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Complex fragment atrial electrograms, not pulmonary vein, the ideal ablation targets for chronic atrial fibrillation
Medical Hypotheses (2008) 70, 349–351
http://intl.elsevierhealth.com/journals/mehy
Complex fragment atrial electrograms, not pulmonary vein, the ideal ablation targets for chronic atrial fibrillation Hailong Tao, Jianzeng Dong, Changsheng Ma
*
Department of Cardiology, AnZhen Hospital, Capital Medical University, Beijing 100029, PR China Received 12 March 2007; accepted 12 March 2007
Summary Complex fragment atrial electrograms (CFAEs) are fractionated or discrete atrial wave fronts that frequently mapped in chronic atrial fibrillation (CAF). The CFAEs areas represent slow conduction and/or functional blocks that play substrate role in AF. Compared with the limited efficacy of pulmonary veins (PVs) oriented ablation strategy for CAF, few attempts of adjunctive ablation on CFAEs gain promising outcome. We hypothesized that CFAEs, not PVs, are the ideal ablation targets for CAF. c 2007 Elsevier Ltd. All rights reserved.
Introduction
Limitation of PVs ablation for CAF
The dominant ablation for AF mainly concentrates on PVs, trigger of AF, and gains success in paroxysmal atrial fibrillation (PAF) but shows limited efficacy for CAF [1–8]. CFAEs are series of fragmented and discrete atrial electrograms that are frequently recorded in CAF. The regions of CFAEs represent slow conduction and key points for functional block of which compose the basis of substrate for AF [9]. Adjunctive or solely ablation on CFAEs has achieved a high level of success in termination of CAF [9,10]. We hypothesized that CFAEs, not PVs are the ideal strategy for CAF ablation.
Temporary AF ablation focuses on PVs and has been proved efficient for paroxysmal AF. But the real success rate for CAF is low (PAF (85%) vs. CAF (68%)) [1–8]. Clinical practices have found that relative amount of CAF can not be terminated by solely PVs ablation [5–7]. Frequent AF recurrence episode for CAF challenges current ablation strategy [5–7,11,12]. Nevertheless, some hybrid therapies which ablate CFAEs or other substrates beyond PVs have been proved to be efficacious for improving termination of CAF [10,12,13].
* Corresponding author. Tel.: +86 10 64456412; fax: +86 10 64456078. E-mail address: [email protected] (C. Ma).
Evidence of CFAEs Many mapping studies of both animals and humans have demonstrated the presence of fragmented or discrete atrial electrograms in AF [14–17]. The
0306-9877/$ - see front matter c 2007 Elsevier Ltd. All rights reserved. doi:10.1016/j.mehy.2007.03.042
350 characteristics of CFAEs are defined as: (1) fractionated electrograms composed of two deflections or more; (2) atrial electrograms with a very short cycle length (6120 ms) [9]. Such complex electrical activity has a relatively short cycle length and heterogeneous temporal and spatial distribution and tissue anisotropy [9]. Areas of CFAEs represent either continuous reentry of the fibrillation waves into the same area or overlap of different wavelets entering the same area at different times [15,18]. The electrophysiological features of CFAEs conform to the basic characters of substrate for AF, heterogeneous conduction and functional block. CFAEs are regarded as markers of the rotor areas that maintain the atrial fibrillation [9].
Relation between CFAEs and CAF Generally understandings, CFAEs represent more complex and irregular electrical activity in CAF. In animal experiments, CFAEs are frequently mapped in induced AF which is stimulated through long duration [11]. Compared to PAF, fragmentation index (FI) which quantify the extent of fragment is higher in CAF (34 ± 9 vs. 27 ± 9%; p = 0.03) [19]. A research that compared the extent of fragment between CAF and PAF has identified more complex and fragmented electrograms are vulnerable in CAF [18]. CFAEs also coincide with high-frequency activity that plays other role in maintaining AF [20]. CFAEs areas are responsible for the perpetuation of CAF [9].
Efficiency of CFAEs ablation Animal experiments have showed that CFAEs are mainly located among mid-atrial septum and ablation in such areas can convert induced AF [21]. Ablation and elimination CFAEs can increase cycle length and promote termination of AF [9]. A study of 121 patients who undergone CFAEs ablation showed curative in 95% of patients during ablation and free of AF in 91% of patients in one year followup. It is noted that in this cohort population, CAF patients cover 52.9% and conversion rate is 91% during ablation. The study also showed that a number of patients benefited from an ablation procedure not involving the pulmonary veins [9].
The hypothesis CFAEs are some specific atrial electrograms characterized by fragmented or multi-deflected wave
Tao et al. fronts and short cycle length. CFAEs are prone to present in CAF and are regarded as markers of the rotor areas that maintain the atrial fibrillation. The areas of CFAEs compose the basis of reentry and promote substrates of CAF. Current ablation focuses on PVs and only gains limited efficiency in CAF. CFAEs ablation concentrates on substrate modification and gains promising outcome. The above evidence supports our hypothesis that CFAEs, not PVs, are the ideal ablation targets for CAF and warrants further clinical trials to investigate if solely CFAEs ablation is sufficient for all AF.
References [1] 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. [2] Kanagaratnam L, Tomassoni G, Schweikert R, Pavia S, Bash D, Beheiry S, et al. Empirical pulmonary vein isolation in patients with chronic atrial fibrillation using a threedimensional nonfluoroscopic mapping system: long-term follow-up. Pacing Clin Electrophysiol 2001;24:1774–9. [3] Haissaguerre M, Jais P, Shah DC, et al. Catheter ablation of chronic atrial fibrillation targeting the reinitiating triggers. J Cardiovasc Electrophysiol 2000;11:2–10. [4] Natale A, Pisano E, Beheiry S, et al. Ablation of right and left atrial premature beats following cardioversion in patients with chronic atrial fibrillation refractory to antiarrhythmic drugs. Am J Cardiol 2000;85:1372–5. [5] Seidl K, Schwacke H, Zahn R, et al. Catheter ablation of chronic atrial fibrillation with noncontact mapping: are continuous linear lesions associated with ablation success? Pacing Clin Electrophysiol 2003;26:534–43. [6] Riccardo Cappato, Hugh Calkins, Shih-Ann Chen, Wyn Davies, Yoshito Iesaka, Jonathan Kalman, et al. Worldwide survey on the methods, efficacy, and safety of catheter ablation for human atrial fibrillation. Circulation 2005;111:1100–5. [7] Nattel S. New ideas about atrial fibrillation 50 years on. Nature 2002;415:219–26. [8] Allessie MA, Konings K, Kirchhof CJHJ, et al. Electrophysiologic mechanisms of perpetuation of atrial fibrillation. Am J Cardiol 1996;77:10A–23A. [9] Koonlawee Nademanee, John McKenzie, Erol Kosar, Mark Schwab, Buncha Sunsaneewitayakul, Thaveekiat Vasavakul, et al. A new approach for catheter ablation of atrial fibrillation: mapping of the electrophysiologic substrate. J Am Coll Cardiol 2004;43:2044–53. [10] Mark D O’Neill, Pierre Jaı ¨s, Yoshihide Takahashi, Anders Jo ¨nsson, Fre ´de ´ric Sacher, Me ´le `ze Hocini, et al. The stepwise ablation approach for chronic atrial fibrillation – evidence for a cumulative effect. J Cardiovasc Electrophysiol 2006;16:153–67. [11] Stabile G, Turco P, La Rocca V, Nocerino P, Stabile E, De Simone A. Is pulmonary vein isolation necessary for curing atrial fibrillation? Circulation 2003;108:657–60. [12] Kottkamp H, Tanner H, Kobza R, et al. Time courses and quantitative analysis of atrial fibrillation episode number and duration after circular plus linear left atrial lesions: trigger elimination or substrate modification: early or delayed cure? J Am Coll Cardiol 2004;44:869–77.
