- Email: [email protected]
Reply to the Editor—Masked Left Atrial Appendage Isolation During Ablation Of Persistent Atrial Fibrillation
LETTERS TO THE EDITOR To the Editor—Left Atrial Appendage Electrical Isolation We read with interest the short communication in Heart Rhythm entitled “Masked left atrial appendage isolation during ablation of persistent atrial fibrillation” by Leftheriotis et al.1 Our group recently reported a series on left atrial appendage (LAA) electrical isolation.2 We believe the LAA is an important and underestimated trigger site of atrial fibrillation that should be targeted when triggers from this structure are demonstrated and after catheter ablation has failed. We do not consider LAA electrical isolation to be a complication of extensive LA burnings. Actually, we intentionally targeted the LAA and achieved satisfactory results during long-term follow-up. The LAA is an extra–pulmonary vein trigger that should be targeted, especially in women and in patients with persistent and long-standing persistent atrial fibrillation. With regard to lifelong warfarin administration in these patients, several considerations should be taken into account. There is no demonstration that electrical isolation of the LAA abolishes contraction of the appendage and exposes the patient to a higher risk for transient ischemic attack/stroke. This consideration is based on our recent results that showed abnormal functionality of the isolated appendage only in 44/34% of the cases. This may be due to a LAA reconnection, the presence of persistent dissociated firing, or left ventricular contraction transmitted to the LAA. In addition, many centers perform extensive ablation for treatment of persistent and long-standing persistent AF, and in many cases it is possible that the LAA was inadvertently isolated, as demonstrated by Leftheriotis et al.1 In those cases where the LAA was isolated inadvertently, no warfarin was used and supposedly no stroke/transient ischemic attack was described. Another important issue suggested by the authors is the potential for a closure device in patients with abnormal LAA function who are interested in discontinuing warfarin. We believe that the possibility of achieving sinus rhythm in patients with long-standing persistent AF (in many cases, due to the CHAD2 score these patients would be maintained on warfarin even after ablation) is of great importance. Luigi Di Biase, MD, PhD*† [email protected] Andrea Natale, MD, FHRS, FACC*
References 1.
2.
Leftheriotis D, Yoshiga Y, Kuck K-H, Ouyang F. Masked left atrial appendage isolation during ablation of persistent atrial fibrillation. Heart Rhythm 2010;8: 137–141. Di Biase L, Burkhardt JD, Mohanty P, et al. Left atrial appendage: an underrecognized trigger site of atrial fibrillation. Circulation 2010;122:109 –118.
Reply to the Editor—Masked Left Atrial Appendage Isolation During Ablation of Persistent Atrial Fibrillation We thank Drs. Di Biase and Natale for their interest in our case report1 and their fruitful discussion. According to their recent publication, the left atrial appendage (LAA), like the pulmonary veins, may harbor arrhythmogenic foci in approximately 30% of patients with long-standing persistent atrial fibrillation (AF), and LAA isolation demonstrates a beneficial effect in this population.2 These data are similar to that of our experience in patients with long-standing persistent AF. Furthermore, our data based on 14 patients after catheter ablation of persistent or long-standing persistent AF also showed that LAA isolation was not associated with complications related with stroke or transient ischemic attack during mean follow-up of 9 ⫾ 5 months.3 In these patients, oral anticoagulation (phenprocoumon) was administered for at least 3 months after ablation. Importantly, formation of thrombi within the LAA was observed in only 2 of these 14 patients, in whom a significant decrease in LAA flow velocity (⬍20 cm/s) was observed. Both patients were suboptimally anticoagulated with international normalized ratio of 1.6 and 1.7, respectively. Interestingly, both patients were in sinus rhythm.3 This observation is in accordance with the report by Di Biase and Natale. Based on thrombus formation within the LAA in our series, LAA isolation was considered a potential complication in our case report. However, there is no consensus on whether LAA isolation will be defined as a complication of catheter ablation of AF. Finally, we agree with the pertinent remark regarding the importance of sinus rhythm preservation in patients with long-standing AF. Similar to the report by Di Biase and Natale,2 75% of our patients with LAA isolation remained in sinus rhythm during the follow-up period.3,4 The use of closure devices in LAA is also an adjunctive tool that should be further studied in the future, especially in patients with severely impaired LAA function.
*Texas Cardiac Arrhythmia Institute St. David’s Medical Center Austin, Texas, USA † University of Foggia, Foggia, Italy 1547-5271/$ -see front matter © 2011 Heart Rhythm Society. All rights reserved.
