The following is a summary of “Placental delayed villous maturation is associated with fetal congenital heart disease,” published in the FEBRUARY 2023 issue of Obstetrics and Gynecology by O’Hare, et al.

The placenta is a vital organ for fetal development and health, but in pregnancies with congenital heart disease, there are often abnormalities in the development and function of the placenta. However, previous research needed standardized diagnostic criteria and control populations, which limited its generalizability and ability to identify specific placental abnormalities associated with congenital heart disease. For a study, researchers aimed to address these limitations by using the Amsterdam criteria to compare placental abnormalities in pregnancies with fetal congenital heart disease to those without and to investigate any differences in placental abnormalities based on cardiac physiology.

From January 2013 to June 2019, a retrospective cohort study was carried out at a single center. The study included infants diagnosed prenatally with moderate-severe congenital heart disease delivered at ≥37 weeks of gestation. A control group born at ≥37 weeks of gestation without fetal congenital heart disease or significant pregnancy complications was also included and matched with the congenital heart disease group based on maternal race and ethnicity and infant sex. The Amsterdam criteria were applied to categorize placental pathology findings into delayed villous maturation, maternal vascular malperfusion, fetal vascular malperfusion, and inflammatory lesions. The study compared the frequency of placental abnormalities between groups and used logistic regression to examine the association of clinical and sociodemographic factors with delayed villous maturation, maternal vascular malperfusion, and fetal vascular malperfusion.

About 194 pregnancies with fetal congenital heart disease and 105 controls were included, and 83% of those with congenital heart disease and 82% of those in the control group were non-Hispanic White. Pregnancies with fetal congenital heart disease showed increased rates of delayed villous maturation (6% vs. 19%; P<.001) and maternal vascular malperfusion (19% vs 34%; P=.007) but not fetal vascular malperfusion (6% vs 10%; P=.23) compared to controls. When compared to controls, infants with congenital heart disease and a 2-ventricle architecture had the highest risks of delayed villous maturation (odds ratio, 5.5; 95% CI, 2.2-15.7; P<.01). 

Infants with 2-ventricle anatomy and newborns with single-ventricle physiology with pulmonic blockage had maternal vascular malperfusion that was 2.2 times greater (P=.02) and 2.9 times higher (P=.02), respectively. In the congenital heart disease group, oligohydramnios was linked to maternal vascular malperfusion, while polyhydramnios was linked to delayed villous maturation, higher maternal body mass index, bigger newborn birth head circumference, and infant breathing support in the delivery room. With regard to infant birth head circumference and infant respiratory support in the delivery room, associations of delayed villous maturation persisted in multivariable models that adjusted for cardiac diagnosis (odds ratio, 1.2; 95% CI, 1.0-1.5; P=.02; and odds ratio, 3.0; 1.3-6.5; P=.007).

Maternal variables may be related to placental maldevelopment in pregnancies with fetal congenital heart disease since they showed greater rates of delayed villous maturation and maternal vascular malperfusion than controls. However, further research was required to ascertain how these anomalies related to the outcomes of postnatal infants.

Reference: ajog.org/article/S0002-9378(22)00645-7/fulltext