Abstract:Purpose of reviewAbnormal uterine artery Doppler (UtAD) studies early in gestation have been associated with adverse pregnancy outcomes. However, their association with complications in the third trimester is weak. We aim to review the prediction ability for perinatal complications of these indices in the third trimester.
Recent findingsAbnormal UtAD waveforms in the third trimester are associated with preeclampsia, small-for-gestational age infants (SGA), preterm birth, perinatal death, and other perinatal co… Show more
“…The persistent increase in the uterine artery impedance in the third trimesters increased the risk of SGA [ 8 ]. UtA examination can be conducted in transvaginal and transabdominal approaches, and transabdominal approach is recommended because most of the studies evaluating the UtA in the third trimester used a transabdominal approach [ 10 ]. Therefore, we performed a systematic review and meta-analysis based on the previously published studies to comprehensively explore the association between transabdominal UtA measurements and the risk of SGA in the first, second, and third trimesters.…”
Background
The association between uterine artery Doppler (UtA) measurements and small for gestational age (SGA) has not been quantitatively analyzed throughout the whole pregnancy. This systematic review and meta-analysis aims to comprehensively explore the association between UtA measurements and SGA in the first, second, and third trimesters.
Methods
Studies were searched from Pubmed, Embase, Cochrane Library, and Web of Science. Weighted mean difference (WMD), odds ratio (OR), and relative risk (RR) with 95% confidence interval (CI) were used as the effect size. Heterogeneity of all effect sizes was tested and quantified using I2 statistics. Sensitivity analysis was conducted for all outcomes, and publication bias was evaluated using Begg’s test.
Results
A total of 41 studies were finally included in our meta-analysis. In the first trimester, mean PI was significantly higher in the SGA group than the non-SGA group (WMD: 0.31, 95%CI: 0.19–0.44). In the second trimester, odds of notch presence (OR: 2.54, 95%CI: 2.10–3.08), mean PI (WMD: 0.21, 95%CI: 0.12–0.30), and mean RI (WMD: 0.05, 95%CI: 0.05–0.06) were higher in the SGA group. Also, abnormal UtA measurements were associated with the increased odds of SGA (all P < 0.05). In the third trimester, PI z-score (WMD: 0.62, 95%CI: 0.33–0.91) and PI MoM (WMD: 0.08, 95%CI: 0.06–0.09) showed a significant increase in the SGA group. The odds of SGA were higher in the women with mean PI > 95% (OR: 6.03, 95%CI: 3.24–11.24).
Conclusions
Abnormal UtA measurements were associated with high odds of SGA, suggesting that UtA might be an adjunctive screening method for SGA in the whole pregnancy.
“…The persistent increase in the uterine artery impedance in the third trimesters increased the risk of SGA [ 8 ]. UtA examination can be conducted in transvaginal and transabdominal approaches, and transabdominal approach is recommended because most of the studies evaluating the UtA in the third trimester used a transabdominal approach [ 10 ]. Therefore, we performed a systematic review and meta-analysis based on the previously published studies to comprehensively explore the association between transabdominal UtA measurements and the risk of SGA in the first, second, and third trimesters.…”
Background
The association between uterine artery Doppler (UtA) measurements and small for gestational age (SGA) has not been quantitatively analyzed throughout the whole pregnancy. This systematic review and meta-analysis aims to comprehensively explore the association between UtA measurements and SGA in the first, second, and third trimesters.
Methods
Studies were searched from Pubmed, Embase, Cochrane Library, and Web of Science. Weighted mean difference (WMD), odds ratio (OR), and relative risk (RR) with 95% confidence interval (CI) were used as the effect size. Heterogeneity of all effect sizes was tested and quantified using I2 statistics. Sensitivity analysis was conducted for all outcomes, and publication bias was evaluated using Begg’s test.
Results
A total of 41 studies were finally included in our meta-analysis. In the first trimester, mean PI was significantly higher in the SGA group than the non-SGA group (WMD: 0.31, 95%CI: 0.19–0.44). In the second trimester, odds of notch presence (OR: 2.54, 95%CI: 2.10–3.08), mean PI (WMD: 0.21, 95%CI: 0.12–0.30), and mean RI (WMD: 0.05, 95%CI: 0.05–0.06) were higher in the SGA group. Also, abnormal UtA measurements were associated with the increased odds of SGA (all P < 0.05). In the third trimester, PI z-score (WMD: 0.62, 95%CI: 0.33–0.91) and PI MoM (WMD: 0.08, 95%CI: 0.06–0.09) showed a significant increase in the SGA group. The odds of SGA were higher in the women with mean PI > 95% (OR: 6.03, 95%CI: 3.24–11.24).
Conclusions
Abnormal UtA measurements were associated with high odds of SGA, suggesting that UtA might be an adjunctive screening method for SGA in the whole pregnancy.
Fetal growth restriction (FGR), which most commonly results from suboptimal placental function, substantially increases risks for adverse perinatal and long-term outcomes. The only “treatment” that exists is delivery, which averts stillbirth but does not improve outcomes in survivors. Furthermore, the potential long-term consequences of FGR to the fetus, including cardiometabolic disorders, predispose these individuals to developing FGR in their future pregnancies. This creates a multi-generational cascade of adverse effects stemming from a single dysfunctional placenta, and understanding the mechanisms underlying placental-mediated FGR is critically important if we are to improve outcomes and overall health. The mechanisms behind FGR remain unknown. However, placental insufficiency derived from maldevelopment of the placental vascular systems is the most common etiology. To highlight important mechanistic interactions within the placenta, we focus on placental vascular development in the setting of FGR. We delve into fetoplacental angiogenesis, a robust and ongoing process in normal pregnancies that is impaired in severe FGR. We review cellular models of FGR, with special attention to fetoplacental angiogenesis, and we highlight novel integrin-extracellular matrix interactions that regulate placental angiogenesis in severe FGR. In total, this review focuses on key developmental processes, with specific focus on the human placenta, an underexplored area of research.
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