Dionyssios Leftheriotis, MD [email protected] Feifan Ouyang, MD Medizinische Abteilung Asklepios Klinik St. Georg Hamburg, Germany
e2
Heart Rhythm, Vol 8, No 2, February 2011
References 1.
2.
3.
4.
Leftheriotis D, Yoshiga Y, Kuck K-H, Ouyang F. Masked left atrial appendage isolation during ablation of persistent atrial fibrillation. Heart Rhythm 2010;8: 137–141. Di Biase L, Burkhardt JD, Mohanty P, et al. Left atrial appendage: an underrecognized trigger site of atrial fibrillation. Circulation 2010;122:109 – 118. Tilz RR, Chun KR, Schmit B, et al. Catheter ablation of long-standing persistent atrial fibrillation: a lesson from circumferential pulmonary vein isolation. J Cardiovasc Electrophysiol 2010;21:1085–1093. Tilz RR, Schmidt B, Menon S, et al. Left atrial appendage function and clinical outcome after electrical isolation of left atrial appendage in patients undergoing atrial fibrillation ablation. Circulation 2008;118:S694 –S695.
paced morphology. We would like to present this exception as an example of the need to exercise when using this response, especially in ORT where the response depends on multiple variables such as site of pacing, relative distance and conduction time to the His-Purkinje system, and the accessory pathway. Krishnakumar Nair, MD, CCDS† [email protected] Raja Selvaraj, MD* Kah Len Ho, MD† Kumaraswamy Nanthakumar, MD, FRCPC†
To the Editor—His Capture and Entrainment
†
In their article entitled “A novel approach to differentiating orthodromic reciprocating tachycardia from atrioventricular nodal reentrant tachycardia” in the September 2010 issue of Heart Rhythm, Dandamudi et al1 report that in all 23 patients with orthodromic reciprocating tachycardia (ORT) in their study, atrial entrainment occurred before or within one beat after a fully paced right ventricular (RV) complex, whereas in atrioventricular nodal reentrant tachycardia (AVNRT), atrial entrainment occurred more than one beat after a fully paced RV complex. This maneuver is especially useful when RV overdrive pacing terminates tachycardia, making interpretation of the response to pacing termination impossible to use. In AVNRT, atrial entrainment has to occur through the His–Purkinje system. Therefore, antidromic His capture, which results in a fully paced RV complex, necessarily precedes atrial entrainment. In ORT, on the other hand, atrial entrainment can occur by the pathway or by the His-Purkinje system. Entrainment usually occurs through the pathway, followed by orthodromic His capture. A fixed fusion type of RV morphology develops only after orthodromic His capture and therefore typically after atrial entrainment. This is the basis of the maneuver detailed by Dandamudi et al. Because antidromic His capture is essential before atrial entrainment in AVNRT, we agree with the authors that the appearance of a fully paced RV morphology before or within one beat of atrial entrainment excludes AVNRT. However, we disagree with the conclusion that this finding identifies all patients with ORT. Especially in the case of left lateral accessory pathways, the time taken for the RV paced impulse to reach the pathway may be greater than the time needed for the impulse to capture the His. Therefore, the His bundle can be captured retrogradely with a fully paced morphology seen several beats prior to atrial entrainment. We recently reported one such case,2 and this phenomenon can be seen clearly in Figure 2 of our report. This figure shows the beginning of entrainment, and a fully paced RV morphology is seen in beat 3, preceded by antidromic His capture as evidenced by shortening of the H-H interval, His morphology different from anterograde His, and shorter AH interval (compared to Figure 1 in the same report). However, the atrium is entrained two cycles after this fully
Division of Cardiology University Health Network Toronto General Hospital Toronto, Ontario, Canada *Department of Cardiology Jawaharlal Institute of Postgraduate Medical Education and Research Puducherry, India
References 1.
2.
Dandamudi G, Mokabberi R, Assal C, et al. A novel approach to differentiating orthodromic reciprocating tachycardia from atrioventricular nodal reentrant tachycardia. Heart Rhythm 2010;7:1326 –1329. Nair K, Selvaraj R, Farid T, Nanthakumar K. Antidromic His capture during entrainment of orthodromic AVRT. Pacing Clin Electrophysiol 2010;33:1153– 1156.
