Thrombophilic risk factors for placental stillbirth

Objectives

To define the characteristics of placental stillbirth and the possible contribution of thrombophilic risk factors.

Study design

A prospective cohort study was performed. Women diagnosed with antenatal stillbirth (>20 weeks) of singleton pregnancies between 2006 and 2008 were referred postpartum for evaluation. Maternal risk factors, fetal, placental and cord abnormalities, and a detailed thrombophilia screening, including inherited and acquired thrombophilia, were evaluated. Fetal autopsy and placental pathology were encouraged.Placental stillbirth was defined as death of a normally-formed fetus with evidence of intrauterine fetal growth restriction, oligohydramnios, placental abruption and/or histological evidence of placental contribution to fetal death. Pregnancy characteristics and thrombophilia profiles were compared between placental and non-placental stillbirth cases.

Results

Sixty-seven women with stillbirth comprised the study group. Placental stillbirth was evident in 33/67 (49.3%). Significantly more women with placental stillbirth were nulliparous, when compared with non-placental stillbirth women (21/33 vs. 9/34, p = 0.002). Mean gestational age was lower for placental, compared with non-placental stillbirth (31.1 ± 6.1 weeks vs. 33.9 ± 4.8 weeks, p = 0.04), as was birth weight. Thirty-six of the 67 women (53.7%) tested positive for at least one thrombophilia. The prevalence of maternal thrombophilia was higher for placental stillbirth women (63.6%), and even higher (69.6%) for women after preterm (<37 weeks) placental stillbirth. Factor V Leiden and/or prothrombin G20210A mutation were much more prevalent in placental versus non-placental stillbirth women (OR 3.06, 95% CI 1.07-8.7).

Conclusions

Placental stillbirth comprises a unique subgroup with specific maternal characteristics. Maternal thrombophilia is highly prevalent, especially in preterm placental stillbirth. This may have implications for the management strategy in future pregnancies in this subgroup.     

Inherited thrombophilias and pre-eclampsia in Brazilian women

OBJECTIVE: The aim of the present study was to compare the distribution of G1691A, G20210A and C677T mutations in pre-eclamptic Brazilian women and in matched control women with an uncomplicated normal pregnancy. STUDY DESIGN: these mutations were investigated by PCR-RFLP in 83 normal pregnancies (control group) and in 30 pre-eclamptic pregnant women (severe form). RESULTS: G1691A mutation was detected neither in the control group nor in pre-eclamsia women. G20210A mutation was detected in heterozygosis in 3 (3.61%) control subjects, but not in pre-eclampsia group. C677T mutation was detected in homozygosis in 6 (7.23%) control subjects and 2 (6.67%) pre-eclamptic women and in heterozygosis in 31 (37.3%) control subjects and 12 (40%) pre-eclamptic women. Differences in the mutation frequencies detected in the two groups were not statistically significant. CONCLUSION: No correlation was observed between pre-eclampsia and presence of G1691A, G20210A and C677T mutations in Brazilian women.     

Factor V Leiden and prothrombin 20210 G-A mutations in controls and in patients with thromboembolic events during pregnancy or the puerperium

Factor V Leiden and prothrombin 20210 G-A mutations are independent risk factors for venous thrombosis. We studied the frequency of these mutations in 35 patients who had thromboembolic events during pregnancy and puerperium, and in 32 women who had a history of uncomplicated pregnancy, delivered either vaginally or by cesarean section, and did not have a past history of thromboembolism. Factor V Leiden mutation was present in 7 patients (20%) in the study group. Of these 7 patients, 1 was homozygote, whereas the remaining 6 were heterozygote for the mutation. Prothrombin 20210 G-A mutation was present in 2 patients (5.7%) in the study group. In the control group none of the 32 patients was positive for the factor V Leiden and prothrombin 20210 G-A mutations. Our findings indicate that the factor V Leiden mutation is an important risk factor for thromboembolic disease during pregnancy or puerperium.     

