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    • Introduction Atrial fibrillation AF is a

    2019-05-20

    Introduction Atrial fibrillation (AF) is a common cardiac arrhythmia that becomes more prevalent with age [1] and is associated with an increased long-term risk of stroke, purinergic receptors failure, and all-cause mortality [2]. Since Einthoven recorded the electrograms in 1906 [3], AF has widely been recognized as “absolute arrhythmia”, although the mechanisms of AF are still uncertain. The activation patterns that underlie the irregular electrical activity that occurs during AF have traditionally been described as disorganized or random [4–10]. The mechanisms of AF are considered to be random or spiral reentry without fixed circuits, as observed in the accessory pathways of Wolff–Parkinson–White (WPW) syndrome. Thus, the target of AF ablation is not the substrate, but instead the trigger in general, although the ablation target of accessory pathways is typically not the trigger. Therefore, in patients with long-standing AF in which the substrate is supposedly more important than the trigger, “rate control” is more common than “rhythm control.” However, studies based predominantly on statistical methods have provided evidence that AF is not entirely random [11,12], and Madapati and colleagues reported that stable microreentrant sources were the most likely underlying mechanism of AF in a sheep model [13]. Thus, the mechanisms of AF are still controversial, particularly in humans. After the Atrial Fibrillation Follow-up Investigation of Rhythm Management (AFFIRM) [14] and Resynchronization–Defibrillation for Ambulatory Heart Failure Trial (RAFT) [15] demonstrated that the strategy of maintaining sinus rhythm with antiarrhythmic drugs was not better than that of rate control in conjunction with anticoagulation, the development of catheter ablation emerged as an alternative approach for treating AF patients without antiarrhythmic drugs. Shortly after Swartz et al. introduced the catheter-based Maze procedure [16], Haissaguerre and colleagues published a paper revealing that the pulmonary veins (PVs) are an important source of triggering foci for paroxysmal AF [17]. The initial ablative approach was to focally ablate the culprit PV identified as the triggering site initiating AF [17,18], and electrophysiologists began to isolate the electrical connections of all 4 veins from the left atrial (LA) muscle. To avoid PV stenosis and to attempt to include more AF substrate in the isolated areas, numerous investigators now perform PV isolation (PVI) further away from the PV ostia, thereby creating wider areas of LA ablation. A recent consensus of world-renowned experts in AF ablation stated that PVI is a cornerstone of catheter ablation of the AF, and most laboratories perform PVI as the primary approach for patients with paroxysmal AF [19]. Its success rate in the paroxysmal AF subset ranges from 38% to 70% after a single procedure and 65% to 90% after repeated procedures. However, PVI alone is not effective for treating patients with persistent AF [19]. In these patients, additional linear lesions are intended to eliminate additional arrhythmogenic substrate and to prevent large atrial reentrant circuits that are potentially involved in perpetuation of AF; complete linear lesions have been shown to improve outcomes [20]. PVI in addition to ablation at the roof and mitral isthmus achieved sinus rhythm in 69% of patients with persistent AF compared with only 20% of patients who underwent PVI alone [21]. Linear ablation in addition to PVI was demonstrated to be effective in preventing atrial tachycardia after circumferential PV ablation for paroxysmal AF [22], whereas macroreentrant arrhythmias that occur during follow-up are frequently related to gaps in previous linear lesions [23,24]. The ideal approach to identify target sites of AF ablation would be to find substrates that perpetuate the arrhythmia. In the past, it was believed that AF substrates could not be mapped since reentrant circuits underlying the substrate are random and not amenable to point-to-point or endocardial mapping. However, recent observational studies by Nademanee et al. have demonstrated that substrates serving as “AF perpetuators” can be identified by searching for areas that have complex fractionated atrial electrograms (CFAEs) [25,26]. During sustained AF, CFAEs are often recorded in specific areas of the atria, and exhibit temporal and spatial stability [25,27]. By ablating areas that have persistent CFAE recording, these studies showed that AF was terminated in over 85% of patients, and the procedure yielded a very good long-term outcome in both paroxysmal and chronic AF patients [25,26]. Although 8 years have passed since the first report was published, CFAE-guided ablation has not been fully understood until now. An excellent review of CFAE-ablation was previously published by Nademanee et al. [28], thus this review will focus on the practical aspects of CFAE-ablation combined with or without PVI and will describe some representative cases to provide guidance for CFAE-ablation.