Reply to the Editor—Differentiating Orthodromic Reciprocating Tachycardia From Atrioventricular Nodal Reentrant Tachycardia In our series,1 there were 15 left free-wall accessory pathways, with the remaining being either septal (right or left) or right free-wall accessory pathways (APs). In all patients with left free-wall APs, we were able to demonstrate acceleration of the tachycardia cycle length (TCL) to the paced cycle length (PCL) with the first fixed morphology right ventricular (RV) paced beat. However, we also showed that with most septal and right free-wall pathways, TCL was accelerated to the PCL even prior to achieving fixed RV pacing morphology. In order for our maneuver to work, it is critical to assess all QRS morphologies to determine the first fixed RV paced morphology beat. Also, it is important that synchronized pacing be performed because asynchronous pacing could reset atrioventricular nodal reentry tachycardia (AVNRT) or orthodromic reentry tachycardia (ORT) based on timing of the RV pacing stimulus. Finally, the first entrained atrial complex is determined by a fixed RV pacing stimulus to atrial electrogram interval. These factors will clearly determine which fixed RV morphology stimulus beat entrained the first atrial complex during tachycardia. It is likely that with left lateral APs, there could be exceptions where acceleration of TCL to the PCL with fixed RV fusion could
References 1.
2.
Leftheriotis D, Yoshiga Y, Kuck K-H, Ouyang F. Masked left atrial appendage isolation during ablation of persistent atrial fibrillation. Heart Rhythm 2010;8: 137–141. Di Biase L, Burkhardt JD, Mohanty P, et al. Left atrial appendage: an underrecognized trigger site of atrial fibrillation. Circulation 2010;122:109 –118.
Reply to the Editor—Masked Left Atrial Appendage Isolation During Ablation of Persistent Atrial Fibrillation We thank Drs. Di Biase and Natale for their interest in our case report1 and their fruitful discussion. According to their recent publication, the left atrial appendage (LAA), like the pulmonary veins, may harbor arrhythmogenic foci in approximately 30% of patients with long-standing persistent atrial fibrillation (AF), and LAA isolation demonstrates a beneficial effect in this population.2 These data are similar to that of our experience in patients with long-standing persistent AF. Furthermore, our data based on 14 patients after catheter ablation of persistent or long-standing persistent AF also showed that LAA isolation was not associated with complications related with stroke or transient ischemic attack during mean follow-up of 9 ⫾ 5 months.3 In these patients, oral anticoagulation (phenprocoumon) was administered for at least 3 months after ablation. Importantly, formation of thrombi within the LAA was observed in only 2 of these 14 patients, in whom a significant decrease in LAA flow velocity (⬍20 cm/s) was observed. Both patients were suboptimally anticoagulated with international normalized ratio of 1.6 and 1.7, respectively. Interestingly, both patients were in sinus rhythm.3 This observation is in accordance with the report by Di Biase and Natale. Based on thrombus formation within the LAA in our series, LAA isolation was considered a potential complication in our case report. However, there is no consensus on whether LAA isolation will be defined as a complication of catheter ablation of AF. Finally, we agree with the pertinent remark regarding the importance of sinus rhythm preservation in patients with long-standing AF. Similar to the report by Di Biase and Natale,2 75% of our patients with LAA isolation remained in sinus rhythm during the follow-up period.3,4 The use of closure devices in LAA is also an adjunctive tool that should be further studied in the future, especially in patients with severely impaired LAA function.
*Texas Cardiac Arrhythmia Institute St. David’s Medical Center Austin, Texas, USA † University of Foggia, Foggia, Italy 1547-5271/$ -see front matter © 2011 Heart Rhythm Society. All rights reserved.
Dionyssios Leftheriotis, MD [email protected] Feifan Ouyang, MD Medizinische Abteilung Asklepios Klinik St. Georg Hamburg, Germany
e2
Heart Rhythm, Vol 8, No 2, February 2011
References 1.
2.
3.
4.
Leftheriotis D, Yoshiga Y, Kuck K-H, Ouyang F. Masked left atrial appendage isolation during ablation of persistent atrial fibrillation. Heart Rhythm 2010;8: 137–141. Di Biase L, Burkhardt JD, Mohanty P, et al. Left atrial appendage: an underrecognized trigger site of atrial fibrillation. Circulation 2010;122:109 – 118. Tilz RR, Chun KR, Schmit B, et al. Catheter ablation of long-standing persistent atrial fibrillation: a lesson from circumferential pulmonary vein isolation. J Cardiovasc Electrophysiol 2010;21:1085–1093. Tilz RR, Schmidt B, Menon S, et al. Left atrial appendage function and clinical outcome after electrical isolation of left atrial appendage in patients undergoing atrial fibrillation ablation. Circulation 2008;118:S694 –S695.
