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Bronchopulmonary dysplasia-associated pulmonary hypertension: clues from placental pathology.
OBJECTIVES: Bronchopulmonary dysplasia (BPD) and the associated complication of pulmonary hypertension (PH) leads to increased mortality and a longer length of stay among survivors. Placental histopathology may give early clues of subsequent events. The objective was to evaluate the relationship of maternal vascular underperfusion (MVU) changes on placental histopathology with subsequent development of BPD-associated PH in a cohort of extremely premature infants.
STUDY DESIGN: In a cohort of preterm infants '⩽28 weeks' gestational age (GA) and with 'severe' BPD, this retrospective study evaluated specific placental histopathological changes and assessed the relationship with subsequent development of PH. 'Severe' BPD was defined as the need for ⩾30% oxygen and/or positive pressure ventilation at 36 weeks postmenstrual age. Placental and echocardiographic assessments were done by investigators masked to the grouping and clinical outcomes.
RESULTS: Fifty six infants with severe BPD formed the cohort; PH was noted in 22 (39.3%) infants. The GA of the infants with and without PH was comparable (25.8±1.6 vs 25.8±1.3 weeks, P=0.9). On placental histopathological examination, 13 (23%) had features of MVU. On univariate logistic regression, the presence of changes consistent with MVU increased the relative risk of subsequent BPD-associated PH by 2.75 (95% confidence interval 1.56 to 4.85, P=0.004). The significance persisted after adjustment for GA. Stratification by the presence or absence of fetal growth restriction, yielded nonsignificant associations (P=0.17).
CONCLUSION: Based on the results of the present study, specific placental histopathological changes may give early clues to the subsequent development of BPD-associated PH.
STUDY DESIGN: In a cohort of preterm infants '⩽28 weeks' gestational age (GA) and with 'severe' BPD, this retrospective study evaluated specific placental histopathological changes and assessed the relationship with subsequent development of PH. 'Severe' BPD was defined as the need for ⩾30% oxygen and/or positive pressure ventilation at 36 weeks postmenstrual age. Placental and echocardiographic assessments were done by investigators masked to the grouping and clinical outcomes.
RESULTS: Fifty six infants with severe BPD formed the cohort; PH was noted in 22 (39.3%) infants. The GA of the infants with and without PH was comparable (25.8±1.6 vs 25.8±1.3 weeks, P=0.9). On placental histopathological examination, 13 (23%) had features of MVU. On univariate logistic regression, the presence of changes consistent with MVU increased the relative risk of subsequent BPD-associated PH by 2.75 (95% confidence interval 1.56 to 4.85, P=0.004). The significance persisted after adjustment for GA. Stratification by the presence or absence of fetal growth restriction, yielded nonsignificant associations (P=0.17).
CONCLUSION: Based on the results of the present study, specific placental histopathological changes may give early clues to the subsequent development of BPD-associated PH.
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