Background-Catheter ablation of atrial fibrillation (AF) became an effective therapy for patients with drug-refractory AF, and the indications have broadened to include nonparoxysmal AF patients. However, data about the long-term effectiveness of ablation in patients with nonparoxysmal AF are lacking. The aim of the present study was to investigate the long-term outcomes of catheter ablation in patients with nonparoxysmal AF. Methods and Results-A total of 88 nonparoxysmal AF patients who received a stepwise catheter ablation (isolation of the pulmonary veins plus substrate modification) from 2006 to 2008 were enrolled. Freedom of recurrence was defined as the absence of atrial arrhythmias without using any antiarrhythmic agents after the catheter ablation. There were 63 patients (71.6%) with recurrences (47 patients with AF and 16 patients with atrial flutter/atrial tachycardia) after the initial procedure during a median follow-up period of 36.8 months. A CHADS 2 score of ≥3 and the left atrial (LA) diameter were significant predictors of recurrences in the multivariable analysis. Of the patients with CHADS 2 scores of ≥3 and an LA dimension ≥44 mm, all had recurrences within 1 year after the initial procedure. The overall recurrence-free rate could increase to 47.7% after the second procedure and 51.1% after the third procedure. Conclusions-The long-term recurrence-free rate of ablation in nonparoxysmal AF was only 28.4% after a single procedure, and multiple procedures were necessary to raise the recurrence-free rate. The CHADS 2 score and LA dimension may help us to identify patients who will have recurrences after catheter ablations of nonparoxysmal AF.(Circ Arrhythm Electrophysiol. 2012;5:514-520.)

The CHADS(2) and CHA(2)DS(2)-VASc scores are useful predictors of adverse events after catheter ablation of AF.

In-stent restenosis reflects the interaction of a cascade of molecular and cellular events occurring within the vessel wall. Coronary stenting induces localized injury to the vessel wall, which leads to the release of thrombogenic, vasoactive, and lymphocytes mitogenic factors that result in processes causing re-narrowing at the injured site. Three major processes have been identified that lead to the in-stent restenosis: neointimal hyperplasia, elastic recoil, and negative arterial remodeling. The most important one is intimal hyperplasia. As the time course of neointimal hyperplasia is unknown, a causal relationship between the development of new blood vessels and clinical restenosis cannot be firmly established.

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