Placental Bed Spiral Arteries Research Articles

Spiral artery remodeling and maternal cardiovascular risk: the spiral artery remodeling (SPAR) study.

Women with a history of placental bed disorders, including preeclampsia and intrauterine growth restriction have an increased long-term risk of cardiovascular disease (CVD). Further, similarities exist between atherosclerosis and abnormalities observed in placental bed spiral arteries in pregnancies affected by preeclampsia and intrauterine growth restriction, such as acute atherosis and defective remodeling. This suggests a common pathophysiological pathway underlying both disorders. The aim of this study was to investigate vascular and inflammatory lesions in the placental bed of women with preeclampsia and normal pregnancy using a systematic approach to characterize lesions of the placental bed, and relate spiral artery pathology to postpartum CVD risk assessment. Placental bed punch biopsies were performed following caesarean section and systematically studied to assess vascular pathology, arterial remodeling, and the presence of CD3, CD56, and CD68 cells. In addition, levels of modifiable CVD risk factors were assessed immediately postpartum. We found fewer spiral arteries with complete remodeling in women with preeclampsia than in the control group (21 vs. 68%; P = 0.008). Further, women with preeclampsia showed less presence of CD3 cells in both the decidua and the myometrium. Preliminary findings of CVD risk factor assessment postpartum suggest a correlation between acute atherosis and higher triglyceride and low-density lipoprotein cholesterol levels. Systematic study of vascular pathology in uterine spiral artery biopsy samples in relation to CVD risk factors provides valuable insight into the link between cardiovascular health and placental bed disorders.

20 Defective placental bed vascular remodeling precedes manifestations of superimposed preeclampsia in stroke-prone spontaneously hypertensive rats

Introduction Pregnant women suffering from chronic hypertension are at increased risk of developing superimposed preeclampsia (SPE), often associated with poor fetal and maternal outcomes. Most animal models available to date reproduce ‘de novo' PE-like features through different experimental approaches, but the development of a SPE syndrome in pregnant animals with pre-existing arterial hypertension has been greatly overlooked in basic research pertaining hypertensive pregnancies. Objectives To characterize timed pregnancies in the Stroke Prone Spontaneously Hypertensive Rat (SHRSP) strain, a well-known model for essential hypertension, focusing on the development of clinical, fetal and placental manifestations of SPE. Methods SHRSP and Wistar Kyoto (WKY) females (10–12weeks old, N =5animals/day analyzed) were mated to congenic males and checked daily for vaginal plugs, denoted as gestation day (GD) 1. Blood pressure (BP) was determined by the tail-cuff method pre-mating and on the morning of GD1, 7, 9, 13, 17 and 19. On the selected dates, females were housed in metabolic cages for collection of 24h urine samples. Following collection of blood samples, animals were euthanized and implantation sites isolated for morphological analyzes. Fetal and placental weights were recorded on GD 18 and GD20. Results Compared to WKY, the SHRSP exhibited a significant elevation of baseline hypertension towards the last third of pregnancy (i.e, from GD13 to GD20) together with increased protein excretion, considered diagnostic hallmarks for SPE. Renal compromise was also evident as a progressive decrease of urinary output and histopathological changes in the glomerular and tubulointerstitial compartments of SHRSP kidneys. The SHRSP offspring were growth restricted and morphometrical analyzes showed underlying abnormal placentation, including signs of placental insufficiency such as decreased fetal to placental weight ratio and hypertrophy of the labyrinth layer linked to defective vascularization. Notably, our analysis also showed that the onset of the maternal syndrome was preceded by incomplete remodeling of the placental bed spiral arteries, which showed luminal narrowing and decreased densities of perivascular uterine NK cells at GD14 followed by defective infiltration of endovascular trophoblasts at GD18. Conclusion Our data confirms the characterization of pregnant SHRSP as a model reproducing clinical diagnostic traits and the underlying placental pathology observed in preeclampsia superimposed on chronic hypertension. This novel model provides an attractive system for interventional studies and dissection of the multifactorial origins of hypertensive disorders of pregnancy.

