Key result
Fetal congenital heart defects are linked to ~4.4-fold higher odds of abnormal cord insertion.
Why the study?
The heart and placenta share key developmental pathways involving PlGF and VEGFR-1, but placental pathology and PlGF/VEGFR-1 expression patterns in pregnancies with fetal congenital heart defects needed evaluation.
Case-Control (n=102)
Blind analysis of histological sections
No
Odds Ratio: 4.38 (95% CI 1.78–11.23)
Altered placental growth factor expression and increased placental gross and microscopic pathologies in CHD pregnancies support the involvement of placental-mediated mechanisms and the heart-placenta axis in the development of congenital heart defects.
Association with placental defects supports heart-placenta axis in CHD; hypothesis-generating and should not yet change practice.
The heart and placenta have simultaneous embryologic development, the interactions between the two organs representing the heart-placental axis. They both share key developmental pathways, one of which involves the placental growth factor (PlGF) and its receptor, vascular endothelial growth factor receptor-1 (VEGFR-1). The aim of this study was to evaluate the placental pathology and the expression patterns of PlGF and VEGFR-1 in pregnancies with fetuses with congenital heart defects (CHDs). We analyzed placental gross and microscopic alterations between placentas from pregnancies with CHD fetuses and pregnancies with structurally normal heart fetuses. We also performed the immunohistochemical (IHC) assessment of the placental expression of PlGF and VEGFR-1 in the two groups. We discovered significant gross placental abnormalities in pregnancies with CHD fetuses, including a shorter umbilical cord, marginal or velamentous umbilical cord insertion, and a lower fetal-to-placental weight ratio. Also, 88.2% of the placentas in the CHD group displayed microscopic pathologic aspects. We demonstrated significant placental immunostaining for PlGF and VEGFR-1 in the syncytiotrophoblast and decidual cells compared to villous endothelial cells. We identified a lower placental IHC expression of PlGF in pregnancies with CHD fetuses compared to controls but no differences in the placental immunostaining pattern for VEGFR-1 between the two groups. Our study uncovered a potential role played by the PlGF/VEGFR-1 pathway in the development of CHDs through placental-mediated mechanisms.
No takes yet. Share an insight, caveat, or question.
Bolunduț et al. (2025) conducted a case-control in Fetal congenital heart defects (n=102). Fetal congenital heart defects vs. Structurally normal heart fetuses was evaluated on Marginal or velamentous umbilical cord insertion (OR 4.38, 95% CI 1.78-11.23). Fetal congenital heart defects were associated with significant placental abnormalities, including a 4.38-fold increased odds of marginal or velamentous umbilical cord insertion.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: