- Email: [email protected]
The type of atrial fibrillation recurrence after catheter ablation for persistent atrial fibrillation: What does it mean?
Letters to the Editor [5] Tadamura E, Yamamuro M, Kubo S, et al. Multimodality imaging of cardiac sarcoidosis before and after steroid therapy. Circulation 2006;113:e771–3. [6] Hiraga H, Yuwai K, Hiroe M. Guideline for the diagnosis of cardiac sarcoidosis: study report on diffuse pulmonary disease (in Japanese). Jpn Ministry of Health Welfare; 199323–4. Tadamura E, Yamamuro M, Kubo S, et al. Multimodality imaging of cardiac sarcoidosis before and after steroid therapy. Circulation 1993;113:e771–3.
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[7] Japanese Ministry of Health and Welfare. Diagnostic standard and guidelines for sarcoidosis. Jpn J Sarcoidosis Granulomatous Disord 2007;27:89–102. [8] Cleland JG, Daubert JC, Erdmann E, et al. The effect of cardiac resynchronization on morbidity and mortality in heart failure. N Engl J Med 2005;352:1539–49. [9] Banba K, Kusano KF, Nakamura K, et al. Relationship between arrhythmogenesis and disease activity in cardiac sarcoidosis. Heart Rhythm 2007;4:1292–9.
http://dx.doi.org/10.1016/j.ijcard.2014.07.042 0167-5273/© 2014 Elsevier Ireland Ltd. All rights reserved.
The type of atrial fibrillation recurrence after catheter ablation for persistent atrial fibrillation: What does it mean? Basri Amasyali a,⁎, Ayhan Kilic b, Adnan Dogan a a b
Dumlupinar University, School of Medicine, Department of Cardiology, 43000 Kütahya, Turkey Gulhane Medical Academy, Department of Cardiology, Ankara, Turkey
a r t i c l e
i n f o
Article history: Received 10 May 2014 Accepted 5 July 2014 Available online 12 July 2014 Keywords: Atrial fibrosis Atrial fibrillation Catheter ablation
Catheter ablation of persistent atrial fibrillation (AF) remains a challenging procedure and a very fast growing topic in the field of cardiology. We read with great interest the article written by Sairaku and colleagues addressing the effect of the type of AF recurrence on the result of the second ablation procedure. They have studied 18 and 19 patients who underwent the second ablation procedure for paroxysmal and persistent AF as the recurrence form, respectively. They have found that AF recurrence was less likely to occur after the second session in patients with recurrent paroxysmal AF than in those with recurrent persistent AF (17% vs. 53%, p = 0.032) during a follow-up period of 49 ± 19 months [1]. I would like to discuss the results of this study through a window of “atrial fibrosis”. Although the study design employed by Sairaku and colleagues does not contain a method for quantitative appreciation of atrial fibrosis, we believe that discussion of this aspect would be beneficial for better understanding of the issue. In other words, it would have been beneficial to know the differences between the extent and distribution patterns of atrial fibrosis in patients with recurrent paroxysmal AF and recurrent persistent AF. A recently published study from Lo et al. emphasizes the importance of atrial fibrosis in this subject. In this study, left atrial volume was the only factor to predict the recurrence type of AF (i.e., paroxysmal versus persistent AF) after the initial ablation. Voltage mapping suggested that a reverse electric and structural remodeling occurred after the ablation of chronic AF when the recurrence was paroxysmal AF [2]. Extensive evidence indicates that structural remodeling, particularly interstitial fibrosis, is an important contributor to the substrate of AF [3]. In historical perspective, actually, the presence of fibrosis has been described already years ago by Spach and Boineau as a potential
⁎ Corresponding author. Tel.: +90 274 265 2031; fax: +90 274 265 2016. E-mail address: [email protected] (B. Amasyali).
