Titre
Pulmonary and systemic vascular dysfunction in young offspring of mothers with preeclampsia.
Type
article
Institution
UNIL/CHUV/Unisanté + institutions partenaires
Périodique
Auteur(s)
Jayet, Pierre-Yves
Auteure/Auteur
Rimoldi Stefano, F.
Auteure/Auteur
Stuber, Thomas
Auteure/Auteur
Salmòn Carlos, S.
Auteure/Auteur
Hutter, Damian
Auteure/Auteur
Rexhaj, Emrush
Auteure/Auteur
Thalmann, Sébastien
Auteure/Auteur
Schwab, Marcos
Auteure/Auteur
Turini, Pierre
Auteure/Auteur
Sartori-Cucchia, Céline
Auteure/Auteur
Nicod, Pascal
Auteure/Auteur
Villena, Mercedes
Auteure/Auteur
Allemann, Yves
Auteure/Auteur
Scherrer, Urs
Auteure/Auteur
Sartori, Claudio
Auteure/Auteur
Liens vers les personnes
Liens vers les unités
ISSN
1524-4539[electronic], 0009-7322[linking]
Statut éditorial
Publié
Date de publication
2010
Volume
122
Numéro
5
Première page
488
Dernière page/numéro d’article
494
Langue
anglais
Résumé
BACKGROUND: Adverse events in utero may predispose to cardiovascular disease in adulthood. The underlying mechanisms are unknown. During preeclampsia, vasculotoxic factors are released into the maternal circulation by the diseased placenta. We speculated that these factors pass the placental barrier and leave a defect in the circulation of the offspring that predisposes to a pathological response later in life. The hypoxia associated with high-altitude exposure is expected to facilitate the detection of this problem.
METHODS AND RESULTS: We assessed pulmonary artery pressure (by Doppler echocardiography) and flow-mediated dilation of the brachial artery in 48 offspring of women with preeclampsia and 90 offspring of women with normal pregnancies born and permanently living at the same high-altitude location (3600 m). Pulmonary artery pressure was roughly 30% higher (mean+/-SD, 32.1+/-5.6 versus 25.3+/-4.7 mm Hg; P<0.001) and flow-mediated dilation was 30% smaller (6.3+/-1.2% versus 8.3+/-1.4%; P<0.0001) in offspring of mothers with preeclampsia than in control subjects. A strong inverse relationship existed between flow-mediated dilation and pulmonary artery pressure (r=-0.61, P<0.001). The vascular dysfunction was related to preeclampsia itself because siblings of offspring of mothers with preeclampsia who were born after a normal pregnancy had normal vascular function. Augmented oxidative stress may represent an underlying mechanism because thiobarbituric acid-reactive substances plasma concentration was increased in offspring of mothers with preeclampsia.
CONCLUSIONS: Preeclampsia leaves a persistent defect in the systemic and the pulmonary circulation of the offspring. This defect predisposes to exaggerated hypoxic pulmonary hypertension already during childhood and may contribute to premature cardiovascular disease in the systemic circulation later in life.
METHODS AND RESULTS: We assessed pulmonary artery pressure (by Doppler echocardiography) and flow-mediated dilation of the brachial artery in 48 offspring of women with preeclampsia and 90 offspring of women with normal pregnancies born and permanently living at the same high-altitude location (3600 m). Pulmonary artery pressure was roughly 30% higher (mean+/-SD, 32.1+/-5.6 versus 25.3+/-4.7 mm Hg; P<0.001) and flow-mediated dilation was 30% smaller (6.3+/-1.2% versus 8.3+/-1.4%; P<0.0001) in offspring of mothers with preeclampsia than in control subjects. A strong inverse relationship existed between flow-mediated dilation and pulmonary artery pressure (r=-0.61, P<0.001). The vascular dysfunction was related to preeclampsia itself because siblings of offspring of mothers with preeclampsia who were born after a normal pregnancy had normal vascular function. Augmented oxidative stress may represent an underlying mechanism because thiobarbituric acid-reactive substances plasma concentration was increased in offspring of mothers with preeclampsia.
CONCLUSIONS: Preeclampsia leaves a persistent defect in the systemic and the pulmonary circulation of the offspring. This defect predisposes to exaggerated hypoxic pulmonary hypertension already during childhood and may contribute to premature cardiovascular disease in the systemic circulation later in life.
PID Serval
serval:BIB_A686C996980F
PMID
Open Access
Oui
Date de création
2010-08-25T09:14:42.840Z
Date de création dans IRIS
2025-05-21T00:41:23Z