Increased Apoptosis in First Trimester Extravillous Trophoblasts from Pregnancies at Higher Risk of Developing Preeclampsia

Preeclampsia complicates 5 to 10% of pregnancies and is a leading cause of maternal and fetal mortality and morbidity. Although the cause is unknown, inadequate invasion and remodeling of maternal uterine arteries by extravillous trophoblasts (EVTs) in the first trimester is a common feature. Uterine spiral artery resistance as detected by Doppler ultrasound is commonly used in the second trimester to identify pregnancies destined to develop preeclampsia. Correlation between high uterine resistance and the failure of trophoblast invasion has been reported as early as 12 weeks. However, the reason for this failure has not been established. Understanding the processes involved would significantly improve our diagnostic potential. In this study, we correlated increased first trimester uterine artery resistance with a biological abnormality in trophoblast function. EVTs derived from high-resistance pregnancies were more sensitive to apoptotic stimuli than those from normal-resistance pregnancies. Survival of EVTs from high-resistance pregnancies could be increased by nitric oxide, whereas inhibition of nitric oxide in cells from normal-resistance pregnancies increased apoptotic sensitivity. This predates the onset of symptoms by several weeks and provides evidence for a mechanism responsible for the incomplete uterine vessel remodeling and the differences in artery resistance between preeclamptic and normal pregnancies.

P-360: The risk of pre-eclampsia is decreased in women with endometriosis

Studies on unexplained infertility and pregnancy outcome indicate an increased risk of adverse pregnancy outcome. In this study, we investigated whether endometriosis (E) increases the risk of pre-eclampsia (PE). Retrospective, case-control study. The incidence of PE was determined in 245 women with clinical and/or laparoscopic evidence of E and in 274 control women, matched for age and parity, without clinical and/or laparoscopic evidence of E. Outcome measurements were based on obstetrical records and where not available, on patient’ questionnaire. PE was defined when after 20 weeks gestation a bloodpressure >140/90 and proteinuria >300mg/24h were noted in a normotensive woman. Statistical analysis was performed with the SPSS program using the chi-quare and Fisher’s Exact tests. PE occurred in the E group (2/245, 0.8%) significantly less than in the control group (16/274, 5.8%) (P=0.002; OR=7.5, 95%CI 1.7-33.3). During the first pregnancy PE occurred in the endometriosis group (2/170, 1.2%) significantly less than in the control group (13/187, 7.0%) (P=0,007; OR=6.3, 95%CI 1.4-28.6). In the subgroup of patients who had undergone laparoscopy PE occurred significantly less in the E group (2/168, 1.2%) than in the control group (4/54, 7.4%) (P=0.032; OR=6.6, 95%CI= 1.2-37). Odds ratios were adjusted for maternal age, calendar year of the index event, place of delivery and multiple pregnancies. We report for the first time that women with E have a significantly lower risk of PE than those without E. Although the underlying mechanisms remain to be elucidated, other studies have shown that E is associated with increased endometrial angiogenesis and vascular perfusion in the late secretory phase of the cycle, which could facilitate remodeling of the placental bed spiral arteries during endovascular trophoblast invasion. Our findings further support the notion that the endometrial microenvironment prior to conception is an important determinant of pregnancy outcome.

Mechanisms regulating cytotrophoblast invasion in normal pregnancy and pre‐eclampsia

