Class IC antiarrhythmic drug induced atrial flutter: electrocardiographic and electrophysiological findings and their importance for long term outcome after right atrial isthmus ablation

Abstract

Objective-To describe the electrocardiographic and electrophysiological findings of new atrial flutter developing in patients taking class IC antiarrhythmic drugs for recurrent atrial fibrillation, and to report the long term results of right atrial isthmus ablation in relation to the ECG pattern of spontaneous atrial flutter. Design-Retrospective analysis. Setting-Tertiary care academic hospital. Patients-24 consecutive patients with atrial fibrillation (age 54 (12) years; 5 female, 19 male) developing atrial flutter while taking propafenone (n = 12) or flecainide (n = 12). Results-The ECG was classified as typical (n = 13; 54%) or atypical atrial flutter (n = 8) or coarse atrial fibrillation (n = 3). Counterclockwise atrial flutter was the predominant arrhythmia. Acute success after isthmus ablation was similar in patients with typical (12/13) and atypical (8/8) atrial flutter. After long term follow up (13 (6) months, range 6-26 months), continuation of antiarrhythmic drug treatment appeared to result in better control of recurrences of atrial fibrillation in patients with typical atrial flutter (11/13) than in those with atypical atrial flutter (4/8), but the diVerence was not significant. Ablation for coarse atrial fibrillation was unsuccessful. Conclusions-New atrial flutter developing in patients taking class IC antiarrhythmic drugs for recurrent atrial fibrillation has either typical or atypical flutter wave morphology on ECG. The endocardial activation pattern and the acute results of ablation suggest that the flutter circuit was located in the right atrium and that the isthmus was involved in the re-entry mechanism. There appeared to be better long term control of recurrent atrial fibrillation in patients with typical (85%) as compared with atypical atrial flutter (50%). Patients developing coarse atrial fibrillation may not be candidates for this strategy. (Heart 2001;85:424-429)

Potassium Channel Blockade Enhances Atrial Fibrillation–Selective Antiarrhythmic Effects of Optimized State-Dependent Sodium Channel Blockade

“…4,[20][21][22][23] However, proarrhythmic effects, particularly in patients with ischemic heart disease, and poor long-term sinus rhythm maintenance limit their clinical use. 4,[24][25][26][27][28] Similarly, KCBs such as dofetilide and ibutilide are moderately efficacious anti-AF drugs. 29 Unfortunately, the risk of QT prolongation and ventricular tachyarrhythmias associated with KCBs, particularly in the setting of bradycardia or hypokalemia, are major limiting factors.…”

Antiarrhythmic Drug Therapy for Atrial Fibrillation

“…It has mild negative inotropic effects and, like propafenone, is associated with a significant incidence of atrial flutter. 15,16 Dizziness and visual disturbance represent the common noncardiovascular side effects seen in 5% to 10% of patients taking flecainide. 17 Propafenone has ␤ blocking in addition to sodium channel blocking activity.…”

“…It is renally cleared and is prescribed twice daily unless the creatinine clearance is between 30 and 60 mL/min, in which case it should be dosed daily. 16 The usual dose range is 160 to 480 mg/d in divided dosages. It is generally started at a dose of 80 mg twice daily and uptitrated with attention to QT prolongation.…”

Randomized Study Comparing Combined Pulmonary Vein–Left Atrial Junction Disconnection and Cavotricuspid Isthmus Ablation Versus Pulmonary Vein–Left Atrial Junction Disconnection Alone in Patients Presenting With Typical Atrial Flutter and Atrial Fibrillation

“…9 -11 In this subset of patients with both AF and AFL, CTI ablation and continuation of antiarrhythmic drugs (AADs) has been reported to achieve successful control of both arrhythmias and is still considered an effective and acceptable treatment approach. [12][13][14] Recently, however, it has been demonstrated that in patients with clinical evidence of both AF and typical AFL, AF is induced by triggers from pulmonary vein (PV) foci in Ͼ85% of cases. 15, 16 Kumagai et al 16 suggested that focal activation originating from the PVs may trigger AFL and concluded that CTI ablation combined with PV isolation should be considered in such patients.…”