Abstract
BACKGROUND: Fetal growth restriction (FGR) and late-onset preeclampsia (late-onset PE) reflect placental dysfunction but exhibit distinct maternal hemodynamics within the “maternal cardiovascular-placental-fetal unit”. INTRODUCTION: Our objective was to investigate the correlation between fetal-placental Doppler indices and maternal cardiac function in pregnant women with late-onset PE or FGR. METHODS: A total of 90 pregnant women at 35–39⁺⁶ weeks of gestation were enrolled and divided into three groups: Control (n = 30), FGR (n = 30), and late-onset PE (n = 30). Doppler ultrasonography was used to measure uterine artery pulsatility indices(UtA-PI), umbilical artery pulsatility indices(UA-PI) Z-scores, and middle cerebral artery pulsatility indices(MCA-PI) Z-scores, alongside maternal hemodynamic parameters, including cardiac output (CO), peripheral vascular resistance (PVR), left ventricular mass (LVM), and left atrial anteroposterior diameter (LAAPD).The Kruskal-Wallis test was used to compare characteristics among the three groups. Spearman’s rank correlation analysis was employed to assess relationships between maternal cardiac output/peripheral vascular resistance and fetal-placental Doppler indices in the three subgroups. Partial Spearman rank correlation analysis adjusting for maternal age and BMI was used to evaluate independent associations. RESULTS: FGR neonates had the lowest birth weights (p < 0.05). The FGR group showed reduced CO, LVM, LAAPD (p < 0.05) but elevated PVR, UtA-PI, UA-PI Z-scores (p < 0.05). Late-onset PE exhibited preserved cardiac function (CO, LVM, LAAPD comparable to controls, p > 0.05) but significantly higher CO, LVM, LAAPD than FGR (p < 0.05). No significant differences in MCA-PI Z-scores were observed across groups. UtA-PI negatively correlated with CO (ρ=−0.396, p < 0.001) but positively with PVR (ρ = 0.371, p < 0.001). UA-PI Z-score negatively correlated with CO (ρ=−0.257, p = 0.015). However, MCA-PI Z-scores showed no correlation with CO and PVR.Notably, 90% of FGR cases clustered in the low-CO/high-UtA-PI quadrant. CONCLUSIONS: In direct response to our primary aim investigating maternal-fetal hemodynamic coupling, we conclude that: FGR manifests as maternal hemodynamic failure (low-CO/high-UtA-PI) causing placental hypoperfusion; Late-onset PE presents volume overload with preserved uteroplacental function; Dual UtA-PI and CO assessment provides phenotype-specific biomarkers to guide targeted therapy. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s12884-025-07848-x.