Abstract 4372906: Impact of Maternal Gestational Diabetes on Offspring Cardiac Function: A Systematic Review and Meta-Analysis

Abstract

Background: Gestational diabetes mellitus (GDM) affects 6–12% of pregnancies globally and is linked to adverse fetal cardiac remodeling. Offspring exposed to GDM in utero show altered myocardial performance index (MPI) and increased left ventricular mass index (LVMI). We performed a systematic review and meta-analysis to assess the impact of maternal GDM on neonatal and early childhood cardiac structure and function. Methods: A PRISMA-compliant search was conducted across PubMed, Scopus, and Web of Science (last updated April 2024) for studies comparing echocardiographic parameters in GDM-exposed vs non-GDM-exposed offspring. Inclusion criteria: (1) human subjects, (2) reported MPI or LVMI, (3) GDM diagnosed per WHO/ADA criteria, and (4) echocardiography performed <12 years of age. Pooled effect sizes were computed using a random-effects model (Hedges’ g). Heterogeneity assessed via I2, and subgroup analyses explored term vs preterm outcomes and GDM treatment status. Results: 13 studies (n = 1,621 offspring) met inclusion. GDM-exposed offspring had significantly higher LVMI (Hedges’ g = 0.51; 95% CI: 0.34–0.67) and abnormal MPI (Hedges’ g = 0.59; 95% CI: 0.43–0.75) compared to controls. The effect was most pronounced in third trimester GDM and insulin-treated cohorts. Heterogeneity was moderate (I = 48%). Subgroup analysis showed greater dysfunction in boys vs girls (p = 0.04). Meta-regression revealed stronger MPI alteration with increasing maternal HbA1c (β = 0.22, p = 0.003). No evidence of publication bias was observed. Conclusion: In utero exposure to maternal GDM is associated with early subclinical LV dysfunction and remodeling, reflected by elevated MPI and LVMI. These changes may predispose offspring to long-term cardiometabolic risk. Our findings support the utility of early echocardiographic screening in this population and the importance of optimized GDM management to prevent fetal cardiac programming.