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Fetal Echocardiography and Pulsed-wave Doppler Ultrasound in a Rabbit Model of Intrauterine Growth Restriction
Published on: June 29, 2013
Cardiac function in fetal growth restriction
Ilenia Mappa1, Pavjola Maqina1, Victoria Bitsadze1,2
1Division of Maternal and Fetal Medicine, Cristo Re Hospital, Tor Vergata University, Rome, Italy.
Insights
Fetal growth restriction (FGR) impacts fetal development and long-term health due to placental insufficiency. This review explores how early and late FGR uniquely alter fetal cardiac hemodynamics and blood flow.
Area of Science:
- Obstetrics and Gynecology
- Fetal Medicine
- Cardiology
Background:
- Fetal growth restriction (FGR) is a condition where a fetus cannot reach its full growth potential.
- FGR is classified as early (<32 weeks) or late (≥32 weeks) onset, each with distinct pathological mechanisms.
- FGR is linked to adverse short- and long-term outcomes, including neurodevelopmental delay and increased risk of infant and adult complications.
Purpose of the Study:
- To review the modifications in fetal cardiac hemodynamics in early and late-onset FGR.
- To elucidate the distinct mechanisms of cardiac hemodynamic changes in early versus late FGR.
- To highlight the impact of placental insufficiency and chronic fetal hypoxia on fetal cardiac function.
Main Methods:
- This review synthesizes existing literature on fetal cardiac hemodynamics in FGR.
- It analyzes studies focusing on cardiovascular adaptations and maladaptations in early and late FGR.
- The review discusses findings from Doppler ultrasound and other fetal assessment techniques.
Main Results:
- Early-onset FGR involves preferential cardiac output diversion to the brain and heart, with abnormal flow patterns indicating worsening hypoxia.
- Late-onset FGR is characterized by fetal heart remodeling and functional changes, primarily due to reduced umbilical vein flow.
- Both forms of FGR demonstrate significant alterations in fetal cardiac hemodynamic profiles.
Conclusions:
- Fetal growth restriction significantly impacts fetal cardiac hemodynamics, with distinct patterns observed in early and late-onset cases.
- Understanding these hemodynamic alterations is crucial for predicting outcomes and managing pregnancies complicated by FGR.
- Further research into targeted interventions based on specific hemodynamic profiles is warranted.
Abstract:
Fetal growth restriction (FGR) is defined as the inability of the fetus to reach its growth potential. According to the onset of the disease is defined early (<32 weeks) or late (≥32 weeks). FGR is associated with an increased risk of adverse short- and long-term outcomes, including hypoxemic events and neurodevelopmental delay compared to normally grown fetuses and increased risk of complications in the infanthood and adulthood. The underlying cause of FGR is placental insufficiency leading to chronic fetal hypoxia that affects cardiac hemodynamic with different mechanism in early and late onset growth restriction. In early onset FGR adaptive mechanisms involve the diversion of the cardiac output preferentially in favor of the brain and the heart, while abnormal arterial and venous flow manifest in the case of further worsening of fetal hypoxia. In late FGR the fetal heart shows a remodeling of its shape and function mainly related to a reduction of umbilical vein flow. In this review we discuss the modifications occurring at the level of the fetal cardiac hemodynamic in fetuses with early and late FGR.
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