Atrial Fibrillation in the Wolff-Parkinson-White Syndrome

Since the advent of catheter ablation for atrial fibrillation (AF) aiming the pulmonary veins a few years ago, there has been an overwhelming interest and a dramatic increase in AF investigation. AF has a different dimension in the context of the Wolff-Parkinson-White (WPW) syndrome. Indeed, AF may be a nightmare in a young person that has an accessory pathway (AP) with fast anterograde conduction. It may be life-threatening if an extremely rapid ventricular response develops degenerating into ventricular fibrillation. Therefore, it is very important to know the mechanisms involved in the development of AF in the WPW syndrome. There are several possible mechanisms that may be involved in the development of AF in the WPW syndrome, namely, spontaneous degeneration of atrioventricular reciprocating tachycardia into AF, the electrophysiological properties of the AP, the effects of AP on atrial architecture, and intrinsic atrial muscle vulnerability. Focal activity, multiple reentrant wavelets, and macroreentry have all been implicated in AF, perhaps under the further influence of the autonomic nervous system. AF can also be initiated by ectopic beats originating from the pulmonary veins, and elsewhere. Several studies demonstrated a decrease incidence of AF after successful elimination of the AP, suggesting that the AP itself may play an important role in the initiation of AF. However, since AF still occurs in some patients with the WPW syndrome even after successful ablation of the AP, there should be other mechanisms responsible for the development of AF in the WPW syndrome. There is a clear evidence of an underlying atrial muscle disease in patients with the WPW syndrome. Atrial myocardial vulnerability has been studied performing an atrial endocardial catheter mapping during sinus rhythm, and analizing the recorded abnormal atrial electrograms. This review analizes the available data on this singular setting since AF has a reserved prognostic significance in patients with the WPW syndrome, and has an unusually high incidence in the absence of any clinical evidence of organic heart disease. www.jafib.com 22 May-Jun, 2011 | Vol 4 | Issue 1 Journal of Atrial Fibrillation Featured Review www.jafib.com 23 May-Jun, 2011 | Vol 4 | Issue 1 al 11 by surgical means, and Haissaguerre et al 12by catheter ablation, have documented a reduction in AF inducibility following elimination of the AP in patients with WPW syndrome. Indeed, ablation of the AP is very effective in the abolition of conduction through the AP, and of clinical episodes of atrioventricular reciprocating tachycardia (AVRT) and AF; however, it does not prevent recurrences of AF in certain patients. Therefore, it is very important to determine all possible mechanisms for the development of AF in the WPW syndrome. It is paramount to understand that AF may be lifethreatening in the setting of WPW syndrome with fast anterograde AP conduction, because a rapid ventricular response may develop degenerating into ventricular fibrillation .13 Several mechanisms responsible for the development of AF in the WPW syndrome were investigated in detail, namely, the spontaneous degeneration of AVRT into AF, the electrical properties of the AP, the effects of AP on atrial architecture, and the intrinsic atrial muscle vulnerability.14-22Considering all the mechanisms proposed to explain the development of atrial fibrillation in the WPW syndrome, this review analizes the available data on this singular and interesting topic since AF has a reserved prognostic significance in patients with the WPW syndrome, and has an unusually high incidence in the absence of any clinical evidence of organic heart disease. Electrophysiological properties of the accessory pathway in the WPW syndrome Anterograde and retrograde electrophysiologic properties of the AP have been well investigated. The coexistence of a functional retrograde AP and sustained episodes of AVRT has been found to play an important role in triggering AF in patients with the WPW syndrome. 13, 23 In the electrophysiologic laboratory, it is relatively common to observe spontaneous degeneration of induced AVRT into AF in WPW patients. AF has a different dimension in the context of the WPW syndrome [Figure 1]. It may be a nightmare in a young person that has an AP with fast anterograde conduction. AF may be life-threatening if an extremely rapid ventricular response develops degenerating into ventricular fibrillation. There is clear data to support that retrograde conduction to the atrium through multiple AP, or multifiber AP during AVRT can initiate AF. The incidence of spontaneous degeneration of induced AVRT into AF has been reported to be in the range of 16% to 26%, 13 and it was found to occur in a similar proportion in patients with conFigure 1: Atrial fibrillation in the Wolff-Parkinson-White syndrome 12 lead electrocardiographic recording in a patient with induced atrial fibrillation in the manifest Wolff-Parkinson-White syndrome. There is an evident very rapid ventricular rate. Reprinted with permission from Avalos Morel P, Centurión OA, Bianco Cáceres HF et al. Rev Soc Parag Cardiol 2005;2:159-168. cealed WPW, and manifest WPW syndrome.24 Frequent tachycardias seem to promote an electrical remodeling and an increased atrial vulnerability to AF. For example, AVRT can increase atrial vulnerability as a result of a shortened atrial cycle length, increased sympathetic tone and atrial stretch due to hemodynamic changes that occur during AVRT. In this regard, Chen et al 25 observed that the cycle lenght of reciprocating tachycardia at the time of electrophysiologic study was significantly shorter in WPW patients with than without AF. This finding suggests that it is easier to develop AF in a rapid episode of sustained AVRT. Successful surgical or transcatheter ablation of the AP in patients without organic heart disease has been demonstrated to prevent future occurrence of AF in the majority of patients.11, 13 This fact is well documented by long-term follow-up studies after successful AP ablation that demonstrated significantly reduced incidences of spontaneous AF. The recurrence rate of spontaneous AF after successful ablation of the AP is reported to be in the range of 6% to 10%. 11-13 However, Hamada et al. made a very interesting observation in this respect. They observed that clinical episodes of AF recurred in 71% of their patients whose AF remained inducible immediately postablation, however, in none of the patients who remained uninducible postablation .26 Threrefore, there is a high incidence of AF recurrence in a subgroup of patients whose AF remained inducible despite successful ablation of the AP. A detailed examination of this subgroup of patients prone to develop AF could shed more light in the understanding of the mechanisms for the genesis of AF in WPW patients despite successful AP ablation. Atrial double potentials and retrograde AP conduction. NHsieh et al 17 investigated the influence of atrial double potentials in the genesis of AF in patients with WPW syndrome. Double atrial potentials recorded in the coronary sinus are not an unusual phenomenon in patients with supraventricular tachyarrhythmias, and they have shown to potentiate the occurrence of atrial tachycardias. They demonstrated that patients with the WPW syndrome, especially with a left lateral bypass tract, had a higher incidence of double atrial potentials and induced AF than patients with AVNRT. Furthermore, WPW patients with double atrial potentials had a higher incidence of induced AF than those WPW patients without double atrial potentials. Campbell et al 23 demonstrated a high incidence rate of AF that was initiated with incremental right ventricular pacing and premature ventricular contraction (PVC). They described in detail the role of retrograde multiple AP as a mechanism of premature atrial contraction that initiates atrial repetitive fir Hsieh et al 17 investigated the influence of atrial double potentials in the genesis of AF in patients with WPW syndrome. Double atrial potentials recorded in the coronary sinus are not an unusual phenomenon in patients with supraventricular tachyarrhythmias, and they have shown to potentiate the occurrence of atrial tachycardias. They demonstrated that patients with the WPW syndrome, especially with a left lateral bypass tract, had a higher incidence of double atrial potentials and induced AF than patients with AVNRT. Furthermore, WPW patients with double atrial potentials had a higher incidence of induced AF than those WPW patients without double atrial potentials. Campbell et al 23 demonstrated a high incidence rate of AF that was initiated with incremental right ventricular pacing and premature ventricular contraction (PVC). They described in detail the role of retrograde multiple AP as a mechanism of premature atrial contraction that initiates atrial repetitive firing or intratrial reentry in the vulnerable period of the atrium during AVRT .23 They stated that intermittent retrograde conduction over a second AP with faster conduction caused early atrial depolarization in a critical and vulnerable period of the atrium, setting the scenario for reentry to occur. Spontaneous occurrence of PVC depolarizes the atrium in a retrograde manner that can cause AF to develop. Iesaka et al 27 hypothesized that during AVRT, the complex excitation inputs into the atrium over the retrograde multiple or multifiber AP could trigger AF. They identified retrograde multiple and multifiber AP based on the results of electrophysiologic studies and radiofrequency catheter ablation. The incidence of clinical PAF, as well as, induced AF was significantly greater in the multiple AP patients. However, the incidence of clinical AVRT was similar between multiple and single AP Journal of Atrial Fibrillation Featured Review www.jafib.com 24 May-Jun, 2011 | Vol 4 | Issue 1 patients. The incidence of AF initiated during ventricular pacing and AVRT was significantly greater in the multiple AP patients. A very interesting finding in this study 27 was that AF inducibility during AVRT and ventricular pacing was eliminated by partial ablation of multiple or multifiber AP. However, AVRT