Journal
AMERICAN JOURNAL OF OBSTETRICS AND GYNECOLOGY
Volume 218, Issue 2, Pages S869-S879Publisher
MOSBY-ELSEVIER
DOI: 10.1016/j.ajog.2017.12.012
Keywords
cardiovascular disease; echocardiography; epigenetics; fetal growth restriction and fetal programming
Categories
Funding
- Instituto de Salud Carlos III integrados en el Plan Nacional de I+D+I [PI14/00226, PI15/00130, INT16/00168]
- por el ISCIII-Subdireccion General de Evaluacion y el Fondo Europeo de Desarrollo Regional (FEDER)
- AGAUR 2014 SGR grant [928]
- la Caixa Foundation (Spain)
- Cerebra Foundation for the Brain Injured Child (Carmarthen, Wales, UK)
- European Union [2013-0040]
- predoctoral governmental Bolivar Gana con Ciencia grant from Colombia
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In the modern world, cardiovascular disease is a leading cause of death for both men and women. Epidemiologic studies consistently have suggested an association between low birthweight and/or fetal growth restriction and increased rate of cardiovascular mortality in adulthood. Furthermore, experimental and clinical studies have demonstrated that sustained nutrient and oxygen restriction that are associated with fetal growth restriction activate adaptive cardiovascular changes that might explain this association. Fetal growth restriction results in metabolic programming that may increase the risk of metabolic syndrome and, consequently, of cardiovascular morbidity in the adult. In addition, fetal growth restriction is strongly associated with fetal cardiac and arterial remodeling and a subclinical state of cardiovascular dysfunction. The cardiovascular effects ocurring in fetal life, includes cardiac morphology changes, subclinical myocardial dysfunction, arterial remodeling, and impaired endothelial function, persist into childhood and adolescence. Importantly, these changes have been described in all clinical presentations of fetal growth restriction, from severe early- to milder late-onset forms. In this review we summarize the current evidence on the cardiovascular effects of fetal growth restriction, from subcellular to organ structure and function as well as from fetal to early postnatal life. Future research needs to elucidate whether and how early life cardiovascular remodeling persists into adulthood and determines the increased cardiovascular mortality rate described in epidemiologic studies.
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