BACKGROUND:The benefits of closing the ductus arteriosus in very preterm infants have not been convincingly shown in numerous clinical trials. Because a large untreated ductus arteriosus can cause death from congestive heart failure in infants born at term, we need to explain why this might not occur in premature infants born at <28 weeks’ gestation.
METHODS:Based on information in the literature, I have commented on the possible relationship between the pulmonary vasculature and the shunt through the patent ductus arteriosus.
RESULTS:Many of these infants have bronchopulmonary dysplasia, in which animal and human studies have shown a reduced number of capillaries and small pulmonary arteries as well as reduction in vascular endothelial growth factor (VEGF) and platelet endothelial cell adhesion molecule-1 (PECAM-1). Both of these import angiogenic factors. Some who do not have bronchopulmonary dysplasia may have a restricted pulmonary vascular bed.
CONCLUSIONS:The increased pulmonary vascular resistance in very premature infants may restrict pulmonary blood flow even if the ductus is large, thus reducing the urgency for ductus closure.