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Fetal cardiac remodeling and dysfunction is associated with both preeclampsia and fetal growth restriction.

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BACKGROUND Preeclampsia and fetal growth restriction share some pathophysiological features and are both associated with placental insufficiency. Fetal cardiac remodeling has extensively been described in fetal growth restriction, whereas little… Click to show full abstract

BACKGROUND Preeclampsia and fetal growth restriction share some pathophysiological features and are both associated with placental insufficiency. Fetal cardiac remodeling has extensively been described 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 to uncomplicated pregnancies. STUDY DESIGN This was a prospective observational study including pregnancies complicated by normotensive fetal growth restriction (FGR, n=36), preeclampsia with a normally grown fetus (PE, n=35), preeclampsia with fetal growth restriction (PE-FGR, 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 (BNP) 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), FGR 0.31 (0.26-0.34), PE 0.31 (0.29-0.33) and PE-FGR 0.28 (0.26-0.33); p<0.001] and more spherical right ventricles [right ventricular sphericity index: uncomplicated pregnancies 1.42 (1.25-1.72), FGR 1.29 (1.22-1.72), PE 1.30 (1.33-1.51) and PE-FGR 1.35 (1.27-1.46); p=0.04] and hypertrophic ventricles [relative wall thickness: uncomplicated pregnancies 0.55 (0.48-0.61), FGR 0.67 (0.58-0.8), PE 0.68 (0.61-0.76), and PE-FGR 0.66 (0.58-0.77); p<0.001]. Signs of myocardial dysfunction were also observed, with increased myocardial performance index [uncomplicated pregnancies 0.78 z-scores (0.32-1.41), FGR 1.48 (0.97-2.08), PE 1.15 (0.75-2.17) and PE-FGR 1.45 (0.54-1.94); p<0.001] and higher cord blood BNP [uncomplicated pregnancies 14.2 (8.4-30.9) pg/mL, FGR 20.8 (13.1-33.5) pg/mL, PE 31.8 (16.4-45.8) pg/mL and PE-FGR 37.9 (15.7-105.4) pg/mL; P<0.001] and Troponin I as compared to uncomplicated pregnancies. CONCLUSIONS 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.

Keywords: growth restriction; uncomplicated pregnancies; preeclampsia fetal; fetal growth; growth

Journal Title: American journal of obstetrics and gynecology
Year Published: 2019

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