The placental bed underlies the placenta and includes the decidua basalis and underlying myometrium containing the uterine spiral arteries. For successful human haemochorial placentation, the placental bed spiral arteries must undergo considerable alterations. These physiological modifications are thought to be brought about by the interaction of invasive cytotrophoblast with the spiral artery vessel wall. Failure of spiral artery transformation is thought to play an important role in the sequence of events that gives rise to pre-eclampsia. The mechanisms that control human trophoblast invasion in normal, let alone abnormal pregnancy, are still poorly understood. Much of the information on the early physiological changes within the placental bed comes from studies on intact hysterectomy specimens.(1) Details of such events in late pregnancy and in pregnancies complicated by pre-eclampsia and fetal growth restriction are principally derived from the study of placental bed biopsies taken at Caesarean section. The methods of sampling the placental bed have been reviewed elsewhere.(2) Many investigators have relied on in vitro models of trophoblast invasion. In vitro models can be extremely useful in dissecting out some of these processes but may be open to artefacts. The mechanisms underlying normal and failed trophoblast invasion appear to be complex. In this manuscript the mechanisms that control the invasion of trophoblast into the decidua and myometrium are reviewed. Along with this is a review of the purported mechanisms underlying failed spiral artery transformation. Particular emphasis has been placed on topics that have been best studied.

Divergent trophoblast invasion and apoptosis in placental bed spiral arteries from pregnancies complicated by maternal anemia and early-onset preeclampsia/intrauterine growth restriction

Impaired trophoblast invasion into spiral arteries is associated with early-onset intrauterine growth restriction and preeclampsia. We compared trophoblast invasion into spiral arteries in pregnancies with maternal anemia or early-onset preeclampsia/intrauterine growth restriction and related these findings to trophoblast apoptosis. Full-thickness uterine wall samples were obtained from women with early-onset preeclampsia/intrauterine growth restriction (n = 6), normal pregnancies (n = 5), and chronic anemia (n = 8). Trophoblast invasion into the walls of spiral arteries was quantified by morphometric analysis of paraffin sections stained with anticytokeratin 18, antiactin, and anticytokeratin 18 neoepitope (M30) antibodies. Trophoblast invasion into spiral arteries was increased in anemic pregnancies (mean [SD]: 206 [46] cell profiles/mm2) and severely impaired in preeclamptic/intrauterine growth restriction pregnancies (17 [6]), compared with normal subjects (149 [52]). Spiral artery lumen area was increased in anemia (0.07 [0.03] mm2) versus normal pregnancies (0.09 [0.04] mm2) and reduced in preeclampsia/intrauterine growth restriction (0.04 [0.02] mm2). Trophoblast apoptosis was similar in anemic (4.2% [3.4%]) and normal (5.0% [1.9%]) pregnancies but increased in preeclampsia/intrauterine growth restriction (12% [5.6%]). Trophoblast invasion into the placental bed in early-onset preeclampsia/intrauterine growth restriction is limited by increased apoptosis, resulting in narrower spiral arteries, which is in contrast to findings in anemia.

Priming and remodelling of human placental bed spiral arteries during pregnancy – A Review

It is now well known that in order to establish human hemochorial placentation and to provide a progressive increase in blood supply to the growing fetus, the uterine spiral arteries must undergo considerable alterations. This physiological modification is thought to be brought about by the interaction of invasive cytotrophoblast with the spiral artery vessel wall. Despite intensive research our understanding of the mechanisms that control human trophoblast invasion in normal, let alone abnormal pregnancy, are still poorly understood. This is partly due to difficulties in obtaining "true" placental bed biopsies and most investigators have relied on in vitro models of trophoblast invasion. Clearly interpretation of such studies must be tempered with a degree of caution. This review outlines why the placental bed is important, how we can sample and study it, what morphology actually occurs in the placental bed spiral arteries during pregnancy and then briefly summarise the findings on the placental bed in pre-eclampsia.

The decidual suction method: a new way of collecting decidual tissue for functional and morphological studies

Background. Studies of extravillous trophoblasts and placental bed spiral arteries are essential for a better understanding of pathological pregnancies such as preeclampsia, intrauterine growth restriction and diabetes mellitus. A major challenge is to obtain representative and sufficient tissue for morphological and functional investigations. Currently, tissue material is mostly harvested by placental bed biopsy (PBB). We describe a new suction method to obtain a larger volume of decidual tissue from the placental bed. Methods. Tissue was harvested in 51 cesarean sections by vacuum suction of the placental bed. Sections from formalin-fixed, paraffin-embedded tissue were routinely stained with hematoxylin and eosin (H&E), immunostained with a panel of antibodies and morphologically examined for the presence of trophoblasts and spiral arteries. The results were compared with those from archive material from PBBs and placental basal plate sections (BPSs). Short-term adverse events were registered for the study patients. Long-term complications were registered from medical charts of 151 women having undergone the decidual suction method (DSM), with a follow-up of 38–60 months. Results. In 86% (n = 44), one random section from the decidual suction material demonstrated at least one spiral artery. In 37% (n = 19), six or more spiral arteries were present. All sections revealed extravillous trophoblasts. No short- or long-term morbidity was recorded. Conclusions. The decidual suction method represents an important improvement in the work to obtain sufficient decidual tissue for morphological and functional studies of extravillous trophoblast function and spiral artery adaptation. The method is safe, as no short- or long-term complications were registered.

The Effects of Angiogenic Growth Factors on Extravillous Trophoblast Invasion and Motility

There is accumulating evidence that deficient trophoblast invasion of the placental bed spiral arteries is crucial to the pathogenesis of pre-eclampsia and intrauterine growth restriction. However, the factors which regulate the process of trophoblast invasion remain unclear. We have investigated whether extravillous trophoblast invasion and motility are mediated by the angiogenic growth factors, vascular endothelial growth factor (VEGF) and placental growth factor (PlGF).The SGHPL-4 extravillous trophoblast cell line was utilized. Expression of mRNA for the receptors of VEGF and PlGF (KDR and flt-1) was determined using the reverse transcriptase polymerase chain reaction. An in vitro model of invasion assessed the number and length of trophoblast processes invading into an extracellular matrix. The motility of cells under standard culture conditions was also quantified. The effect of the addition of VEGF and PlGF (±heparin) on trophoblast invasion and motility was determined. The effect of VEGF and PlGF (±heparin) on SGHPL-4 cell proliferation was assessed by cell counts at 24, 48 and 72h post-addition of growth factor.The SGHPL-4 cells expressed mRNA for the flt-1 but not the KDR receptor. The addition of VEGF resulted in a significant decrease in the number of trophoblast processes formed (P< 0.02); this effect was not influenced by the addition of heparin. However, there was no effect on the length of processes formed in response to VEGF (±heparin). The addition of PlGF had no effect on either the number or the length of processes formed. The addition of VEGF increased the motility of the SGHPL-4 cells (P< 0.002); the addition of heparin prevented this VEGF-induced increase in motility. The addition of PlGF had no effect on SGHPL-4 motility (±heparin). Neither growth factor had any effect on the proliferative ability of SGHPL-4 cells.Contrary to our hypothesis, we did not find that the angiogenic growth factors, VEGF and PlGF, mediated the in vitro invasion of trophoblast cells into an extracellular matrix. However, VEGF did increase trophoblast motility. Our findings of an effect of VEGF on trophoblast motility (and possibly invasion) suggests the presence of functional receptors, which can mediate the actions of VEGF. Caution must be exercised before any extrapolation to the in vivo situation, however, it could be speculated that the increased motility in response to VEGF may be an initial response to attract trophoblast cells to the decidua, and that VEGF might then limit the degree to which trophoblast cells invade.

Histopathological study of placental bed biopsy in placenta previa

To study placental bed biopsy changes in placenta previa and normally implanted placenta. Fifty placental bed biopsies from 50 patients with placenta previa and 50 placental bed biopsies from normally implanted placenta were taken at cesarean section. Placental bed biopsy was stained with hematoxyline and eosin for histological examination. Both the groups were compared for trophoblastic invasion and vascular changes of placental bed spiral arteries. Statistical analysis was done by Chi-square test. Placenta bed biopsy was representative in 42/50 (84%) biopsy samples of the study group (placenta previa) and 35/50 (70%) of the control group (normally located placenta). Trophoblastic giant cell migration into decidua was present in 100% of representative samples of both the groups while migration into myometrium was seen in 66.67% and 51.14% of samples of study and control group. Average number of trophoblastic giant cells per sample was significantly higher in placenta previa (decidua 41.3%, myometrium 52%) than the control group (decidua 17.4%; myometrium 14.5%). Trophoblastic giant cell infiltration into myometrial spiral arterioles was higher in placenta previa (81.83 cells per vessel). Percentage of myometrial spiral arterioles showing physiological changes was significantly higher in the study group (50.39%) compared to the control group (21.14%). Incidence of inflammatory cell infiltration was higher in the study group (42.86%). Hemorrhage into decidua and myometrium were seen in biopsy samples of the placenta previa. Placenta previa is associated with significantly higher trophoblastic giant cell infiltration and physiological changes of the myometrial spiral arterioles.

Interaction of interstitial trophoblast with placental bed capillaries and venules of normotensive and pre-eclamptic pregnancies

While endovascular trophoblast invasion of the human placental bed spiral arteries has been studied extensively, no information is available on the interaction between interstitially invading trophoblast and uterine capillaries and venules. Placental bed biopsies of eight normotensive and 15 pre-eclamptic patients were double-immunostained for cytokeratin and the endothelial marker CD31, providing satisfactory staining results in six and 10 biopsies, respectively. Interstitial trophoblast tissue density did not differ between the two series of biopsies, implying that this pathway of invasion is not impaired in pre-eclampsia. Both groups showed a similar incidence of approach of non-arterial vascular structures by perivascular trophoblast. Differences in CD31 staining intensity were noticed in different vascular cross-sections. Lower staining intensity was related to the presence of perivascular trophoblast. Because of the identity of CD31 with the platelet-endothelial cell adhesion molecule (PECAM)-1, the trophoblast-dependent downregulation of CD31 may play a role in the control of leukocytic traffic within the placental bed. The phenomena described in this paper did not show any difference between the normotensive and pre-eclamptic patients, implying that interaction of interstitial trophoblast with venous and capillary structures is not related to the pathogenesis of pre-eclampsia.

A study of placental bed spiral arteries and trophoblast invasion in normal and severe pre-eclamptic pregnancies.

To investigate trophoblast invasion and vascular changes in placental bed spiral arteries in normal and severe pre-eclamptic pregnancies. A histological and immunohistochemical study of placental bed biopsies containing spiral arteries. The University Hospital, Leuven, Belgium. Twenty-one placental bed biopsies from 21 normal pregnancies and 24 placental bed biopsies from 24 severe pre-eclamptic pregnancies, taken at caesarean section. Histological and immunohistochemical appearance of spiral arteries (stained with haematoxylin and eosin), periodic acid schiff, and a monoclonal antibody to low molecular weight cytokeratin. One hundred and twenty-seven spiral arteries were studied. In the 21 biopsies from clinically normal pregnancies at term, 100% of the decidual spiral arteries and 76% of the myometrial arteries showed trophoblast invasion. In the 24 biopsies from women with severe pre-eclampsia, trophoblast invasion was seen in 44% and 18% of the decidual and myometrial segments, respectively. Endovascular trophoblast invasion was complete, partial or isolated. A variety of morphological features was present not only in different spiral arteries from the same biopsy but also in different segments of the same artery. The vascular change most commonly associated with normal pregnancies was physiological change and subintimal thickening of both segments of the spiral arteries. In pre-eclampsia medial disorganisation and hyperplasia in the myometrial arteries and acute atherosis in decidual arteries were common. Endovascular trophoblast did not show an all or none invasive phenomenon in normal and pre-eclamptic pregnancies. More decidual than myometrial arteries were invaded in both groups of patients, and there was a gradient in the percentage of decidual and myometrial arteries invaded from normal pregnancy to pre-eclampsia. Morphological features in one spiral artery may not necessarily be representative of all of those in a placental bed.

