Europace Advance Access published online on August 28, 2008
Europace, doi:10.1093/europace/eun238
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Electroanatomic mapping in the catheter ablation of premature atrial contractions with a non-pulmonary vein origin
1 Division of Cardiovascular Disease, University of Alabama at Birmingham, VH B147, 1670 University Boulevard, 1530 3rd Avenue South, Birmingham, AL 35294-0019, USA; 2 Division of Cardiology, Aichi Prefectural Cardiovascular and Respiratory Center, Ichinomiya, Japan; 3 Department of Cardiology, Nagoya University Graduate School of Medicine, Nagoya, Japan
Manuscript submitted 5 May 2008. Accepted after revision 21 July 2008.
* Corresponding author. Tel: +1 205 975 4724; fax: +1 205 975 4720. E-mail address: takumi-y{at}fb4.so-net.ne.jp
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Symptomatic premature atrial contractions (PACs) may be a target for catheter ablation. However, mapping of PACs with an atrial origin may not be easy because of erratic incidence and different sites of origin. Although the technique and efficacy of electroanatomic mapping has been established in stable arrhythmias, electroanatomic mapping of PACs in intermittent arrhythmias has not yet been reported. This article describes a manoeuvre for mapping PACs using an electroanatomic mapping system. Our experience has demonstrated that electroanatomic mapping using an auto-freeze map is feasible during PACs and may be an option for catheter ablation of PACs.
Key Words: Electroanatomic mapping, Premature atrial contraction, Non-pulmonary vein, Radiofrequency catheter ablation
Premature atrial contractions (PACs) may be a target for catheter ablation because they are sometimes symptomatic and may initiate atrial fibrillation (AF).1
,2 Premature atrial contractions arising from the pulmonary veins (PVs) may be easily treated by PV isolation.3,4 However, mapping of PACs with a non-PV origin may not be easy because of the erratic incidence and different sites of origin of the PACs. Although the technique and efficacy of electroanatomic mapping has been established in stable arrhythmias,5–7 they have not been fully established in intermittent arrhythmias.8 In this article, a manoeuvre to map PACs by using an electroanatomic mapping system is described.
Before electroanatomic mapping, a multipolar catheter was introduced into the coronary sinus (CS) as a reference. An additional mapping catheter was also placed in the His-bundle region, and/or oesophagus and simultaneous recordings from those catheters were used in order to differentiate the multiple PACs. Intra-cardiac recordings from the CS catheter were obtained during both sinus rhythm and PACs, and the averaged cycle length of sinus rhythm and averaged coupling interval of the targeted PACs were measured. Electroanatomic mapping was performed using an ablation catheter (Navi-StarTM, Biosense Webster, Diamond Bar, CA, USA) as previously reported.7,8 The spatial resolution was set with a fill threshold of 10–15 mm, and detailed mapping was performed so as not to have any defects in the electroanatomic map. The maximum value point of the electrode pair of the CS catheter was used as the reference against which the local activation time was measured. With this setting, the electrode pair of the CS catheter that recorded an atrial electrogram larger than the ventricular electrogram was selected. Electroanatomic mapping of the PACs was performed by using the auto-freeze feature of the CARTOTM system (Biosense Webster) (Figure 1). The auto-freeze feature allowed for the automatic selection and analysis of intermittent arrhythmias such as premature ventricular contractions8 or PACs. If the coupling between the sinus rhythm and the arrhythmia beats was set as expected from the pattern of the arrhythmia's appearance, the auto-freeze map could automatically collect the electroanatomic data of the arrhythmic beats, satisfying the given requirements. The duration of the coupling interval was usually set between the coupling interval of the PACs –50 ms and sinus rhythm –50 ms (Figure 2). This setting did not allow the auto-freeze map to capture sinus beats when the sinus rate oscillated within 50 ms, but allowed capture of the PACs when the coupling interval oscillated within 50 ms (Figure 2). It did not, however, allow the auto-freeze map to capture different PACs with coupling intervals shorter than that of the target PACs –50 ms, such as PACs induced by a mapping catheter or with longer coupling intervals than that of sinus rhythm –50 ms (Figure 2). When multiple PACs were observed, mapping of the PACs with the shortest coupling interval was performed first, and the longer coupling interval of another PAC was used instead of the cycle length of the sinus rhythm. The earliest activation site during the PACs was identified on the activation map made by the electroanatomic map using the auto-freeze map. When PACs were infrequent, electroanatomic mapping of the atrium was first performed during sinus rhythm in order to create a geometry of the atrium (Figure 3). Following that, electroanatomic mapping was performed in a limited area of interest revealed by the coarse mapping.