Prothrombin G20210A mutation in cases with recurrent miscarriage: a study of the mediterranean population

Background: Thrombophilic predisposition may be one of the underlying causes of recurrent miscariage (RM). The purpose of this study was to evaluate the Prothrombin G20210A mutation in cases with history of RM. Material and methods: A total of 104 cases, 55 with diagnosis of RM and 49 control cases, were included in this controlled study. In all cases, in addition to full examination tests, Prothrombin 20210A mutation analysis was carried out by means of Polymerase Chain Reaction (PCR). Results: Mean number of the abortion was 3.51±0.74 in the RM group and 0.08±0.27 in the control group (p<0.05). As a consequence of comprehensive examinations, in 24 (43.6%) of 55 RM cases at least one etiologic factor was put forth. Prothrombin G20210A mutation was observed in six (10.9%) cases of the RM group and one (2.04%) in the control group (p<0.05). Four of the six cases (66.7%) of Prothrombin G20210A mutation had a subsequent pregnancy. Among these four pregnancies, there was one spontaneous loss at 14 weeks of gestation and one severe pre-eclampsia. Conclusion: Our data together with literature suggest that Prothrombin G20210A mutation may be associated with RM. We recommend this genetic testing as a screening tool for women with history of RM.     

Oxidative stress in midpregnancy as a predictor of gestational hypertension and pre-eclampsia

OBJECTIVES: To explore the relationship between the levels of maternal oxidative stress and glycaemia during pregnancy and to compare the predictive values of 8-epimer of prostaglandin F(2alpha) (8-isoPGF(2alpha)) and mean arterial pressure (MAP) in midpregnancy for the development of hypertensive complications in later pregnancy. DESIGN: Prospective observational study as an ancillary study to the Hyperglycaemia and Adverse Pregnancy Outcome (HAPO) study. SETTING: Obstetric clinics and wards of a university teaching hospital in Hong Kong. POPULATION: Selected women with singleton pregnancies attending the antenatal clinic. METHODS: Pregnant women who met HAPO inclusion criteria were recruited for the study. Glucose tolerance was assessed by a 75-g 2-hour oral glucose tolerance test (OGTT) at 24-32 weeks of gestation. Fasting plasma samples for 8-isoPGF(2alpha) estimation and urine samples for 8-isoPGF(2alpha) and 2,3-dinor 8-isoPGF(2alpha) assays were collected and blood pressures measured during the OGTT visit. Random plasma and urine samples were also obtained at 34-37 weeks. Glucose results were unblinded to the attending obstetrician if limits preset under the HAPO protocol were met. MAIN OUTCOME MEASURES: Maternal plasma 8-isoPGF(2alpha) and urinary 8-isoPGF(2alpha) and 2,3-dinor 8-isoPGF(2alpha) both at the time of OGTT (24-32 weeks) and at 34-37 weeks of gestation. Incidence of pre-eclampsia and gestational hypertension. RESULTS: Of the 408 women who attended for OGTT at 24-32 weeks, two met the glucose criteria for unblinding and 25 had missing 8-isoPGF(2alpha) values and thus were excluded from analysis. Of the 381 women, 338 (88.7%) attended for random plasma samples at 34-37 weeks. Significant correlations were observed between maternal fasting plasma isoprostane and both fasting (r= 0.20; P < 0.001) and 2-hour (r= 0.39; P < 0.001) plasma glucose levels at the time of OGTT. Gestational hypertension/pre-eclampsia occurred in 17 (4.2%) women, and at the time of OGTT, they had significantly higher fasting plasma 8-isoPGF(2alpha) (P < 0.001), urine 8-isoPGF(2alpha) (P < 0.005) and urine 2,3-dinor 8-isoPGF(2alpha) to creatinine ratios (P < 0.001), as well as higher MAP (P < 0.001) than women who remained normotensive. At 34-37 weeks, only random plasma 8-isoPGF(2alpha) was significantly higher (P < 0.001) among the women with gestational hypertension/pre-eclampsia. CONCLUSIONS: Plasma markers of oxidative stress were positively correlated with plasma glucose at the time of OGTT (24-32 weeks). Women who subsequently developed gestational hypertension/pre-eclampsia had significantly higher plasma and urine markers of oxidative stress at the time of OGTT but only higher plasma markers at 34-37 weeks. Plasma 8-isoPGF(2alpha) appears to be a very good predictor of subsequent gestational hypertension/pre-eclampsia when measured at the time of OGTT, but its ability to discriminate deteriorates as pregnancy advances.     

Thrombophilic genes alterations as risk factor for recurrent pregnancy loss

Objective: The important polymorphisms leading to inherited thrombophilia are Factor V Leiden (FVL), Prothrombin G20210A and MTHFR C677T and A1298C. The frequencies also the correlation among these polymorphisms and RPL have been reported controversially in various populations. Our clinic is one of the referral centers in reproductive biomedicine in which patients in all over Iran refer to; thus the results of this study could be considered clinically beneficial. Besides, in the present study, not only the frequency of specific but also multiple thrombophilic gene alterations were compared in Iranian women with RPL and a control group.

