? But this is just a consequence of how placentas develop: the trophoblast burrow into the maternal spiral arteries during initial implantation. Their normal development is known to be compromised in preeclampsia; PE placentas on biopsy have developed with inadequate remodeling. http://atvb.ahajournals.org/content/25/1/102.full.pdf
is one discussion but there are hundreds if you search strings like "trophoblast spiral artery first trimester". It starts Remodeling of the uterine arteries is a key event in early pregnancy. In the first trimester of pregnancy, a subpopulation of fetal trophoblast cells, the extravillous trophoblast, invade the uterine wall (interstitial invasion) and its blood vessels (endovascular invasion) as far as the myometrial segments. In the uterine spiral arteries, the trophoblasts interdigitate between the endothelial cells (ECs), replacing the endothelial lining and most of the musculoelastic tissue in the vessel walls. This creates a high-flow, low-resistance circulation that increases maternal blood flow to the placental villi at the maternal–fetal interface... Defective remodeling of the spiral arteries is associated with pregnancies complicated by preeclampsia and intrauterine growth restriction (IUGR) and is proposed to lead to an overall state of oxidative stress or fluctuations in oxygen concentrations analogous to hypoxia-reperfusion within the placental environment...
Is that what I wasn't explaining?
ETA: also useful: a Google Image search of "spiral artery remodeling preeclampsia"
ETA: also useful: http://dmm.biologists.org/content/5/1/9.longIt is clear from placental samples examined at term, as well as from Doppler ultrasound study of placental perfusion, that the remodeling of spiral arteries is incomplete in patients with preeclampsia. Fewer trophoblast cells are present within the spiral arterioles, and the vessel walls remain stiff (Khong et al., 1986; Aquilina and Harrington, 1996). Although, by definition, preeclampsia can be diagnosed only after the 20th week of pregnancy (and clinically typically presents even later), this vascular remodeling occurs during the first two trimesters. In normal pregnancies, endovascular extravillous cytotrophoblast cells have been identified by 9 weeks of gestation (Craven et al., 1998), and intervillous blood flow is not established until 10–12 weeks of gestation (Caniggia et al., 2000; Burton et al., 2009). Thus, poor trophoblast invasion is an early event in disease progression, although it has not been determined whether it is the cause of preeclampsia or a result of another underlying problem.