What is the role of medications in the treatment of pediatric atrial flutter?

Updated: Feb 04, 2019
  • Author: M Silvana Horenstein, MD; Chief Editor: Syamasundar Rao Patnana, MD  more...
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Drug therapy of atrial flutter in children can be classified under the 3 broad headings of ventricular rate control, acute conversion, and chronic suppression.

Digoxin is relatively safe for preventing rapid conduction of atrial flutter via the atrioventricular (AV) node to the ventricles, and some evidence indicates that this reduces symptomatology during flutter. Nevertheless, digoxin is unlikely to be particularly effective in the acute conversion or prevention of atrial flutter recurrence. It is devoid of negative inotropic effects (as is amiodarone) and is useful to control ventricular rate when using propafenone, flecainide, or procainamide.

Intravenous procainamide has been used with variable success to effect acute conversion of atrial flutter to sinus rhythm. Procainamide infusion should be preceded by digitalization to prevent procainamide-induced acceleration of AV node conduction to the ventricles.

The Vaughan Williams class III agents ibutilide and dofetilide may be used for acute conversion of atrial flutter and fibrillation. Both are more effective than other medications in converting atrial flutter, but their use is associated with QT prolongation with a nontrivial risk of induction of torsade de pointes polymorphic ventricular tachycardia. Clinical experience in adults is limited, and efficacy, dosing, and safety in children have not been established.

A relatively more recent drug, dronedarone, a less-lipophilic amiodarone analog, has been shown to prevent recurrence of atrial flutter and atrial fibrillation in adult patients, according to several multicenter trials. However, it increases mortality in patients with decompensated heart failure and therefore should be avoided in such cases. [21] Safety and efficacy of this drug have not been confirmed in patients younger than 18 years.

Fetal atrial flutter is the second most common intrauterine tachyarrhythmia. Treatment is aimed at controlling ventricular rate and, thus, avoiding hydrops fetalis. First-line treatment is digoxin administered to the mother, which provides a conversion rate to sinus rhythm of 45-52%. In addition, its positive inotropic effect may be beneficial. More recently, a retrospective study involving data from 21 fetuses with supraventricular tachycardia and 2 cases of atrial flutter suggests that flecainide may be effective and safe as first-line therapy for fetal supraventricular tachycardia. [22]  Of 17 fetuses treated with flecainide monotherapy, 15 converted to sinus rhythm while 2 were refractory.

Sotalol has also been used in numerous cases with success,  including children with incessant tachyarrhythmias. [23]  Maternal drug levels were not reliable predictors of successful therapy. [24, 25] Flecainide alone or in combination with digoxin is used as second-line treatment, although one study suggests that flecainide may be an effective first-line therapy for fetal supraventricular tachycardia. [26]  Fetal atrial flutter in a structurally normal heart seldom recurs after conversion before or after birth, and postnatal suppressive antiarrhythmic therapy may not be necessary.

Flutter in patients with repaired or palliated structural congenital lesions is more likely to recur, and long-term antiarrhythmic therapy aimed at flutter suppression is often instituted after the first or the second flutter episode.

Vaughan Williams class IC (eg, flecainide, propafenone) or class III (eg, sotalol, amiodarone) agents have been prescribed with variable success. Some authors have cautioned against use of flecainide in this setting, but the data are equivocal. Combinations of agents occasionally succeed after failure of single-agent therapy.

Use of antiarrhythmic agents other than digoxin for the long-term suppression of atrial flutter in sinus node disease (a frequent coexisting finding) is particularly controversial. In patients with atrial flutter who have had the Mustard procedure, treatment with quinidine was associated with case reports of sudden death. This resulted in the recommendation of antibradycardia pacing initiation before antiarrhythmic drug therapy in these patients. This recommendation has gradually broadened to encompass other antiarrhythmic agents in patients with other types of repaired congenital heart disease.

Diltiazem can provide rapid, consistent, and safe temporary ventricular rate control in children.

Antibradycardia pacing may be directly advantageous in flutter suppression by reducing the frequency of flutter-inducing pauses and premature beats. It also provides a safety factor for more aggressive antiflutter drug therapy.

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