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Published on: January 26, 2024
Placental pathologic changes of maternal vascular underperfusion in bronchopulmonary dysplasia and pulmonary
K K Mestan1, J Check1, L Minturn2
1Department of Pediatrics, Division of Neonatology, Northwestern University Feinberg School of Medicine, Ann & Robert H. Lurie Children's Hospital, 225 East Chicago Avenue, Box #45, Chicago, IL, 60611, USA.
Insights
Maternal vascular underperfusion (MVU) in the placenta is linked to bronchopulmonary dysplasia (BPD) in premature infants. This placental finding may identify infants at higher risk for developing pulmonary hypertension (PH).
Area of Science:
- Neonatal Medicine
- Perinatal Pathology
- Pediatric Pulmonology
Background:
- Bronchopulmonary dysplasia (BPD) is a common chronic lung disease in infants.
- BPD-associated pulmonary hypertension (PH) is a severe complication impacting long-term health.
- Chronic fetal hypoxia-ischemia is implicated in BPD and PH development.
Purpose of the Study:
- To investigate the association between placental maternal vascular underperfusion (MVU) and BPD.
- To determine if MVU is further associated with PH in infants with BPD.
Main Methods:
- Retrospective cohort study of premature infants (≤28 weeks gestation).
- BPD defined by oxygen requirement at 36 weeks corrected gestational age.
- PH identified via echocardiogram review; placental slides reviewed for MVU.
Main Results:
- 121 of 283 infants had MVU; 55% developed BPD, 20% had PH.
- MVU was significantly associated with increased BPD risk (aOR=2.6).
- Specific MVU sublesions correlated with PH development.
Conclusions:
- Placental MVU may indicate intrauterine hypoxia-ischemia in infants who develop BPD.
- MVU identifies infants with increased risk for developing PH.
- Findings support earlier, targeted therapies for BPD and associated PH.
Introduction:
Bronchopulmonary dysplasia (BPD) is the most common chronic lung disease of infancy, and BPD-associated pulmonary hypertension (PH) is a serious complication that can negatively impact later childhood health. There is growing evidence that lung injury leading to BPD and PH is due to chronic fetal hypoxia-ischemia. The purpose of this study was to investigate whether placental pathologic changes of maternal vascular underperfusion (MVU) are associated with BPD, and further increased with PH.
Methods:
We conducted a 5-year retrospective cohort study of premature infants born ≤28 weeks. BPD was defined as persistent oxygen requirement at 36 weeks corrected gestational age. PH was identified using a standardized algorithm of echocardiogram review. Archived placental slides underwent standardized masked histopathologic review. Logistic regression modeling was performed, taking into account important maternal and infant covariates.
Results:
Among 283 births, 121 had MVU, of which 67 (55%) developed BPD, and 24 (20%) had PH. Among the common neonatal complications of extreme prematurity, BPD was the only outcome that was increased with MVU (P < 0.001). After adjustment for birth weight, fetal growth restriction, preeclampsia and other factors, infants with MVU were more likely to develop BPD (adjusted odds ratio = 2.6; 95% confidence interval = 1.4, 4.8). Certain MVU sublesions (fibrinoid necrosis/acute atherosis and distal villous hypoplasia/small terminal villi) were increased with PH (P < 0.001).
Discussion:
Placental MVU may identify BPD infants who were exposed to intrauterine hypoxia-ischemia, which increases their risk for development of PH disease.
Conclusions:
Our findings have important implications for providing earlier and more effective therapies for BPD.
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