Highlights: What are the main findings? Fetal growth restriction (FGR) induces early and persistent myocardial remodeling, including reduced cardiomyocyte number, fibrosis, altered ventricular geometry, and subclinical systolic–diastolic dysfunction detectable from fetal life. These cardiac and vascular changes can be identified with advanced fetal and neonatal imaging and are associated with increased cardiovascular and metabolic risk from childhood to adulthood. What are the implications of the main findings? FGR should be considered an early-life cardiovascular risk condition, requiring a life-course perspective that integrates obstetric, neonatal, and cardiology follow-up. Early identification of high-risk fetuses and infants may enable targeted surveillance and preventive strategies to reduce long-term cardiovascular morbidity. Background/Objectives: Fetal growth restriction (FGR), historically termed intrauterine growth restriction (IUGR), is a multifactorial condition in which the fetus fails to reach its genetically determined growth potential, most often due to placental insufficiency. Beyond its link with increased perinatal morbidity and mortality, FGR has been associated with long-term cardiovascular risk through early-life programming. The developing fetal heart is vulnerable to chronic hypoxia and nutrient deprivation, potentially inducing structural and functional alterations with lifelong consequences. This narrative review summarizes and critically appraises experimental and clinical evidence on the impact of FGR on myocardial development and cardiovascular health from fetal life to adulthood. Methods: We conducted a narrative review using a structured literature search of studies published in the last 15 years in PubMed and Scopus, focusing on experimental, imaging, and epidemiological research evaluating cardiac structure, function, and long-term cardiovascular outcomes in FGR. Evidence from fetal and neonatal echocardiography, including Doppler and speckle-tracking techniques, as well as molecular and histological studies, was examined. No statistical meta-analysis was performed. Results: FGR has been associated with reduced cardiomyocyte number, altered myocardial architecture, increased interstitial fibrosis, and persistent ventricular remodeling. Functional studies suggest early impairments in systolic and diastolic performance, with alterations in cardiac energy metabolism and epigenetic regulation. Advanced imaging may enable detection of subclinical cardiac dysfunction in utero and early postnatally. Epidemiological data suggest an increased risk of hypertension, ischemic heart disease, heart failure, and metabolic disorders in adulthood among individuals born growth-restricted. Conclusions: FGR represents an early cardiovascular risk condition. Improved understanding of fetal cardiac programming may help refine risk stratification, surveillance, and preventive strategies to reduce long-term cardiovascular morbidity in individuals born growth-restricted.
The Impact of Fetal Growth Restriction on Myocardial Development from Fetal Life to Early Childhood: A Narrative Review
Calcaterra, Valeria;
2026-01-01
Abstract
Highlights: What are the main findings? Fetal growth restriction (FGR) induces early and persistent myocardial remodeling, including reduced cardiomyocyte number, fibrosis, altered ventricular geometry, and subclinical systolic–diastolic dysfunction detectable from fetal life. These cardiac and vascular changes can be identified with advanced fetal and neonatal imaging and are associated with increased cardiovascular and metabolic risk from childhood to adulthood. What are the implications of the main findings? FGR should be considered an early-life cardiovascular risk condition, requiring a life-course perspective that integrates obstetric, neonatal, and cardiology follow-up. Early identification of high-risk fetuses and infants may enable targeted surveillance and preventive strategies to reduce long-term cardiovascular morbidity. Background/Objectives: Fetal growth restriction (FGR), historically termed intrauterine growth restriction (IUGR), is a multifactorial condition in which the fetus fails to reach its genetically determined growth potential, most often due to placental insufficiency. Beyond its link with increased perinatal morbidity and mortality, FGR has been associated with long-term cardiovascular risk through early-life programming. The developing fetal heart is vulnerable to chronic hypoxia and nutrient deprivation, potentially inducing structural and functional alterations with lifelong consequences. This narrative review summarizes and critically appraises experimental and clinical evidence on the impact of FGR on myocardial development and cardiovascular health from fetal life to adulthood. Methods: We conducted a narrative review using a structured literature search of studies published in the last 15 years in PubMed and Scopus, focusing on experimental, imaging, and epidemiological research evaluating cardiac structure, function, and long-term cardiovascular outcomes in FGR. Evidence from fetal and neonatal echocardiography, including Doppler and speckle-tracking techniques, as well as molecular and histological studies, was examined. No statistical meta-analysis was performed. Results: FGR has been associated with reduced cardiomyocyte number, altered myocardial architecture, increased interstitial fibrosis, and persistent ventricular remodeling. Functional studies suggest early impairments in systolic and diastolic performance, with alterations in cardiac energy metabolism and epigenetic regulation. Advanced imaging may enable detection of subclinical cardiac dysfunction in utero and early postnatally. Epidemiological data suggest an increased risk of hypertension, ischemic heart disease, heart failure, and metabolic disorders in adulthood among individuals born growth-restricted. Conclusions: FGR represents an early cardiovascular risk condition. Improved understanding of fetal cardiac programming may help refine risk stratification, surveillance, and preventive strategies to reduce long-term cardiovascular morbidity in individuals born growth-restricted.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
