Key result
Fetal growth restriction is linked to ~1.8 L/min lower maternal cardiac output versus controls.
Why the study?
Fetal growth restriction (FGR) is associated with maternal cardiovascular maladaptation, but its relationship with cardiac function, biomarkers, and fetoplacental dysfunction, as well as variation by FGR onset, remained incompletely characterized.
Observational (n=140)
Fetal growth restriction is characterized by a maternal low-output, high-resistance cardiovascular phenotype accompanied by markedly elevated circulating NT-proBNP and GDF-15 concentrations.
Answers are grounded in this paper and cite their sources.
May support maternal hemodynamic evaluation in fetal growth restriction; extends observational links but requires trials before guiding care.
Background/Objectives: Fetal growth restriction (FGR) is associated with maternal cardiovascular maladaptation, but its relationship with cardiac function, biomarkers and fetoplacental dysfunction remains incompletely characterized. We aimed to characterize the maternal cardiovascular phenotype associated with FGR and its variation according to onset. Methods: This prospective study included 140 singleton pregnancies: 59 with FGR (10 early-onset; 49 late-onset) and 81 controls. Assessments included maternal hemodynamics, echocardiography, circulating biomarkers, fetoplacental Doppler indices and neonatal outcomes. Analyses comprised group comparisons, multivariable regression, correlations and exploratory biomarker ROC analyses. Results: After adjustment for gestational age at the corresponding assessment, maternal age, body mass index, preeclampsia and chronic hypertension, FGR was associated with lower cardiac output (−1.84 L/min; 95% CI, −2.13 to −1.55), higher systemic vascular resistance (+530 dyn·s·cm−5; 95% CI, 429–632) and altered relaxation indices. NT-proBNP and GDF-15 concentrations were 191% (95% CI, 141–250%) and 125% (95% CI, 92–164%) higher, respectively. Early-onset FGR showed greater abnormalities in selected hemodynamic and relaxation parameters and higher GDF-15 than late-onset FGR; e′, E/e′, and NT-proBNP did not differ significantly. Apparent within-cohort AUCs for FGR discrimination were 0.991 for NT-proBNP and 0.961 for GDF-15. Selected cardiovascular parameters correlated with fetoplacental Doppler indices and perinatal outcomes. Early-onset FGR had the highest NICU admission rate and longest neonatal hospitalization among survivors, alongside substantially earlier delivery. Conclusions: FGR was associated with a low-output, high-resistance maternal cardiovascular phenotype and elevated biomarkers. Onset-related comparisons remain exploratory and were not validated by the gestational-age-restricted sensitivity analysis, which included only late-onset FGR. Incremental predictive value beyond fetal biometry and Doppler assessment and benefits for clinical management remain to be established.
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Minciună et al. (2026) conducted an observational in Fetal growth restriction (FGR) (n=140). Fetal growth restriction (FGR) vs. Controls (uncomplicated singleton pregnancies) was evaluated on Maternal cardiac output (MD -1.84 L/min, 95% CI -2.13 to -1.55). Fetal growth restriction was associated with lower maternal cardiac output and higher systemic vascular resistance (+530 dyn·s·cm−5) vs controls.
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