Fetal umbilical artery velocity waveforms and subsequent neonatal outcome

Trudinger, Brian J.; Cook, Colleen M.; Giles, Warwick B.; Ng, Sher M.; Fong, E. A.; Connelly, Anita; Wilcox, Wendy R.

doi:10.1111/j.1471-0528.1991.tb13428.x

Cited by 170 publications

(79 citation statements)

References 24 publications

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“…Uterine artery Doppler velocimetry was defined as abnormal if the mean (average of right and left) resistance index (RI) was above the 95th percentile for gestational age (using the reference range proposed by Kurmanavicius et al) [165]. Umbilical artery Doppler velocimetry was defined as abnormal if either the pulsatility index (PI) was above the 95th percentile for gestational age (using the reference range proposed by Arduini and Rizzo) [166] or in the presence of abnormal waveforms (absent or reversed end-diastolic velocities) [167]. The patients were classified into the following groups: (1) normal Doppler velocimetry in the uterine and umbilical arteries; (2) Doppler abnormalities in the uterine arteries alone; (3) Doppler abnormalities in umbilical arteries alone; or (4) Doppler abnormalities in both vessels.…”

Section: Doppler Velocimetrymentioning

confidence: 99%

Maternal plasma concentrations of sST2 and angiogenic/anti-angiogenic factors in preeclampsia

Stampalija

Chaiworapongsa

Romero

et al. 2013

The Journal of Maternal-Fetal & Neonatal Medicine

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Objectives: Angiogenic/anti-angiogenic factors have emerged as one of the promising biomarkers for the prediction of preeclampsia. Since not all patients with preeclampsia can be identified by these analytes, the search for additional biomarkers continues. The soluble form of ST2 (sST2), a protein capable of binding to interleukin (IL)-33 and thus contributing to a Th1-biased immune response, has been reported to be elevated in maternal plasma of women with preeclampsia. The aims of this study were to examine: (1) differences in maternal plasma concentrations of sST2 and IL-33 between women diagnosed with preeclampsia and those having uncomplicated pregnancies; (2) the relationship between sST2, umbilical and uterine artery Doppler velocimetry, and the severity of preeclampsia; and (3) the performance of sST2 and angiogenic/anti-angiogenic factors in identifying patients with preeclampsia at the time of diagnosis. Methods: This cross-sectional study included women with preeclampsia (n ¼ 106) and women with an uncomplicated pregnancy (n ¼ 131). Plasma concentrations of sST2, IL-33, soluble vascular endothelial growth factor receptor (sVEGFR)-1, soluble endoglin (sEng) and placental growth factor (PlGF) were determined by enzyme linked immune sorbent assay. Area under the receiver operating characteristic curve (AUC) for the identification of preeclampsia was examined for each analyte. Results: (1) Patients with preeclampsia had a higher mean plasma concentrations of sST2 than those with an uncomplicated pregnancy (p50.0001), while no significant difference in the mean plasma concentration of IL-33 between the two groups was observed; (2) the magnitude of this difference was greater in early-onset, compared to late-onset disease, and in severe compared to mild preeclampsia; (3) sST2 plasma concentrations did not correlate with the results of uterine or umbilical artery Doppler velocimetry (p ¼ 0.7 and p ¼ 1, respectively) among women with preeclampsia; (4) sST2 correlated positively with plasma concentrations of sVEGFR1-1 and sEng (Spearman's Rho ¼ 0.72 and 0.63; each p50.0001), and negatively with PlGF (Spearman's Rho ¼ À0.56, p50.0001); and (5) while the AUC achieved by sST2 and angiogenic/anti-angiogenic factors in identifying women with preeclampsia at the time of diagnosis were non-significantly different prior to term (537 weeks of gestation), thereafter the AUC achieved by sST2 was significantly less than that achieved by angiogenic/anti-angiogenic factors. Conclusions: Preeclampsia is associated with increased maternal plasma concentrations of sST2. The findings that sST2 concentrations do not correlate with uterine or umbilical artery Doppler velocimetry in women with preeclampsia suggest that elevated maternal plasma sST2 concentrations in preeclampsia are not related to the increased impedance to flow in the uteroplacental circulation. The performance of sST2 in identifying preeclampsia at the time of diagnosis prior to 37 weeks of gestation was comparable to that of angiogenic/anti-angiogenic f...

