Catheter Ablation in Neonate with Heart Failure Due to Incessant Atrioventricular Reentrant Tachycardia

Abstract The atrioventricular (AV) reentrant tachycardia (AVRT) is the most common cause of supraventricular tachycardia (SVT) in the young pediatric population. Some newborns might present with congestive heart failure and require interventional treatment. Catheter ablation in small infants (<6 months and <5 kg) is still poorly performed and controversial due to high complications rate in this group of patients.1 We report a case of a 28 days old infant (3,5 kg) with a drug-refractory left accessory pathway mediated tachycardia and severe hemodynamic compromise, who underwent catheter ablation. Radiofrequency ablation should be part of the therapeutic arsenal in a context of drug-resistant supraventricular tachycardia with hemodynamic compromise, despite the greater risks of complications in this special population.

Comparison of electrophysiologic effects and efficacy of single-dose intravenous and long-term oral amiodarone therapy in patients with AV nodal reentrant tachycardia.

Electrophysiologic effects and the efficacy of single-dose intravenous (i.v.) amiodarone were compared with those of long-term oral therapy in 9 patients of AV nodal reentrant tachycardia (AVNRT) utilising slow pathway (SP) for anterograde and fast pathway (FP) for retrograde conduction. Electrophysiologic data were obtained by programmed electrical stimulation (PES) before, 15 to 30 minutes after i.v. amiodarone (5 mg/kg body-weight over 10 minutes) and a mean of 64.6 +/- 23.7 days after oral therapy, on a maintenance dose of 200 to 400 mg daily. There was no significant influence on the sinus cycle length and infranodal conduction (HV) by i.v. or oral amiodarone as compared to pre-drug values. AV nodal conduction, evaluated by AH interval, increased significantly and comparably with both (8% after i.v., 10% after oral; p = NS). Anterograde conduction through SP, as evidenced by pacing cycle length producing AH block, was prolonged by both (31% after i.v., 52% after oral; p = NS). Oral amiodarone, however, was more effective than i.v. in lengthening the effective refractory period (ERP) of anterograde FP (45% vs 17%, p < 0.05). Although both depressed retrograde conduction significantly, long-term oral amiodarone was more effective in prolonging the paced cycle length (PCL) producing ventriculoatrial (VA) block (79% vs 50%; p < 0.05) and ERP of VA conduction system (72% vs 42%; p < 0.01). AVNRT was successfully terminated in 7 patients after i.v. amiodarone. However, tachycardia was reinducible in 3 patients after i.v. and in none after long-term oral therapy. None had clinical recurrence of tachycardia on maintenance oral therapy. The mean concentration of the drug was 3.1 +/- 1.81 micrograms/ml after i.v. and 1.3 +/- 0.47 micrograms/ml after oral therapy (p < 0.05). These results. suggest that i.v. amiodarone terminated AVNRT by depressing both anterograde and retrograde limbs of the reentrant circuit and eventually blocking one of these. Oral therapy prevented recurrence and reinducibility by its predominant effect in prolonging refractoriness of the atrium and ventricle, and depressing conduction through the retrograde FP. It is concluded that i.v. amiodarone is an effective drug in acute termination of tachycardia mediated by AV nodal reentry and that long-term oral therapy is excellent in preventing recurrence and reinducibility of tachycardia. There are significant differences in the electrophysiologic properties and mechanism of action between the two forms, not influenced by the blood levels of amiodarone.