Interaction between pulmonary vasculature and the patent ductus arteriosus in very premature infants.

Abstract

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. 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. 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. 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.