Association of severe placental insufficiency and systemic venous pressure rise in the fetus with increased neonatal cardiac troponin T levels.
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.


METHODS
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.


CONCLUSIONS
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.
Mäkikallio
K
K
Departments of Obstetrics and Gynecology and Physiology, University of Oulu, Oulu, Finland.
Vuolteenaho
O
O
Jouppila
P
P
Räsänen
J
J
D000328:Adult; D001724:Birth Weight; D001783:Blood Flow Velocity; D009202:Cardiomyopathies / Q000097:blood / Q000209:etiology*; D005260:Female; D005333:Fetus / Q000502:physiology*; D005865:Gestational Age; D006801:Humans; D006863:Hydrogen-Ion Concentration; D006973:Hypertension / Q000097:blood / Q000150:complications; D007231:Infant, Newborn; D010927:Placental Insufficiency / Q000150:complications* / Q000503:physiopathology; D011225:Pre-Eclampsia / Q000097:blood / Q000150:complications; D011247:Pregnancy; D011248:Pregnancy Complications; D011673:Pulsatile Flow; D020107:Troponin T / Q000097:blood*; D014469:Umbilical Arteries; D014599:Uterus / Q000098:blood supply; D014690:Venous Pressure
D020107:Troponin T