Methods: The patients group comprised 330 women with three or more consecutive RPLs. The control population included 350 women with at least one child and no history of pregnancy loss. FVL, Prothrombin G20210A and MTHFR C677T polymorphisms were analyzed by Strip assay kit. MTHFR A1298C was genotyped by PCR-RFLP.

Results: The frequencies of FVL, Prothrombin G20210A, MTHFR C677T and MTHFR A1298C mutations in patients were 8.48, 4.24, 45.45 and 59.39%, and in controls were 2.86, 2.86, 34.28 and 6%, respectively.

Conclusions: The present data showed that FVL, MTHFR polymorphisms also combined with thrombophilic gene mutations have a strong association with RPL.     

Routine investigations might be useful in pre-eclampsia, but not in gestational hypertension

BACKGROUND: Women referred to secondary care with suspected pregnancy-induced hypertension (PIH) are commonly investigated with blood tests and cardiotocography (CTG), regardless of the clinical severity of their condition. Over-investigation might lead to inappropriate intervention. AIMS: To investigate how often abnormal blood test and CTG results occur in women with pre-eclampsia and gestational hypertension and in women who do not have pregnancy-induced hypertension. METHODS: Retrospective case note review of 526 consecutive women referred with suspected pregnancy-induced hypertension to a district hospital. The frequency of abnormal test results and the pregnancy outcomes were analysed according to clinical classification. RESULTS: 36% of women referred did not meet the clinical criteria for a diagnosis of pregnancy-induced hypertension. Abnormalities of platelet count and/or liver function were seen in 11% of women with pre-eclampsia and in less than 2% of women with gestational hypertension and in a similar proportion of women who did not have pregnancy-induced hypertension. Gestational hypertension was associated with increased induction and caesarean birth rates, but not with low birthweight or preterm delivery. Progression from gestational hypertension to pre-eclampsia was not predicted by blood test abnormalities. Support for the routine use of antenatal CTG was not found. CONCLUSIONS: A clinical diagnosis of pregnancy-induced hypertension should be confirmed before blood tests are ordered. The incidence of test abnormalities was only increased in pre-eclampsia and in gestational hypertension before term. CTG might only be of use in selected cases.     

Management of late preterm and early-term pregnancies complicated by mild gestational hypertension/pre-eclampsia

Gestational hypertension/pre-eclampsia is the most frequent obstetrical complication, complicating 26%-29% of all gestations in nulliparous women. In general, the diagnosis of mild gestational hypertension/pre-eclampsia is made at 38 weeks or more in approximately 80% of cases. For many years, the optimal timing of delivery for patients with mild gestational hypertension/pre-eclampsia at 37-0/7 to 39-6/7 weeks was unclear. Recently, investigators of the HYPITAT (Pregnancy-induced hypertension and pre-eclampsia after 36 weeks: induction of labor versus expectant monitoring: A comparison of maternal and neonatal outcome, maternal quality of life and costs) randomized trial evaluated maternal and neonatal complications in patients at 36-40 weeks' gestation who were randomized to either induction of labor or expectant monitoring. The results of this trial revealed that induction of labor at or after 37-0 weeks was associated with lower rate of maternal complications without increased rates of either cesarean delivery or neonatal complications. In contrast, the optimum management for those with mild hypertension/pre-eclampsia with stable maternal and fetal conditions at 34-0/7 to 36-6/7 weeks remains uncertain. Therefore, there is urgent need for research to evaluate the reasons for late preterm birth in such women as well as for a randomized trial to evaluate the optimal timing for delivery in such patients.     

