A study led at Vall d’Hebron Institute of Research (VHIR), in collaboration with the Kings College University Hospital of London, provides first evidence of abnormal angiogenesis in human with congenital heart defects (CHD) that could contribute to the development of some of these diseases. The finding, published in the "http://eurheartj.oxfordjournals.org/content/early/2013/10/23/eurheartj.eht389.abstract?sid=c3a7fc6e-3786-4cc4-9dea-1d37ae288dc5" European Heart Journal, may allow the development of novel predictive strategies and open a window of research opportunities into novel preventive therapeutics in these patients. CHD are present in 8 per 1,000 live births worldwide and are only detected in the 50% of cases during pregnancy. Abnormalities of the heart and great arteries are the most common congenital defects, and one of the main causes of neonatal deaths. Despite significant advances in the understanding of mechanisms determining heart formation, the causes of CHD remain undefined in the vast majority of cases.Nonetheless, this study carried out in the Placental Insufficiency Unit of Vall d’Hebron University Hospital (HUVH) by researchers from the Maternal Fetal Medicine group and the group of the CIBBIM- Nanomedicine Lysosomal Storage Diseases and Cell Pathophysiology, demonstrates that there is an intrinsically angiogenic impairment in CHD that appears to be present in both the maternal and foetal circulation and foetal heart. Angiogenesis plays an essential role in the embryogenic development, because it is the physiological process through which new blood vessels and the heart are formed.65 pregnant women were studiedThe second stage of the study was carried out between June 2010 and September 2012 at the Foetal Medicine Unite of HUVH, over 65 pregnant women carrying a foeatus with a major CHD. Researchers determined maternal serum levels of pIGF, sFIt and soluble endoglin (sEng) in the second and third trimesters of pregnancy, in order to ascertain whether such changes are related to foetal cord angiogenic and antiangiogenic markers and perinatal results. The results of the study confirm the outcomes from animal studies and strongly suggest an excessive anti-angiogenic signaling in the embryogenic period that could contribute to the development of some CHD, such as Tetralogy of Fallot or some defects in the atrioventricular septum. According to Dr. Elisa Llurba, who is the principal investigator of the study, they have demonstrated that “the problem is not only in the foetus, but also in the placenta, as we have already seen the angiogenic alteration in the blood of pregnant women”. In that sense, she assures that this study “opens a new window in the prediction and prevention of these diseases, since we could, in the future, diagnose CHD in early stages through a blood test to the mother".