paced morphology. We would like to present this exception as an example of the need to exercise when using this response, especially in ORT where the response depends on multiple variables such as site of pacing, relative distance and conduction time to the His-Purkinje system, and the accessory pathway. Krishnakumar Nair, MD, CCDS† [email protected] Raja Selvaraj, MD* Kah Len Ho, MD† Kumaraswamy Nanthakumar, MD, FRCPC†
To the Editor—His Capture and Entrainment
†
In their article entitled “A novel approach to differentiating orthodromic reciprocating tachycardia from atrioventricular nodal reentrant tachycardia” in the September 2010 issue of Heart Rhythm, Dandamudi et al1 report that in all 23 patients with orthodromic reciprocating tachycardia (ORT) in their study, atrial entrainment occurred before or within one beat after a fully paced right ventricular (RV) complex, whereas in atrioventricular nodal reentrant tachycardia (AVNRT), atrial entrainment occurred more than one beat after a fully paced RV complex. This maneuver is especially useful when RV overdrive pacing terminates tachycardia, making interpretation of the response to pacing termination impossible to use. In AVNRT, atrial entrainment has to occur through the His–Purkinje system. Therefore, antidromic His capture, which results in a fully paced RV complex, necessarily precedes atrial entrainment. In ORT, on the other hand, atrial entrainment can occur by the pathway or by the His-Purkinje system. Entrainment usually occurs through the pathway, followed by orthodromic His capture. A fixed fusion type of RV morphology develops only after orthodromic His capture and therefore typically after atrial entrainment. This is the basis of the maneuver detailed by Dandamudi et al. Because antidromic His capture is essential before atrial entrainment in AVNRT, we agree with the authors that the appearance of a fully paced RV morphology before or within one beat of atrial entrainment excludes AVNRT. However, we disagree with the conclusion that this finding identifies all patients with ORT. Especially in the case of left lateral accessory pathways, the time taken for the RV paced impulse to reach the pathway may be greater than the time needed for the impulse to capture the His. Therefore, the His bundle can be captured retrogradely with a fully paced morphology seen several beats prior to atrial entrainment. We recently reported one such case,2 and this phenomenon can be seen clearly in Figure 2 of our report. This figure shows the beginning of entrainment, and a fully paced RV morphology is seen in beat 3, preceded by antidromic His capture as evidenced by shortening of the H-H interval, His morphology different from anterograde His, and shorter AH interval (compared to Figure 1 in the same report). However, the atrium is entrained two cycles after this fully
Division of Cardiology University Health Network Toronto General Hospital Toronto, Ontario, Canada *Department of Cardiology Jawaharlal Institute of Postgraduate Medical Education and Research Puducherry, India
References 1.
2.
Dandamudi G, Mokabberi R, Assal C, et al. A novel approach to differentiating orthodromic reciprocating tachycardia from atrioventricular nodal reentrant tachycardia. Heart Rhythm 2010;7:1326 –1329. Nair K, Selvaraj R, Farid T, Nanthakumar K. Antidromic His capture during entrainment of orthodromic AVRT. Pacing Clin Electrophysiol 2010;33:1153– 1156.
Reply to the Editor—Differentiating Orthodromic Reciprocating Tachycardia From Atrioventricular Nodal Reentrant Tachycardia In our series,1 there were 15 left free-wall accessory pathways, with the remaining being either septal (right or left) or right free-wall accessory pathways (APs). In all patients with left free-wall APs, we were able to demonstrate acceleration of the tachycardia cycle length (TCL) to the paced cycle length (PCL) with the first fixed morphology right ventricular (RV) paced beat. However, we also showed that with most septal and right free-wall pathways, TCL was accelerated to the PCL even prior to achieving fixed RV pacing morphology. In order for our maneuver to work, it is critical to assess all QRS morphologies to determine the first fixed RV paced morphology beat. Also, it is important that synchronized pacing be performed because asynchronous pacing could reset atrioventricular nodal reentry tachycardia (AVNRT) or orthodromic reentry tachycardia (ORT) based on timing of the RV pacing stimulus. Finally, the first entrained atrial complex is determined by a fixed RV pacing stimulus to atrial electrogram interval. These factors will clearly determine which fixed RV morphology stimulus beat entrained the first atrial complex during tachycardia. It is likely that with left lateral APs, there could be exceptions where acceleration of TCL to the PCL with fixed RV fusion could