Discussion
Fetal heart rate monitoring remains an important part of antenatal care, and as seen in our case, the tachycardia was first detected by routine fetal heart rate check.5 Fetal AF accounts for roughly 25-30 of all fetal tachyarrhythmias and is associated with variable AV conduction. There are congenital structural anomalies that may occur with AF including hypoplastic left heart syndrome, atrioventricular septal defect, pulmonary atresia and Ebstein’s anomaly. Both SVT and fetal AF have similar incidence of hydrops fetalis averaging 40% and similar mortality rate of 10%. Studies have shown that hydropic foetuses with fetal AF have higher ventricular rates than the non-hydropic ones, but no difference in the atrial rates.6
Most cases of fetal AF occur in the third trimester as seen in our case, with the median age presentation of 32 weeks. The ventricles are protected during fetal AF by the AV node which is not part of the intra-atrial re-entrant circuit. This is achieved by variably blocking the AV conduction, with 2:1 AV block present in over 80% of patients with fetal AF.4,7 This finding is in keeping with our patient who had 2:1 block. Fetal AF could easily be diagnosed by clinicians using the M-mode ultrasound with the apical four-chamber heart view. Both the atria and ventricles should be clearly identified in relation to the spine and descending aorta as landmarks. The focus should not be to get the ventricular rate only in fetal tachyarrhythmia using the power Doppler button. With the M-mode across both either atrium or ventricle, their respective rates could be measured and the variable conduction pattern also. It is very important to make the right diagnosis before proceeding to treatment especially in low resource setting or general hospitals without paediatric cardiologist services. In our case, the initial diagnosis was thought to be fetal SVT before the patient was referred. This is because no simultaneous atrial reading was taken. This is one of the major reasons of writing this report for educational purposes. Secondly, it is known that up to 20% of fetal tachyarrhythmia is associated with cardiac anomaly, hence the need to perform fetal echocardiography before deciding on management option.3,8 This informs the need of multidisciplinary team management with neonatologists, paediatric cardiologist, and obstetricians. At term pregnancies, the babies should not just be delivered based on fetal distress without these considerations as the outcomes may be untoward. This is well exemplified in this case.
Based on the points highlighted above, the antenatal management of fetal AF depends on several factors including fetal gestational age, presence of fetal hydrops or features of heart failure, and associated structural heart disease. The risk of hydrops in fetal AF is said to be more with a ventricular rate of over 210 bpm. There was no hydrops in our case even though the ventricular heart rate was 260 bpm.6 The development of associated cardiac anomaly is associated with poorer neonatal outcome, hence the advantage of early detection and treatment. Although prenatal treatment of fetal AF with transplacental antiarrhythmic medications is the most common documented method of treatment, this is not always the case.9 At term or late preterm gestation, delivery of the foetus with postnatal treatment is often considered as a better choice.3,10 This obviates the adverse effects of the medication on the mother and the risk of transplacental treatment on the foetus. This explains the basis of our postnatal treatment modality.
The commonly used antiarrhythmic drugs include digoxin as first choice and sotalol, flecainide, amiodarone, verapamil, procainamide as second choice.2,11 Studies show that there is a significantly better response to sinus rhythm prenatally when digoxin is used in non-hydropic foetuses (80%), compared with 43% in hydropic foetuses.8,12
It is important to remember that spontaneous conversion to sinus rhythm does happen in fetal AF postnatally, although this was not observed in our case.13 The ECG done postnatally confirmed the neonate was still in AF (Figure 1), hence the use of synchronised cardioversion which successfully resulted in sinus rhythm (Figure 2). Digoxin was continued as an antiarrhythmic prophylaxis. After sinus rhythm is achieved postnatally, one may monitor to see if there is recurrence with AF before instituting prophylaxis, or electively treat for 6 months to 1 year.10 However, the risk of AF recurrence is very rare beyond the neonatal period. In our case, digoxin was given for the first 28 days and to be continued for the first 6 months at least with follow up.