Childhood cardiac function after severe maternal red cell isoimmunization

To estimate the long-term effects of anemia on the fetal heart by echocardiography of children who received intrauterine blood transfusions for red cell isoimmunization.

Surviving children who received intrauterine transfusions during the period from 1992 to 2003 were identified. Children matched for age and sex were chosen for the control group to create a 1:1 case-control study design. A clinical interview, physical examination, and echocardiography assessment (corrected for body surface area) were performed.

Twenty-five children were recruited for the case group and matched to 25 healthy children for the control group. Children in the case group had received a median of four intrauterine transfusion procedures (range 1-7), with a median gestation at initial intrauterine transfusion of 28 weeks (range 22-34 weeks). Hydrops was present in 32%. Median initial hemoglobin was 76 g/L (range 25-133 g/L). Median gestation at delivery was 36 weeks (range 29-38 weeks). The median age of children in the case group was 10.1 years (range 3.6-15.8 years) and of those in the control group was 10.5 years (range 3.8-16.4 years; P=.122). There was no difference in body surface area, baseline heart rate, systolic blood pressure, or diastolic blood pressure between children in the case group and those in the control group. Echocardiography demonstrated three main differences: children in the case group had 9% less left atrial area (95% confidence interval [CI] 2-16% less; P=.02), 10% less ventricular mass (95% CI 1-19% less; P=.039), and an average 11 ms less mitral valve atrial duration (95% CI 3-19 ms less; P=.009) than did those in the control group. These results did not alter when adjusted for isoimmunization severity.

Fetal anemia secondary to red cell isoimmunization is associated with a reduction in left ventricular mass and left atrial area in childhood, although resting ventricular function is maintained. We speculate this may be secondary to the prenatal effects of anemia on cardiomyocyte proliferation and differentiation.

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