Objective: To evaluate a management protocol of fetal supraventricular tachycardia (SVT) based on prior identification of the underlying mechanism. Design and setting: Prospective study in a mother-child tertiary university centre. Patients: During a consecutive 36 month period, 18 fetuses with sustained SVT underwent a superior vena cava/ascending aorta (SVC/AA) Doppler investigation in an attempt to determine the atrioventricular (AV) relation and to treat the arrhythmia according to a pre-established management protocol. Main outcome measure: Rate of conversion to sinus rhythm. Results: Seven fetuses had short ventriculoatrial tachycardia, five of these with a 1:1 AV conduction suggesting re-entrant tachycardia. The first choice drug was digoxin and all were converted. One fetus had AV dissociation leading to the diagnosis of junctional ectopic tachycardia, which was resistant to digoxin and sotalol; amiodarone achieved postnatal conversion. One fetus had SVT and first or second AV block; the diagnosis was atrial ectopic tachycardia (AET), which responded to sotalol given as a drug of first choice. Seven fetuses had long ventriculoatrial tachycardia: one with sinus tachycardia (no treatment), one with permanent junctional reciprocating tachycardia (PJRT), and three with AET. The first choice drug was sotalol and all were converted. One AET was classified postnatally as PJRT. Six fetuses had intra-atrial re-entrant tachycardia: five with 2:1 AV conduction and one with variable block. The first choice drug was digoxin. Conversion was achieved in all but one, who died after birth from advanced cardiomyopathy. Conclusion: The electrophysiological mechanisms of fetal SVT can be clarified with SVC/AA Doppler. The proposed management protocol has so far yielded a good rate of conversion to sinus rhythm.

Objective To study the impact of well-controlled, uncomplicated

Experimental studies in animals using Doppler ultrasound suggest that hemodynamic disturbances during fetoplacental circulatory insufficiency will be detected at an earlier and less severe stage in the aortic isthmus compared to the umbilical artery. In cases in which more severe impairment of the placental circulation was achieved, reverse flow was recorded in the aortic isthmus before its appearance in the umbilical artery. The present study was undertaken to investigate whether the same findings could be demonstrated in the aortic isthmus of the human fetus. The video recordings of 100 fetuses with abnormal umbilical artery pulsatility index were reviewed. Qualitative abnormalities of the Doppler waveform, i.e., absence or reversal of end-diastolic velocities, were more frequently found in the aortic isthmus (absent 28%, reversed 41%) compared to the fetal end of the umbilical artery (absent 20%, reversed 19%; p < 0.0001) and also more frequently found in the fetal end compared to the placental end (absent 13%, reversed 2%; p < 0.0001). This study confirms our previous observations of the aortic isthmus as a site for early detection of fetoplacental hemodynamic disturbances. Reverse diastolic flow in the isthmus could direct poorly oxygenated blood from the descending aorta towards the carotid arteries and the brain. Further prospective studies are needed to establish the clinical value of these findings in terms of perinatal morbidity and, more importantly, of long-term neurological impairment.

ABSTRACT