Fetal tachyarrhythmias are an important cause of fetal morbidity and mortality. The majority of fetal tachyarrhythmias are due to atrioventricular reentrant type of supraventricular tachycardia and atrial flutter. Fetal echocardiography remains the main toot of diagnosing and discerning the mechanism of tachyarrhythmia. The goals of therapy for fetal arrhythmias are to restore sinus rhythm, resolve heart failure, and postpone delivery before term. Although there is no anonymity in the approach to the drug treatment of fetal tachycardia, digoxin is the most commonly employed first-line antiarrhythmic drug for supraventricular tachycardia. In digoxin nonresponders, flecainide (± digoxin) controls tachyarrhythmia with high conversion rate. A combination of digoxin and sotalol has proved effective therapy for atrial flutter, but the proarrhythmic side effect of sotalol on the fetus has been a concern. Amiodarone has emerged as a second-line treatment after digoxin failure in nonhydropic fetuses and the most effective treatment for drug-refractory fetal tachycardia accompanied by hydrops. Both the fetus and mother should be closely monitored for the response and adverse effect of the treatment. The antiarrhythmic treatment for supraventricular tachycardia should be continued after birth and during infancy due to the high incidence of postnatal recurrence.
|Number of pages||8|
|Journal||Current Treatment Options in Cardiovascular Medicine|
|State||Published - Oct 2004|