cause of atrial activation abnormalities that may underlie the initiation and perpetuation of reentrant arrhythmias [4]. Importantly, postmortem structural analyses recently suggested that age-related changes per se were unlikely to be the sole cause of advanced fibrosis underlying AF [5]. Moreover, Mahnkopf et al. recently described the delayed enhancement magnetic resonance imaging (MRI) evaluation of the left atrial substrate in patients with “lone” AF. Interestingly, a substantial portion of these “lone” AF patients showed a mild or even moderate degree of left atrial fibrosis [6]. Additionally, the entity of “fibrotic atrial cardiomyopathy” has lately been formulated to underline the importance of this feature [7]. Thus, atrial fibrosis seems to be an important consideration in the work-up of patients with persistent AF undergoing catheter ablation. It has been suggested that atrial fibrosis, as determined by delayed enhancement MRI, was independently associated with increased likelihood of recurrent arrhythmia in patients with AF undergoing catheter ablation [3]. Fibrosis promotes AF by interrupting fiber-bundle continuity and causing local conduction disturbances [8]. Atrial fibrosis appears to be a common endpoint of a wide range of AF-promoting conditions. Furthermore, AF also appears to promote atrial fibrosis, which contributes importantly to resistance to treatment in patients with long-standing arrhythmia [9,10]. In the study by Sairaku et al., the rate of pulmonary vein (PV) reconnection is relatively higher in the group with recurrent paroxysmal AF, although not statistically significantly (94% vs. 79%, p = 0.19). Still, the phenomenon of PV reconnection seems to have clinical significance, because a significant proportion of these patients have enjoyed an AF-free period after the PV isolation in the second intervention [1]. This shows us that at least some of the triggers responsible for the paroxysmal AF attacks in these patients originate from the reconnecting PVs. Also, it can be said that the atrial substrate perpetuating AF in patients with recurrent paroxysmal AF was more likely abolished by the initial PV isolation when compared to the patients with recurrent persistent AF, as suggested also by Sairaku et al. [1]. This makes us think that the substrate leading to AF in patients with persistent AF, i.e. atrial fibrosis, can exhibit significant individual variations in terms of localization and/or extent. According to one study, AF was terminated during ablation outside the LA in nearly 40% of the cases, suggesting that a non-PV mechanism was operative in a substantial proportion of these patients [11]. That's why different additional ablation strategies have been used to achieve substrate modification in persistent AF although there is consensus that PV isolation targeting the arrhythmia trigger is the basic step. Probably because of this controversy, we still don't have a satisfactory answer for
526
Letters to the Editor
the question “Is isolation of PVs required for ablating persistent AF?”. PV isolation seems to be required in patients with recurrent paroxysmal AF after ablation for persistent AF. This is supported by the study of Sairaku and colleagues, as well as others, and these patients seem to have a significantly better outcome compared to those with recurrent persistent AF [1,12]. Additionally, it has also been suggested that PV isolation along with ablation of non-PV triggers was adequate for treatment of persistent AF, and that additional substrate modification did not improve single procedural efficacy [13]. However, PV isolation was not required according to other authors who targeted elimination of complex fractionated electrograms, or autonomic ganglion plexus for ablation of persistent AF [14,15]. More recently, Narayan et al. reported that focal impulse and rotor mapping and ablation without PV isolation, with the aid of computerized mapping, was sufficient to terminate persistent AF [16]. The sites of successful ablation were often outside the PVs and included right-sided rotors in a quarter of cases, which supports the findings of Wu et al. [11,16]. Ablation strategies in persistent AF differ significantly among centers, mainly because of the scarcity of knowledge about the factors that contribute to the establishment of persistent or permanent AF. After the recent appreciation of importance of atrial fibrosis as AF substrate, preprocedural MRI to document the quantity of atrial fibrosis is being increasingly used. In conclusion, it would have been logical to build an ablation strategy as to assess the amount and localization of substrate for persistent AF, i.e. atrial fibrosis, before the procedure, and merge this information with real-time electrogram signals obtained during the procedure. 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 [3,17,18]. 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. There are no conflicts of interest to declare. References [1] Sairaku A, Yoshida Y, Hirayama H, Kihara Y. Conversion from persistent to paroxysmal atrial fibrillation after pulmonary vein isolation is a good sign. Int J Cardiol 2014;173:322–3.
http://dx.doi.org/10.1016/j.ijcard.2014.07.041 0167-5273/© 2014 Elsevier Ireland Ltd. All rights reserved.
