OBJECTIVE: The aim of this study was to test the hypothesis that severe placental insufficiency and a rise in fetal systemic venous pressure are associated with fetal myocardial cell damage, which in turn leads to increased neonatal troponin T levels. STUDY DESIGN: Sixty-six neonates born after uncomplicated pregnancy and delivery were included in the control group. Study groups 1 and 2 consisted of 32 and 5 neonates, respectively, born to women with hypertensive disorder. In study group 1 the fetal intra-abdominal portion of the umbilical vein showed normal nonpulsatile blood flow pattern in every case. In study group 2 all the fetuses had atrial pulsations in the intraabdominal umbilical vein. After delivery blood samples were collected from the umbilical arteries, and cardiac troponin T concentrations were measured with commercially available enzyme-linked immunosorbent assay kits. A clinically significant troponin T level was set at >/=0.10 ng/mL. RESULTS: In study group 1 the maternal main uterine arterial blood flow pattern was normal in 30 cases and abnormal in 2 cases. Umbilical artery blood velocity waveforms were normal in 26 fetuses, 4 fetuses had a decreased diastolic blood flow, 1 fetus had an absent diastolic blood flow pattern, and 1 fetus had a retrograde diastolic blood flow pattern. In study group 2 maternal uterine arterial Doppler findings were abnormal in every case, and all the fetuses had retrograde diastolic blood flow pattern in the umbilical artery. Neonatal troponin T levels were <0.10 ng/mL in the control group (0-0.14 ng/mL) and in study group 1 (0-0.16 ng/mL), except for 1 case in each group. Every neonate in study group 2 had a troponin T level >0.10 ng/mL, with the range from 0.11 to 0.35 ng/mL. In study group 2 troponin T concentrations were significantly higher (P <.0001) than in either the control group or study group 1. CONCLUSION: Neonatal troponin T levels are not clinically significantly increased in normal pregnancies and in pregnancies complicated by maternal hypertensive disorder but with normal fetal umbilical venous return. Neonatal troponin T concentrations are significantly increased in the presence of abnormal umbilical venous return, which indicates myocardial cell damage.
OBJECTIVE: The aim of this study was to test the hypothesis that severe placental insufficiency and a rise in fetal systemic venous pressure are associated with fetal myocardial cell damage, which in turn leads to increased neonatal troponin T levels. STUDY DESIGN: Sixty-six neonates born after uncomplicated pregnancy and delivery were included in the control group. Study groups 1 and 2 consisted of 32 and 5 neonates, respectively, born to women with hypertensive disorder. In study group 1 the fetal intra-abdominal portion of the umbilical vein showed normal nonpulsatile blood flow pattern in every case. In study group 2 all the fetuses had atrial pulsations in the intraabdominal umbilical vein. After delivery blood samples were collected from the umbilical arteries, and cardiac troponin T concentrations were measured with commercially available enzyme-linked immunosorbent assay kits. A clinically significant troponin T level was set at >/=0.10 ng/mL. RESULTS: In study group 1 the maternal main uterine arterial blood flow pattern was normal in 30 cases and abnormal in 2 cases. Umbilical artery blood velocity waveforms were normal in 26 fetuses, 4 fetuses had a decreased diastolic blood flow, 1 fetus had an absent diastolic blood flow pattern, and 1 fetus had a retrograde diastolic blood flow pattern. In study group 2 maternal uterine arterial Doppler findings were abnormal in every case, and all the fetuses had retrograde diastolic blood flow pattern in the umbilical artery. Neonatal troponin T levels were <0.10 ng/mL in the control group (0-0.14 ng/mL) and in study group 1 (0-0.16 ng/mL), except for 1 case in each group. Every neonate in study group 2 had a troponin T level >0.10 ng/mL, with the range from 0.11 to 0.35 ng/mL. In study group 2 troponin T concentrations were significantly higher (P <.0001) than in either the control group or study group 1. CONCLUSION: Neonatal troponin T levels are not clinically significantly increased in normal pregnancies and in pregnancies complicated by maternal hypertensive disorder but with normal fetal umbilical venous return. Neonatal troponin T concentrations are significantly increased in the presence of abnormal umbilical venous return, which indicates myocardial cell damage.