inducibility remained in most patients with partial ablation of the multiple o multifiber AP. The incidence of induced AF after total ablation was similar between patients with multiple or single AP. The authors based on their findings indicate that the existence of a retrograde multiple or multifiber AP is strongly related to AF inducibility. In addition, the complex excitation inputs into the atrium over the retrograde multiple or multifiber AP is necessary to trigger AF. Retrograde conduction of PVC to the atrium in the WPW syndrome caused multiple episodes of PAF in a patient without previous arrhythmias after having a myocardial infarction .15 During the electrophysiological study the patient presented two spontaneous episodes of AF initiated by PVC conducted to the atria through the AP. After successful catheter ablation of the AP the patient did not present arrhythmia recurrences, although he had multiple PVCs recorded in a 24 Hs Holter monitoring. 15 It may be argued that atrial vulnerability could be a predisposing factor in this kind of patients with a previous myocardial infarction. The impairment of the diastolic left ventricular function could modify the electrophysiological properties of the atria because of an increase in atrial pressure and atrial stretch. However, the fact that the patient did not have AF episodes after catheter ablation of the AP is against this mechanism being the only element responsible for the arrhythmia episodes. This interesting single case clearly demonstrates how complex is the mechanism to develop AF in the WPW syndrome. The authors 15hypothesize that PVCs with a short coupling interval resulted in VA conduction to the atria and activated the left atrium during the atrial vulnerable phase, thereby precipitating the onset of AF. This hypothesis is supported by two facts: first, AF episodes were experienced only after myocardial infarction in the presence of an AP. This could be related to a possible increase in the appearance of PVCs with different origins and coupling intervals. Second, new AF episodes were not experienced after successful AP ablation despite the fact that Holter monitoring performed after ablation demonstrated the presence of frequent polymorphic PVCs. In this regard, Jackman et al. observed multiple retrograde conductions over separate AP branches during AVRT and reentry originating from the branching networks. They indicated that microreentry mimicking atrial flutter or fibrillation could originate within the branching networks of the AP strands and that this may account for the unusually high incidence of AF in the WPW syndrome.28 In their study, they utilized closely spaced orthogonal catheter electrodes in the coronary sinus and found electrophysiologic evidence for a branching or multifiber structure of the left free wall AP. However, this finding has not been comfirmed in a large population. Moreover, this finding was indirectly contradicted by other mapping studies of AF initiation in patients with the WPW syndrome. 13, 29, 30 These two studies demonstrated that the onset of AF was more frequently initiated near the high right atrium regardless of the AP location .13, 29, 30 Fujimura et al 13 showed that most episodes of AF started at a high right atrial site regardless of AP location, with only 19% of AF episodes starting at the electrode site in the coronary sinus closest to the AP Intraatrial wavefront collision and anterograde AP conduction There are several studies that stressed the relation between anterograde conduction properties of the AP and AF in the WPW syndrome. 13, 24, 3032 Ong et al. performed an atrial mapping study using a multiple electrode array during surgery and suggested a possible mechanism of sustaining atrial fibrillation in patients with WPW syndrome .30 They demonstrated that wavefront collisions between incoming atrial wavefronts via an AP during non-preexcited beats generated new wavefronts to help perpetuate AF. This concept of intraatrial wavefront collision possibly explains susceptibility to AF in patients with multiple AP. Multiple and asynchronous wavefronts could be generated by conduction over multiple AP or widely separated strands forming multifiber AP during AVRT. The wavefronts collision in the atrium could be a mechanism for induction and perpetuation of AF. Although, it seems a plausible conception the exact electrophysiologic mechanism remains to be clarified in detail. Fujimura et al 13 observed that the anterograde AP effective refractory period (ERP) was shorter in Journal of Atrial Fibrillation Featured Review www.jafib.com 25 May-Jun, 2011 | Vol 4 | Issue 1 plain the lower incidence of AF in the concealed WPW group, since shortening of the cycle length is known to increase atrial vulnerability. Therefore, the genesis of AF in the WPW syndrome can not be solely attributed to the ocurrence of AVRT. Intra-atrial or inter-atrial conduction disturbances may be a possible explanation for the longer cycle length of AVRT in patients with manifest WPW syndrome. The anterograde AP conduction properties distinguished patients with and without AF. It is