Key result
Fetal isovolumetric contraction time remained normal (30 ms) during fetal supraventricular tachycardia (200 bpm), indicating ICT is constant during tachycardia if cardiac function is maintained.
Case Report (n=1)
No
Fetal isovolumetric contraction time remains constant during supraventricular tachycardia if cardiac function is maintained, and its subsequent prolongation may signal deteriorating fetal condition.
May flag fetal decompensation if ICT prolongs in SVT; single-case data leaves open prospective validation.
We report the measurement of the isovolumetric contraction time in a fetus (fetal ICT) presenting with supraventricular tachycardia (SVT) at 37 weeks' gestation. A 44-year-old woman was referred to our hospital because of fetal tachyarrhythmia. Her family and own history were unremarkable and her previous six pregnancies had been uneventful. On ultrasound, the estimated fetal birth weight was 2310 g and the amniotic fluid index was 11.5 cm. The umbilical artery Doppler flow study showed an S/D ratio of 2.6. The fetal heart rate (FHR) was 205 bpm (Figure 1a) and this was shown to be an SVT by M-mode echocardiography. No hydropic change was noted in the fetus, indicating adequate cardiac function. The fetal ICT was measured using a continuous Doppler device (FD-390, Toitu, Tokyo, Japan), as previously reported1-3, with a B-mode ultrasound system (SonoSite 180PLUS; SonoSite, Tokyo, Japan) to ensure the correct alignment to record a Doppler signal from the mitral and aortic valves. While the FHR was 200 bpm, the fetal ICT was 30 ms (an average of three measurements; normal mean ± SD, 29 ± 2.49 ms) (Figure 2). At 37 weeks, the mother was prescribed oral digoxin (250 µg three times a day) to correct the fetal arrhythmia before delivery, and the FHR returned to normal 5 days later. The maternal digoxin level was monitored from 37 + 3 weeks onwards and remained mostly in the maternal therapeutic range until delivery (Figure 2). The fetal ICT was also monitored, and increased progressively from 23.5 at 37 + 5 weeks to 36 ms prior to delivery (Figure 2). Labor was induced at 39 weeks because of a lack of fetal growth on ultrasound. The appearance of late decelerations on the cardiotocogram (CTG) in labor (Figure 1b), at a cervical dilatation of 2 cm, prompted emergency Cesarean section. A 2500-g male was delivered, with Apgar scores of 9 and 9 at 1 and 5 min, respectively. The baby continued to do well in the first neonatal week. Cardiotocographic (CTG) findings of this case. (a) CTG at 37 + 3 weeks' gestation; the baseline fetal heart rate (FHR) was 205 bpm. (b) CTG at induction of labor at 39 + 0 weeks; the baseline FHR was 125 bpm and late decelerations were noted after uterine contractions. Sequential changes in fetal isovolumetric contraction time (ICT) (a) and heart rate (b), and maternal serum digoxin level (c). At 37 + 4 weeks' gestation, the fetal ICT and heart rate at the time of ICT measurement were 30 ms and 200 bpm, respectively. Fetal ICT was shortened to 24 ms after correction of the tachyarrhythmia, and then gradually lengthened to 36 ms (a). FHR returned to 134 bpm 5 days after maternal digoxin administration (b). Maternal serum digoxin levels are plotted with the adult therapeutic range shown for reference (1.0–2.6 mmol/L) (c). The ICT, which is the time interval between the onset of ventricular contraction and cardiac ejection, has been established as an index of cardiac contractility. We have reported previously that the Doppler cardiac signal can be used to measure the fetal ICT non-invasively in human fetuses, by using frequency filters1-3. We have validated this measure in fetal lambs, showing that our Doppler system measures the same time period as that measured by invasive procedures to record atrioventricular closure and aortic opening3. The fetal ICT of 30 ms, measured when the FHR was 200 bpm in this case, was within our previously reported normal range2. The presence of an SVT may be associated with a new pacemaker rather than the S-A node. Although in this case the electrical pathway in the heart is different, the mechanical interval, i.e. the ICT, should not be altered significantly. In addition, the fetal ICT is independent of gestational age2. The result from our present case indicates that even if a tachycardia exists, the fetal ICT will show normal values as long as the fetal cardiac contractility is normal. While this result may be predicted, it has not been demonstrated previously in the human fetus. In adults, Ferro et al.4 concluded that the ICT did not change when tachycardia was present. Our case agrees with this result. We have already shown in normal fetuses that the ICT is independent of FHR when FHR is normal (120–160 bpm)2. Based on the result of this case, it also appears that the fetal ICT is constant in the presence of fetal tachycardia, as long as fetal cardiac function is maintained. We have reported previously that prolonged fetal ICT is associated with fetal complications, such as severe intrauterine growth restriction, abnormal CTG and/or the brain-sparing effect2. In our present case, a gradual prolongation of the fetal ICT occurred after correction of the tachyarrhythmia. Based on the fact that the fetus was small and operative delivery by Cesarean for a non-reassuring FHR (late decelerations) was needed, this prolongation of the fetal ICT might be associated with deteriorating fetal condition. Y. Fujita*, B.
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Fujita et al. (2006) conducted a case report in Fetal supraventricular tachycardia (n=1). Fetal tachycardia was evaluated on Fetal isovolumetric contraction time (ICT). Fetal isovolumetric contraction time remained normal (30 ms) during fetal supraventricular tachycardia (200 bpm), indicating ICT is constant during tachycardia if cardiac function is maintained.
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