Complex fragment atrial electrograms, not pulmonary vein [13] Mauricio Arruda, Andrea Natale. Adjunctive role of nonpulmonary venous ablation in the cure of atrial fibrillation. J Cardiovasc Electrophysiol 2006;17:S37–43. [14] Konings KTS, Kirchhof CJHJ, Smeets JRLM, et al. Highdensity mapping of electrically induced atrial fibrillation in humans. Circulation 1994;89:1665–80. [15] Konings KTS, Smeets JLRM, Penn OC, et al. Configuration of unipolar atrial electrograms during electrically induced atrial fibrillation in humans. Circulation 1997;95:1231–41. [16] Gardner PI, Ursell PC, Fenoglio Jr JJ, Wit AL. Electrophysiologic and anatomic basis for fractionated electrograms recorded from healed myocardial infarcts. Circulation 1985;72:596–611. [17] Dillon SM, Allessie MA, Ursell PC, Wit AL. Influences of anisotropic tissue structure on reentrant circuits in the epicardial border zone of subacute canine infarcts. Circ Res 1988;63:182–206.
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[18] Konings KTS, Kirchhof CJHJ, Smeets JRLM, et al. Highdensity mapping of electrically induced atrial fibrillation in humans. Circulation 1994;89:1665–80. [19] Sanders P, Szumowski L, Jaı ¨s P, Nalliah C, Hsu L, Hocini M, et al. Atrial remodeling in paroxysmal versus chronic atrial fibrillation. Comparison of electrogram fragmentation and voltage reduction. Heart Rhythm 2005;2:S21. [20] Prashanthan Sanders, Omer Berenfeld, Me ´le `ze Hocini, Pierre Jaı ¨s, Ravi Vaidyanathan, Li-Fern Hsu, et al. Spectral analysis identifies sites of high-frequency activity maintaining atrial fibrillation in humans. Circulation 2005;112:789–97. [21] Tondo C, Scherlag BJ, Otomo K, Antz M, Patterson E, Arruda M, et al. Critical atrial site for ablation of pacinginduced atrial fibrillation in the normal dog heart. J Cardiovasc Electrophysiol 1997;8:1266–8.
Available online at www.sciencedirect.com
http://intl.elsevierhealth.com/journals/mehy
Complex fragment atrial electrograms, not pulmonary vein, the ideal ablation targets for chronic atrial fibrillation Hailong Tao, Jianzeng Dong, Changsheng Ma
*
Department of Cardiology, AnZhen Hospital, Capital Medical University, Beijing 100029, PR China Received 12 March 2007; accepted 12 March 2007
Summary Complex fragment atrial electrograms (CFAEs) are fractionated or discrete atrial wave fronts that frequently mapped in chronic atrial fibrillation (CAF). The CFAEs areas represent slow conduction and/or functional blocks that play substrate role in AF. Compared with the limited efficacy of pulmonary veins (PVs) oriented ablation strategy for CAF, few attempts of adjunctive ablation on CFAEs gain promising outcome. We hypothesized that CFAEs, not PVs, are the ideal ablation targets for CAF. c 2007 Elsevier Ltd. All rights reserved.
Introduction
Limitation of PVs ablation for CAF
The dominant ablation for AF mainly concentrates on PVs, trigger of AF, and gains success in paroxysmal atrial fibrillation (PAF) but shows limited efficacy for CAF [1–8]. CFAEs are series of fragmented and discrete atrial electrograms that are frequently recorded in CAF. The regions of CFAEs represent slow conduction and key points for functional block of which compose the basis of substrate for AF [9]. Adjunctive or solely ablation on CFAEs has achieved a high level of success in termination of CAF [9,10]. We hypothesized that CFAEs, not PVs are the ideal strategy for CAF ablation.
Temporary AF ablation focuses on PVs and has been proved efficient for paroxysmal AF. But the real success rate for CAF is low (PAF (85%) vs. CAF (68%)) [1–8]. Clinical practices have found that relative amount of CAF can not be terminated by solely PVs ablation [5–7]. Frequent AF recurrence episode for CAF challenges current ablation strategy [5–7,11,12]. Nevertheless, some hybrid therapies which ablate CFAEs or other substrates beyond PVs have been proved to be efficacious for improving termination of CAF [10,12,13].
