(65) Identifying the Incidence of Abnormal Cardiopulmonary Phenotypes Underlying Bronchopulmonary Dysplasia with Pulmonary Hypertension Across Different Gestational Ages

Background: Premature infants are at increased risk of bronchopulmonary dysplasia (BPD) and chronic pulmonary hypertension (cPH). The feasibility and yield of standardized targeted neonatal echocardiography (TNE) screening for infants at risk of BPD associated cPH has not been studied .

Objectives: Identify the incidence of abnormal cardiopulmonary phenotypes underlying cPH in patients with BPD in infants born 21-296/7 weeks gestational age (GA).

Design/Methods: A retrospective analysis was conducted on a cohort of neonates < 30 weeks GA admitted to our NICU in the first 3 postnatal days. Standardized cPH screening is performed at 36 weeks corrected GA or 8 postnatal weeks. Abnormal cardiopulmonary phenotypes [resistance mediated PH, flow mediated PH, post-capillary left ventricular diastolic phenotype, pulmonary vein stenosis] were categorized by consensus based on persistence in 2 consecutive serial TNE studies completed within 4 weeks. The primary outcome was the incidence of abnormal cardiopulmonary profiles across GA groups [21-23 weeks, 24-26 weeks, or 27-29 weeks] and was analyzed using χ2 and Fisher’s exact test.

Results: A cohort of 392 patients were screened, 212 of which met eligibility criteria [Figure 1]. Demographics factors were similar across the GA groups aside from expected lower birthweight in the lower GA groups [Table 1]. The overall incidence of abnormal cardiopulmonary profiles was low [n=32 (15.1%)], but not different between GA subgroups[Table 2]. Of these, 12 had cPH with 9 (4.2%) resistance mediated and 3 (1.4%) flow mediated. There frequency of resistance mediated PH was higher in the 21-23 weeks GA groups, but not statistically significant.

Conclusions: The incidence of abnormal cardiopulmonary phenotypes and cPH at our institution is low, despite the fact that 25% of the cohort is born between 21-23 weeks GA. Future studies should characterize mechanistic risk factors for specific cardiovascular phenotypes.