Jonathan L Hecht1, Zsuzsanna K Zsengeller2, Melissa Spiel3, S Ananth Karumanchi4, Seymour Rosen5. 1. Department of Pathology, Beth Israel Deaconess Medical Center (BIDMC), 330 Brookline Ave, Boston, MA 02215, USA. Electronic address: JLHecht@bidmc.harvard.edu. 2. Department of Medicine, Beth Israel Deaconess Medical Center (BIDMC), 330 Brookline Ave, Boston, MA 02215, USA. Electronic address: zzsengel@bidmc.harvard.edu. 3. Department of Obstetrics and Gynecology, Beth Israel Deaconess Medical Center (BIDMC), 330 Brookline Ave, Boston, MA 02215, USA. Electronic address: mspiel@bidmc.harvard.edu. 4. Department of Obstetrics and Gynecology, Beth Israel Deaconess Medical Center (BIDMC), 330 Brookline Ave, Boston, MA 02215, USA; Department of Medicine, Beth Israel Deaconess Medical Center (BIDMC), 330 Brookline Ave, Boston, MA 02215, USA. Electronic address: sananth@bidmc.harvard.edu. 5. Department of Pathology, Beth Israel Deaconess Medical Center (BIDMC), 330 Brookline Ave, Boston, MA 02215, USA. Electronic address: srosen@bidmc.harvard.edu.
Abstract
INTRODUCTION: In the setting of preeclampsia (PE), decidual vasculopathy (DV) can be seen along the free membranes. METHODS: We describe DV using stains for CD31, CD34, Cd42b, CD68, desmin, fibrin and Masson's trichrome in patients with preeclampsia and fetal growth restriction. RESULTS: We first examined the "membrane roll" sections from the placentas of six patients with preeclampsia. Affected vessels showed endothelial proliferation with detachment. Remodeling of the media was characterized by smooth muscle loss with variable degrees of fibrin deposition. CD31 and CD34 highlighted the prominent endothelium and showed striking particulate staining throughout the media. All of these findings infer a sequence of endothelial injury, fragmentation and repair with incorporation of endothelial components into the vascular wall. We evaluated the frequency of DV by clinical presentation; in cases with PE with and without small for gestational age (SGA) (N = 15), and SGA with and without Doppler flow abnormalities (N = 15). All groups except the SGA without Doppler abnormalities showed DV. Among placentas with DV, the most severely affected group was PE with SGA; the least affected was PE without SGA. DISCUSSION: The association with SGA suggests that the DV is a subacute process of vascular injury that accelerates in the setting of PE. The majority of DV cases were not initially recognized suggesting a role for endothelial markers for DV detection. We also propose that the rampant endothelial injury seems to be a prominent finding in the decidual vessels of subjects with PE complicated by SGA and a similar process in the systemic vasculature may be responsible for the circulating endothelial microparticles reported in such patients.
INTRODUCTION: In the setting of preeclampsia (PE), decidual vasculopathy (DV) can be seen along the free membranes. METHODS: We describe DV using stains for CD31, CD34, Cd42b, CD68, desmin, fibrin and Masson's trichrome in patients with preeclampsia and fetal growth restriction. RESULTS: We first examined the "membrane roll" sections from the placentas of six patients with preeclampsia. Affected vessels showed endothelial proliferation with detachment. Remodeling of the media was characterized by smooth muscle loss with variable degrees of fibrin deposition. CD31 and CD34 highlighted the prominent endothelium and showed striking particulate staining throughout the media. All of these findings infer a sequence of endothelial injury, fragmentation and repair with incorporation of endothelial components into the vascular wall. We evaluated the frequency of DV by clinical presentation; in cases with PE with and without small for gestational age (SGA) (N = 15), and SGA with and without Doppler flow abnormalities (N = 15). All groups except the SGA without Doppler abnormalities showed DV. Among placentas with DV, the most severely affected group was PE with SGA; the least affected was PE without SGA. DISCUSSION: The association with SGA suggests that the DV is a subacute process of vascular injury that accelerates in the setting of PE. The majority of DV cases were not initially recognized suggesting a role for endothelial markers for DV detection. We also propose that the rampant endothelial injury seems to be a prominent finding in the decidual vessels of subjects with PE complicated by SGA and a similar process in the systemic vasculature may be responsible for the circulating endothelial microparticles reported in such patients.
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