CIENCIASMEDICASNEWS: Possible joint pathways of early pre-eclampsia and congenital heart defects via angiogenic imbalance and potential evidence for cardio-placental syndrome

jueves, 12 de diciembre de 2013

Possible joint pathways of early pre-eclampsia and congenital heart defects via angiogenic imbalance and potential evidence for cardio-placental syndrome

Karen Sliwa1,* and
Alexandre Mebazaa2

+ Author Affiliations

¹Hatter Institute for Cardiovascular Research in Africa & IIDMM, Cape Heart Centre, Department of Medicine, Faculty of Health Sciences, University of Cape Town, South Africa
²Inserm 942; University Paris Diderot, PRES Sorbonne Paris Cité; and AP-HP, Hôpitaux Universitaire Saint Louis-Lariboisière, Paris, France

↵*Corresponding author. Hatter Institute for Cardiovascular Research in Africa, Cape Heart Centre, 4th floor Chris Barnard Building, Faculty of Health Sciences, University of Cape Town, Private Bag X3, Observatory, Cape Town, 7935 South Africa. Tel: +27 21 406 6457, Fax: +27 21 6504101, Email: karen.Sliwa-Hahnle@uct.ac.za

This editorial refers to ‘Maternal and foetal angiogenic imbalance in congenital heart defects’, by E. Llurba et al. doi:10.1093/eurheartj/eht389

Foetal vasculogenesis and angiogenesis and maternal angiogenesis are essential requirements for a pregnancy. Decidua-associated vascular changes arise in the inner junctional zone myometrium in early pregnancy, followed by trophoblast invasion with associated remodelling.¹ Decidual natural killer and dendritic cells regulate key developmental processes at the human foetal–maternal interface via human leucocyte antigen (HLA)-C, HLA-E, and HLA-G.² Intervillous flow starts at 7–8 weeks gestation, via connecting channels between maternal myometrial spiral arteries and lacunae in the wall of the implanted cytoblast. Early trophoblast plugging might protect the embryo against high oxygen concentrations, and it has to be postulated that premature loss of those plugs could lead to early miscarriage or early-onset pre-eclampsia.³

In the past decade, extensive research has investigated the abnormalities that can occur in the first trimester of pregnancy that could lead to chorionic regression or small placenta, contributing to intrauterine growth restriction and early-onset pre-eclampsia.⁴ Placental flow defects can occur as early as 12 weeks in women who subsequently develop pre-eclampsia. Hypoxia and reoxygenation episodes can generate reactive oxygen species, leading to placental oxidative stress and placental dysfunction. Although the causes of pre-eclampsia, defined as new hypertension (diastolic blood pressure >90 mmHg) and substantial proteinuria (>300 mg in 24 h) after 20 weeks gestation,⁴ remains largely unknown, the leading hypothesis strongly suggests disturbed placental function in early pregnancy, possibly due to failed interaction between two genetically different organisms.⁴ As a second stage of the foetal–maternal interphase, research by Levine and Karumanchi has shown an increased production of bioactive trophoblast debris, including an excess of syncytiotrophoblast-derived antiangiogenic factors, such as soluble forms of vascular endothelial growth factor (VEGF) receptors, including the VEGF receptor-1, also …

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