Adequate placental development leads normal fetal growth and the future adult health¹. Intrauterine growth restriction, cardiopathy, neuropathy and fetal programming diseases related to maternal alcohol consumption² could be associated with altered placentation³. Our objective was study if perigestational alcohol consumption up to organogenesis produces placental anomaly, through vascular endothelial growth factor (VEGF) deregulation and oxidative stress. Ethanol 10%/ drinking water was administered to mouse females for 15 days before and up to day 10 of gestation, and pregnancy continued with water until gestational day 13 (TF). Control females consumed ethanol-free water (CF). The 27% of TF-feto-placental units had labyrinthine histological abnormalities (disorganized vascularization) and fetal malformations (p<0.001). Labyrinthine growth was diminished (PAS, ImageJ, p<0.05) in TF-placentas as well as myocardial wall thickness of TF-fetus (79% of TF-fetus vs 13% of CF, p<0.001) due to reduced proliferation (Ki67 immunohistochemistry, IHC). VEGF expression (IHC, Western Blot) increased in TF-placentas, but decreased in fetal heart vs CF (p<0.001), together with oxidative stress. In conclusion, perigestational alcohol consumption up to early gestation leads to anomalies in heart-placental axis, suggesting that the prenatal origin of typical cardiopathy of fetal alcoholic spectrum (FASD) would be associated with placental alterations due to maternal alcohol consumption.