Purpose of Study Recent studies have demonstrated that in utero congenital heart disease (CHD) significantly alters the normal growth and development of the fetus. Newly published data demonstrate significant hemodynamic decreases in cardiac output, stroke volume, and ejection fraction in the fetus with CHD; however, the mechanisms by which these changes occur remain unclear. The purpose of this study was to determine the mechanisms of altered in utero hemodynamics by comparing the ventricular ejection dynamics in fetuses with CHD with normal fetuses.
Methods Used A total of 162 fetal echocardiograms were retrospectively examined. Eighty-seven were fetuses with in utero diagnosed CHD and 75 were gestational age matched normal fetuses. The gestational age range was 20 to 37 weeks. Doppler echocardiographic velocity-time plots of the aorta and pulmonary artery were digitized and coupled with 2-dimensional echocardiographic vessel diameter measurements. Measures of ejection dynamics were then derived from the time series data, including stroke volume, cardiac output, ejection time, acceleration time, mean acceleration and net developed force.
Summary of Results Compared to gestational age matched normal fetuses, the CHD fetuses demonstrated a decrease in the net force developed (1.255 ± 0.694, p < .03), prolonged acceleration times (0.243 ± 0.075, p < .002) in the pulmonary artery (0.281 ± 0.075, p < .004) in the aorta), and normal ejection times (0.183 vs. 0.185).
Conclusions Normal ejection times suggest that afterload is not a critical determinate in the observed decreases in cardiac output, stroke volume, and ejection fraction in the fetuses with CHD. The decrease in the net developed force and prolonged acceleration times suggests decreased myocardial function as the major cause of the altered in utero hemodynamics in this population.