Abstract
To assess the influence of isolated congenital heart disease (CHD) on fetal arterial Doppler blood flow velocity waveforms. Doppler flow velocimetry was performed in the umbilical artery and middle cerebral artery in 115 consecutive fetuses with antenatally diagnosed CHD. Gestational age ranged between 19 and 41 weeks. Fetuses with isolated CHD were defined as group A (n = 55), showing cardiogenic hydrops fetalis in six cases; group B included 60 cases complicated by chromosomal or non-chromosomal extracardiac malformation, uteroplacental dysfunction or non-cardiogenic non-immune hydrops fetalis. The control group comprised 100 healthy fetuses of uncomplicated pregnancies. Individual pulsatility index measurements were converted into their Z-scores (delta values) for statistical analysis. In regard to the umbilical artery pulsatility index, 115 fetuses with CHD showed a significantly greater (P < 0.001) difference from the normal mean for gestation (delta values) than the control group. However, 29 of the 33 cases with indices above the 95% reference interval were additionally associated with extracardiac malformations, uteroplacental dysfunction or non-cardiogenic non-immune hydrops fetalis. While fetuses with isolated CHD still showed significantly higher values than healthy fetuses (P < 0.01), only in 4 of 55 (7%) fetuses did the measured umbilical artery pulsatility index exceed the 95% reference interval. There was no significant difference from the control group, in which 4 of 100 cases showed an umbilical artery pulsatility index above the 95% reference interval. Elevated umbilical artery pulsatility indices were seen in only four cases of severe obstruction of the outflow tracts leading to reverse perfusion of the affected great artery and in one case of Ebstein's anomaly with pulmonary insufficiency. Although all four fetuses with isolated CHD and elevated umbilical artery pulsatility index died, 14 of 18 fetuses with lethal outcome had normal pulsatility index values in the umbilical artery. Investigations of the middle cerebral artery blood flow revealed no significant difference between fetuses with and without CHD or any subgroups. This study shows that arterial blood flow velocity waveforms in fetuses with isolated CHD do not show sufficient alterations to be of diagnostic value. Only in severe outflow tract obstructions due to a 'steal effect' or in significant insufficiencies of semilunar valves leading to an impaired 'wind-kessel function' may the special hemodynamic changes induced by CHD result in a significant increase of pulsatility index in the umbilical artery. In the majority of cases with CHD the increase of pulsatility index of umbilical arterial blood flow velocity waveforms, however, results from extracardiac anomalies, especially uteroplacental dysfunction and chromosomal abnormalities. Furthermore, umbilical artery Doppler sonography is not clinically helpful in predicting fetal outcome.
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