[2] Lo LW, Tsao HM, Lin YJ, et al. Different patterns of atrial remodeling after catheter ablation of chronic atrial fibrillation. J Cardiovasc Electrophysiol 2011;22:385–93. [3] Marrouche NF, Wilber D, Hindricks G, et al. Association of atrial tissue fibrosis identified by delayed enhancement MRI and atrial fibrillation catheter ablation: the DECAAF study. JAMA 2014;311:498–506. [4] Spach MS, Boineau JP. Microfibrosis produces electrical load variations due to loss of side-to-side cell connections: a major mechanism of structural heart disease arrhythmias. Pacing Clin Electrophysiol 1997;20:397–413. [5] Platonov PG, Mitrofnova LB, Oshanskaya V, Ho SY. Structural abnormalities in atrial walls are associated with presence and persistency of atrial fibrillation but not with age. J Am Coll Cardiol 2011;58:2225–32. [6] Mahnkopf C, Badger TJ, Burgon NS, et al. Evaluation of the left atrial substrate in patients with lone atrial fibrillation using delayed-enhanced MRI: implications for disease progression and response to catheter ablation. Heart Rhythm 2010;7:1475–81. [7] Kottkamp H. Human atrial fibrillation substrate: towards a specific fibrotic atrial cardiomyopathy. Eur Heart J 2013;34:2731–8. [8] Burstein B, Comtois P, Michael G, et al. Changes in connexin expression and the atrial fibrillation substrate in congestive heart failure. Circ Res 2009;105:1213–22. [9] Burstein B, Qi XY, Yeh YH, Calderone A, Nattel S. Atrial cardiomyocyte tachycardia alters cardiac fibroblast function: a novel consideration in atrial remodeling. Cardiovasc Res 2007;76:442–52. [10] Verheule S, Tuyls E, Gharaviri A, et al. Loss of continuity in the thin epicardial layer because of endomysial fibrosis increases the complexity of atrial fibrillatory conduction. Circ Arrhythm Electrophysiol 2013;6:202–11. [11] Wu LM, Yao Y, Zheng LH, Zhang KJ, Zhang S. Long-term followup of pure linear ablation on persistent atrial fibrillation without circumferential pulmonary vein isolation. J Cardiovasc Electrophysiol 2014;25:471–6. [12] Ammar S, Hessling G, Reents T, et al. Arrhythmia type after persistent atrial fibrillation ablation predicts success of the repeat procedure. Circ Arrhythm Electrophysiol 2011;4:609–14. [13] Dixit S, Marchlinski FE, Lin D, et al. Randomized ablation strategies for the treatment of persistent atrial fibrillation: RASTA study. Circ Arrhythm Electrophysiol 2012;5:287–94. [14] Nademanee K, McKenzie J, Kosar E, et al. A new approach for catheter ablation of atrial fibrillation: mapping of the electrophysiologic substrate. J Am Coll Cardiol 2004;43:2044–53. [15] Nakagawa H, Scherlag BJ, Patterson E, Ikeda A, Lockwood D, Jackman WM. Pathophysiologic basis of autonomic ganglionated plexus ablation in patients with atrial fibrillation. Heart Rhythm 2009;6:S26–34. [16] Narayan SM, Krummen DE, Shivkumar K, Clopton P, Rappel WJ, Miller JM. Treatment of atrial fibrillation by the ablation of localized sources: CONFIRM (conventional ablation for atrial fibrillation with or without focal impulse and rotor modulation) trial. J Am Coll Cardiol 2012;60:628–36. [17] denUijl DW, Delgado V, Bertini M, et al. Impact of left atrial fibrosis and left atrial size on the outcome of catheter ablation for atrial fibrillation. Heart 2011;97:1847–51. [18] McGann C, Akoum N, Patel A, et al. Atrial fibrillation ablation outcome is predicted by left atrial remodeling on MRI. Circ Arrhythm Electrophysiol 2014;7:23–30.