Immunohistochemical Detection of lipoprotein(a) in the wall of placental bed spiral arteries in normal and severe preeclamptic pregnancies

In normal pregnancy trophoblast invades the spiral arteries and produces the physiological fibrinoid degeneration of the vessel wall. In pre-eclampsia, physiological change is restricted and pathological change develops in the non-invaded arteries, including acute atherosis. This study was undertaken to determine if lipoprotein(a) [Lp(a)], which is associated with atherogenesis is present in the wall of spiral arteries that have undergone physiological and pathological change. One hundred and sixteen spiral arteries were examined from 18 normal and 24 severe pre-eclamptic pregnancies. Lp(a) was detected in all atherotic and necrotic lesions, in 57% of spiral arteries with medical disorganization or hyperplasia, and in 45% of those with physiological change. When Lp(a) was detected differences were found in the amount seen: it was most in atherosis, less in necrosis, less still in medical change, and least in physiological change. For the same vascular change generally more Lp(a) was detected in the pre-eclamptic group than in the normal group. The detection of Lp(a) helps to distinguish physiological fibrinoid from atherotic and necrotic fibrinoid. Many atherotic and necrotic areas initially overlooked using standard histology were highlighted using immunohistochemistry. Atherosis can develop in spiral arteries that have been invaded by trophoblast. In those with pre-eclampsia, atherosis was found in 56% of decidual but only in 8% of myometrial spiral arteries. Small areas of necrosis were common in physiologically changed arteries from normal pregnancies.

Immunohistochemical detection of liporpotein(a) in the wall of plancetal bed spiral arteries

Objective: Lipoprotein(a) [Lp(a)] has been localised in the wall of atherosclerotic coronary arteries. Pre-eclampsia is associated with an increased incidence of atherotie lesions in the placental bed spiral arteries. This study was undertaken to determine if Lp(a) is present in these atherotie lesions and in the walls of spiral arteries that have undergone physiological and other pathological changes in pregnancy. Methods: 116 spiral arteries were studied in 42 placental bed biopsies taken from 18 normal and 24 severe pre-eclamptic pregnancies. Standard histology (H&E, PAS) and immunohistochemicai staining using a streptavidin-biotin system (Zymed No. 95-6543) with a monoclonal antibody to apolipoprotein (a), [Lp(a)], (Cappel clone 2-D1) were carried out. Controls were atherosclerotie coronary artery, TBS and a monoclonal antibody to cytokeratin. The amount of Lp(a) detected was scored as negative, faint, light, moderate and heavy. Results: Lp(a) was detected in all spiral arteries with atherosis and necrosis, in 57% with disorganisation or hyperplasia and in 45% with physiological change. 12 spiral arteries did not show any morphological change and Lp(a) was not detected in these. When Lp(a) was detected there was a trend in the amount seen between spiral arteries showing these features: it was most in atherotie vessels, less in areas of necrosis, less still in vessels with medial change and least in vessels with physiological change. In normal pregnancies the amount of Lp(a) when detected was generally less than in the severe pre-eclamptic group for the same category of vascular change. Conclusions: Immunostaining for Lp(a) was sensitive in demonstrating areas of atherosis and necrosis and as a marker may help to distinguish between physiological and atherotic fibrinoid. The prothrombotic property of Lp(a) may play a role which leads to the increase placental infarction seen in pre-eclampsia.

A high uterine artery pulsatility index reflects a defective development of placental bed spiral arteries in pregnancies complicated by hypertension and fetal growth retardation