known that a shorter anterograde AP ERP allows faster ventricular rates during AF, therefore, the associated atrial stretch and hypoxia may contribute to sustaining the arrhythmia. Atrial structural heterogeneities at the AP insertion. There is no detailed data on the structure of atrial tissue around the AP available currently. Most of the histopathological studies in patients with WPW syndrome have delt with the AP itself with no special description of the atrial tissue at the insertion of the AP. It is well known that structural heterogeneities play an important role in atrial reentry due to the influence of unidirectional block and conduction delay. Thus, it is possible that in patients with WPW syndrome, the increased structural heterogeneity created by the presence of the AP may play a role in the generation and maintenance of atrial reentry. 32 In experimental studies of the canine heart model of WPW syndrome, structural differences in the AP apparently affected refractoriness and conduction properties of the AP. 33 It was postulated that the AP is the result of an embriologic fault in the formation of fibrous tissue separating the atria and the ventricles .34 Therefore, developmental abnormalities may also be present in the atrial tissue adjacent to the AP, which may affect the functional electrical properties of the atrium close to the AP insertion. Dispersion of the refractory periods and conduction disturbances apparently occur around the interconnection between different tissues such as the atrium and the AP. Either anatomical or functional properties of the atrial tissue near the AP may play a role in the genesis of AF and may contribute to the Journal of Atrial Fibrillation Featured Review www.jafib.com 26 May-Jun, 2011 | Vol 4 | Issue 1 the group with AF than in the control group, and that there were no significant differences in retrograde properties. Della Bella et al 24also reported similar findings. They found that the anterograde ERP of the AP was significantly shorter in WPW patients with spontaneous AF that in those WPW patients without spontaneous AF. They also found that AF was more frequent in patients with manifest WPW than in those with concealed WPW syndrome. These findings suggest that the retrograde conduction properties of a single AP are not the critical determinants of AF. The study by Asano et al 31 is in accord with this concept. Although they studied symptomatic and asymptomatic patients, they found that the incidence of spontaneous AF in the manifest WPW group was higher than in the concealed WPW group. However, this was not the same for the induction of AVRT in these two groups. The induction of AVRT was 75% in the manifest WPW group compared to 100% in the concealed WPW group. The mean AVRT cycle length was shorter in patients with concealed WPW than in the manifest WPW patients. This fact does not explain the lower incidence of AF in the concealed WPW group, since shortening of Fujimura et al 13 observed that the anterograde AP effective refractory period (ERP) was shorter in the group with AF than in the control group, and that there were no significant differences in retrograde properties. Della Bella et al 24also reported similar findings. They found that the anterograde ERP of the AP was significantly shorter in WPW patients with spontaneous AF that in those WPW patients without spontaneous AF. They also found that AF was more frequent in patients with manifest WPW than in those with concealed WPW syndrome. These findings suggest that the retrograde conduction properties of a single AP are not the critical determinants of AF. The study by Asano et al 31 is in accord with this concept. Although they studied symptomatic and asymptomatic patients, they found that the incidence of spontaneous AF in the manifest WPW group was higher than in the concealed WPW group. However, this was not the same for the induction of AVRT in these two groups. The induction of AVRT was 75% in the manifest WPW group compared to 100% in the concealed WPW group. The mean AVRT cycle length was shorter in patients with concealed WPW than in the manifest WPW patients. This fact does not exJournal of Atrial Fibrillation Featured Review www.jafib.com 27 May-Jun, 2011 | Vol 4 | Issue 1 arrhythmia (62%). Patients with a right free wall AP had a rather low rate of inducible arrhythmia (21%). Patients with left free wall and posteroseptal AP had a 44% and 36% rate of induction, respectively .23-26Patients with a right-sided AP had a lower inducibility of AVRT and a relatively long retrograde ERP over the AP. This allowed only relatively late PVCs to be conducted retrogradely over the AP to the atrium, wich might explain the lower rate of inducibility of AF in these patients. Intrinsic atrial muscle vulnerability in the WPW syndrome The persistance of AF in certain patients with WPW syndrome despite the successful abolition of the AP may be explained by the presence of an underlying atrial disease considering the AP as an innocent bystander .13, different incidence of atrial vulnerability and AF in the WPW syndrome. The anatomy, direction and location of the