Radiofrequency catheter ablation of atrial arrhythmias. Results and mechanisms.

BACKGROUND: Radio frequency catheter ablation is accepted therapy for patients with paroxysmal supraventricular tachycardia and has a low rate of complications. For patients with atrial arrhythmias, catheter ablation of the His bundle has been an option when drugs fail or produce untoward side effects. Although preventing rapid ventricular response, this procedure requires a permanent pacemaker and does not restore the atrium to normal rhythm. Therefore, we evaluated the safety and efficacy of radiofrequency ablation directed at the atrial substrate.

METHODS AND RESULTS: Thirty-seven patients with 42 atrial arrhythmias (mean +/- SD age, 41 +/- 24 years) who had failed a median of three drugs were enrolled. Diagnoses were automatic atrial tachycardia in 12, atypical atrial flutter in 1, typical atrial flutter in 18, reentrant atrial tachycardia in 8, and sinus node reentry in 3 patients. Sites for atrial flutter ablation were based on anatomic barriers in the floor of the right atrium. For automatic atrial tachycardia, the site of earliest activation before the P wave was sought. All with reentrant atrial tachycardia had previous surgery for congenital heart disease and reentry around a surgical scar, anatomic defect, or atriotomy incision and our goal was to identify a site of early activation in a zone of slow conduction. At target sites, 20 to 50 W of radiofrequency energy was delivered during tachycardia between the 4- or 5-mm catheter tip and a skin patch, except in 4 patients with atrial flutter, in whom a catheter with a 10-mm thermistor-embedded tip was used. Procedure end point was inability to reinduce tachycardia. Acute success was achieved in 11 of 12 (92%) with automatic atrial tachycardia, 17 of 18 (94%) with typical atrial flutter, 7 of 8 (88%) with reentrant atrial tachycardia, and 3 of 3 (100%) with sinus node reentry but not in the patient with atypical atrial flutter. For tachycardia involving reentry (reentrant atrial tachycardia and atrial flutter), successful ablation required severing an isthmus of slow conduction. For those with atrial flutter, this was between the tricuspid annulus and the coronary sinus os (10) or posterior (4) or posterolateral (3) between the inferior vena cava (2) or an atriotomy scar (1) and the tricuspid annulus. Deep venous thrombosis occurred in 1 patient. At mean follow-up of 290 +/- 40 days, the ablated arrhythmia recurred in 1 (9%) with automatic atrial tachycardia, 5 (29%) with atrial flutter, and 1 (14%) with reentrant atrial tachycardia, all of whom had successful repeat ablation. Previously undetected arrhythmias occurred in 2 patients who are either asymptomatic or controlled with medication.

CONCLUSIONS: Ablation of automatic and reentrant atrial tachycardia and atrial flutter had a high success rate and caused no complications from energy application. Repeat procedures may be required for long-term success, especially in patients with atrial flutter. The mechanism by which ablation is successful is similar for atrial flutter and other forms of atrial reentry and involves severing a critical isthmus of slow conduction bounded by anatomic or structural obstacles. Automatic arrhythmias are abolished by directing lesions at the focus of abnormal impulse formation.