come. However, in the absence of growth retardation, pre- mature delivery may render better fetus and so a protective eﬀect. Previous publications have already related increased cTnT to a patent ductus arteriousus. El-Khuﬀash and Molloy studied 80 infants with 28-week median gestational age and observed increased cTnT levels in infants with an open ductus which decreased after ductal closure [12]. Important hemodynamic changes may be related to an open ductus arteriousus. There is frequently atrial and ventricular overload and a drop of diastolic blood pressure causing so-called blood ﬂow steel. The blood that ﬂows in the descending aorta during systole comes back through the patent channel towards the pulmonary artery. Large shunts may lead to more than 50% return of blood in the descending aorta, causing hypoperfusion of all systemic arteries, includ- ing the coronary arteries. It is possible that the coronary hypoperfusion will lead to myocardial ischemia, some degree of necrosis and increased cTnT values. Improvement in cardiac overload with a patent ductus may also explain the protective eﬀect of diuretics [13]. The eﬀect of gestational age is still a controversial issue. Diﬀerent from our ﬁndings, previous studies did not show increased cTnT values infants with lower gestational age [3, 10, 12, 14]. Most studies had smaller numbers of VLBW infants, and very few babies below 28 of weeks gestation. In a more recent series from our institution, not published yet, including only babies with less than 1000 g, we have also not found a relationship between cTnT values and gestational age suggesting that these diﬀerences may be population related [15]. Our study is the largest series of very-low-birth-weight newborns studied, with a third-generation cTnT assay. The predominant proﬁle associated with a positive troponin test, was that of an immature baby, intubated in the delivery room, with respiratory distress, and requiring vasoactive drugs. Our ﬁndings conﬁrm previous observations and suggest that cTnT may be a very useful and early marker of myocar- dial injury in very-low-birth-weight newborn infants. References [1] World Health Report 1995, World Health Organization, Gene- va, Switzerland, 1997. [2] D. Trevisanuto, M. Zaninotto, S. Altinier, M. Plebani, and V. Zanardo, “High serum cardiac troponin T concentrations in preterm infants with respiratory distress syndrome,” Acta Paediatrica, vol. 89, no. 9, pp. 1134–1136, 2000. [3] S. J. Clark, P. Newland, C. W. Yoxall, and N. V. Subhedar, “Concentrations of cardiac troponin T in neonates with and without respiratory distress,” Archives of Disease in Childhood, vol. 89, no. 4, pp. F348–F352, 2004. [4] J. S. Alpert, K. Thygesen, J. P. Bassand et al., “Myocardial infarction redeﬁned (a consensus document of the joint Euro- pean society of cardiology/American college of cardiology committee for the redeﬁnition of myocardial infarction),” Journal of the American College of Cardiology, vol. 36, no. 3, pp. 959–969, 2000.