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Increased acinar arterial wall muscle in preterm infants with PROM and pulmonary hypoplasia
1Department of Pediatrics, Children's Mercy Hospital, University of Missouri-Kansas City School of Medicine, USA.
Insights
Premature rupture of fetal membranes (PROM) can cause pulmonary hypoplasia (PH) and pulmonary hypertension in preterm infants. This study found increased pulmonary arterial wall thickness and muscularization in infants with PROM and PH, indicating a high risk for pulmonary hypertension.
Area of Science:
- Neonatal Medicine
- Pediatric Pathology
- Cardiopulmonary Physiology
Background:
- Pulmonary hypoplasia (PH) is a common complication in preterm infants, often linked to premature rupture of fetal membranes (PROM).
- PH is frequently associated with pulmonary hypertension, impacting infant survival and health outcomes.
- Understanding the structural changes in pulmonary vasculature is crucial for managing PH and its complications.
Purpose of the Study:
- To quantify acinar arterial wall thickness and muscularization in preterm infants who died with PH secondary to PROM.
- To compare these vascular changes to age-matched controls without PH.
Main Methods:
- Post-mortem analysis of lung tissue and pulmonary vasculature from 16 preterm infants with PROM and PH.
- Comparison with 16 age-matched control infants.
- Histological assessment of alveolar ductal artery wall thickness and presence of muscle.
Main Results:
- Infants with PROM and PH exhibited significantly thicker alveolar ductal artery walls (15.1% vs. 7.4%, p < 0.0001) compared to controls.
- Ninety-one percent of infants with PH showed muscle in the arterial walls, versus only 18% in the control group.
- These findings indicate increased pulmonary arterial muscularization in infants with PROM and PH.
Conclusions:
- Preterm infants with PROM and subsequent PH demonstrate significant increases in pulmonary arterial muscularization.
- This vascular remodeling places these infants at high risk for developing pulmonary hypertension.
- Early therapeutic interventions aimed at reducing pulmonary vascular resistance are recommended for affected infants.
Abstract:
Pulmonary hypoplasia (PH), secondary to premature rupture of fetal membranes (PROM), is a frequent cause of pulmonary insufficiency in preterm infants. Pulmonary hypoplasia of diverse causes is usually associated with pulmonary hypertension. The objective of this study was to quantitate the acinar arterial wall thickness and muscularization in preterm infants with PROM that died with PH in comparison to age-matched controls. The left lung and pulmonary vasculature were perfused and fixed in a standard method in 16 infants with PROM and PH, and in 16 controls. In infants with PH, the alveolar ductal artery walls were nearly twice as thick as those of controls, 15.1 +/- 5.1% versus 7.4 +/- 1.3%, p < 0.0001. Ninety-one percent had muscle in the wall compared to 18% of controls. We conclude that infants with PROM and PH have increased pulmonary arterial muscularization, placing them at significant risk to have pulmonary hypertension. For these infants, therapy to reduce pulmonary vascular resistance should be instituted early.