Prevalence of thrombophilia in women with severe ovarian hyperstimulation syndrome and cost-effectiveness of screening

OBJECTIVE: To determine the prevalence of markers of thrombophilia in patients with severe ovarian hyperstimulation syndrome (OHSS) and to evaluate the cost-effectiveness of screening for factor V Leiden and prothrombin G20210A mutations in women entering an IVF program. DESIGN: Case-control study and cost-effectiveness analysis. SETTING: University teaching hospital. PATIENT(S): Women undergoing controlled ovarian hyperstimulation for IVF complicated by severe OHSS (group 1, n = 20), women undergoing controlled ovarian hyperstimulation for IVF without development of severe OHSS (group 2, n = 40), and healthy control subjects (group 3, n = 100). INTERVENTION(S): Investigation of markers of thrombophilia. Estimate of number of IVF patients needed to detect a case of severe OHSS and thrombosis associated with thrombophilia genetic mutation was calculated from the available data. MAIN OUTCOME MEASURE(S): Blood samples were analyzed for inherited (resistance to activated protein C due to the factor V Leiden mutation; prothrombin G20210A mutation; deficiencies in antithrombin, protein C, and protein S) and acquired (presence of circulating lupus anticoagulants and/or anticardiolipin antibodies; deficiencies of antithrombin and protein S; acquired protein C resistance) markers of thrombophilia. The cost of preventing one thrombotic event in a patient developing severe OHSS after IVF and having factor V Leiden or prothrombin G20210A mutations was calculated. RESULT(S): None of the OHSS patients or controls had antithrombin, protein C, or free protein S deficiencies. All of them tested negative for antiphospholipid antibodies. No patient in group 1 had the factor V Leiden or prothrombin G20210A mutations. The prothrombin G20210A mutation was detected in 1 out of 40 patients (2.5%) in group 2. Both factor V Leiden and prothrombin G20210A mutations were detected in two of the control subjects (2%) (group 3). The estimated cost of preventing one thrombotic event arising as a consequence of screening for factor V Leiden and prothrombin G20210A mutation is a minimum of 418,970 dollars and 2,430,000 dollars, respectively. CONCLUSION(S): The prevalence of thrombophilia is not increased in women with severe OHSS. Screening for V Leiden and prothrombin G20210A mutation in an IVF general population is not cost-effective.     

Maternal and fetal plasma zinc in pre-eclampsia.

Zinc is important for fetal growth and is involved in several important enzyme systems. Maternal and umbilical plasma zinc concentrations were determined in 52 parturient women with mild and severe pre-eclampsia, and were compared with those obtained from 20 women in labor whose pregnancies had progressed normally. A decrease in maternal as well as umbilical plasma zinc concentrations was observed in pre-eclamptic women, and this decrease was statistically significant in severe pre-eclampsia. The causes of these changes in plasma zinc concentrations in pre-eclampsia were discussed, and the possible adverse effects of zinc deficiency on the mother and fetus were mentioned. Low plasma zinc concentrations in pre-eclampsia may be a sign of zinc deficiency, implying possible risks to the mother and her fetus. It is recommended that maintenance of adequate dietary zinc nutrition during pregnancy, and particularly in pre-eclampsia, is important.     

Inheritance and perinatal consequences of inherited thrombophilia in Greece.

OBJECTIVE: To investigate the impact of inherited thrombophilic factors on the gestational outcome of unselected pregnant women. METHOD: A total of 392 women with spontaneous pregnancy were investigated for Factor V Leiden, prothrombin G20210A, and MTHFR C677T mutations. Adverse pregnancy outcomes were recorded. RESULTS: Thrombophilic genotypes were significantly higher in women with placental abruption. Heterozygocity for Factor V Leiden increased the risk for placental abruption 9.1 times. The MTHFR T677T genotype increased the risk for placental abruption 4.8 times despite folate supplements, and normal serum folate and B(12) levels. Women with inherited thrombophilia and previous obstetric complications were at significant risk for complications in a subsequent pregnancy (P<0.05). CONCLUSION: Women with placental abruption should be screened for thrombophilic factors and plasma homocysteine should be measured. Subgroups of women with inherited thrombophilia and obstetric complications might benefit from prophylactic anticoagulation in subsequent pregnancies.     

Association between maternal serum 25-hydroxyvitamin D level and pre-eclampsia

Objectives: The objective of the study was to evaluate the association of maternal plasma levels of 25-hydroxyvitamin D (25(OH)D) at late second and third trimester and the risk of pre-eclampsia.

Methods: In this prospective cohort study, maternal plasma 25(OH)D levels were measured at late second and third trimester in 77 women who later developed pre-eclampsia (31 non-severe and 46 severe cases) and 180 women without pre-eclampsia.