525
[7] Japanese Ministry of Health and Welfare. Diagnostic standard and guidelines for sarcoidosis. Jpn J Sarcoidosis Granulomatous Disord 2007;27:89–102. [8] Cleland JG, Daubert JC, Erdmann E, et al. The effect of cardiac resynchronization on morbidity and mortality in heart failure. N Engl J Med 2005;352:1539–49. [9] Banba K, Kusano KF, Nakamura K, et al. Relationship between arrhythmogenesis and disease activity in cardiac sarcoidosis. Heart Rhythm 2007;4:1292–9.
http://dx.doi.org/10.1016/j.ijcard.2014.07.042 0167-5273/© 2014 Elsevier Ireland Ltd. All rights reserved.
The type of atrial fibrillation recurrence after catheter ablation for persistent atrial fibrillation: What does it mean? Basri Amasyali a,⁎, Ayhan Kilic b, Adnan Dogan a a b
Dumlupinar University, School of Medicine, Department of Cardiology, 43000 Kütahya, Turkey Gulhane Medical Academy, Department of Cardiology, Ankara, Turkey
a r t i c l e
i n f o
Article history: Received 10 May 2014 Accepted 5 July 2014 Available online 12 July 2014 Keywords: Atrial fibrosis Atrial fibrillation Catheter ablation
Catheter ablation of persistent atrial fibrillation (AF) remains a challenging procedure and a very fast growing topic in the field of cardiology. We read with great interest the article written by Sairaku and colleagues addressing the effect of the type of AF recurrence on the result of the second ablation procedure. They have studied 18 and 19 patients who underwent the second ablation procedure for paroxysmal and persistent AF as the recurrence form, respectively. They have found that AF recurrence was less likely to occur after the second session in patients with recurrent paroxysmal AF than in those with recurrent persistent AF (17% vs. 53%, p = 0.032) during a follow-up period of 49 ± 19 months [1]. I would like to discuss the results of this study through a window of “atrial fibrosis”. Although the study design employed by Sairaku and colleagues does not contain a method for quantitative appreciation of atrial fibrosis, we believe that discussion of this aspect would be beneficial for better understanding of the issue. In other words, it would have been beneficial to know the differences between the extent and distribution patterns of atrial fibrosis in patients with recurrent paroxysmal AF and recurrent persistent AF. A recently published study from Lo et al. emphasizes the importance of atrial fibrosis in this subject. In this study, left atrial volume was the only factor to predict the recurrence type of AF (i.e., paroxysmal versus persistent AF) after the initial ablation. Voltage mapping suggested that a reverse electric and structural remodeling occurred after the ablation of chronic AF when the recurrence was paroxysmal AF [2]. Extensive evidence indicates that structural remodeling, particularly interstitial fibrosis, is an important contributor to the substrate of AF [3]. In historical perspective, actually, the presence of fibrosis has been described already years ago by Spach and Boineau as a potential
⁎ Corresponding author. Tel.: +90 274 265 2031; fax: +90 274 265 2016. E-mail address: [email protected] (B. Amasyali).
