Maternal left ventricular function and adverse neonatal outcomes in women with cardiac disease.
Accepted version
Peer-reviewed
Repository URI
Repository DOI
Change log
Authors
Abstract
PURPOSE: To evaluate the relationship between maternal left ventricular systolic function, utero-placental circulation, and risk of adverse neonatal outcomes in women with cardiac disease. METHODS: 119 women managed in the pregnancy heart clinic (2019-2021) were identified. Women were classified by their primary cardiac condition. Adverse neonatal outcomes were: low birth weight (< 2500 g), small-for-gestational-age (< 10th birth-weight centile), pre-term delivery (< 37 weeks' gestation), and fetal demise (> 20 weeks' gestation). Parameters of left ventricular systolic function (global longitudinal strain, radial strain, ejection fraction, average S', and cardiac output) were calculated and pulsatility index was recorded from last growth scan. RESULTS: Adverse neonatal outcomes occurred in 28 neonates (24%); most frequently in valvular heart disease (n = 8) and cardiomyopathy (n = 7). Small-for-gestational-age neonates were most common in women with cardiomyopathy (p = 0.016). Early pregnancy average S' (p = 0.03), late pregnancy average S' (p = 0.02), and late pregnancy cardiac output (p = 0.008) were significantly lower in women with adverse neonatal outcomes than in those with healthy neonates. There was a significant association between neonatal birth-weight centile and global longitudinal strain (p = 0.04) and cardiac output (p = 0.0002) in late pregnancy. Pulsatility index was highest in women with cardiomyopathy (p = 0.007), and correlated with average S' (p < 0.0001) and global longitudinal strain (p = 0.03) in late pregnancy. CONCLUSION: Women with cardiac disease may not tolerate cardiovascular adaptations required during pregnancy to support fetal growth. Adverse neonatal outcomes were associated with reduced left ventricular systolic function and higher pulsatility index. The association between impaired systolic function and reduced fetal growth is supported by insufficient utero-placental circulation.
Description
Keywords
Journal Title
Conference Name
Journal ISSN
1432-0711