James C Huhta1, Kersti Linask. 1. aPerinatal Cardiology, All Children's Hospital, John Hopkins Medicine, Baltimore, Maryland bDepartment of Pediatrics, USF School of Medicine, Tampa, Florida, USA.
Abstract
PURPOSE OF REVIEW: Provide a rationale for attempting prevention of congenital heart defects (CHDs). RECENT FINDINGS: Prevention of neural-tube defects can be achieved with preconceptional use of folic acid. Extrapolating results from animal studies to human pregnancy shows that folate deficiency as well as one-time exposure to environmental factors in the first 2 to 3 weeks of human gestation can result in severe CHD. Considering that approximately 50% of pregnancies are unplanned, this period of pregnancy can be considered high risk for cardiac, as well as neural, birth defects, as the woman usually is not aware of her pregnancy and may not yet be taking precautionary actions to protect the developing embryo. In mammals, folate supplementation prevents CHD induced by alcohol, by lithium, or by elevation of the metabolite homocysteine. Optimal protection of cardiogenesis was observed to occur with folate supplementation provided on the morning after conception and at higher doses than currently available in prenatal vitamin supplementation. Clinical studies show a similar pattern with high doses of folic acid required to prevent CHD. SUMMARY: Today, all patients with a family history of CHD should discuss the prenatal use of folate supplementation with their obstetricians prior to becoming pregnant.
PURPOSE OF REVIEW: Provide a rationale for attempting prevention of congenital heart defects (CHDs). RECENT FINDINGS: Prevention of neural-tube defects can be achieved with preconceptional use of folic acid. Extrapolating results from animal studies to human pregnancy shows that folatedeficiency as well as one-time exposure to environmental factors in the first 2 to 3 weeks of human gestation can result in severe CHD. Considering that approximately 50% of pregnancies are unplanned, this period of pregnancy can be considered high risk for cardiac, as well as neural, birth defects, as the woman usually is not aware of her pregnancy and may not yet be taking precautionary actions to protect the developing embryo. In mammals, folate supplementation prevents CHD induced by alcohol, by lithium, or by elevation of the metabolite homocysteine. Optimal protection of cardiogenesis was observed to occur with folate supplementation provided on the morning after conception and at higher doses than currently available in prenatal vitamin supplementation. Clinical studies show a similar pattern with high doses of folic acid required to prevent CHD. SUMMARY: Today, all patients with a family history of CHD should discuss the prenatal use of folate supplementation with their obstetricians prior to becoming pregnant.
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