Preeclampsia (PE) is a characterized by de novo hypertension and proteinuria. Women affected with PE have an increased risk of chronic hypertension and premature cardiovascular disease years later. Mice bearing transgenic fetuses overexpressing the human transcription factor STOX1 (storkhead box1) develop a severe preeclamptic phenotype. The molecular analysis of long term cardiovascular risks induced by preeclampsia will be studied using our mouse model. We started with 10 eight to ten-months-old mice, 5 had control gestations and 5 preeclamptic gestations 6 to 8 months earlier. We analyzed heart functional parameters by ultrasonography, in normal and stressed conditions. Then we carried out a transcriptional profile of endothelial cells and hearts of the mice. Fibrosis was evaluated by a histology analysis of the hearts. Finally the cytokine levels in mice plasma will be analyzed on 33 cytokines. The relative mass of the heart of the preeclamptic mice was increased by 11% (p = 0.017), with an important fibrosis. Ultrasonography revealed a lesser morphological adaptation to stress. Under dobutamin aortic peak velocity, blood pressure, and right ventricular outflow are significantly increased. The endothelial cells microarray analysis demonstrate that ∼3073 transcripts (p Our results demonstrate massive quasi-invisible long term effects of preeclampsia, affecting strongly the endothelial cells. Dilatation of hearts and fibrosis indicate a noxious cardiac tissue remodeling in preeclamptic mice. To the best of our knowledge, our study is one of the first to address the molecular effects of preeclampsia in the long term.