Microvessel density in the placental bed among preeclampsia patients (original) (raw)
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Vascular Dysfunction in Preeclampsia
Microcirculation, 2014
Preeclampsia is a complex disorder which affects an estimated 5% of all pregnancies worldwide. It is diagnosed by hypertension in the presence of proteinuria after the 20th week of pregnancy and is a prominent cause of maternal morbidity and mortality. As delivery is currently the only known treatment, preeclampsia is also a leading cause of preterm delivery. Preeclampsia is associated with maternal vascular dysfunction, leading to serious cardiovascular risk both during and following pregnancy. Endothelial dysfunction, resulting in increased peripheral resistance, is an integral part of the maternal syndrome. While the cause of preeclampsia remains unknown, placental ischemia resulting from aberrant placentation is a fundamental characteristic of the disorder. Poor placentation is believed to stimulate the release of a number of factors including pro-and antiangiogenic factors and inflammatory activators into the maternal systemic circulation. These factors are critical mediators of vascular function and impact the endothelium in distinctive ways, including enhanced endothelial oxidative stress. The mechanisms of action and the consequences on the maternal vasculature will be discussed in this review.
Angiogenic imbalance in the pathophysiology of preeclampsia: Newer insights
Seminars in Nephrology, 2004
Angiogenesis is the process of neovascularization from preexisting blood vessels, whereas vasculogenesis is the process of blood vessel generation from angioblast precursor cells. The human placenta undergoes high levels of angiogenesis and vasculogenesis during fetal development. Additionally, the placenta undergoes a process of vascular mimicry (also referred to as pseudovasculogenesis) in which the placental cytotrophoblasts convert from an epithelial to an endothelial phenotype during normal fetal development. Failure of placental angiogenesis and pseudovasculogenesis during placental development has been linked to the pathogenesis of preeclampsia. It currently is believed that soluble factors released by the diseased placenta lead to clinical findings of preeclampsia. This article discusses placental vascular development in health and in disease, with a focus on accumulating recent evidence that the maternal clinical syndrome of preeclampsia is an antiangiogenic state resulting from an excess of anti-endothelial factors liberated by the diseased placenta. Semin Nephrol 24:548 -556
Hypertension in pregnancy, 2014
To evaluate if placental histopathological changes of vascular insufficiency correlate with circulating angiogenic factors in patients with preeclampsia. Subjects were selected from a previous prospective cohort study of preeclampsia based on the availability of plasma anti-angiogenic factor (sFlt1) and pro-angiogenic factor (PlGF) measurements and placental histology specimens. Preeclamptic patients were divided into two groups based on plasma levels of these factors described as a ratio: anti-angiogenic preeclampsia with sFlt1/PlGF ratio ≥85 and normal angiogenic preeclampsia with sFlt1/PlGF < 85. The placental lesions of vascular insufficiency that were studied specifically included atherosis, infarcts, syncytial knots, acute and chronic abruption, hematoma, and fetal thrombosis. The data are shown as median (quartile 1 and quartile 3) or n (%) when appropriate. The anti-angiogenic preeclampsia group (N = 48) presented at an earlier gestational age (weeks) than the normal angi...
Journal of ultrasound in medicine : official journal of the American Institute of Ultrasound in Medicine, 2015
The purpose of this study was to compare the use of vascular indices derived from the whole placenta to those from the placental bed only for predicting preeclampsia and to determine whether the addition of pregnancy-associated plasma protein A (PAPP-A) and mean uterine artery Doppler values improves prediction. We conducted a secondary analysis of a prospective cohort of women with singletons between 11 and 14 weeks' gestation undergoing sonography for aneuploidy screening. Placental vascularization indices from the whole placenta versus the placental bed were combined with first-trimester maternal serum PAPP-A levels, mean uterine artery Doppler values, or the combination of both to predict the development of preeclampsia or early preeclampsia (delivery <34 weeks). The predictive ability of each vascular index was calculated by using areas under receiver operating characteristic curves. The sensitivity of the model for predicting preeclampsia and early preeclampsia at fixed...
Endothelial function and uterine perfusion and subsequent pregnancies complicated by preeclampsia
Revista Médica de Minas Gerais, 2013
Introduction: the pathophysiology of preeclampsia (PE) is based on a deficiency in the process of placentation associated with systemic maternal endothelial dysfunction. The investigation on the occurrence of these phenomena before the onset of PE clinical manifestations can become a new diagnostic method for its prediction. Objectives: to compare the process of placentation and endothelial function in pregnant women at high-risk for PE development, correlating these findings with its further development. Patients and methods: 74 pregnant women underwent flowmediated dilation (DFM) of the brachial artery and Doppler flowmetry of uterine arteries to assess endothelial function and placentation process, respectively. The examinations were performed between 16 and 20 weeks of gestation and patients were followed until the postpartum period. Results: 15 patients had pregnancies complicated by PE and 59 remained normotensive until the postpartum period. Patients who subsequently developed PE presented high values of pulsatility index in uterine arteries (p <0.001), between 16 and 20 weeks gestation, however, the analysis of DFM did not show difference compared to patients who remained normotensive. Conclusion: The observed data suggest that deficiency in the placentation process chronologically precedes the clinical manifestations of PE, which does not occur with endothelial dysfunction.
