Maternal homocysteine and congenital heart defects.

C S i o the Editor: An estimated 80% of congenital heart defects result rom an interaction between susceptibilities in parental and fetal enomes and environmental exposures including maternal lifestyle actors (1). We and others have recently reported that women who ave congenital heart defect-affected pregnancies have alterations n folate metabolism (2). This population-based case-control study as undertaken to determine whether these alterations are associted with specific cardiac phenotypes in their children. The study opulation, eligibility criteria, and methods have been previously ublished (2). Case women had delivered a live-born infant with a nonyndromic septal, conotruncal, or rightor left-sided obstrucive defect confirmed by echocardiogram, or surgical or autopsy eport reviewed by a pediatric cardiologist. Cases were classified nto five defect categories based on anatomical lesion: 1) conotrunal—including transposition of the great arteries, tetralogy of Fallot, runcus arteriosus, double outlet right ventricle, malaligned ventricular eptal defect, and interrupted aortic arch type B; 2) septal—including trial, ventricular, and atrioventricular septal defects; 3) right-sided bstructive—including pulmonary valve stenosis, and pulmonary and ricuspid atresia; 4) left-sided obstructive—including aortic valve tenosis, hypoplastic left heart syndrome and variants, coarctation, and nterrupted aortic arch types A and C lesions; and 5) complex ases—combination of three or more of the above cardiac defects.