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Author Spotlight: Modeling an Aspect of Preeclampsia in Female Mice Using Hypoxic Human Placenta-Derived Small Extracellular Vesicles
Published on: January 26, 2024
Linking maternal and neonatal circulation in preeclampsia
Federica Piani1, Lorenzo Annesi2,3, Daniela Degli Esposti3
1Division of Physiology and Pathophysiology, Otto Loewi Research Center for Vascular Biology, Immunology and Inflammation, Medical University of Graz, Graz, Austria.
Hypertensive disorders of pregnancy, particularly early-onset preeclampsia (EOPE), are major causes of perinatal morbidity and mortality. Although impaired placentation has long been recognized as a key mechanism, increasing evidence highlights the contribution of maternal cardiovascular dysfunction. However, how maternal hemodynamics influences neonatal circulatory transition remains poorly understood. In this prospective study, mother-infant pairs from pregnancies complicated by EOPE were enrolled if the mother had undergone echocardiographic assessment within 3 wk before delivery and the neonate had received continuous hemodynamic monitoring by electrical cardiometry for at least 72 h after birth. Associations between maternal and neonatal hemodynamic parameters were explored using correlation analysis, and generalized linear mixed-effects models (GLMMs) accounted for repeated neonatal measurements, neonatal exposure to dopamine or dobutamine, and patent ductus arteriosus (PDA). Maternal systolic function indices [cardiac output (CO), ejection fraction (EF), and tissue Doppler s' velocities] inversely correlated with neonatal CO in fully adjusted GLMM models. EF was positively associated with neonatal systemic vascular resistance when adjusted for inotropic support (P = 0.010), with attenuation after additional adjustment for PDA (P = 0.052). Overall, maternal systolic impairment in EOPE was associated with higher neonatal CO, indicating a compensatory increase in neonatal cardiac performance, whereas changes in neonatal vascular tone were minimal. These findings provide the first quantitative evidence of maternal-neonatal hemodynamic coupling and support the value of integrated cardiovascular assessment of both mother and newborn in hypertensive pregnancies.NEW & NOTEWORTHY This study provides the first evidence that maternal cardiovascular maladaptation in preeclampsia is directly mirrored in neonatal hemodynamics. Newborns displayed a compensatory rise in cardiac output in response to maternal systolic dysfunction, whereas changes in neonatal vascular tone remained minimal. Although maternal and neonatal circulations are traditionally examined independently, these findings underscore a tightly linked maternal-fetal hemodynamic dyad, offering new insight into the physiological continuity that spans the perinatal transition.
Hypertensive disorders of pregnancy, particularly early-onset preeclampsia (EOPE), are major causes of perinatal morbidity and mortality. Although impaired placentation has long been recognized as a key mechanism, increasing evidence highlights the contribution of maternal cardiovascular dysfunction. However, how maternal hemodynamics influences neonatal circulatory transition remains poorly understood. In this prospective study, mother-infant pairs from pregnancies complicated by EOPE were enrolled if the mother had undergone echocardiographic assessment within 3 wk before delivery and the neonate had received continuous hemodynamic monitoring by electrical cardiometry for at least 72 h after birth. Associations between maternal and neonatal hemodynamic parameters were explored using correlation analysis, and generalized linear mixed-effects models (GLMMs) accounted for repeated neonatal measurements, neonatal exposure to dopamine or dobutamine, and patent ductus arteriosus (PDA). Maternal systolic function indices [cardiac output (CO), ejection fraction (EF), and tissue Doppler s' velocities] inversely correlated with neonatal CO in fully adjusted GLMM models. EF was positively associated with neonatal systemic vascular resistance when adjusted for inotropic support (P = 0.010), with attenuation after additional adjustment for PDA (P = 0.052). Overall, maternal systolic impairment in EOPE was associated with higher neonatal CO, indicating a compensatory increase in neonatal cardiac performance, whereas changes in neonatal vascular tone were minimal. These findings provide the first quantitative evidence of maternal-neonatal hemodynamic coupling and support the value of integrated cardiovascular assessment of both mother and newborn in hypertensive pregnancies.NEW & NOTEWORTHY This study provides the first evidence that maternal cardiovascular maladaptation in preeclampsia is directly mirrored in neonatal hemodynamics. Newborns displayed a compensatory rise in cardiac output in response to maternal systolic dysfunction, whereas changes in neonatal vascular tone remained minimal. Although maternal and neonatal circulations are traditionally examined independently, these findings underscore a tightly linked maternal-fetal hemodynamic dyad, offering new insight into the physiological continuity that spans the perinatal transition.
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