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Author Spotlight: Effect of Left Atrial Ligation on Avian Embryonic Hearts and HLHS Implications
Published on: June 16, 2023
Hypoplastic left heart syndrome is associated with structural and vascular placental abnormalities and leptin
Helen N Jones1, Stephanie K Olbrych2, Kathleen L Smith3
1Divisions of Pediatric Surgery, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, USA.
Insights
Placentas from fetuses with hypoplastic left heart syndrome (HLHS) show abnormal structure and reduced weight. These placental abnormalities may contribute to fetal growth issues in HLHS pregnancies.
Area of Science:
- Cardiovascular Pathology
- Developmental Biology
- Placental Biology
Background:
- Hypoplastic left heart syndrome (HLHS) is a severe congenital heart defect linked to fetal growth problems.
- While genetic and environmental factors are implicated, the placenta's role in HLHS pathogenesis remains unclear.
Purpose of the Study:
- To systematically investigate placental characteristics in HLHS cases, with and without associated growth abnormalities.
Main Methods:
- Analysis of placental tissues from HLHS singleton births and gestational age-matched controls.
- Assessment of gross pathology, parenchymal morphology, vascular architecture, and leptin signaling.
- Correlation with clinical data including birth weight and placental pathology reports.
Main Results:
- HLHS placentas exhibited significantly reduced weight and increased fibrin deposition compared to controls.
- Micropathological findings included increased syncytial nuclear aggregates, decreased terminal villi, and reduced vasculature.
- Elevated leptin expression was observed in syncytiotrophoblast and endothelial cells of HLHS placentas.
Conclusions:
- Abnormal placental morphology in HLHS suggests an immature structure potentially caused by vascular issues.
- Increased placental leptin may represent a compensatory mechanism for vascular abnormalities.
- Further research on fetal and placental angiogenesis is crucial for understanding HLHS and related growth deviations.
Introduction:
Hypoplastic left heart syndrome (HLHS) is a severe cardiovascular malformation (CVM) associated with fetal growth abnormalities. Genetic and environmental factors have been identified that contribute to pathogenesis, but the role of the placenta is unknown. The purpose of this study was to systematically examine the placenta in HLHS with and without growth abnormalities.
Methods:
HLHS term singleton births were identified from a larger cohort when placenta tissue was available. Clinical data were collected from maternal and neonatal medical records, including anthropometrics and placental pathology reports. Placental tissues from cases and controls were analyzed to assess parenchymal morphology, vascular architecture and leptin signaling.
Results:
HLHS cases (n = 16) and gestational age-matched controls (n = 18) were analyzed. Among cases, the average birth weight was 2993 g, including 31% that were small for gestational age. When compared with controls, gross pathology of HLHS cases demonstrated significantly reduced placental weight and increased fibrin deposition, while micropathology showed increased syncytial nuclear aggregates, decreased terminal villi, reduced vasculature and increased leptin expression in syncytiotrophoblast and endothelial cells.
Discussion:
Placentas from pregnancies complicated by fetal HLHS are characterized by abnormal parenchymal morphology, suggesting immature structure may be due to vascular abnormalities. Increased leptin expression may indicate an attempt to compensate for these vascular abnormalities. Further investigation into the regulation of angiogenesis in the fetus and placenta may elucidate the causes of HLHS and associated growth abnormalities in some cases.
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