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We sought to determine if increased placental vascular impedance to flow is associated with changes in fetal cardiac function using spatiotemporal image correlation and virtual organ computer-aided analysis.A cross-sectional study was performed in fetuses with umbilical artery pulsatility index95th percentile (abnormal [ABN]). Ventricular volume (end-systole, end-diastole), stroke volume, cardiac output (CO), adjusted CO, and ejection fraction were compared to those of 184 normal fetuses.A total of 34 fetuses were evaluated at a median gestational age of 28.3 (range, 20.6-36.9) weeks. Mean ventricular volumes were lower for ABN than normal cases (end-systole, end-diastole) with a proportionally greater decrease for left ventricular volume (vs right). Mean left and right stroke volume, CO, and adjusted CO were lower for ABN (vs normal) cases. Right ventricular volume, stroke volume, CO, and adjusted CO exceeded the left in ABN fetuses. Mean ejection fraction was greater for ABN than normal cases. Median left ejection fraction was greater (vs right) in ABN fetuses.Increased placental vascular impedance to flow is associated with changes in fetal cardiac function.

The objective of this study was to quantify fetal cardiovascular parameters using spatiotemporal image correlation (STIC) and virtual organ computer-aided analysis (VOCAL).A cross-sectional study was performed in normal pregnancies (19-42 weeks) to evaluate ventricular volume, stroke volume (SV), cardiac output (CO), and ejection fraction (EF). The CO was also expressed as a function of estimated fetal weight and biometric parameters.The following results were found: (1) 184 STIC datasets; (2) with advancing gestation, ventricular volume, SV, CO, and adjusted CO increased, whereas EF decreased; (3) right ventricular (RV) volume was larger than the left ventricular (LV) volume in systole (0.50 vs 0.27 mL; P.001) and diastole (1.20 vs 1.03 mL; P.001); (4) there were no differences between the LV and RV in SV, CO, or adjusted CO; and (5) LV EF was greater than the RV EF (72.2 vs 62.4%; P.001).Normal fetal cardiovascular physiology is characterized by a larger RV volume and a greater LV EF, resulting in similar LV and RV SV and CO.

The objective of the study was to determine whether eclampsia has a different circulating profile of angiogenic (placental growth factor [PlGF]) and antiangiogenic factors (soluble vascular endothelial growth factor receptor-1 [sVEGFR-1] and soluble endoglin [sEng]) from severe preeclampsia.This cross-sectional study included pregnant women in the following groups: (1) normal pregnancy (n = 40); (2) severe preeclampsia (n = 40); and (3) eclampsia (n = 20). Maternal serum PlGF, sVEGFR-1, and sEng concentrations were determined using an enzyme-linked immunosorbent assay.The study results included the following: (1) the median concentration of sVEGFR-1 and sEng was higher and of PlGF was lower in severe preeclampsia or eclampsia than in normal pregnancy (P.001 for all); and (2) the median concentrations of these 3 analytes did not differ significantly between patients with severe preeclampsia and those with eclampsia.Eclampsia is associated with higher maternal circulating concentrations of sVEGFR-1 and sEng and lower concentrations of PlGF than normal pregnancy but with similar concentrations to severe preeclampsia. These findings suggest that eclampsia shares a common pathogenic pathway as severe preeclampsia.

The mechanism of mouse parturition is thought to involve myometrial infiltration by amniotic fluid (AF) macrophages, activated by surfactant protein-A (SP-A). In humans, the concentration of AF SP-A decreases during labor, and no fetal macrophages are found in the myometrium after labor. Therefore, it appears that the mechanisms of labor in mice and humans are different. We investigated a potential role for SP-A in human pregnancy and parturition by examining SP-A expression patterns in AF and amnion. High molecular weight (HMW; >250 kD) oligomeric SP-A was increased in AF with advancing gestation. Interestingly, these oligomers were more abundant in placental amnion before labor at term, while they increased primarily in reflected amnion during labor (p

