Cardiol Rev. 2025 Apr 18. doi: 10.1097/CRD.0000000000000918. Online ahead of print.
ABSTRACT
Preeclampsia (PE), a hypertensive disorder affecting up to 8% of pregnancies, has been associated with cardiac structural and functional changes in offspring. Studies suggest that neonates exposed to PE in utero may exhibit increased left ventricular mass, myocardial hypertrophy, and disrupted myocardial compaction. However, the long-term cardiovascular effects remain inconsistent across studies, with some evidence indicating an elevated risk of systolic and diastolic dysfunction persisting into adolescence and adulthood. The multifactorial nature of PE complicates the establishment of clear causality, as mechanisms likely involve placental insufficiency, angiogenic imbalance, oxidative stress, and epigenetic modifications. Research indicates that fetal developmental programming due to adverse intrauterine conditions plays a critical role in shaping offspring cardiovascular outcomes. Independent of fetal growth restriction, PE exposure has been linked to altered cardiac remodeling and increased vascular resistance. Despite this growing body of evidence, knowledge gaps remain regarding the molecular pathways linking PE to cardiovascular outcomes in offspring. This review synthesizes findings on the cardiac manifestations of offspring exposed to PE and underscores the need for further research to better understand the interplay of maternal hypertension and fetal cardiovascular development. By increasing awareness among healthcare providers, this review aims to highlight opportunities for early intervention in this at-risk population.
PMID:40249186 | DOI:10.1097/CRD.0000000000000918