Results: The mean gestational age of the timing of the blood sampling was 31.1?±?4.4 at control group, 32.6?±?5.7 at non-severe pre-eclamptic group and 32.3?±?5.4 at severe pre-eclamptic group. The mean 25(OH)D concentration was significantly low in severe pre-eclampsia group (5.8?±?4.5?ng/ml) than non-severe pre-eclampsia (11.8?±?7.3?ng/ml, p?=?0.039) and control groups (14.9?±?12.0?ng/ml, p?<?0.0001). There was no statistically significant difference in 25(OH)D concentration between non-severe pre-eclamptic and control groups (p?=?0.404). In women with 25(OH)D concentration <20?ng/ml, a 12.45-fold increase in the odds of severe pre-eclampsia were detected.

Conclusion: Women with severe pre-eclampsia had low serum 25(OH)D levels. The correlation between maternal 25(OH)D levels and aspartate aminotransferase, alanine transaminase, serum creatinine levels, platelet count were not determined. 25(OH)D levels may be used as an independent predictive marker of severe pre-eclampsia.     

Clinical and pathogenetic features of early- and late-onset pre-eclampsia

Background: PE is present in ～2–8% of all pregnant women worldwide. Placental bed disorders at early and late PE have been not carried out yet. However, these studies help to explore details of the pathogenesis of PE, and to optimize the prognosis and obstetric management.

Objective: To identify clinical and morphological differences between early- and late-onset PE based on a comprehensive observation of pregnant women with regard to morphological and immunohistochemical characteristics of the placental bed.

Materials and methods: One hundred fifty patients aged 18–43 years old delivered by cesarean section due to severe PE. The samples of placental bed tissue were studied by morphological and immunohistochemical methods.

Results: The violation of invasion trophoblast, remodeling of spiral arteries were expressed in early onset PE; the degree of compensation of chronic hypoxia tissue in the area of the placental site was typical for late PE and was absent of an early onset PE.

Conclusion: Our studies confirm the need for separation of early- and late-onset PE, being justified in terms of different pathogenetic mechanisms of formation, and therefore the possibility of therapeutic effects, duration of pregnancy prolongation, forecasting, search early diagnostic markers of the disease, and personalized approaches.     

Association of pre-eclampsia with the R563Q mutation of the beta-subunit of the epithelial sodium channel

The R563Q mutation of the beta-subunit of the epithelial sodium channel (ENaC) is associated with hypertension in black and mixed ancestry (MA) men and women in South Africa. The frequency of the R563Q mutation in black and MA women with pre-eclampsia (n= 230) and in controls (n= 198) was studied. The R563Q mutation was found in 7.8% of the women with pre-eclampsia and in 2.6% of controls (P= 0.014). This remained significant if the black women were analysed separately (P= 0.031). We have demonstrated that a genetic variant of the ENaC is associated with pre-eclampsia. This has implications for understanding the pathogenesis and treatment of pre-eclampsia.     

Alterations in placental pendrin expression in pre-eclampsia

Abstract

Introduction: Pendrin is an integral membrane protein and plays a key role in extracellular fluid volume and blood pressure control. We aimed to investigate the relationship between pendrin immunostaining intensity in normal and pre-eclamptic placental tissue.

Methods: Fifty-six placental tissues, of which 26 were in pre-eclamptic, and 30 were in control group were evaluated by immunohistochemical staining. Positive immunostaining was evaluated using a semiquantitative score: 0, negative; +, mild; ++, moderate; and +++, intense.

Results: There was more positive immunstaining in the pre-eclamptic placenta compared to the controls (p?<?0.001). A significant positive correlation was observed between immunostaining level and diastolic blood pressure (r?=?0.533, p?=?0.005) in the pre-eclamptic group. However, no significant correlation was observed between any condition and immunostaining level in the control group.

Conclusions: Placentas in the pre-eclamptic group were significantly more immunostained with pendrin than were those in the control group. In addition, a positive correlation between immunostaining intensity with pendrin and both systolic and diastolic blood pressure were observed. Pendrin may play a role in the mechanism of severe hypertension in women with pre-eclampsia.     