Adiponectin, an anti-inflammatory and anti-diabetogenic adipokine, has an important regulatory effect on both the innate and adaptive limbs of the immune response. The objective of this study was to determine whether adiponectin is present in amniotic fluid (AF) and if its concentration changes with gestational age, in the presence of labor, and in the presence of intra-amniotic infection (IAI) in patients with spontaneous preterm labor (PTL) and intact membranes.This cross-sectional study included 468 patients in the following groups: (1) women in the mid-trimester of pregnancy (14-18 weeks) who underwent amniocentesis for genetic indications and delivered a normal neonate at term (n = 52); (2) normal pregnant women at term with (n = 49) and without (n = 41) spontaneous labor; (3) patients with an episode of PTL and intact membranes who were classified into: (a) PTL who delivered at term (n = 149); (b) PTL who delivered preterm (37 weeks gestation) without IAI (n = 108); and (c) PTL with IAI (n = 69). Adiponectin concentration in AF was determined by ELISA.(1) The median AF adiponectin concentration at term was significantly higher than in the mid-trimester (35.6 ng/ml, interquartile range [IQR] 26.4-52.7 vs. 29.9 ng/ml, IQR 19.9-35.2; p = 0.01); (2) among women with PTL and intact membranes, the median AF adiponectin concentration was significantly higher in patients with IAI than in those without IAI who delivered either at term (54.3 ng/ml, 39.0-91.8 vs. 50.1 ng/ml, 33.2-72.8; p = 0.02) or preterm (47.6 ng/ml, 32.6-74.6; p = 0.01); and (3) among women at term, there was no significant difference in the median AF adiponectin concentration between those with and without labor (33.7 ng/ml, IQR 21.7-53.9 vs. 35.6 ng/ml, IQR 26.4-52.7; respectively p = 0.5).(1) Adiponectin is a physiologic constituent of AF; and (2) adiponectin concentrations in AF are increased significantly with advancing gestation and in the presence of IAI. Collectively, these findings suggest that adiponectin plays a dynamic role in normal gestation and in the presence of IAI.

Circulating soluble human leukocyte antigen-G (sHLA-G) has been associated with pregnancy complications, and determination of sHLA-G concentrations in amniotic fluid (AF) has been reported in normal pregnancies. Our aim was to determine if the AF concentrations of sHLA-G change with advancing gestation, spontaneous labor at term, and in patients with spontaneous preterm labor (PTL) with intact membranes, as well as in those with preterm prelabor rupture of membranes (PROM), in the presence or absence of intra-amniotic infection/inflammation (IAI).This cross-sectional study included the following groups: (1) mid-trimester (n = 55); (2) normal pregnancy at term with (n = 50) and without (n = 50) labor; (3) spontaneous PTL with intact membranes divided into: (a) PTL who delivered at term (n = 153); (b) PTL who delivered preterm without IAI (n = 108); and (c) PTL with IAI (n = 84); and (4) preterm PROM with (n = 46) and without (n = 44) IAI. sHLA-G concentrations were determined by ELISA. Non-parametric statistics were used for analysis.(1) Among patients with PTL, the median AF sHLA-G concentration was higher in patients with IAI than in those without IAI or women that delivered at term (p0.001 for both comparisons); (2) Similarly, patients with preterm PROM and IAI had higher median AF sHLA-G concentrations than those without IAI (p = 0.004); (3) Among patients with PTL and delivery, those with histologic chorioamnionitis and/or funisitis had a higher median AF sHLA-G concentration than those without histologic inflammation (p0.001); and (4) The median AF sHLA-G concentration did not change with advancing gestational age.AF sHLA-G concentrations are elevated in preterm parturition associated to IAI as well as in histologic chorioamnionitis. We propose that sHLA-G may participate in the regulation of the host immune response against intra-amniotic infection.

Human parturition is characterized by the activation of genes involved in acute inflammatory responses in the fetal membranes. Manganese superoxide dismutase (Mn SOD) is a mitochondrial enzyme that scavenges reactive oxygen species (ROS). Mn SOD is up-regulated in sites of inflammation and has an important role in the down-regulation of acute inflammatory processes. Therefore, the aim of this study was to determine the differences in Mn SOD mRNA expression in the fetal membranes in patients with term and preterm labor (PTL) as well as in acute chorioamnionitis.Fetal membranes were obtained from patients in the following groups: (1) term not in labor (n = 29); (2) term in labor (n = 29); (3) spontaneous PTL with intact mebranes (n = 16); (4) PTL with histological chorioamnionitis (n = 12); (5) preterm prelabor rupture of the membranes (PPROM; n = 17); and (6) PPROM with histological chorioamnionitis (n = 21). Mn SOD mRNA expression in the membranes was determined by quantitative real-time reverse transcription-polymerase chain reaction.(1) Mn SOD mRNA expression was higher in the fetal membranes of patients at term in labor than those not in labor (2.4-fold; p = 0.02); (2) the amount of Mn SOD mRNA in the fetal membranes was higher in PTL than in term labor or in PPROM (7.2-fold, p = 0.03; 3.2-fold, p = 0.03, respectively); (3) Mn SOD mRNA expression was higher when histological chorioamnionitis was present both among patients with PPROM (3.8-fold, p = 0.02) and with PTL (5.4-fold, p = 0.02) than in patients with these conditions without histological chorioamnionitis; (4) expression of Mn SOD mRNA was higher in PTL with chorioamnionitis than in PPROM with chorioamnionitis (4.3-fold, p = 0.03).The increase in Mn SOD mRNA expression by fetal membranes in term labor and in histological chorioamnionitis in PTL and PPROM suggests that the fetus deploys anti-oxidant mechanisms to constrain the inflammatory processes in the chorioamniotic membranes.