cause of atrial activation abnormalities that may underlie the initiation and perpetuation of reentrant arrhythmias [4]. Importantly, postmortem structural analyses recently suggested that age-related changes per se were unlikely to be the sole cause of advanced fibrosis underlying AF [5]. Moreover, Mahnkopf et al. recently described the delayed enhancement magnetic resonance imaging (MRI) evaluation of the left atrial substrate in patients with “lone” AF. Interestingly, a substantial portion of these “lone” AF patients showed a mild or even moderate degree of left atrial fibrosis [6]. Additionally, the entity of “fibrotic atrial cardiomyopathy” has lately been formulated to underline the importance of this feature [7]. Thus, atrial fibrosis seems to be an important consideration in the work-up of patients with persistent AF undergoing catheter ablation. It has been suggested that atrial fibrosis, as determined by delayed enhancement MRI, was independently associated with increased likelihood of recurrent arrhythmia in patients with AF undergoing catheter ablation [3]. Fibrosis promotes AF by interrupting fiber-bundle continuity and causing local conduction disturbances [8]. Atrial fibrosis appears to be a common endpoint of a wide range of AF-promoting conditions. Furthermore, AF also appears to promote atrial fibrosis, which contributes importantly to resistance to treatment in patients with long-standing arrhythmia [9,10]. In the study by Sairaku et al., the rate of pulmonary vein (PV) reconnection is relatively higher in the group with recurrent paroxysmal AF, although not statistically significantly (94% vs. 79%, p = 0.19). Still, the phenomenon of PV reconnection seems to have clinical significance, because a significant proportion of these patients have enjoyed an AF-free period after the PV isolation in the second intervention [1]. This shows us that at least some of the triggers responsible for the paroxysmal AF attacks in these patients originate from the reconnecting PVs. Also, it can be said that the atrial substrate perpetuating AF in patients with recurrent paroxysmal AF was more likely abolished by the initial PV isolation when compared to the patients with recurrent persistent AF, as suggested also by Sairaku et al. [1]. This makes us think that the substrate leading to AF in patients with persistent AF, i.e. atrial fibrosis, can exhibit significant individual variations in terms of localization and/or extent. According to one study, AF was terminated during ablation outside the LA in nearly 40% of the cases, suggesting that a non-PV mechanism was operative in a substantial proportion of these patients [11]. That's why different additional ablation strategies have been used to achieve substrate modification in persistent AF although there is consensus that PV isolation targeting the arrhythmia trigger is the basic step. Probably because of this controversy, we still don't have a satisfactory answer for
526
Letters to the Editor
the question “Is isolation of PVs required for ablating persistent AF?”. PV isolation seems to be required in patients with recurrent paroxysmal AF after ablation for persistent AF. This is supported by the study of Sairaku and colleagues, as well as others, and these patients seem to have a significantly better outcome compared to those with recurrent persistent AF [1,12]. Additionally, it has also been suggested that PV isolation along with ablation of non-PV triggers was adequate for treatment of persistent AF, and that additional substrate modification did not improve single procedural efficacy [13]. However, PV isolation was not required according to other authors who targeted elimination of complex fractionated electrograms, or autonomic ganglion plexus for ablation of persistent AF [14,15]. More recently, Narayan et al. reported that focal impulse and rotor mapping and ablation without PV isolation, with the aid of computerized mapping, was sufficient to terminate persistent AF [16]. The sites of successful ablation were often outside the PVs and included right-sided rotors in a quarter of cases, which supports the findings of Wu et al. [11,16]. Ablation strategies in persistent AF differ significantly among centers, mainly because of the scarcity of knowledge about the factors that contribute to the establishment of persistent or permanent AF. After the recent appreciation of importance of atrial fibrosis as AF substrate, preprocedural MRI to document the quantity of atrial fibrosis is being increasingly used. In conclusion, it would have been logical to build an ablation strategy as to assess the amount and localization of substrate for persistent AF, i.e. atrial fibrosis, before the procedure, and merge this information with real-time electrogram signals obtained during the procedure. 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 [3,17,18]. 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. There are no conflicts of interest to declare. References [1] Sairaku A, Yoshida Y, Hirayama H, Kihara Y. Conversion from persistent to paroxysmal atrial fibrillation after pulmonary vein isolation is a good sign. Int J Cardiol 2014;173:322–3.
http://dx.doi.org/10.1016/j.ijcard.2014.07.041 0167-5273/© 2014 Elsevier Ireland Ltd. All rights reserved.
