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Objectives This study aimed to evaluate the impact, safety, and success of atrial fibrillation (AF) ablation in adults with congenital heart disease (ACHD) transferring ablation strategies established in normal hearts. Background AF is an emerging arrhythmia in ACHD. Methods Fifty-seven consecutive ACHD (median age 51.1 ± 14.8 years) with drug-refractory AF were analyzed who underwent catheter ablation between 2004 and 2017. CHD was classified according to its complexity into mild (61.4%), moderate (17.5%), and severe (21.1%) lesions. AF ablation was performed in 104 procedures following a sequential ablation approach. Results Of the 57 patients, 30 underwent corrective surgery, 6 underwent palliative surgery, 5 had catheter interventions, and 16 were natural survivors. Follow-up was available for all patients (median 41 ± 36 months). The median duration of cyanosis was 9.2 ± 19.7 years, and the time of volume or pressure overload prior to corrective surgery or intervention was 26.1 ± 21.2 years and 18.1 ± 15.8 years, respectively. The Kaplan-Meier estimate for arrhythmia-free survival following the index ablation procedure was 63% for 1 year and 22% for 5 years. Performing subsequent ablation procedures (2.0 ± 0.5), the Kaplan-Meier estimate significantly improved, with 99% for 1 year and 83% for 5 years (p Conclusions AF ablation strategies established in normal hearts can be transferred to ACHD. The treatment is safe and effective with acceptable long-term results. Varying anatomical pre-conditions and the heterogeneous population itself are challenging and contribute toward a higher reablation rate. Therefore, AF ablation in ACHD should be reserved for dedicated and highly specialized teams.

This study aimed to evaluate the impact, safety, and success of atrial fibrillation (AF) ablation in adults with congenital heart disease (ACHD) transferring ablation strategies established in normal hearts.AF is an emerging arrhythmia in ACHD.Fifty-seven consecutive ACHD (median age 51.1 ± 14.8 years) with drug-refractory AF were analyzed who underwent catheter ablation between 2004 and 2017. CHD was classified according to its complexity into mild (61.4%), moderate (17.5%), and severe (21.1%) lesions. AF ablation was performed in 104 procedures following a sequential ablation approach.Of the 57 patients, 30 underwent corrective surgery, 6 underwent palliative surgery, 5 had catheter interventions, and 16 were natural survivors. Follow-up was available for all patients (median 41 ± 36 months). The median duration of cyanosis was 9.2 ± 19.7 years, and the time of volume or pressure overload prior to corrective surgery or intervention was 26.1 ± 21.2 years and 18.1 ± 15.8 years, respectively. The Kaplan-Meier estimate for arrhythmia-free survival following the index ablation procedure was 63% for 1 year and 22% for 5 years. Performing subsequent ablation procedures (2.0 ± 0.5), the Kaplan-Meier estimate significantly improved, with 99% for 1 year and 83% for 5 years (p 0.01). Five patients died during follow-up due to their underlying CHD condition or underwent transplantation.AF ablation strategies established in normal hearts can be transferred to ACHD. The treatment is safe and effective with acceptable long-term results. Varying anatomical pre-conditions and the heterogeneous population itself are challenging and contribute toward a higher reablation rate. Therefore, AF ablation in ACHD should be reserved for dedicated and highly specialized teams.

For treatment of chronic atrial and junctional ectopic tachycardia, standard antiarrhythmic therapy has been shown to be ineffective in most patients. Both the intravenous efficacy and the oral efficacy of 2 class IC antiarrhythmic drugs, encainide and flecainide, were studied in 16 patients with atrial ectopic tachycardia and in 3 patients with junctional ectopic tachycardia, using exercise testing, 24-hour long-term electrocardiography and programmed electrical stimulation. All patients had been previously treated unsuccessfully with several antiarrhythmic drugs. In 5 patients, tachycardia was persistent; in the remaining patients, it occurred intermittently for more than 12 hours/day. Intravenous encainide, in doses ranging from 0.3 to 2.0 mg/kg body weight, was given to 5 patients with atrial ectopic tachycardia, and it terminated atrial ectopic tachycardia in all patients. Intravenous flecainide was given to 9 patients, and it terminated atrial tachycardia in 4 and slowed the tachycardia rate in 2. It terminated junctional tachycardia in 2 patients and slowed tachycardia rate in 1. During a follow-up period of 10 +/- 5 months, oral encainide, in dosages between 150 and 225 mg/day, completely suppressed atrial ectopic activity in 4 patients. In the remaining patient, encainide reduced the number of tachycardia episodes markedly but had to be withdrawn because of intolerable side effects. During a 12 +/- 11-month (median 6) follow-up, oral flecainide at dosages between 200 and 300 mg/day, completely suppressed ectopic activity in 7 patients and improved symptoms in 5. Only 1 patient failed to respond to oral flecainide. The results of this study indicate that both encainide and flecainide are effective in the treatment of chronic ectopic atrial and junctional tachycardia.