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The efficacy of the present mapping technique was examined in selected patients who had symptomatic and drug-refractory PACs exhibiting the following clinical presentations: frequent incidence (on average >5 b.p.m.), single or two P-wave morphologies, a stable coupling interval of the main PACs on the surface electrocardiogram, and few and short episodes of AF. Electroanatomic mapping using an auto-freeze map was performed in seven patients with non-PV PAC origins, and the origins of eight PACs were found: four were located in the left atrial posterior wall, two in the crista terminalis, and two in the mitral annulus (Figures 1 and 3). Three of those PACs initiated AF during the electrophysiological study. All PACs were eliminated by one or two radiofrequency applications with guidance from the electroanatomic map. Thereafter, no PACs could be induced by burst atrial pacing (to a cycle length as short as 200 ms) during an isoproterenol infusion (2–4 µg/min). No complications occurred. The fluoroscopy time and procedure time (defined as the time from the beginning of the electroanatomic mapping to the last radiofrequency application) were 27.5 ± 9.1 and 46.3 ± 11.3 min, respectively. Follow-up was performed at 2 weeks, 1 month, and every month thereafter, using 24 h Holter and cardiac recordings. All patients who reported symptoms were given an event monitor to document the cause of the symptoms. All the seven patients were free of atrial arrhythmias without any anti-arrhythmic drugs during more than 1 year of follow-up.
Two of the seven cases revealed possible problems during electroanatomic mapping using the auto-freeze map. In the first case, the configuration of the atrial electrograms recorded from the CS catheter during sinus rhythm differed greatly from that during the PACs (Figure 4). Here, the maximum value point of the electrode pair of the CS catheter was used as the reference because the atrial electrogram was larger than the ventricular electrogram during sinus rhythm. However, an atrial electrogram smaller than the ventricular electrogram was recorded from the same electrode pair of the CS catheter during the PACs (Figure 4). Consequently, the PACs could not be captured by an auto-freeze map. Therefore, when the electrode pair of the CS catheter was determined as the reference, attention had to be paid to the change in the atrial electrograms in the reference during sinus rhythm and the PACs. If all the electrode pairs of the CS catheter are not available for the change in the atrial electrograms, using another mapping catheter or the maximal or minimal dV/dt point as the reference can be an option. In the second case, PACs were induced during isoproterenol infusion. The isoproterenol infusion also caused an acceleration of sinus rhythm during mapping, and thereafter sinus beats were also captured by the auto-freeze map.
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Our experience demonstrated that electroanatomic mapping using an auto-freeze map was feasible and effective for the selected PACs. The present non-fluoroscopic mapping technique may reduce the fluoroscopic time when compared with the standard electrophysiological mapping technique. Simultaneous multisite mapping using a non-contact balloon or basket catheter may be helpful for identifying the origins of PACs, especially with low and irregular incidence.9
–13 However, the simultaneous multi-site mapping technique may have several disadvantages as against the mapping technique presented here. The movement of the ablation catheter may be compromised in the limited atrial space with the non-contact balloon inflated. Contact mapping with a basket catheter may have limited accessibility. In non-contact balloon mapping, as the distance from the non-contact balloon to the mapping points increases, the accuracy of mapping decreases.14 Therefore, especially in the left atrium where positioning of a non-contact balloon is anatomically limited, there may be some less accurate mapping areas. In addition, the mapping technique presented here has advantages over the mapping technique using a non-contact balloon or basket catheter, such as the use of fewer mapping catheters and lesser risk of thrombosis. Therefore, we believe that electroanatomic mapping using an auto-freeze map may be an option for catheter ablation of PACs. The mapping technique presented here may have potential limitations. In electroanatomic mapping, catheter stability may be the main challenge. Recording a point only during PACs may not allow for eliminating respiratory movements, and the PACs themselves may influence mapping catheter stability. If the presence of multiple PAC origins is not recognised by the auto-freeze modality or by the activation sequences recorded by the multipolar catheters, it may result in a misleading map with a wide area of early activation. However, we think that adding more detailed mapping in the area of interest exhibiting early activation may overcome these potential limitations.