[2] Lo LW, Tsao HM, Lin YJ, et al. Different patterns of atrial remodeling after catheter ablation of chronic atrial fibrillation. J Cardiovasc Electrophysiol 2011;22:385–93. [3] Marrouche NF, Wilber D, Hindricks G, et al. Association of atrial tissue fibrosis identified by delayed enhancement MRI and atrial fibrillation catheter ablation: the DECAAF study. JAMA 2014;311:498–506. [4] Spach MS, Boineau JP. Microfibrosis produces electrical load variations due to loss of side-to-side cell connections: a major mechanism of structural heart disease arrhythmias. Pacing Clin Electrophysiol 1997;20:397–413. [5] Platonov PG, Mitrofnova LB, Oshanskaya V, Ho SY. Structural abnormalities in atrial walls are associated with presence and persistency of atrial fibrillation but not with age. J Am Coll Cardiol 2011;58:2225–32. [6] Mahnkopf C, Badger TJ, Burgon NS, et al. Evaluation of the left atrial substrate in patients with lone atrial fibrillation using delayed-enhanced MRI: implications for disease progression and response to catheter ablation. Heart Rhythm 2010;7:1475–81. [7] Kottkamp H. Human atrial fibrillation substrate: towards a specific fibrotic atrial cardiomyopathy. Eur Heart J 2013;34:2731–8. [8] Burstein B, Comtois P, Michael G, et al. Changes in connexin expression and the atrial fibrillation substrate in congestive heart failure. Circ Res 2009;105:1213–22. [9] Burstein B, Qi XY, Yeh YH, Calderone A, Nattel S. Atrial cardiomyocyte tachycardia alters cardiac fibroblast function: a novel consideration in atrial remodeling. Cardiovasc Res 2007;76:442–52. [10] Verheule S, Tuyls E, Gharaviri A, et al. Loss of continuity in the thin epicardial layer because of endomysial fibrosis increases the complexity of atrial fibrillatory conduction. Circ Arrhythm Electrophysiol 2013;6:202–11. [11] Wu LM, Yao Y, Zheng LH, Zhang KJ, Zhang S. Long-term followup of pure linear ablation on persistent atrial fibrillation without circumferential pulmonary vein isolation. J Cardiovasc Electrophysiol 2014;25:471–6. [12] Ammar S, Hessling G, Reents T, et al. Arrhythmia type after persistent atrial fibrillation ablation predicts success of the repeat procedure. Circ Arrhythm Electrophysiol 2011;4:609–14. [13] Dixit S, Marchlinski FE, Lin D, et al. Randomized ablation strategies for the treatment of persistent atrial fibrillation: RASTA study. Circ Arrhythm Electrophysiol 2012;5:287–94. [14] Nademanee K, McKenzie J, Kosar E, et al. A new approach for catheter ablation of atrial fibrillation: mapping of the electrophysiologic substrate. J Am Coll Cardiol 2004;43:2044–53. [15] Nakagawa H, Scherlag BJ, Patterson E, Ikeda A, Lockwood D, Jackman WM. Pathophysiologic basis of autonomic ganglionated plexus ablation in patients with atrial fibrillation. Heart Rhythm 2009;6:S26–34. [16] Narayan SM, Krummen DE, Shivkumar K, Clopton P, Rappel WJ, Miller JM. Treatment of atrial fibrillation by the ablation of localized sources: CONFIRM (conventional ablation for atrial fibrillation with or without focal impulse and rotor modulation) trial. J Am Coll Cardiol 2012;60:628–36. [17] denUijl DW, Delgado V, Bertini M, et al. Impact of left atrial fibrosis and left atrial size on the outcome of catheter ablation for atrial fibrillation. Heart 2011;97:1847–51. [18] McGann C, Akoum N, Patel A, et al. Atrial fibrillation ablation outcome is predicted by left atrial remodeling on MRI. Circ Arrhythm Electrophysiol 2014;7:23–30.