Transplacental metoprolol for fetal supraventricular tachycardia.

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We report the successful use of metoprolol in two fetuses with supraventricular tachycardia (SVT) that were refractory to flecainide monotherapy. The first fetus was diagnosed at 20 weeks' gestation with persistent SVT and hydrops (heart rate of 250–280 bpm, 1:1 atrioventricular conduction, short ventriculoatrial time interval). Oral flecainide (100 mg four times/day) led to resolution of hydrops, but treatment was complicated by high flecainide levels (> 820 µg/L) and PR-interval and QT-interval prolongation (200 ms and 460 ms, respectively). Lowering the flecainide dose led to recurrence of SVT and hydrops. Following multispecialist and patient discussions, oral metoprolol (50 mg three times/day) was added at 31 + 0 weeks' gestation. Within 2 days, the fetal heart rate was 202 bpm and hydrops resolved. Within 6 days, normal sinus rhythm (heart rate, 119 bpm) was restored (Figure 1). Maternal systolic blood pressure (BP) remained > 90 mmHg and no side effects were experienced. A healthy infant (birth weight, 2.9 kg) was delivered in sinus rhythm at 38 + 2 weeks' gestation. A brief period of atrioventricular re-entry tachycardia (AVRT) occurred after birth and there was intermittent pre-excitation (Wolff–Parkinson–White pattern). Cord-blood concentration of metoprolol was 0.16 mg/L (therapeutic range, 0.02–0.34 mg/L), confirming placental transfer. A second case of short ventriculoatrial SVT (heart rate, 230 bpm) in a non-hydropic fetus at 34 + 6 weeks' gestation was also treated with metoprolol (50 mg three times/day) following failure to convert to sinus rhythm after 5 days of flecainide therapy, despite maternal concentration > 700 µg/L. Conversion to sinus rhythm occurred within 3 days (heart rate, 123 bpm). Maternal systolic BP readings were > 95 mmHg. Fetal growth velocity was maintained and the baby was delivered in sinus rhythm at 37 + 5 weeks (birth weight, 3.0 kg). AVRT recurred in infancy. Uncontrolled fetal SVT with hydrops has a high mortality rate1, 2 and requires prompt and effective treatment. The choice of therapy depends on the type of arrhythmia, presence of hydrops and institutional experience2, 3. Some drugs, for example, digoxin, have poor placental transfer in the presence of hydrops, so flecainide or sotalol are used widely as the first-line therapy in hydropic fetuses2, 3. In refractory cases, additional or alternative antiarrhythmic agents are controversial because of the potential for drug interaction and maternal side effects. Flecainide, sotalol and amiodarone all prolong the QT interval, with a potential risk of maternal arrhythmia, and substituting a drug involves a period of treatment cessation which is challenging in hydropic fetuses in which there is an urgency to control the SVT. Postnatally, beta-blockers can be combined with flecainide to control SVT in neonates, but their use for fetal SVT has been reported in only one case4. The primary electrophysiological advantage of beta-blockers is the lack of pro-arrhythmogenic effect, which is in contrast with other antiarrhythmic agents used for fetal SVT. Metoprolol is a selective beta-1-adrenoreceptor antagonist which equilibrates across the placenta and could be considered5. There have been concerns regarding beta-blockers leading to fetal growth restriction; this is likely to be related to a reduction in maternal BP rather than a direct causal relationship and may be principally related to prolonged use of atenolol, rather than all beta-blockers. The safe use of beta-blockers is reflected in pregnancy guidelines which suggest their use to treat maternal SVT6 and hypertension in pregnancy7. Study of the utility and safety profile of metoprolol for fetal SVT is required if widespread use is to be considered. In conclusion, the judicious use of metoprolol for flecainide-resistant fetal SVT may be considered under cardiological supervision and with close monitoring of fetal growth and maternal BP.