Abstract
Early injury to the lung circulation leads to the rapid development of pulmonary hypertension (PH) after premature birth. PH in bronchopulmonary dysplasia (BPD) results from increased vascular tone and abnormal vasoreactivity, hypertensive remodeling, and decreased vascular growth. The development of PH is sometimes a serious complication of BPD that can significantly impact the morbidity and mortality rates of preterm infants. Despite a gradual reduction in pulmonary arterial pressure postnatally, approximately a quarter of BPD infants have echocardiographic evidence of PH later. The pathogenesis of PH in BPD is very complex and multifactorial, often resulting from interactions between genetic and environmental or acquired factors (both prenatal and postnatal). Antenatal risk factors such as intrauterine growth retardation, maternal preeclampsia, and oligohydramnios suggest compelling evidence for the fetal origins of PH. Despite the potential importance of PH in preterm infants, the pathophysiology and the risk factors of PH in infants with BPD are still poorly understood. I have reviewed recent progress in research concerning the pathophysiology including the risk factors of PH in infants with BPD.
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