Hybrid theraphy for atrial fibrillation

See page 565 for the article to which this Editorial refers Atrial fibrillation is the most frequently occurring sustained tachyarrhythmia and is associated with heart failure and thromboembolic complications [1] . Although a considerable amount of research is presently being conducted to develop effective nonpharmacological treatment options for patients with atrial fibrillation, antiarrhythmic drugs remain the mainstay of therapy for atrial fibrillation. It has been known for many years that some patients with atrial fibrillation develop atrial flutter after treatment with antiarrhythmic drugs [2] . Although little is known about the mechanisms by which antiarrhythmic drugs may change atrial fibrillation into atrial flutter, a growing body of evidence indicates that radiofrequency catheter ablation of drug-induced atrial flutter may provide an effective new way of treating paroxysmal atrial fibrillation [3–5] . In this issue Reithmann et al. [6] add further knowledge to this topic by elegantly describing their experience with radiofrequency catheter ablation of the isthmus between the tricuspid annulus and the inferior caval vein in 10 patients who developed atrial flutter after amiodarone therapy for paroxysmal atrial fibrillation. They compared their findings in these 10 patients to the results of isthmus ablation in 28 patients with isolated atrial flutter and 54 patients with both atrial flutter and fibrillation. Successful isthmus ablation, as assessed by the presence of bi-directional isthmus block, could be achieved in more than 90% of all patients. After a relatively short follow-up of 83 months, the occurrence of paroxysmal atrial fibrillation was similar in patients with drug-induced atrial flutter and patients with isolated atrial flutter (20% and 25%, respectively) and significantly higher (76%) in patients with both atrial flutter and atrial fibrillation before isthmus ablation. From this and other similar studies it can be concluded that hybrid therapy consisting of isthmus ablation and continuation of antiarrhythmic drug treatment is an effective means to control both drug-induced atrial flutter and paroxysmal atrial fibrillation. A change from atrial fibrillation to atrial flutter has been observed most commonly with Class Ic drugs such as flecainide and propafenone and the Class III drug amiodarone [3–5,7] . Previous studies have documented a conversion from atrial fibrillation to symptomatic atrial flutter during treatment with antiarrhythmic drugs in about 10% or more of