International Journal of Pediatrics Variables Weight (g) GA (weeks) CRIB (Me) SNAPPE (Me) Apgar 1 min (Me) Apgar 5 min (Me) Days on MV Days on CPAP Total Time of O2 Days in hospital Variables Prenatal steroids Abnormal Doppler EOT (delivery room) DMH Use of surfactant Hypotension PDA Use of indomethacin Use of dopamine Use of dobutamine Use of diuretics Cardiac dysfunction Cardiac overload 1124 ± 292 30 ± 2.0 3.1 ± 3.4 18.5 ± 16.4 6.7 ± 1.9 8.5 ± 1.0 3.91 ± 9.1 5.3 ± 7.9 16.1 ± 25.4 54.2 ± 27.9 Troponin (−) 74% 54% 25% 55% 45% 24% 42% 34% 24% 27% 42% 15% 28% Table 2: Neonatal variables versus cardiac troponin T results. Troponin (−) n = 70 Troponin (+) n = 46 Table 3: Neonatal variables versus cardiac troponin T results. 953 ± 301 28 ± 2.2 5.5 ± 4.3 27 ± 17.4 5.3 ± 2.2 7.9 ± 1.3 12.5 ± 20.1 12.9 ± 12.2 37.3 ± 43.1 75.14 ± 43.7 Troponin (+) 77% 37% 53% 80% 76% 34% 74% 60% 52% 54% 58% 40% 47% 3 P value P < 0.003 P < 0.01 P < 0.001 P < 0.01 P < 0.01 P < 0.01 P < 0.01 P < 0.001 P < 0.002 P < 0.006 P value P < 0.9 P < 0.12 P < 0.005 P < 0.01 P < 0.002 P < 0.30 P < 0.01 P < 0.01 P < 0.004 P < 0.005 P < 0.13 P < 0.03 P < 0.05 conﬁrmed the clinical usefulness of troponin T in patients with acute coronary syndrome establishing the diagnosis of ischemia, myocardial necrosis, and the prognosis of acute myocardial infarct. Due to the absolute speciﬁcity of cTnT regarding the myocardial tissue and its high sensitivity, even in microscopic regions, for myocardial necrosis, the American College of Cardiology and the European Society of Cardiology recommended cardiac troponins as the best biological markers for myocardial infarct [4]. There are several studies published on the behavior of cTnT in newborns, in diﬀerent clinical situations, and its value in diagnosing cardiovascular dysfunction. Adamcova´ et al. studying the cTnT in the blood cord of newborns suggested that its increase would indicate fetal distress and myocardial compromise. These authors evaluated cord blood cTnT in 15 healthy term newborns and found plasma concentrations of 0.05 ± 0.04 ng/mL in 10 of the 15 infants studied. Among these, 5 showed higher concentrations of cTnT (0.19 ± 0.07 ng/mL) [5]. In 2000, Trevisanuto et al. described high cTnT con- centrations in preterm infants with respiratory distress and suggested that it was due to myocardial damage. They also observed a signiﬁcant relationship of troponin T levels with the use of vasopressors, mechanical ventilation, and high oxygenation index in patients with respiratory distress syndrome. The mean plasma troponin was 0.38 ng/mL in patients with respiratory distress versus 0.13 ng/mL in patients without respiratory distress (P < 0.01) [2]. These same authors, in a subsequent study, compared the cTnT, cTnl, and CKMB concentrations in the blood cord of 85 healthy full-term newborns and in blood samples of their mothers’ right after birth. The concentrations of cTnT and cTnl were higher than the detection limit in 2 (2.3%) and 41 (48.2%), respectively. Two mothers (2.3%) had cTnT levels higher than the detection limit; none showed increase in the cTnl levels. These authors concluded that cTnT in the blood cord is often above the detection limit at birth, while the cTnl is more often undetectable and comparable to that of healthy mothers. Therefore, these cardiac regulatory proteins are of neonatal origin and are not inﬂuenced by maternal levels [6]. Several publications have attempted to correlate in- creased cTnT with other markers of myocardial dysfunction and echocardiographic abnormalities. Cruz et al. studied 27 ELBW infants and measured cTnt in the ﬁrst 48 hours of life. They observed increased levels in infants with low Apgar scores and requiring inotropic support. cTnT did not correlate with simultaneous echocardiographic measures of cardiac function [7]. Costa et al. And Rajakumar et al. in two