OBSTETRICS Abnormal vascular architecture at the placental-maternal interface in placenta increta Frédéric Chantraine, MD; Silvia Blacher, PhD; Sarah Berndt, PhD; José Palacios-Jaraquemada, MD, PhD; Nanette Sarioglu, MD; Michelle Nisolle, MD, PhD; Thorsten Braun, MD; Carine Munaut, PhD; Jean-Michel Foidart, MD, PhD OBJECTIVE: The objective of the study was to characterize the vascular architecture at the placental-maternal interface in pregnancies compli- cated by placenta increta and normal pregnancies. STUDY DESIGN: Vessel numbers and cross-section area density and spatial and area distributions in 13 placenta-increta placental beds were compared with 9 normal placental beds using computer-assisted image analysis of whole-slide CD31 immunolabeled sections. RESULTS: The total areas occupied by vessels in normal and placenta- increta placental beds were comparable, but vessels were significantly sparser and larger in the latter. Moreover, placenta-increta–vessel dis- tributions (area and distance from the placental–myometrial junction) were more heterogeneous. CONCLUSION: Size and spatial organization of the placenta-increta vascular architecture at the placental-maternal interface differed from normal and might partially explain the severe hemorrhage observed during placenta-increta deliveries. Key words: placenta increta, placental bed, vessel architecture, virtual imaging Cite this article as: Chantraine F, Blacher S, Berndt S, et al. Abnormal vascular architecture at the placental-maternal interface in placenta increta. Am J Obstet Gynecol 2012;207:188.e1-9. I n accordance with the American So- ciety of Maternal-Fetal Medicine rec- ommendations, placenta accreta defines abnormally invasive placental implanta- tion. 1 This severe obstetrical complica- tion, often responsible for life-threaten- ing hemorrhage during delivery, affects 1 in 533 to 2510 deliveries. 2,3 Its 10-fold increased incidence over the past 50 years has been associated with the rising cesarean section rate. 4 Furthermore, the hysterectomy rate for accreta placenta- tion increased by 23% between 1994 and 2007. 5 A history of cesarean section re- mains the dominant maternal risk factor to develop placenta accreta and other complications in subsequent pregnan- cies. 6,7 When placenta previa is present, the risk of placenta accreta increases from 3% for patients with a history of 1 cesarean section to 40-67% for those with 3 or more cesarean sections. 8 A de- fect in the decidua, resulting in the direct adhesion of chorionic villi to the myo- metrium is suspected to be the main cause of placenta accreta. 9 We and others provided functional, echographic, and anatomical evidence of an extensive vascular anastomotic network in the subplacental myome- trium during normal pregnancy. 10-13 This network provides the placental in- tervillous blood supply and creates ar- teriovenous shunts in the subplacental myometrium. 10 After delivery, passive uterine retraction and active myome- trium contractions create a physiolog- ical tourniquet that stop the circula- tion in the terminal segments of this network, which open in the villous chamber, thereby preventing postpar- tum haemorrhage. A precise definition of the vascular architecture at the placenta-maternal interface is lacking in women with pla- centa accreta. Only a few studies have characterized in vivo the uteroplacen- tal vascularization for patients with placenta increta using 3-dimensional (3D) color power Doppler or 3D- angiography. 14,15 Because women with placenta ac- creta are at high risk of early postpar- tum hemorrhage, we analyzed in this study the vessel distribution in their placental bed in comparison with that of normal pregnancies. We combined high-resolution virtual imaging of whole-tissue sections and computer- assisted image analysis to avoid inter- and intraobserver variability of the conventional optical microscopy and hot spot analysis. 16 From the Department of Obstetrics and Gynecology, Centre Hospitalier Universitaire, Hôpital la Citadelle (Drs Chantraine, Nisolle, and Foidart), and the Laboratory of Tumor and Development Biology, Centre Hospitalier Universitaire, GIGA-Cancer, University of Liège (Drs Chantraine, Blacher, Berndt, Nisolle, Munaut, and Foidart), Liège, Belgium; J. J. Naon Morphological Institute, School of Medicine, University of Buenos Aires, Buenos Aires, Argentina (Dr Palacios-Jaraquemada); and the Department of Pathology, Charité Campus Virchow-Klinikum (Dr Sarioglu), and the Department of Obstetrics, Charité Campus Virchow-Klinikum (Dr Braun), Berlin, Germany. Received April 6, 2012; revised May 23, 2012; accepted June 28, 2012. This study was supported by grants from the Fonds National de la Recherche Scientifique, Belgium. The authors report no conflict of interest. Reprints: Frédéric Chantraine, MD, Service de Gynécologie-Obstétrique, Centre Hospitalier Régional Citadelle, ULg, 1, Blv 12ème de Ligne, B-4000 Liège, Belgium. fchantraine@chu.ulg.ac.be. 0002-9378/$36.00 • © 2012 Mosby, Inc. All rights reserved. • http://dx.doi.org/10.1016/j.ajog.2012.06.083 Research www. AJOG.org 188.e1 American Journal of Obstetrics & Gynecology SEPTEMBER 2012