Placental bed spiral arteries in the hypertensive disorders of pregnancy
Bjog-an International Journal of Obstetrics and Gynaecology, 1991
Objective— The investigation of the histology of the placental bed spiral arteries in normal pregnancy and in pregnancies complicated by hypertension, with or without proteinura.Design— An observational study, based on women having caesarean sections for clinical reasons.Subjects— 17 normal pregnant women, 43 with gestational hypertension, of whom 39 had proteinuria, 17 with chronic hypertension, of whom 6 had proteinuria, and 5 with unclassified hypertension.Interventions— Placental bed biopsies obtained during caesarean section.Main outcome measures— Histological appearance of sections stained with haematoxylin and eosin PAS and Lendrum's MSB.Results— Biopsies containing spiral arteries were obtained from 6 normotensive and 44 hypertensive women. Trophoblastic invasion was present in 5 of the 6 normotensive biopsies but absent in the majority of those with hypertension. Subintimal proliferation was seen in all the normotensive biopsies but in only 8 of 28 from those with gestational hypertension and proteinuria. Other features seen predominantly or only in the hypertensive biopsies, in order of frequency, were medial hyperplasia, fibrin deposits, acute atherosis, endothelial vacuolation and thrombosis.Conclusion— Absence of physiological changes may not be peculiar to preeclampsia but may be associated or even a result of various forms of hypertension in pregnancy. Spiral arteries show a spectrum of changes in hypertensive pregnancies that do not appear to bear a clear-cut relation to the clinical signs.
Background: Preeclampsia occurs in 3-5% of pregnancies and is a major cause (12-20 %) of maternal mortality in developed countries. It is the leading cause of preterm birth and intra-uterine growth restrictions (IUGR). Objective: The study was designed to determine and demonstrate the ultra structural changes of endothelial cells in placenta of women suffering from hypertensive disease. Patients & Methods: Placental samples were obtained from two groups of pregnant women groups (preeclamptic and normal pregnant women). The specimens were fixed in 2.5% gluteraldehyde and preceded for electron microscopic examination. Results: Placenta of women with preeclampsia has shown marked degenerative changes in both endothelial and trophoblastic cells. These changes were represented by precipitation of fibrin with the accumulation of platelets in capillary lumen. Abundance of collagen fibers precipitate in the apical region of both endothelial cells and trophoblasts, with thickening of endothelial basement membrane. Conclusion: All histological changes or lesions obstruct the continuous conduction from maternal surface of the trophoblasts through fetal capillary endothelium causing endothelial dysfunction.
Bjog-an International Journal of Obstetrics and Gynaecology, 2000
Objective To determine the correlation between placental bed biopsy findings, and blood levels of the vascular cell adhesion molecule (VCAM-1) and fibronectin in pre-eclampsia/eclampsia, and to evaluate the relationship between these variables and severity of the disease.Design A prospective case-control study.Setting Department of Obstetrics and Gynaecology, Cerrahpasa Medical Faculty, Istanbul.Sample Thirty-five women with pre-eclampsia/eclampsia were compared with 25 healthy women with uncomplicated pregnancies. Twenty-one placental bed biopsies from pre-eclamptic pregnancies were compared with 17 from normal pregnancies.Main outcome measures Peripheral venous blood levels of VCAM-1 and fibronectin, measured by enzyme-linked immunoassay and radial immune diffusion technique.Results In pre-eclampsia/eclampsia, blood VCAM-1 and fibronectin levels were higher than in normal pregnancy. Levels of both fibronectin and VCAM-1 correlated significantly with the diastolic blood pressure (r= 0.49 and r= 0.65, P < 0.001). There was also a significant direct linear correlation between plasma fibronectin and VCAM-1 levels (r= 0.57, P < 0.001). Normotensive women all had normal placental bed biopsy findings and the incidence of pathological placental bed biopsy findings increased with the severity of the pre-eclampsia.Conclusion Inadequate trophoblastic invasion of spiral arteries, and elevated levels VCAM-1 and fibronectin were found in women with pre-eclampsia. The magnitude of defective trophoblastic invasion, and blood levels of VCAM-1 and fibronectin correlate with the clinical severity of pre-eclampsia.