Why the study?
Does maternal preeclampsia cause fetal cardiac cell damage as measured by umbilical artery biomarkers?
Does maternal preeclampsia cause fetal cardiac cell damage as measured by umbilical artery biomarkers?
Severe maternal preeclampsia is associated with elevated fetal NT-proBNP and homocysteine levels, suggesting potential in-utero cardiac cell damage and endothelial injury.
May indicate fetal cardiac stress in severe preeclampsia; hypothesis-generating and requires prospective validation before clinical implications.
OBJECTIVE: To determine whether preeclampsia causes fetal cardiac cell damage by assessing umbilical artery NT-proBNP, cardiac troponin I and homocysteine. METHODS: A cross-sectional study with 73 fetuses between 26 and 40 weeks of gestation was performed. Thirty-three healthy mothers' fetuses were control group (Group I). While 12 mildly pre-eclamptic mothers' fetuses constituted Group II, 28 fetuses of severe pre-eclamptic mothers were Group III. RESULTS: Umbilical cord mean NT-proBNP levels of Group I, II and III are 520.8 ± 404.5 pg/ml; 664.2 ± 215.9 pg/ml; and 1932.8 ± 2979.5 pg/ml, respectively (p = 0.0001). The number of neonates with NT-proBNP > 500 pg/mL that indicates severe cardiac damage is higher in Group III (p = 0.001). The mean homocysteine levels are also statistically significantly higher in Group III. Cardiac troponin I levels are not different between the groups (p = 0.46). CONCLUSION: Increased NT-proBNP and homocysteine might not only indicate some degree of in-utero cardiac cell damage but also feto-placental endothelial injury in the fetuses of severe pre-eclamptic mothers. Our finding that shows no evidence of correlation between cardiac troponin I levels with cell damage and endothelial injury requires further research.
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Akil et al. (2015) studied this question.
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