Conflict of interest: T.Y. is supported by a research grant from Boston Scientific and St Jude Medical. H.T.M., A.E.E., V.J.P., and G.N.K. have participated in catheter research funded by Biosense-Webster and Irvine Biomedical. A.E.E. has received honoraria from, and served on Events Committees for, Boston Scientific and St Jude Medical. G.N.K. has received honoraria from Medtronic, Boston Scientific, and St Jude Medical. The electrophysiology fellowship programme at the University of Alabama at Birmingham receives funding support from Boston Scientific and Medtronic. The other authors report no conflicts.
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[1] Haissaguerre M, Jais P, Shah DC, Takahashi A, Hocini M, Quiniou G, et al. Spontaneous initiation of atrial fibrillation by ectopic beats originating in the pulmonary veins. N Engl J Med (1998) 339:659–66.
[2] Chen SA, Hsieh MH, Tai CT, Prakash VS, Yu WC, Hsu TL, et al. Initiation of atrial fibrillation by ectopic beats originating from pulmonary veins: electrophysiologic characteristics, pharmacologic responses, and effects of radiofrequency ablation. Circulation (1999) 100:1879–86.
[3] Haissaguerre M, Shah DC, Jais P, Hocini M, Yamane T, Deisenhofer I, et al. Electrophysiological breakthroughs from the left atrium to the pulmonary veins. Circulation (2000) 102:2463–5.
[4] Oral H, Knight BP, Tada H, Ozaydin M, Chugh A, Hassan S, et al. Pulmonary vein isolation for paroxysmal and persistent atrial fibrillation. Circulation (2002) 105:1077–81.
[5] Gepstein L, Hayam G, Ben-Haim SA. A novel method for non-fluoroscopic catheter-based electroanatomic mapping of the heart: in vitro and in vivo accuracy results. Circulation (1997) 95:1611–22.
[6] Dixit S, Gerstenfeld EP, Callans DJ, Marchlinski FE. Electrocardiographic patterns of superior right ventricular outflow tract tachycardias: distinguishing septal and free-wall sites of origin. J Cardiovasc Electrophysiol (2003) 14:1–7.[CrossRef][Web of Science][Medline]
[7] Varanasi S, Dhala A, Blanck Z, Deshpande S, Akhtar M, Sra J. Electroanatomic mapping for radiofrequency ablation of cardiac arrhythmias. J Cardiovasc Electrophysiol (1999) 10:538–44.[Web of Science][Medline]
[8] Yamada T, Murakami Y, Yoshida N, Okada T, Toyama J, Yoshida Y, et al. Efficacy of electroanatomic mapping in the catheter ablation of premature ventricular contractions originating from the right ventricular outflow tract. J Interv Card Electrophysiol (2007) 19:187–94.[CrossRef][Web of Science][Medline]
[9] Schmitt C, Ndrepepa G, Weber S, Schmieder S, Weyerbrock S, Schneider M, et al. Biatrial multisite mapping of atrial premature complexes triggering onset of atrial fibrillation. Am J Cardiol (2002) 89:1381–7.[CrossRef][Web of Science][Medline]
[10] Ndrepepa G, Weber S, Karch MR, Schneider MA, Schreieck JJ, Schömig A, et al. Electrophysiologic characteristics of the spontaneous onset and termination of atrial fibrillation. Am J Cardiol (2002) 90:1215–20.[CrossRef][Web of Science][Medline]
[11] Yamada T, Murakami Y, Okada T, Murohara T. Focal atrial fibrillation associated with multiple breakout sites at the crista terminalis. Pacing Clin Electrophysiol (2006) 29:207–10.[CrossRef][Medline]
[12] Yamada T, Murakami Y, Okada T, Yoshida N, Ninomiya Y, Toyama J, et al. Non-pulmonary vein epicardial foci of atrial fibrillation identified in the left atrium after pulmonary vein isolation. Pacing Clin Electrophysiol (2007) 30:1323–30.[CrossRef][Medline]
[13] Rha SW, Kim YH, Hong MK, Ro YM, Choi CU, Suh SY, et al. Mechanisms responsible for the initiation and maintenance of atrial fibrillation assessed by non-contact mapping system. Int J Cardiol (2008) 124:218–26.[CrossRef][Web of Science][Medline]
[14] Schilling RJ, Peters NS, Davies DW. Feasibility of a noncontact catheter for endocardial mapping of human ventricular tachycardia. Circulation (1999) 99:2543–52.
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