Adiponectin and insulin resistance in early- and late-onset pre-eclampsia

OBJECTIVE: To evaluate the importance of adiponectin and insulin resistance in early- and late-onset pre-eclampsia. DESIGN: A nested case-control study in 72 pregnant women who participated in the first-trimester Down-syndrome-screening programme and who delivered at our hospital. SETTING: University Hospital, Department of Obstetrics and Gynecology. POPULATION: Pregnant women: 36 women with pre-eclampsia of which 20 late onset and 16 early onset were compared with 36 uncomplicated pregnancies who delivered at term. METHODS: In all the women, insulin resistance was calculated by the homeostasis model assessment ratio (HOMA-IR) and plasma adiponectin was determined using an enzyme-linked immunosorbent assay. MAIN OUTCOME MEASURES: Insulin resistance and adiponectin concentration. RESULTS: First-trimester plasma adiponectin mean levels in the whole pre-eclampsia group were significantly lower than that in the control group (8.4 +/- 3.3 versus 14.8 +/- 4.6 microgram/ml; P < 0.001), whereas first-trimester mean HOMA-IR values were significantly higher in the pre-eclampsia group than that in the control group (2.0 +/- 1.1 versus 1.0 +/- 0.4; P= 0.01). Plasma adiponectin concentrations at delivery in the pre-eclampsia group were significantly higher than that in the control group (9.2 +/- 3.7 versus 7.8 +/- 2.6 microgram/ml; P= 0.04). First-trimester plasma adiponectin mean concentrations in the late-onset subgroup were significantly lower compared with the concentrations in early-onset subgroup (6.2 +/- 1.4 microgram/ml versus 11.1 +/- 3.2 microgram/ml; P < 0.001), and there was a significant difference in adiponectin plasma values only between women in the late-onset pre-eclampsia group versus those in the control group (P < 0.001). First-trimester mean HOMA-IR values were significantly higher in the late-onset subgroup compared with that of the early-onset subgroup (2.5 +/- 1.3 versus 1.3 +/- 0.3; P= 0.02), and there was a significant difference only between the control group versus the late-onset subgroup (P= 0.001). CONCLUSIONS: First-trimester adiponectin and HOMA-IR values seem to select two completely different populations: early- and late-onset pre-eclampsia, which might suggest a different pathogenesis.     

Genetics of suspected thrombophilia in Serbian females with infertility,including three cases,homozygous for FII 20210A or FV 1691A mutations

Reproductive failure (recurrent foetal loss, unexplained infertility and IVF implantation failure) may be, in a number of cases, explained by thrombophilia, either acquired or inherited. Several genes contribute to thrombophilia, some with major effect (Factor V, Factor II), and some with minor effect (MTHFR, PAI-1, ATIII, etc.). The aim of this study was to estimate frequency of thrombophilia-associated genotypes (FII20210G?>?A, FV1691G?>?A, MTHFR677C?>?T and PAI-1 -675 4G/5G) in a group of 1631 Serbian women experiencing reproductive failure, and compare it with a healthy, female control group. Our results showed marginally significant (p?=?0.050) differences in allele frequencies between patients and controls for the FV1691 mutations. For the FII20210G?>?A, although the statistical significance was not achieved (p?=?0.076), we found higher frequency of variant allele in patients compared to controls (1.87% vs. 0.38%, respectively) which may point to a possible role of this polymorphism in thrombotic events. For the MTHFR677C?>?T and PAI-1 -675 4G/5G, we found no difference in distributions of genotype or allele frequencies between these two groups (p?>?0.05). For three subjects with very rare genotypes (two patients homozygous for FV1691G?>?A and one patient homozygous for FII20210G?>?A) we performed additional biochemical analyses for haemostasis, as well as genotyping of two polymorphisms (MTHFR1298A?>?C and ATIII786G?>?A).     

Left atrial mechanical functions in pre-eclampsia

AIM: To assess the effect of short-term pressure overload on left atrial (LA) mechanical function in pre-eclampsia. METHODS: Twenty women with pre-eclampsia and 17 age-matched healthy pregnant women were included. LA volumes were measured echocardiographically at the time of mitral valve opening (Vmax), onset of atrial systole (p-wave at the electrocardiography = Vp) and mitral valve closure (Vmin) according to the biplane area-length method. RESULTS: The mean age, gestational age, weight and body surface area were similar in pre-eclampsia and controls. The ventricular septal and posterior wall thickness were greater in pre-eclampsia (P < 0.001). There were no significant differences in LA diameter, Vmax, Vmin, Vp, LA-passive emptying volume, LA-passive emptying fraction, LA-active emptying volume, LA-active emptying fraction, conduit volume, LA-total emptying volume and LA-total emptying fraction between the groups. CONCLUSION: Left atrial mechanical function didn't change in pre-eclampsia. We conclude that short-lasting pressure overload is not capable of inducing changes in LA function.