Association of Atrial Septal Defects and Bronchopulmonary Dysplasia in Premature Infants - 23/10/18
Abstract |
Objective |
To evaluate the association between the presence of an atrial septal defect (ASD) and the odds of developing bronchopulmonary dysplasia (BPD) in premature infants.
Study design |
We identified a cohort of infants that underwent at least one echocardiogram assessment, birth weight 501-1249 g, and gestational age 23-30 weeks discharged from the neonatal intensive care unit from 2004 to 2016. We used a BPD risk estimator to calculate the predicted risk of developing BPD at 6 postnatal ages within the first 28 days of life. We examined the association between the presence of an ASD and the development of BPD using 2 multivariable logistic regression models for each BPD risk severity on each postnatal day. The first model adjusted for predicted BPD risk and the second added therapeutic interventions for BPD.
Results |
Of 20 496 infants from 228 NICUs who met inclusion criteria, 8892 (43%) were diagnosed with BPD and 1314 (6%) had an ASD. BPD was present in 48% of infants with an ASD and 43% of infants without an ASD. In infants with an ASD, the OR of developing BPD was higher after adjusting for predicted risk of BPD plus therapeutic interventions, regardless of postnatal age or predicted BPD risk severity.
Conclusions |
The presence of an ASD was associated with an increased odds of BPD in this cohort. Future trials should consider ASD as a potentially modifiable risk factor in this vulnerable population.
Le texte complet de cet article est disponible en PDF.Keywords : chronic lung disease, congenital heart disease, pulmonary hypertension
Abbreviations : ASD, BPD, CHD, FiO2, NICHD, NICU, PDA, PH
Plan
| Funded, in part, by the National Institute of Child Health and Human Development (NICHD) (5R25HD076475-05). K.K. receives research support from the National Institutes of Health (NIH) (5T32HD043029-15 and 4T32HD043029-14). E.T. receives research support from the NIH (4T32HD043029-14). R.G. receives research support from the NICHD (HHSN275201000003I), National Institute of Allergy and Infectious Diseases (NIAID) (HHSN272201300017I), and Food and Drug Administration (FDA) (HHSF223201610082C). P.S. receives research support from the NIH (1R21HD080606-01A1), NICHD (HHSN275201000003I), ECHO Program (1U2COD023375-01), and FDA (1R18FD005292-01); he also receives research support from Industry for Neonatal and Pediatric Drug Development (coi.jsp). D.B. receives support from the NIH (2K24HD058735-06), NICHD (HHSN275201000003I), NIAID (HHSN272201500006I), ECHO Program (1U2COD023375-01), and National Center for Advancing Translational Sciences (NCATS) (1U24TR001608-01); he also receives research support from Cempra Pharmaceuticals (subaward to HHSO100201300009C) and industry for neonatal and pediatric drug development (coi.jsp). M.L. receives research support from the FDA (R01FD005101), National Heart, Lung, and Blood Institute (NHLBI) (R34HL124038), ECHO Program (U2COD023375), NICHD (U10HD040492), and the U.S. government for his work in neonatal clinical pharmacology (Government Contract HHSN267200700051C). C.H. receives research support from the NICHD (1K23HD090239) and the U.S. government for his work in pediatric and neonatal clinical pharmacology (Government Contract HHSN267200700051C); he also receives research support from industry for pediatric drug development (conflict-of-interest/). The other authors declare no conflicts of interest. |
Vol 202
P. 56 - novembre 2018 Retour au numéro
Article précédent
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