Maternal and foetal angiogenic imbalance in congenital heart defects

Animal models showed that angiogenesis is related to abnormal heart development. Our objectives were to ascertain whether a relationship exists between congenital heart defects (CHDs) and angiogenic/anti-angiogenic imbalance in maternal and foetal blood and study the expression of angiogenic factors...

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Published in:European heart journal 2014-03, Vol.35 (11), p.701-707
Main Authors: Llurba, Elisa, Sánchez, Olga, Ferrer, Queralt, Nicolaides, Kypros H, Ruíz, Aina, Domínguez, Camen, Sánchez-de-Toledo, Joan, García-García, Belén, Soro, Gemma, Arévalo, Silvia, Goya, Maria, Suy, Anna, Pérez-Hoyos, Santiago, Alijotas-Reig, Jaume, Carreras, Elena, Cabero, Lluís
Format: Article
Language:English
Subjects:
Adult
Antigens, CD - metabolism
Case-Control Studies
Endoglin
Female
Fetal Blood - chemistry
Fetus - metabolism
Heart Defects, Congenital - embryology
Humans
Neovascularization, Physiologic - physiology
Placenta Growth Factor
Pregnancy
Pregnancy Complications, Cardiovascular - metabolism
Pregnancy Proteins - metabolism
Receptors, Cell Surface - metabolism
Vascular Endothelial Growth Factor A - metabolism
Vascular Endothelial Growth Factor Receptor-1 - metabolism
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Summary:Animal models showed that angiogenesis is related to abnormal heart development. Our objectives were to ascertain whether a relationship exists between congenital heart defects (CHDs) and angiogenic/anti-angiogenic imbalance in maternal and foetal blood and study the expression of angiogenic factors in the foetal heart. Maternal and cord blood placental growth factor (PlGF), soluble fms-like tyrosine kinase-1 (sFlt-1) and soluble endoglin (sEng) were compared in 65 cases of CHD and 204 normal controls. Angiogenic factor expression and markers of hypoxia were measured in heart tissue from 23 CHD foetuses and 8 controls. In the CHD group, compared with controls, plasma PlGF levels were significantly lower (367 ± 33 vs. 566 ± 26 pg/mL; P < 0.0001) and sFlt-1 significantly higher (2726 ± 450 vs. 1971 ± 130 pg/mL, P = 0.0438). Foetuses with CHD had higher cord plasma sFlt-1 (442 ± 76 vs. 274 ± 26 pg/mL; P = 0.0285) and sEng (6.76 ± 0.42 vs. 4.99 ± 0.49 ng/mL, P = 0.0041) levels. Expression of vascular endothelial growth factor (VEGF), sFlt-1, markers of chronic hypoxia, and antioxidant activity were significantly higher in heart tissue from CHD foetuses compared with normal hearts (VEGF, 1.59-fold; sFlt-1, 1.92-fold; hypoxia inducible factor (HIF)-2α, 1.45-fold; HO-1, 1.62-fold; SOD1, 1.31-fold). An intrinsically angiogenic impairment exists in CHD that appears to be present in both the maternal and foetal circulation and foetal heart. Our data suggest that an imbalance of angiogenic-antiangiogenic factors is associated with developmental defects of the human heart.
ISSN:0195-668X
1522-9645
DOI:10.1093/eurheartj/eht389