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

Kaarin Mäkikallio, Olli Vuolteenaho, Pentti Jouppila, Juha Rasanen

Research output: Contribution to journalArticle

56 Citations (Scopus)

Abstract

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, 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.

Original languageEnglish (US)
Pages (from-to)726-731
Number of pages6
JournalAmerican Journal of Obstetrics and Gynecology
Volume183
Issue number3
DOIs
StatePublished - 2000
Externally publishedYes

Fingerprint

Placental Insufficiency
Troponin T
Venous Pressure
Fetus
Umbilical Arteries
Umbilicus
Umbilical Veins
Mothers
Pregnancy
Newborn Infant
Control Groups
Enzyme-Linked Immunosorbent Assay

Keywords

  • Doppler ultrasonography
  • Fetal heart
  • Fetal hemodynamics
  • Physiology
  • Preeclampsia

ASJC Scopus subject areas

  • Medicine(all)
  • Obstetrics and Gynecology

Cite this

Association of severe placental insufficiency and systemic venous pressure rise in the fetus with increased neonatal cardiac troponin T levels. / Mäkikallio, Kaarin; Vuolteenaho, Olli; Jouppila, Pentti; Rasanen, Juha.

In: American Journal of Obstetrics and Gynecology, Vol. 183, No. 3, 2000, p. 726-731.

Research output: Contribution to journalArticle

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N2 - 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, 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.

AB - 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, 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.

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KW - Fetal hemodynamics

KW - Physiology

KW - Preeclampsia

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