Fetal Growth Restriction Results in Remodeled and Less Efficient Hearts in Children

TLDR

Fetal growth restriction affects 5–10 % of newborns and is linked to higher adult cardiovascular mortality, possibly through metabolic programming that predisposes to obesity, diabetes, and hypertension. The study seeks to determine whether FGR causes persistent cardiac changes in childhood and, if confirmed, to evaluate interventions that could mitigate such remodeling. Cardiovascular assessment was performed at a mean age of 5 years on 80 FGR children and 120 matched controls, with measurements of cardiac structure and function. FGR children exhibited globular hearts with increased transverse diameters, reduced stroke volume compensated by higher heart rate, subclinical systolic and diastolic dysfunction, elevated blood pressure, thicker intima‑media, and all these abnormalities intensified with greater growth restriction.

Abstract

Fetal growth restriction (FGR) affects 5% to 10% of newborns and is associated with increased cardiovascular mortality in adulthood. The most commonly accepted hypothesis is that fetal metabolic programming leads secondarily to diseases associated with cardiovascular disease, such as obesity, diabetes mellitus, and hypertension. Our main objective was to evaluate the alternative hypothesis that FGR induces primary cardiac changes that persist into childhood.Within a cohort of fetuses with growth restriction identified in fetal life and followed up into childhood, we randomly selected 80 subjects with FGR and compared them with 120 normally grown fetuses, matched for gender, birth date, and gestational age at birth. Cardiovascular assessment was performed in childhood (mean age of 5 years). Compared with control subjects, children with FGR had a different cardiac shape, with increased transversal diameters and more globular cardiac ventricles. Although left ejection fraction was similar among the study groups, stroke volume was reduced significantly, which was compensated for by an increased heart rate to maintain output in severe FGR. This was associated with subclinical longitudinal systolic dysfunction (decreased myocardial peak velocities) and diastolic changes (increased E/E' ratio and E deceleration time). Children with FGR also had higher blood pressure and increased intima-media thickness. For all parameters evaluated, there was a linear increase with the severity of growth restriction.These findings suggest that FGR induces primary cardiac and vascular changes that could explain the increased predisposition to cardiovascular disease in adult life. If these results are confirmed, the impact of strategies with beneficial effects on cardiac remodeling should be explored in children with FGR.