AP may play a role in the genesis of AF in the WPW syndrome. The AP may run in an oblique course rather than perpendicular to the transverse plane of the atrioventricular groove. As a result, the fibers may have an atrial insertion point that is transversely several centimeters removed from the point of ventricular attachment. The AP may occasionally exist as broad bands of tissue rather than discrete hair-like structures. Other than the anatomy of the AP, the location of the AP is better related to induction of AF. Several studies found different induction rates of AF depending on the exact location of the AP [23-26]. It was shown that patients with an anteroseptal AP had a high rate of inducible Figure 2: Atrial endocardial mapping sites The upper part of the figure shows 12 endocardial mapping sites in the right atrium. The atrial endocardial electrograms were recorded in each patient from the anterior, lateral, posterior and medial aspects of the high right atrium (a,b,c,d), mid right atrium (e,f,g,h) and low right atrium (i,j,k,l). SVC= superior vena cava; IVC= inferior vena cava; Ao= aorta; PA= pulmonary artery; LA= left atrium; RV= right ventricle; LV= left ventricle. The lower part of the figure show 2 atrial endocardial electrograms to distinguish an abnormal atrial electrogram (A) with 10 fragmented deflections and 130 ms in duration, from a normal atrial electrogram (B) with 2 deflections and 80 ms in duration. Reprinted with permission from Centurion OA et al. Influence of advancing age on fractionated right atrial endocardial electrograms. Am J Cardiol 2005;96:239-242. 28Patients with the WPW syndrome associated with AF were found to have a high incidence of electrophysiological abnormalities of the atrial muscle. This intrinsic atrial muscle vulnerability certainly plays an important role in the occurrence of AF in these patients. AF has a particular prognostic significance in patients with the WPW syndrome, and its incidence is unusually high in the absence of any clinical evidence of organic heart disease. Ablation of the AP is very effective in the abolition of conduction through the AP, and it has been shown that recurrences of AF after succesful AP ablation occur at a low incidence. Haissaguerre et al 12have documented a reduction in AF inducibility following catheter ablation in patients with WPW syndrome. Sharma et al 11 found a reduction in AF inducibility following elimination of AP by surgical ablation. Other studies have also demonstrated a reduction in AF inducibility after successful AP ablation .1113 Indeed, ablation of the AP is very effective in the elimination of clinical episodes of AVRT and AF; however, it does not prevent recurrences of AF in certain patients. Therefore, it is very important to determine all possible mechanisms for the development of AF in the WPW syndrome patients. An explanation suggested, in certain patients, is the presence of an underlying intrinsic atrial disease. 13, 28 In the absence of structural atrial disease, clinical electrophysiologic studies have not clearly defined atrial features that can predict spontaneous occurrence of AF. Some investigators have studied the atrial vulnerability showing that the induction of sustained episodes of AF was more frequent in patients with a history of spontaneous AF. Others have analyzed the atrial electrophysiological substrate that may predispose to AF. They evaluated atrial refractoriness, intra-atrial and interatrial conduction times, and several electrophysiological parameters elicited with programmed atrial stimulation with single extrastimulus. Important information about intrinsic atrial muscle vulnerability was obtained by atrial endocardial electrograms morphology recorded by atrial endocardial catheter mapping during sinus rhythm (Figure 2). Atrial refractorines dispersion. Nonhomogeneity of ERP of contiguous cells causes a slower conduction velocity of the stimulus that propagates through partially repolarized cells, allowing the genesis of unidirectional blocks and the appearance of multiple reentries. 35 In experimental studies with a computer model of AF, Moe et al 35 demonstrated that an atrial condition characterized by short and nonhomogeneous atrial ERP, associated to intra-atrial conduction disturbances, is considered an important factor in the appearance and maintenance of AF. These findings were later corroborated by other investigators. 