Introduction: The development of PIH is associated with a defective trophoblast invasion and conversion of spiral arteries into low-resistance uteroplacental arteries. Hypertension may then be a compensatory response to a defective uteroplacental perfusion. Similar mechanisms may operate in IUGR. Aim: To compare uterine artery Doppler blood flow measurements with placental bed histology. The hypothesis was that placental bed vessel pathology plays a role for a raised flow resistance. Materials and Methods: After blood flow measurements, a placental bed biopsy was taken at CS in 26 complicated (study group) and 29 uncomplicated pregnancies (control group). Results: The uterine artery PI was significantly more often abnormally high in the study group compared with the control group, and also in hypertensive pregnancies compared with normotensive IUGR pregnancies. Physiological vessel changes were found in all controls but were absent in 76% of study cases. Physiological changes were significantly more often absent in SGA than in AGA newborns. Absence of physiological changes were significantly more often found in cases with an abnormally high PI. Discussion: The results link together circulatory and structural pathophysiological changes of the uteroplacental unit. A defective physiological conversion of the spiral arteries was associated with an increased uterine flow resistance. Conclusion: This study gave further support for the existence of a triad of defective placental bed vessel maturation, increased uteroplacental flow resistance, and hypertension.

Placental bed spiral arteries in the hypertensive disorders of pregnancy

The investigation of the histology of the placental bed spiral arteries in normal pregnancy and in pregnancies complicated by hypertension, with or without proteinura. An observational study, based on women having caesarean sections for clinical reasons. 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. Placental bed biopsies obtained during caesarean section. Histological appearance of sections stained with haematoxylin and eosin PAS and Lendrum's MSB. 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. 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.

Histological characteristics of placental bed spiral arteries related to the clinical classification of hypertensive disorders in human pregnancy

Histological characteristics of placental bed spiral arteries related to the clinical classification of hypertensive disorders in human pregnancy

Inadequate maternal vascular response to placentation in pregnancies complicated by pre-eclampsia and by small-for-gestational age infants.

An examination of the maternal vascular response to placentation shows that physiological changes in the placental bed normally extend from the decidua into the inner myometrium. In pre-eclampsia and in a proportion of pregnancies with small-for-gestational age infants (SGA) the physiological changes are restricted to the decidual segments alone. In addition, complete absence of physiological changes throughout the entire length of some spiral arteries is seen in pre-eclampsia and SGA. This new observation is confirmed in a study of basal plates of placentas from abnormal pregnancies. Intraluminal endovascular trophoblast may be seen in the placental bed spiral arteries in the third trimester in pre-eclampsia and SGA, a feature not seen beyond the second trimester in normal pregnancy. These findings point to a defect in the normal interaction between migratory trophoblast and maternal uterine tissues in pre-eclampsia and in SGA.

Uteroplacental arterial changes related to interstitial trophoblast migration in early human pregnancy

Morphometric and statistical techniques were used to assess the relation of myometrial interstitial trophoblast to the uteroplacental vasculature in 27 intact hysterectomy specimens ranging from 8 to 18 weeks' gestation. It was found that the volume density of cytotrophoblast in the myometrium and in particular the proximity of such trophoblast to the placental bed spiral arteries correlated significantly with morphological alterations in these vessels. The changes included swelling of endothelium, hypertrophy of individual medial smooth muscle cells, and oedema and disruption of the architecture of the vessel wall as a time-related continuum. Some of the changes, such as swollen endothelium and basophilia of medial smooth muscle cells were noted also in spiral arteries in the non-placental bed endometrium but to a considerably less extent than in the placental bed. Intimal vacuolation was common to placental bed and non-placental bed arteries, increased with gestational age and can be considered as a non-specific feature. The migration of endovascular trophoblast into the myometrial spiral arteries in the second trimester occurred only when these arteries had been considerably altered in their morphology. These findings indicate that migratory interstitial cytotrophoblast probably has a role to play in the preparation of the myometrial segments of the uteroplacental arteries for the second wave of endovascular trophoblast migration that occurs in the second trimester of human pregnancy.

Fetal growth retardation and the maternal arterial supply of the human placenta in the absence of sustained hypertension.

In five patients with fetal growth retardation in pregnancies with no or only a moderate and transient rise in blood pressure, vascular lesions in the placental bed spiral arteries were found. These lesions are characterized by less well developed physiological morphological changes, by extensive intimal thickening, by fibrinoid degeneration of the media and by acute atherosis. the recurrent fetal growth retardation in these pregnancies may be the first clinical manifestation of underlying reno-vascular disease.