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Published on: November 8, 2018
Maternal serum placental growth factor at 11-13 weeks' gestation and fetal cardiac defects
E Llurba1, A Syngelaki, O Sánchez
1Department of Obstetrics, Maternal-Fetal Medicine Unit, Vall d'Hebron University Hospital, Universitat Autònoma de Barcelona, Barcelona, Spain. ellurba@vhebron.net
Insights
Maternal serum placental growth factor (PlGF) is lower in pregnancies with fetal heart defects, indicating impaired placental angiogenesis. This suggests a potential early marker for these conditions.
Area of Science:
- Obstetrics and Gynecology
- Fetal Medicine
- Reproductive Biology
Background:
- Placental growth factor (PlGF) is a key marker of placental angiogenesis.
- Fetal heart defects are a significant concern in prenatal diagnostics.
- Understanding early markers for fetal abnormalities is crucial for improved outcomes.
Purpose of the Study:
- To investigate the association between maternal serum PlGF levels and isolated fetal major heart defects.
- To determine if PlGF can serve as an early indicator of placental angiogenesis issues in pregnancies with fetal heart defects.
Main Methods:
- Maternal serum PlGF, PAPP-A, and UtA-PI were measured at 11-13 weeks gestation.
- Data from 68 cases with fetal heart defects and 340 controls were analyzed.
- Biomarker levels were adjusted for covariates and compared between groups.
Main Results:
- Median PlGF multiples of the median (MoM) were significantly lower in the fetal heart defect group compared to controls (P < 0.0001).
- Low PlGF was associated with conotruncal and valve defects, but not left ventricular outflow tract obstruction.
- No significant differences were found in PAPP-A-MoM or UtA-PI-MoM between groups.
Conclusions:
- Pregnancies with isolated fetal heart defects show evidence of impaired placental angiogenesis.
- This impairment occurs independently of compromised placental perfusion or function.
- Maternal serum PlGF may be a valuable marker for detecting early placental abnormalities in fetal heart defect cases.
Objective:
To investigate the relationship between fetal heart defects and maternal serum placental growth factor (PlGF), a marker of placental angiogenesis.
Methods:
Maternal serum PlGF, pregnancy-associated plasma protein-A (PAPP-A) and uterine artery pulsatility index (UtA-PI) at 11-13 weeks' gestation were compared in 68 cases of isolated fetal major heart defects and 340 normal controls. Variables were converted into multiples of the median (MoM) after adjustment for gestational age, maternal age, racial origin, weight, parity and method of conception, and then compared between groups. The cardiac defects included 11 cases of obstruction of the left ventricular outflow tract (LVOT), 25 conotruncal abnormalities and 32 valve defects.
Results:
The median PlGF-MoM in the heart defect group was lower than in controls (0.80 (interquartile range (IQR), 0.57-1.08) vs 1.00 (IQR, 0.79-1.32); P < 0.0001). Low PlGF levels were observed in the presence of conotruncal and valve defects but not in the presence of LVOT defects. There was no significant difference between the group with fetal heart defects and controls in PAPP-A-MoM (0.95 (IQR, 0.68-1.28) vs 1.01 (IQR, 0.70-1.39); P = 0.292) or UtA-PI-MoM (1.01 (IQR, 0.84-1.28) vs 0.99 (IQR, 0.80-1.20); P = 0.396).
Conclusion:
In pregnancies with isolated fetal heart defects there is evidence of impaired placental angiogenesis in the absence of impaired placental perfusion and function.
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