2026-07-10 | Hemodynamic phenotyping of bronchopulmonary dysplasia: from transitional circulation to precision cardiopulmonary care.

Bronchopulmonary dysplasia (BPD) remains one of the most important complications of extreme prematurity and a leading cause of long-term respiratory, cardiovascular, and neurodevelopmental morbidity. Increasing evidence suggests that BPD should be viewed not only as a parenchymal lung disorder but as a complex cardiopulmonary syndrome involving disrupted vascular development, abnormal transitional circulation, and ventricular dysfunction. This review aimed to summarize current evidence on the hemodynamic mechanisms underlying BPD, emphasizing pulmonary vascular disease (PVD), bronchopulmonary dysplasia-associated pulmonary hypertension (BPD-PH), phenotype-based classification, and implications for precision management. A narrative review of experimental, translational, and clinical studies was performed, focusing on pulmonary vascular development, transitional hemodynamics, patent ductus arteriosus, ventricular function, targeted neonatal echocardiography, and biomarker-based risk stratification in preterm infants. Evidence regarding phenotypic classification and individualized therapeutic strategies was also examined. Emerging evidence demonstrates that abnormal pulmonary vascular growth begins early, often during the transitional circulatory period, and is aggravated by hyperoxia, mechanical ventilation, inflammation, placental dysfunction, and altered pulmonary blood flow. Prolonged exposure to hemodynamically significant left-to-right shunts, particularly patent ductus arteriosus, may contribute to pulmonary overcirculation, edema, and vascular remodeling. Elevated pulmonary vascular resistance leads to right ventricular pressure overload, while left ventricular diastolic dysfunction and pulmonary venous congestion further worsen pulmonary edema and gas exchange. Early hemodynamic assessment using targeted neonatal echocardiography and biomarkers such as NT-proBNP enables detection of subclinical PVD and ventricular dysfunction during the first days of life. Phenotype-based classification reveals overlapping parenchymal, interstitial, congestive, vascular, and airway components, supporting individualized cardiopulmonary management. BPD is increasingly recognized as a heterogeneous cardiopulmonary syndrome in which disturbed hemodynamics and impaired cardiopulmonary coupling play central roles in disease progression and prognosis. Early hemodynamic phenotyping may improve risk stratification, support precision-guided interventions, and offer new opportunities to prevent PVD, BPD-PH, and long-term cardiopulmonary sequelae in extremely preterm infants.

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2026-07-09 | Diuretics for Preventing Bronchopulmonary Dysplasia in Preterm Infants: A Systematic Review and Meta-Analysis.

Randomized controlled trials (RCTs) have not demonstrated that diuretics prevent bronchopulmonary dysplasia (BPD), but recent observational studies warrant an updated synthesis. We evaluated the preventive effects and safety of diuretics in preterm infants at risk of developing BPD. MEDLINE, Embase, Cochrane CENTRAL, and CINAHL were searched through June 2025. We included randomized and non-randomized studies of various diuretic classes with different routes, dosing regimens, and treatment durations. The risk of bias was assessed using the RoB 2 and ROBINS-I, and the certainty of evidence using GRADE. Random-effects models were used to calculate the risk ratios and 95% confidence intervals. Forty studies, including six randomized controlled trials (RCTs), were analyzed. Furosemide was the most frequently used diuretic. The RCTs predominantly focused on short-term changes in lung mechanics and did not demonstrate any preventive effect of diuretics on BPD. The meta-analysis showed no significant effects of diuretics on death or BPD (RR, 1.10; 95% CI, 0.77-1.59) or mortality (RR, 0.44; 95% CI, 0.19-1.04). Electrolyte abnormalities were not significantly increased (RR, 1.51; 95% CI, 0.81-2.83). Non-randomized studies have reported a potential reduction in BPD occurrence. However, the overall certainty of the evidence is low to very low due to the small sample sizes and confounding. The current evidence does not confirm that diuretics prevent BPD. Given the uncertainty of the current evidence and the favorable safety profiles, adequately powered RCTs are needed to explore the potential role of diuretics in BPD prevention.

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