Patent Ductus Arteriosus and Bronchopulmonary Dysplasia-Associated Pulmonary Hypertension: A Bayesian Meta-Analysis

Eduardo Villamor1, Elke van Westering-Kroon1, Gema E Gonzalez-Luis2

  • 1Division of Neonatology, Department of Pediatrics, MosaKids Children's Hospital, Maastricht University Medical Center (MUMC+), School for Oncology and Reproduction (GROW), Maastricht University, Maastricht, The Netherlands.

JAMA Network Open
|November 28, 2023
PubMed

Insights

Prolonged exposure to patent ductus arteriosus (PDA) is linked to a higher risk of pulmonary hypertension in extremely preterm infants. Monitoring and managing PH risk in these infants is crucial for clinical decisions.

Area of Science:

  • Neonatal Medicine
  • Pediatric Cardiology
  • Pulmonary Hypertension Research

Background:

  • Bronchopulmonary dysplasia (BPD) is frequently complicated by pulmonary vascular disease and secondary pulmonary hypertension (PH).
  • The development of BPD-associated PH (BPD-PH) is complex, influenced by prenatal and postnatal factors disrupting pulmonary vascular growth.
  • Recent studies suggest a potential association between patent ductus arteriosus (PDA) and the risk of BPD-PH.

Approach:

  • A Bayesian model-averaged (BMA) meta-analysis was conducted to investigate the association between PDA and BPD-PH.
  • Searches of PubMed and Embase up to April 2023 identified studies involving infants with gestational age ≤32 weeks reporting data on PDA and BPD-PH risk.
  • Data extraction and synthesis followed PRISMA and MOOSE guidelines, with BMA used for effect size calculations and Bayes factors (BFs) to quantify evidence.

Key Points:

  • Analysis of 32 studies (8513 infants) revealed varying levels of evidence for PDA's association with BPD-PH.
  • Extreme evidence supported an association for surgically ligated/catheter-occluded PDA (BF10=294.9) and prolonged PDA exposure (dichotomous: BF10=11.80; continuous: BF10=113.60).
  • Weak evidence supported an association for any PDA (BF10=2.90), moderate for hemodynamically significant PDA (BF10=3.77), and weak evidence favored the null hypothesis for medically treated PDA (BF10=0.55).

Conclusions:

  • The findings suggest that prolonged PDA exposure may increase the risk of pulmonary vascular disease in extremely preterm infants.
  • This highlights the importance of monitoring for PH in high-risk preterm infants with extended PDA exposure.
  • Clinical decisions regarding PDA management should incorporate the assessed risk of PH.
Abstract