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Pulmonary hypoplasia associated with congenital heart diseases: a fetal study
Isabelle Ruchonnet-Metrailler1, Bettina Bessieres2, Damien Bonnet3
1AP-HP, Hôpital Necker-Enfants Malades, Service de Pneumologie Pédiatrique, Centre de Référence pour les Maladies Respiratoires Rares de l'Enfant, Paris, France.
Insights
Congenital heart diseases with right outflow obstruction significantly increase the risk of fetal pulmonary hypoplasia (PH). This condition appears to be independent of pulmonary vascular abnormalities, suggesting other mechanisms are involved.
Area of Science:
- Fetal medicine
- Cardiology
- Pulmonology
Background:
- Fetal pulmonary vasculature abnormalities can impact lung development.
- Congenital heart diseases (CHDs) are suspected to be linked to pulmonary hypoplasia (PH).
Purpose of the Study:
- To determine the prevalence of PH in fetuses with CHDs.
- To assess if CHDs with right outflow obstruction pose the highest risk for impaired lung growth.
Main Methods:
- Prospective examination of fetuses with CHDs (post-termination) for heart and lung defects.
- Classification of CHDs into five pathophysiological groups.
- Analysis of lung weight (LW), body weight (BW), LW/BW ratio, and immunohistochemical evaluation of CD31 and VEGF.
Main Results:
- Fetuses with CHDs and right outflow obstruction showed significantly lower LW/BW ratios.
- Pulmonary hypoplasia (PH) was detected in 13% of fetuses and strongly associated with right outflow obstruction (p<0.03).
- Right outflow obstruction was present in 60% of fetuses with PH, versus 32% without PH.
Conclusions:
- CHDs with right outflow obstruction are a significant risk factor for prenatally acquired PH.
- Fetal PH occurrence is not linked to pulmonary vascular abnormalities, suggesting perfusion-independent mechanisms.
Background:
Abnormalities of the fetal pulmonary vasculature may affect lung morphogenesis. Postnatal studies have suggested that pulmonary hypoplasia (PH) may be associated with congenital heart diseases (CHDs).
Objective:
To determine the prevalence of PH associated with CHDs, and to evaluate whether CHDs with right outflow obstruction were associated with the highest risk of lung growth impairment.
Methods:
Between January 2006 and December 2010, fetuses with CHD obtained following the termination of pregnancies due to fetal abnormalities were examined in a prospective manner for the detection of heart and lung defects. CHDs were classified into five pathophysiological groups. Lung weight (LW), body weight (BW), and LW/BW ratio were analyzed for each case. The expression of CD31 and VEGF in the lung was evaluated by immunohistochemistry.
Results:
Fetuses with CHDs and right outflow obstruction had significantly lower LW for a given BW, and significantly lower LW/BW ratios for a given gestational age. When defining PH as a fetal LW/BW ratio <0.015 before 28 weeks, and <0.012 after 28 weeks, PH was detected in 15 of the 119 fetuses analyzed (13%). It was significantly associated with CHD with right outflow obstruction, independently of chromosomal abnormalities and associated extracardiac abnormalities (p<0.03). Right outflow obstruction was detected in 60% of the fetuses with CHD and PH, but in only 32% of those with CHD but no PH. In fetuses with right outflow obstruction, no difference was observed between those with PH and those without PH, in terms of the ratio of pulmonary artery diameter to aortic diameter, lung CD31 expression, or lung VEGF expression.
Conclusion:
CHDs with right outflow obstruction are a significant risk factor for prenatally acquired PH. The occurrence of fetal PH is not correlated with abnormalities of the pulmonary vasculature, suggesting the involvement of perfusion-independent mechanisms.
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