* Corresponding author. Tel.: +86 10 64456412; fax: +86 10 64456078. E-mail address: [email protected] (C. Ma).
Evidence of CFAEs Many mapping studies of both animals and humans have demonstrated the presence of fragmented or discrete atrial electrograms in AF [14–17]. The
0306-9877/$ - see front matter c 2007 Elsevier Ltd. All rights reserved. doi:10.1016/j.mehy.2007.03.042
350 characteristics of CFAEs are defined as: (1) fractionated electrograms composed of two deflections or more; (2) atrial electrograms with a very short cycle length (6120 ms) [9]. Such complex electrical activity has a relatively short cycle length and heterogeneous temporal and spatial distribution and tissue anisotropy [9]. Areas of CFAEs represent either continuous reentry of the fibrillation waves into the same area or overlap of different wavelets entering the same area at different times [15,18]. The electrophysiological features of CFAEs conform to the basic characters of substrate for AF, heterogeneous conduction and functional block. CFAEs are regarded as markers of the rotor areas that maintain the atrial fibrillation [9].
Relation between CFAEs and CAF Generally understandings, CFAEs represent more complex and irregular electrical activity in CAF. In animal experiments, CFAEs are frequently mapped in induced AF which is stimulated through long duration [11]. Compared to PAF, fragmentation index (FI) which quantify the extent of fragment is higher in CAF (34 ± 9 vs. 27 ± 9%; p = 0.03) [19]. A research that compared the extent of fragment between CAF and PAF has identified more complex and fragmented electrograms are vulnerable in CAF [18]. CFAEs also coincide with high-frequency activity that plays other role in maintaining AF [20]. CFAEs areas are responsible for the perpetuation of CAF [9].
Efficiency of CFAEs ablation Animal experiments have showed that CFAEs are mainly located among mid-atrial septum and ablation in such areas can convert induced AF [21]. Ablation and elimination CFAEs can increase cycle length and promote termination of AF [9]. A study of 121 patients who undergone CFAEs ablation showed curative in 95% of patients during ablation and free of AF in 91% of patients in one year followup. It is noted that in this cohort population, CAF patients cover 52.9% and conversion rate is 91% during ablation. The study also showed that a number of patients benefited from an ablation procedure not involving the pulmonary veins [9].
The hypothesis CFAEs are some specific atrial electrograms characterized by fragmented or multi-deflected wave
Tao et al. fronts and short cycle length. CFAEs are prone to present in CAF and are regarded as markers of the rotor areas that maintain the atrial fibrillation. The areas of CFAEs compose the basis of reentry and promote substrates of CAF. Current ablation focuses on PVs and only gains limited efficiency in CAF. CFAEs ablation concentrates on substrate modification and gains promising outcome. The above evidence supports our hypothesis that CFAEs, not PVs, are the ideal ablation targets for CAF and warrants further clinical trials to investigate if solely CFAEs ablation is sufficient for all AF.