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Section: Doppler Velocimetrymentioning

confidence: 99%

Maternal plasma concentrations of sST2 and angiogenic/anti-angiogenic factors in preeclampsia

Stampalija

Chaiworapongsa

Romero

et al. 2013

The Journal of Maternal-Fetal & Neonatal Medicine

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“…31,45,[55][56][57][58][59][60] Even when controlling for gestational age at delivery some series have reported a significant association between abnormal umbilical artery flow and the perinatal results. 31,55,60 In addition, the occurrence of perinatal death in the presence of a normal umbilical flow is very uncommon. 55,57,61 Thus, Doppler of the umbilical artery flow could be considered a riskdiscriminator tool in the management of SGA fetuses.…”

Section: Iugr Versus Normal-sgamentioning

confidence: 99%

“…31,55,60 In addition, the occurrence of perinatal death in the presence of a normal umbilical flow is very uncommon. 55,57,61 Thus, Doppler of the umbilical artery flow could be considered a riskdiscriminator tool in the management of SGA fetuses. Evidence supports those SGA fetuses with normal Doppler benefit from a non-intensive follow-up.…”

Section: Iugr Versus Normal-sgamentioning

confidence: 99%

“…[55][56][57] There is an extensive body of evidence that those SGA fetuses with abnormal umbilical artery flow are at higher risk of adverse perinatal outcome than those with normal flow. 31,45,[55][56][57][58][59][60] Even when controlling for gestational age at delivery some series have reported a significant association between abnormal umbilical artery flow and the perinatal results. 31,55,60 In addition, the occurrence of perinatal death in the presence of a normal umbilical flow is very uncommon.…”

Section: Iugr Versus Normal-sgamentioning

confidence: 99%

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Ultrasound and Doppler Management of Intrauterine Growth Restriction

Carrera¹,

Figueras²,

Meler³

2010

Donald School Journal of Ultrasound in Obstetrics and Gynecology

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“…We have recently studied the origins of the vascular pathology in the fetal umbilical placental circulation. This may be identified antenatally by a 'high resistance' waveform pattern of the umbilical artery flow velocity waveforms 5,6 . Thrombosis and vessel obliteration are seen on histological study 7,8 .…”

Section: Introductionmentioning

confidence: 99%

Gene expression of nitric oxide synthase by human umbilical vein endothelial cells: the effect of fetal plasma from pregnancy with umbilical placental vascular disease

Wang¹

2003

BJOG: An International Journal of Obstetrics and Gynaecology

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Objective To determine whether endothelial cell injury would be produced by factor(s) released into the fetal circulation, manifested by altered messenger RNA expression of nitric oxide synthase. Design Case -control study.Setting University teaching hospital.Samples Fetal plasma was collected from 34 normal pregnancies, 44 pregnancies with umbilical placental vascular disease identified by an abnormal umbilical Doppler and 11 pregnancies with maternal pre-eclampsia but with normal umbilical Doppler studies. Methods Aliquots from a common culture of human umbilical vein endothelial cells (HUVECs) were incubated with fetal plasma from the members of the three patient groups. The total RNA was extracted from the endothelial cells and mRNA for nitric oxide synthase was measured by reverse transcription and semi-quantitative polymerase chain reaction (RT-PCR). This was standardised by comparison of the amplified inducible nitric oxide synthase (iNOS) or endothelial constitutive nitric oxide synthase (ecNOS) to glyceraldehyde 3-phosphate dehydrogenase (GAPDH). Main outcome measure Endothelial cell gene expression of iNOS and ecNOS.Results The mRNA expression of iNOS and ecNOS were significantly higher ( P < 0.05) in HUVECs stimulated by fetal plasma from pregnancies with umbilical placental vascular disease [iNOS 1.12 (0.16); ecNOS 1.78 (0.18)] when compared with normal pregnancies [iNOS 0.56 (0.06); ecNOS 1.06 (0.10)]. In the maternal pre-eclampsia group, the NOS expression [iNOS 0.76 (0.11); ecNOS 1.39 (0.26)] did not differ from normal pregnancy. In the vascular disease group, there was no difference in NOS expression between the subgroups with and without maternal pre-eclampsia. Conclusions Our study demonstrates that umbilical placental vascular disease is associated with a factor(s) in fetal plasma that produces an increase in the expression of iNOS and ecNOS mRNA by endothelial cells. Our findings raise the possibility that the release of factors causing an up-regulation of iNOS and ecNOS in the endothelium in the fetal placenta may occur as part of an inflammatory response of the vascular endothelium to injury.

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Fetal umbilical artery velocity waveforms and subsequent neonatal outcome

Cited by 170 publications

References 24 publications

Maternal plasma concentrations of sST2 and angiogenic/anti-angiogenic factors in preeclampsia

Maternal plasma concentrations of sST2 and angiogenic/anti-angiogenic factors in preeclampsia

Ultrasound and Doppler Management of Intrauterine Growth Restriction

Gene expression of nitric oxide synthase by human umbilical vein endothelial cells: the effect of fetal plasma from pregnancy with umbilical placental vascular disease

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