Can We Do a Prospective Trial for Fetal Tachycardia?

Abstract

Jaeggi and colleagues1 have added to the literature with their extensive assessment of 159 fetal tachyarrhythmia cases collected from 3 institutions over a 10-year period. However, before we comment on their study, it is worth reviewing some of the relevant issues for management of fetal arrhythmias. An estimated 0.4% to 0.6% of pregnancies have a fetal arrhythmia at some point during the pregnancy.2,3 Although the vast majority are not of clinical significance and require no treatment, a much smaller percentage have a sustained tachyarrhythmia that can be life-threatening to the fetus. The most frequent serious arrhythmias in the fetus are supraventricular, most commonly from atrioventricular reentry tachycardia involving an accessory atrioventricular connection (supraventricular tachycardia [SVT]) or atrial flutter, but occasionally from atrioventricular node reentry (also SVT) or ectopic atrial tachycardia.2,3 Here, we refer to all these mechanisms together as supraventricular a rrhythmias (SVAs) and the subgroups of interest as SVT or atrial flutter. Importantly, SVAs can lead to tachycardia-induced cardiomyopathy because of prolonged decreased cardiac output and myocardial fatigue, which can lead to hydrops fetalis and rare fetal death,2,3 as reviewed by Jaeggi et al.1 Treatment options include careful observation, maternal drug therapy, or delivery of the fetus. Article see p 1747 More than 20 studies have looked at outcomes of drug therapy for fetal SVA, some of which are reviewed by Jaeggi et al.1 The most commonly used antiarrhythmics are digoxin, flecainide, sotalol, and amiodarone, but many drugs have been used less frequently, and results vary widely. In the studies using digoxin as first-line therapy, successful conversion has been reported in 50% to 100% of fetuses without hydrops, but only 0% to 20% of patients with hydrops.4–9 Flecainide has resulted in sinus rhythm in …