Abstract:By adjusting for factors linked to adult pulmonary hypertension, namely congenital heart defects, pulmonary diseases and premature birth, we were able to show that other unknown factors may influence the risk for pulmonary hypertension among adults who were born premature.
“…However, a recent Swedish registry review of adults with PAH identified premature birth as an independent risk factor for the development of adult onset PAH. 108 It is highly probable that additional, currently unrecognized, perinatal and developmental factors also affect late development of PH. Fig.…”
Section: Long-term Implications For Early Diagnosis and Treatment Of mentioning
Pediatric pulmonary vascular disease (PVD) and pulmonary hypertension (PH) represent phenotypically and pathophysiologically diverse disease categories, contributing substantial morbidity and mortality to a complex array of pediatric conditions. Here, we review the multifactorial nature of pediatric PVD, with an emphasis on improved recognition, phenotyping, and endotyping strategies for pediatric PH. Novel tailored approaches to diagnosis and treatment in pediatric PVD, as well as the implications for long-term outcomes, are highlighted.
“…However, a recent Swedish registry review of adults with PAH identified premature birth as an independent risk factor for the development of adult onset PAH. 108 It is highly probable that additional, currently unrecognized, perinatal and developmental factors also affect late development of PH. Fig.…”
Section: Long-term Implications For Early Diagnosis and Treatment Of mentioning
Pediatric pulmonary vascular disease (PVD) and pulmonary hypertension (PH) represent phenotypically and pathophysiologically diverse disease categories, contributing substantial morbidity and mortality to a complex array of pediatric conditions. Here, we review the multifactorial nature of pediatric PVD, with an emphasis on improved recognition, phenotyping, and endotyping strategies for pediatric PH. Novel tailored approaches to diagnosis and treatment in pediatric PVD, as well as the implications for long-term outcomes, are highlighted.
“…Infants born in different eras of neonatology show similar long‐term impairment in lung function, airway obstruction, structural abnormalities of the gas transfer and pulmonary function . However, in a recent study we found that premature birth in the pre‐surfactant era was associated with an increased risk of adult PH even after adjustments were made for these risk factors . Our working hypothesis was that PH was associated with premature birth also in the post‐surfactant era.…”
Section: Introductionmentioning
confidence: 81%
“…In a previous study, we found an increased risk of PH in adults born preterm . This study covered mainly the 1970s and 1980s, which was a period when surfactant was not in regular clinical use and is called the “pre‐surfactant era.” The first successful trial of endotracheal surfactant administration to preterm infants was performed in the 1980s and surfactant treatment was later proven to reduce the need for supplemental oxygen and ventilator support as well as the risk of neonatal death.…”
“…Long term, preterm birth is associated with an 8.5‐fold increased risk for developing pulmonary hypertension (defined as a mean pulmonary artery pressure ≥25 mmHg) in childhood and adolescence, and a 3.1‐fold increased risk in adulthood, even after adjusting for confounding factors such as acute pulmonary disorders, congenital heart defects, congenital diaphragmatic hernia and chromosomal disorders (Naumburg et al . , ). At rest, otherwise healthy young adults born preterm exhibit increased vascular stiffness with elevations in resting mean pulmonary arterial pressure (Goss et al .…”
Development of the pulmonary circulation is a critical component of fetal lung development, and continues throughout infancy and childhood, marking an extended window of susceptibility to vascular maldevelopment and maladaptation. Perinatal vascular insults may result in abnormal vascular structure or function, including decreased angiogenic signaling and vascular endowment, impaired vasoreactivity through increased pulmonary artery endothelial dysfunction and remodeling, or enhanced genetic susceptibility to pulmonary vascular disease through epigenetic modifications or germline mutations. Although some infants develop early onset pulmonary hypertension, due to the unique adaptive capabilities of the immature host many do not have clinically evident early pulmonary vascular dysfunction. These individuals remain at increased risk for development of late-onset pulmonary hypertension, and may be particularly susceptible to secondary insults. This review will address the role of perinatal vascular insults in the development of late pulmonary vascular dysfunction with an effort to highlight areas of critical research need.
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