H. Meneses, L. Guedes-Martins
2026.4.9CURRENT CARDIOLOGY REVIEWS
Abstract
Congenital heart defects are the most common malformations in newborns and the leading cause of morbidity and mortality due to congenital abnormalities. As a result of genetic susceptibility and environmental exposure, a few of these anomalies could be prevented by managing modifiable risk factors. Given that maternal obesity is a predisposing factor for obstetric and fetal complications, this review aims to explore its association with congenital heart disease, while addressing mechanisms underlying its pathophysiology at the cellular and molecular levels. For this purpose, a series of searches was carried out on the PubMed database, and additional articles were identified via citation searches. Studies suggest a 17 - 32% increase in risk of the offspring developing a congenital heart defect when compared to normal weight mothers, with an estimate of 7% increased risk per 5 kg/m2 body mass index rise. This review highlights the role of placental dysfunction, a pro-inflammatory state, systemic oxidative stress, and decreased adiponectin, all caused by maternal obesity, in disrupting fetal cardiac development and leading to the development of congenital heart disease. Overall, obesity seems to impair essential cellular processes involved in cardiogenesis, inflicting long-lasting damage to fetal cells. Literature remains inconsistent regarding the role of confounding factors, such as gestational weight gain, gestational diabetes and maternal diet. Further investigation is needed concerning preconceptional and gestational prevention and management strategies suited for these mothers. This narrative review aims to offer an integrated overview of maternal obesity and its physiological consequences, with a particular focus on placental function, fetal cardiac development, and the risk of congenital heart disease.
Citation format
MENESES, H.; GUEDES-MARTINS, L. Maternal obesity and risk of congenital heart defects. CURRENT CARDIOLOGY REVIEWS, 2026, 22.