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Article type: Article Commentary
Authors: Hoffman, Julien I.E.; *
Affiliations: Department of Pediatrics, University of California, San Francisco, CA, USA
Correspondence: [*] Address for correspondence: Julien I.E. Hoffman, M.D., 925 Tiburon Boulevard, Tiburon CA 94920, USA. Tel.: +1 415 497 6741; E-mail: jiehoffman@gmail.com.
Abstract: 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.
Keywords: Angiogenesis, VEGF, pulmonary vascular resistance, bronchopulmonary dysplasia
DOI: 10.3233/NPM-190278
Journal: Journal of Neonatal-Perinatal Medicine, vol. 14, no. 2, pp. 159-161, 2021
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