Objective — to study a change in the architectonics of fetal surface veins of the placenta and the structure of the latter in cytomegalovirus infection in pregnant women. Material and methods. Placentas were studied and divided in 3 groups: 1) 35 placentas from women with physiological pregnancy; 2) 37 placentas from women with an exacerbation of latent cytomegalovirus infection and with chronic compensated placental insufficiency; 3) 30 placentas from those with an exacerbation of latent cytomegalovirus infection and with chronic subcompensated placental insufficiency. After X-ray contrasting the fetal surface veins of the placenta and collecting its sections for morphological analysis, the changes in the blood vessels were compared with the structure of the villous chorion. Results. As compared with Group 2, Group 3 showed reductions in placental weights and placental areas, as well as cotyledon asymmetry and a preponderance of anatomical forms with weak vascular contrasting along with the more frequent emergence of areas of varicosity, contraction, and inflammation of the umbilical vein, as well as the placental fetal surface veins. The investigators more often detected collagenization, fibrinoid degradation, and the increased stromal volume of the stem villi, fibrinoid deposition around the latter, and decreases in the proportion of the intervillous space and syncytiotrophoblast; dilatation of the veins and narrowing of the arteries of the stem villi; pronounced plethora of terminal villi and their avascular forms, intermediate immature villi, chorioamnionitis, deciduitis, pseudonecrosis, calcifications, as well as hemorrhages in the intervillous space. Conclusion. In the development of subcompensated placental insufficiency in women who have experienced an exacerbation of latent cytomegalovirus infection in the second trimester of pregnancy, an important role is assigned to anatomical and pathological changes in the umbilical, fetal surface, and villous chorionic veins, which indicate the development of fetoplacental hypertension, the deceleration of blood flow, and the longer contact of the pathogen with the endothelium and syncytiotrophoblast.