References [1] 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. [2] Kanagaratnam L, Tomassoni G, Schweikert R, Pavia S, Bash D, Beheiry S, et al. Empirical pulmonary vein isolation in patients with chronic atrial fibrillation using a threedimensional nonfluoroscopic mapping system: long-term follow-up. Pacing Clin Electrophysiol 2001;24:1774–9. [3] Haissaguerre M, Jais P, Shah DC, et al. Catheter ablation of chronic atrial fibrillation targeting the reinitiating triggers. J Cardiovasc Electrophysiol 2000;11:2–10. [4] Natale A, Pisano E, Beheiry S, et al. Ablation of right and left atrial premature beats following cardioversion in patients with chronic atrial fibrillation refractory to antiarrhythmic drugs. Am J Cardiol 2000;85:1372–5. [5] Seidl K, Schwacke H, Zahn R, et al. Catheter ablation of chronic atrial fibrillation with noncontact mapping: are continuous linear lesions associated with ablation success? Pacing Clin Electrophysiol 2003;26:534–43. [6] Riccardo Cappato, Hugh Calkins, Shih-Ann Chen, Wyn Davies, Yoshito Iesaka, Jonathan Kalman, et al. Worldwide survey on the methods, efficacy, and safety of catheter ablation for human atrial fibrillation. Circulation 2005;111:1100–5. [7] Nattel S. New ideas about atrial fibrillation 50 years on. Nature 2002;415:219–26. [8] Allessie MA, Konings K, Kirchhof CJHJ, et al. Electrophysiologic mechanisms of perpetuation of atrial fibrillation. Am J Cardiol 1996;77:10A–23A. [9] Koonlawee Nademanee, John McKenzie, Erol Kosar, Mark Schwab, Buncha Sunsaneewitayakul, Thaveekiat Vasavakul, et al. A new approach for catheter ablation of atrial fibrillation: mapping of the electrophysiologic substrate. J Am Coll Cardiol 2004;43:2044–53. [10] Mark D O’Neill, Pierre Jaı ¨s, Yoshihide Takahashi, Anders Jo ¨nsson, Fre ´de ´ric Sacher, Me ´le `ze Hocini, et al. The stepwise ablation approach for chronic atrial fibrillation – evidence for a cumulative effect. J Cardiovasc Electrophysiol 2006;16:153–67. [11] Stabile G, Turco P, La Rocca V, Nocerino P, Stabile E, De Simone A. Is pulmonary vein isolation necessary for curing atrial fibrillation? Circulation 2003;108:657–60. [12] Kottkamp H, Tanner H, Kobza R, et al. Time courses and quantitative analysis of atrial fibrillation episode number and duration after circular plus linear left atrial lesions: trigger elimination or substrate modification: early or delayed cure? J Am Coll Cardiol 2004;44:869–77.
Complex fragment atrial electrograms, not pulmonary vein [13] Mauricio Arruda, Andrea Natale. Adjunctive role of nonpulmonary venous ablation in the cure of atrial fibrillation. J Cardiovasc Electrophysiol 2006;17:S37–43. [14] Konings KTS, Kirchhof CJHJ, Smeets JRLM, et al. Highdensity mapping of electrically induced atrial fibrillation in humans. Circulation 1994;89:1665–80. [15] Konings KTS, Smeets JLRM, Penn OC, et al. Configuration of unipolar atrial electrograms during electrically induced atrial fibrillation in humans. Circulation 1997;95:1231–41. [16] Gardner PI, Ursell PC, Fenoglio Jr JJ, Wit AL. Electrophysiologic and anatomic basis for fractionated electrograms recorded from healed myocardial infarcts. Circulation 1985;72:596–611. [17] Dillon SM, Allessie MA, Ursell PC, Wit AL. Influences of anisotropic tissue structure on reentrant circuits in the epicardial border zone of subacute canine infarcts. Circ Res 1988;63:182–206.
351
[18] Konings KTS, Kirchhof CJHJ, Smeets JRLM, et al. Highdensity mapping of electrically induced atrial fibrillation in humans. Circulation 1994;89:1665–80. [19] Sanders P, Szumowski L, Jaı ¨s P, Nalliah C, Hsu L, Hocini M, et al. Atrial remodeling in paroxysmal versus chronic atrial fibrillation. Comparison of electrogram fragmentation and voltage reduction. Heart Rhythm 2005;2:S21. [20] Prashanthan Sanders, Omer Berenfeld, Me ´le `ze Hocini, Pierre Jaı ¨s, Ravi Vaidyanathan, Li-Fern Hsu, et al. Spectral analysis identifies sites of high-frequency activity maintaining atrial fibrillation in humans. Circulation 2005;112:789–97. [21] Tondo C, Scherlag BJ, Otomo K, Antz M, Patterson E, Arruda M, et al. Critical atrial site for ablation of pacinginduced atrial fibrillation in the normal dog heart. J Cardiovasc Electrophysiol 1997;8:1266–8.
Available online at www.sciencedirect.com