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Published on: June 29, 2013
Fetal cardiac remodeling and dysfunction is associated with both preeclampsia and fetal growth restriction
Lina Youssef1, Jezid Miranda1, Cristina Paules1
1Fetal Medicine Research Center, BCNatal-Barcelona Center for Maternal-Fetal and Neonatal Medicine (Hospital Clínic and Hospital Sant Joan de Deu), Institut Clinic de Ginecologia, Obstetricia i Neonatologia, IDIBAPS, University of Barcelona, and Centre for Biomedical Research on Rare Diseases (CIBER-ER), Barcelona, Spain.
Insights
Preeclampsia and fetal growth restriction cause similar fetal heart remodeling and dysfunction, regardless of fetal size. This suggests a shared pathway impacting fetal cardiovascular adaptation in these high-risk pregnancies.
Area of Science:
- Perinatology
- Fetal Cardiology
- Maternal-Fetal Medicine
Background:
- Preeclampsia and fetal growth restriction (FGR) share placental insufficiency pathophysiology.
- Fetal cardiac remodeling is well-documented in FGR, but less is known in preeclampsia, especially with normally grown fetuses.
Purpose of the Study:
- To compare fetal cardiac structure and function in pregnancies with preeclampsia and/or FGR versus uncomplicated pregnancies.
Main Methods:
- Prospective observational study involving 4 groups: normotensive FGR, preeclampsia with normal growth, preeclampsia with FGR, and uncomplicated pregnancies.
- Fetal echocardiography was performed, and cord blood biomarkers (B-type natriuretic peptide, troponin I) were measured at delivery.
Main Results:
- Fetuses in preeclampsia and/or FGR groups exhibited similar cardiac remodeling, including larger hearts and more spherical right ventricles.
- Signs of myocardial dysfunction were observed, with increased myocardial performance index and elevated cord blood B-type natriuretic peptide and troponin I levels compared to controls.
Conclusions:
- Fetal cardiac remodeling and dysfunction patterns in preeclampsia are similar to those in FGR, irrespective of fetal growth.
- Further research is needed to understand the mechanisms of fetal cardiac adaptation in these conditions.
Background:
Preeclampsia and fetal growth restriction share some pathophysiologic features and are both associated with placental insufficiency. Fetal cardiac remodeling has been described extensively in fetal growth restriction, whereas little is known about preeclampsia with a normally grown fetus.
Objective:
To describe fetal cardiac structure and function in pregnancies complicated by preeclampsia and/or fetal growth restriction as compared with uncomplicated pregnancies.
Study Design:
This was a prospective, observational study including pregnancies complicated by normotensive fetal growth restriction (n=36), preeclampsia with a normally grown fetus (n=35), preeclampsia with fetal growth restriction (preeclampsia with a normally grown fetus-fetal growth restriction, n=42), and 111 uncomplicated pregnancies matched by gestational age at ultrasound. Fetal echocardiography was performed at diagnosis for cases and recruitment for uncomplicated pregnancies. Cord blood concentrations of B-type natriuretic peptide and troponin I were measured at delivery. Univariate and multiple regression analysis were conducted.
Results:
Pregnancies complicated by preeclampsia and/or fetal growth restriction showed similar patterns of fetal cardiac remodeling with larger hearts (cardiothoracic ratio, median [interquartile range]: uncomplicated pregnancies 0.27 [0.23-0.29], fetal growth restriction 0.31 [0.26-0.34], preeclampsia with a normally grown fetus 0.31 [0.29-0.33), and preeclampsia with fetal growth restriction 0.28 [0.26-0.33]; P<.001) and more spherical right ventricles (right ventricular sphericity index: uncomplicated pregnancies 1.42 [1.25-1.72], fetal growth restriction 1.29 [1.22-1.72], preeclampsia with a normally grown fetus 1.30 [1.33-1.51], and preeclampsia with fetal growth restriction 1.35 [1.27-1.46]; P=.04) and hypertrophic ventricles (relative wall thickness: uncomplicated pregnancies 0.55 [0.48-0.61], fetal growth restriction 0.67 [0.58-0.8], preeclampsia with a normally grown fetus 0.68 [0.61-0.76], and preeclampsia with fetal growth restriction 0.66 [0.58-0.77]; P<.001). Signs of myocardial dysfunction also were observed, with increased myocardial performance index (uncomplicated pregnancies 0.78 z scores [0.32-1.41], fetal growth restriction 1.48 [0.97-2.08], preeclampsia with a normally grown fetus 1.15 [0.75-2.17], and preeclampsia with fetal growth restriction 0.45 [0.54-1.94]; P<.001) and greater cord blood B-type natriuretic peptide (uncomplicated pregnancies 14.2 [8.4-30.9] pg/mL, fetal growth restriction 20.8 [13.1-33.5] pg/mL, preeclampsia with a normally grown fetus 31.8 [16.4-45.8] pg/mL and preeclampsia with fetal growth restriction 37.9 [15.7-105.4] pg/mL; P<.001) and troponin I as compared with uncomplicated pregnancies.
Conclusion:
Fetuses of preeclamptic mothers, independently of their growth patterns, presented cardiovascular remodeling and dysfunction in a similar fashion to what has been previously described for fetal growth restriction. Future research is warranted to better elucidate the mechanism(s) underlying fetal cardiac adaptation in these conditions.
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