Placental mesenchymal dysplasia (PMD) is an uncommon vascular anomaly of the placenta characterized by mesenchymal stem villous hyperplasia. Its main sonographic feature is a thickened placenta with hypoechoic areas, and an accurate sonographic diagnosis is challenging. The aim of this study was to report 2 cases of PMD and discuss the differential diagnosis of its sonographic features.Cases of placental masses were studied by 2-dimensional (2D), 3-dimensional (3D), and color Doppler imaging.In case 1, a thick placenta with multiple hypoechoic areas was noted at 13 weeks' gestation. At 19 weeks, the multicystic area, clearly demarcated from a normal-looking placenta, measured 6.5 x 8.5 cm and enlarged gradually. The patient gave birth to a 625-g female neonate after spontaneous labor at almost 26 weeks' gestation. In case 2, a first sonographic examination at 25 weeks' gestation revealed a thickened placenta with hypoechoic areas and a fetus with a single umbilical artery and a ventricular septal defect. At 27 weeks, the abnormal area of the placenta measured 14.5 x 7.5 cm. At 32 weeks' gestation, a caesarean delivery was performed because of a nonreassuring fetal heart tracing, and a 1415-g female neonate was delivered. Both cases were evaluated by 2D, 3D, and color Doppler imaging, and the pathologic features of both placentas were consistent with PMD.Placental mesenchymal dysplasia should be considered in the differential diagnosis of every placental mass, especially in cases of multicystic placental lesion with lack of high-velocity signals inside the lesion, and a normal karyotype.

Objective: Adipose tissue dysfunction, characterized by dysregulation of adipokines production and/or secretion, has been implicated in the pathophysiology of type-2 diabetes mellitus, a metabolic complication closely related to gestational diabetes mellitus (GDM). Recently, an association between circulating maternal visfatin, a novel adipokine with metabolic and immunoregulatory properties, and impaired glucose metabolism as well as with altered fetal growth, has been proposed. The aims of this study were to determine whether there is an association between maternal plasma visfatin concentration, GDM, and a large-for-gestational-age (LGA) newborn. // Study design: This cross-sectional study, included pregnant women at term in the following groups: 1) normal pregnancy and an appropriate-for-gestational-age (AGA) neonate (n=54); 2) normal pregnancy and an LGA newborn (n=47); 3) GDM and an AGA newborn (n=56); 4) GDM and an LGA newborn (n=45). The study population was further stratified by first trimester BMI (

Objective: Adipose tissue has now emerged as a powerful endocrine organ via the production of adipokines. Visfatin, a novel adipokine with diabetogenic and immuno-modulatory properties has been implicated in the pathophysiology of insulin resistance in patients with obesity and Type-2 diabetes mellitus. The aim of this study was to determine whether there are changes in the maternal plasma concentration of visfatin with advancing gestation and as a function of maternal weight. Study design: In this cross-sectional study, maternal plasma concentrations of visfatin were determined in normal weight and overweight/obese pregnant women in the following gestational age groups: 1) 11–14 weeks (n=52); 2) 19–26 weeks (n=68); 3) 27–34 weeks (n=93); and 4) >37 weeks (n=60). Visfatin concentrations were determined by ELISA. Non parametric statistics were used for analysis. Results: 1) The median maternal plasma visfatin concentration was higher in pregnant women between 19–26 weeks of gestation than that of those between 11–14 weeks of gestation (P