36 In a landmark paper from Allesie’s laboratory, Konings KT et al 37 described various types of AF in humans with the WPW syndrome. They induced AF by rapid atrial pacing in 25 patients with WPW syndrome undergoing surgery for interruption of their AP. The free wall of the right atrium was mapped using a spoon-shaped electrode containing 244 unipolar electrodes. Based on the complexity of atrial activation, they defined three types of AF. In type I (40%), single broad wave fronts propagated uniformly across the RA. Type II (32%) was characterized by one or two nonuniformly conducting wavelets, whereas in type III (28%), activation of the RA was highly fragmented and showed three or more different wavelets that frequently changed their direction of propagation as a result of numerous arcs of functional conduction block. They found significant differences among the three types of AF in median intervals, variation in AF intervals, incidence of electrical inactivity, and reentry, and average conduction velocity during AF. Therefore, they could demonstrate that from type I to type III, the frequency and irregularity of AF increased, and the incidence of continuous electrical activity and reentry became higher. These various types of AF in humans appear to be characterized by different numbers and dimensions of the intra-atrial reentrant circuits. Clinical electrophysiology has identified several atrial features that may Journal of Atrial Fibrillation Featured Review www.jafib.com 28 May-Jun, 2011 | Vol 4 | Issue 1 www.jafib.com 29 May-Jun, 2011 | Vol 4 | Issue 1 Journal of Atrial Fibrillation Featured Review AF was reduced following elimination of the AP by surgical cryoablation. However, these parameters were unchanged in patients that had their AP ablated by radiofrequency catheter ablation. Although, they could not clearly explain these different findings with the different ablation techniques, they argued that the prolongation of the atrial ERP played a key factor in the decrease of the AF induction rate in those patients ablated by surgical cryoablation. Probably, the larger myocardial injury created by surgical cryoablation, or dissection of the atrioventricular sulcus may be related to the lower incidence of AF. Another factor that might have influenced is that the radiofrequency applications were mainly delivered on the ventricular side of the atrioventricular valve annulus, while surgical cryoablations were performed directly on the atrial tissue. Therefore, the injury of the atrial tissue was greater in this latter group of patients. The resulting prolongation of the atrial ERP may prevent capture of short coupled premature atrial excitation and, therefore, may result in prevention of atrial electrical disorganization and AF. Tsuji et al 38 also showed that the occurrence of AF depends on a short atrial ERP, and AF mainly originated in the high right atrium regardless of the AP location. Atrial response to programmed stimulation. The induction of AF during electrophysiological testing makes its evaluation difficult and may lead to the undiserable need for antiarrhythmic agents or electrical cardioversion. On the other hand, the induction of AF with programmed atrial stimulation with single extrastimulus is not always successful even in patients with clinically documented AF. Besides the use of rapid burst pacing of the atrium may induce nonspecific AF. Therefore, the analysis of other atrial electrophysiological parameters is useful as indicators of potential atrial vulnerability. There are several atrial electrophysiological parameters relating to AF which are elicited with atrial programmed stimulation. The inducibility of AF, fragmented atrial activity, repetitive atrial firing, and intraatrial lead to the appearance and maintainance of AF, sometimes with conflicting results. These different results may be due to multiple factors, including different stimulation protocols and nonhomogeneous groups of patients. Some investigators reported short atrial ERP in patients with PAF, 38 while others did not. 39 Thus, it is controversial to utilize atrial ERP as a useful measure of atrial vulnerability. Several studies have shown conflicting results regarding refractoriness in AF. The measurement of atrial ERP in AF patients in only one site does not necessarily represent atrial refractoriness since these patients have a wide dispersion of atrial refractoriness. Therefore, it is not comparable in different sites of the atrium neither in different patients. It has been shown that the atrial ERP physiologically shortens with increasing heart rate. 40This rate adaptation is less evident in AF patients, as well as, in isolated cellular preparations. Riccardi et al 41 evaluated the rate adaptation of ERP in WPW patients with and without AF, analyzing the gradient between two different atrial pacing cycle lengths. They found that the functional refractory period increased in most AF patients (81%) with an increase of the atrial stimulation rate, while this absent rate adaptation was observed only in few patients (24%) without AF. The functional refractory period expresses the time needed for the electrical stimulus to be conducted from the distal pair of electrodes to the proximal pair of electrodes, so it is a local intraatrial conduction parameter in a relative refractory condition. The fact that WPW patients with AF showed higher values of refractory periods which became even higher with increasing heart rate ,41 suggests the concept of AF as based on slow con conduction through partially recovered myocardium. The ablation technique utilized for the AP ablation may produce different results regarding atrial vulnerability and AF induction. Muraoka et al 42 observed that the atrial ERP was prolonged, the zones of atrial vulnerability were narrowed and the induction rate of