Cardiac changes in fetuses secondary to immune hemolytic anemia and their relation to hemoglobin and catecholamine concentrations in fetal blood.

OBJECTIVES: Immune hemolytic anemia in the fetus may cause cardiac decompensation and intrauterine death. Postnatally, norepinephrine (noradrenaline) is released in chronic heart failure, and may lead to myocardial hypertrophy. The aim of this study was to determine fetal cardiac changes associated with immune hemolytic anemia by means of echocardiography, and to relate them to fetal hemoglobin and norepinephrine levels.
DESIGN: Thirty anemic fetuses underwent a total of 76 umbilical venous transfusions. Before the procedure, fetal echocardiography was performed, and end-diastolic myocardial wall thicknesses and ventricular dimensions together with Doppler flow patterns at the atrioventricular and semilunar valves were measured. Fetal hemoglobin, epinephrine and norepinephrine concentrations were determined before the transfusion. Statistical analysis of this prospective study comprised descriptive statistics including linear regression and correlation analyses. Two samples of measurements were compared by the Mann-Whitney U test.
RESULTS: The mean hemoglobin concentration before the first transfusion was 6.9 g% at a mean gestational age of 26.8 weeks. Norepinephrine values were elevated in comparison to a reference range, and were higher than epinephrine values. The most striking echocardiographic finding was myocardial hypertrophy of all ventricular walls. Mean blood flow velocities were increased; at the left ventricle, they were negatively related to the hemoglobin concentrations, and positively to the norepinephrine values.
CONCLUSIONS: Fetal myocardial hypertrophy in anemia may be the result of an augmented cardiac workload, indicated by the increased left ventricular mean velocities. This reaction reflects the redistribution of blood flow that may depend on hemoglobin and norepinephrine concentrations.