Pediatr Res. 2026 Jun 27. doi: 10.1038/s41390-026-05260-5. Online ahead of print.
ABSTRACT
BACKGROUND: Premature birth is associated with altered pulmonary vascular development and raised pulmonary artery pressures (PAPs). Arrested alveolar and vascular development reduce lung surface area, which can be assessed by the diffusion capacity of the lung for carbon monoxide (DLCO) and the carbon monoxide transfer coefficient (K). We hypothesise that abnormal DLCO and K would be associated with higher PAPs in school-aged children METHODS: We enroled participants born premature ( < 29 weeks gestation) from the United Kingdom Oscillation Study and age-matched term-born children. Echocardiography was performed, including estimates of systolic and mean PAP (SPAP and MPAP) and spirometry and DLCO measurements were made. An abnormal result was Z score <-1.64 and severely abnormal Z score <-1.96 RESULTS: One hundred ninety-two participants were assessed at 12 (range 10-14) years; 60% born prematurely. Fifty-eight children had severely abnormal K (95% preterm) which was associated with a higher SPAP (p < 0.001) and MPAP (p < 0.001)) and a lower forced expiratory volume in one second to forced vital capacity ratio (FEV/FVC) (p < 0.001).
CONCLUSION: Low K was associated with higher SPAP and MPAP and lower FEV/FVC in school-aged children born premature. We speculate early and serial assessments of lung function with K may identify subjects born preterm at high risk for pulmonary hypertension who would benefit from cardiac assessment.
IMPACT: Premature birth is associated with altered pulmonary vascular development and raised pulmonary artery pressures (PAPs), contributing to increased risk for late cardiopulmonary disease. Abnormal K was associated with higher PAPs in school-aged children born premature. Assessment of K might identify individuals born prematurely who are at greater risk for late cardiopulmonary disease as adults and potentially benefit from cardiac assessment and intervention to prevent progression to higher PAPs and more severe right ventricular dysfunction in early adulthood.
PMID:42365168 | DOI:10.1038/s41390-026-05260-5