Atrial mass reduction in radiofrequency catheter ablation for long-standing persistent atrial fibrillation: do we really ablate the sick or the healthy tissue?

We read with great interest the article written by Seong Woo Han and colleagues addressing the effect of atrial mass reduction on the clinical outcomes after radiofrequency catheter ablation for longstanding persistent atrial fibrillation (AF). They have compared linear ablation and defragmentation and found that only conduction block through linear lines and pulmonary vein isolation (PVI) positively influence the clinical outcomes for long-standing persistent atrial fibrillationwhile the amount of atrial mass reduction did not influence the clinical outcome [1]. Wewould like to discuss two distinct issues: complex-fractionated atrial electrogram (CFAE) and definition of atrial mass reduction. As known, after the breakthrough for AF ablation that came from Haissaguerre et al., when they described pulmonary veins as important sources of focal AF, significant advances were made in the field of catheter ablation of AF [2]. Catheter ablation approaches initially involved PVI, followed by wider areas of ablation including the antral regions, and this strategy was adopted by virtually everyone. However, ablation strategies still differ significantly among laboratories in the settings of long-standing persistent AF cases. These strategies extend from linear ablation of left atrium to ablation of regions of CFAE, ganglionic plexuses, areas outside the left atrium like the cavotricuspid isthmus, to isolation of superior vena cava and coronary sinus. One or more of these ablation approaches are accepted in different laboratories in the ablation procedures of patients with long-standing persistent AF. CFAE was first described by Nademanee et al. [3]. Subsequently, automatic software was developed to identify areas of CFAE and several different algorithms are being used to define CFAE areas in the clinical studies. Although these software programs were developed to aid in rapid and objective identification of areas of CFAE, they are handicapped with the inconsistency among different products [4]. Results of studies have also been inconsistent probably as a result of this discrepancy [4,5]. AlthoughNademanee described success rates of up to 90% in the mid-term follow-up, other studies have reported much less success rates only in the range of 30–35% [3–6]. Thus, this raises the issue if the results would have been different had Seong Woo Han and colleagues used another software. It seems that much more research is needed to improve our knowledge gap regarding CFAE. Another issue I would like to discuss is that it may be argued whether it is appropriate to calculate the proportion of atrial mass reduction during CFAE-guided ablation by dividing the total atrium size by the lesion size. The lack of reliable transmurality with catheter ablation may reduce the value of the definition of “atrial mass reduction” regarding the effectiveness in catheter ablation for AF. In the case of linear lesions, we can prove the efficacy of transmural lesions objectively through demonstration of bidirectional conduction block. However, in the case of CFAE-guided ablation, the end point of “local fractionated potentials were abolished” does not necessarily mean effective transmural lesion. Even if we completed linear ablation lines anatomically guided by 3-D mapping system, almost always there is a need to give additional energy application to create bidirectional conduction block at the ablation line. The only important issue here is effective detection and ablation of the critical substrate producing and sustaining AF, the sine qua non of the arrhythmia. These critical substrates are ganglionic plexuses for some authors, regions of CFAE, empirically created roof lines, linear lesions involving anterior or posterior walls of the atrium or the mitral isthmus for others. The important issue here is to find which definition correctly defines regions of critical substrates in situations involving complex pathophysiological features like persistent AF. Since the more aggressive and wider the ablation, the more fibrosis we leave behind, we need to find the best strategy to plan the best hit. Recent studies have found that AF ablation attempts are less likely to be successful in the presence of extensive atrial fibrosis [7]. There is the possibility that we will have iatrogenically created patients with excessive atrial fibrotic burdens unlikely to benefit from more effective novel AF ablation practices to be developed in the future, unless we develop gold standard strategies and guidance as soon as possible.