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ScienceDirect Journal of Electrocardiology 48 (2015) 445 – 449 www.jecgonline.com
Late onset of exercise induced focal ventricular tachycardia originating from the ventricular end of an A–V accessory pathway after elimination of conduction☆,☆☆,★,★★ Chenni S. Sriram, MD, Mario D. Gonzalez, MD, PhD, FHRS, Gerald V. Naccarelli, MD, FHRS, Jerry C. Luck, MD⁎ Division of Electrophysiology, Heart & Vascular Institute, Penn State Milton S. Hershey Medical Center, Hershey, PA, United States
Abstract
The authors report the unique case of remote onset of exercise induced focal ventricular tachycardia in a 40-year old male patient that originated from the ventricular end of an accessory atrioventricular pathway 18 months after a successful ablation. There was no residual conduction across the pathway after the first ablation. The ventricular tachycardia (VT) was mapped to and successfully ablated at the same site where the ventricular end of the pathway was previously ablated. The VT morphology was similar to that of the pre-excited QRS beats noted before. Thus far, in all reported cases of accessory pathway related automaticity there was intact conduction over the pathway or acute injury to it. To the best of our knowledge a case similar to our patient is not yet reported. © 2015 Elsevier Inc. All rights reserved.
Keywords:
Accessory pathway; Automaticity; Pre-excitation; Ventricular tachycardia; Wide QRS tachycardia
Case report A 40-year-old male who underwent a successful radiofrequency ablation of a mid-septal atrioventricular (A–V) accessory pathway presented 18 months later with exercise induced palpitations and documented wide complex tachycardia (Fig. 1A). He had a 22 year history of ventricular pre-excitation and narrow complex tachycardia with a structurally normal heart. He underwent an electrophysiological study 18 months earlier at our institution because of recurrent symptomatic narrow complex tachycardia refractory to flecainide therapy as well as rapid pre excited atrial fibrillation. Both orthodromic A–V reentrant tachycardia and atrial fibrillation were induced. The ☆ Disclosures: Dr. Mario D. Gonzalez is a consultant for Biosense Webster and Janssen Pharmaceuticals. He has also received research grants and fellowship support from Biosense Webster. Dr. Gerald V. Naccarelli is a consultant for Daiichi-Sankyo, Biosense-Webster, Janssen, Otsuka Pharmaceutical, Bristol Myers Squibb, Glaxo-Smith-Kline, Boehringer-Ingelheim, Pfizer, and Sanofi Aventis. However, none of these entities provided any support for this study. ☆☆ None of the other listed authors have any financial interest to disclose. ★ The authors report no conflicts of interest. The authors alone are responsible for the content and writing of this paper. ★★ Acknowledgments and Sources of Funding: None. ⁎ Corresponding author at: Penn State Heart & Vascular Institute, Milton S. Hershey Medical Center, Penn State University, 500 University Drive, Hershey, PA 17033, United States. E-mail address: [email protected]
http://dx.doi.org/10.1016/j.jelectrocard.2014.10.001 0022-0736/© 2015 Elsevier Inc. All rights reserved.
shortest pre-excited RR interval during atrial fibrillation was 250 milliseconds. The earliest antegrade ventricular activation was recorded just across the tricuspid annulus, 5 mm above of the superior edge of the coronary sinus ostium. The earliest retrograde atrial activation was just above the ostium, 5 mm below the catheter recording the His bundle potential. A single application of radiofrequency energy targeting the ventricular insertion site of the mid-septal A–V accessory pathway eliminated both antegrade and retrograde conduction. There was no residual pathway conduction or automaticity even during isoproterenol administration (8 micrograms per minute). After a long asymptomatic period of 18 months, he began to experience palpitations during exercise. A treadmill exercise stress test showed no evidence of pre-excitation either at baseline or up to stage 5 of a Bruce treadmill test protocol. However, 90 seconds into the recovery phase he developed a wide QRS tachycardia consistent with a ventricular tachycardia (Fig. 1A). Sinus P waves were followed by progressively shorter P-R intervals and progressive ventricular fusion. Since the rate of the ventricular tachycardia (VT) and sinus tachycardia were similar, both rhythms alternated with each other. Abrupt transition from sinus tachycardia to VT occurred after spontaneous premature ventricular complexes (Fig. 1B). The morphology of the VT resembled the pre-excited QRS noted during sinus rhythm prior to the first ablation. In Fig. 2A and B, we show the pre-excited QRS morphology prior to first ablation.
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C.S. Sriram et al. / Journal of Electrocardiology 48 (2015) 445–449
A
B
Fig. 1. A. Exercise induced ventricular tachycardia. Onset of ventricular tachycardia occurs 90 seconds into recovery of exercise stress test (stage 5, Bruce protocol). The first 6 sinus P waves in the figure (small arrows) have a cycle length of 410 ms and are followed by a progressively shorter P-R interval and progressive ventricular fusion (large arrow). The P waves are eventually buried in the QRS. B. Transition for ventricular tachycardia into sinus tachycardia and back into ventricular tachycardia. Note that since the sinus cycle length was similar to the ventricular tachycardia cycle length, both rhythms alternated with each other. A ventricular premature complex (arrow) facilitates the conversion from sinus to ventricular tachycardia.
A repeat electrophysiological study showed no evidence of pre-excitation or retrograde conduction over an accessory pathway during parahisian and differential ventricular pacing. Nonsustained runs of VT (cycle length 400–430 milliseconds) were repeatedly induced with atrial burst pacing during isoproterenol infusion at 8 micrograms per minute (Fig. 3). Isorhythmic dissociation was clearly documented (Fig. 3). His bundle and VT beat dissociation is shown in Figs. 4 and 5. This would eliminate the possibility of AVNRT with left bundle branch block aberrancy as an alternative explanation. The QRS morphology of the VT was similar to that of maximally pre excited beats during atrial fibrillation documented during the first electrophysiological study (Fig. 6). Mapping of the right ventricle during VT identified a focal origin (Fig. 4) at the tricuspid annulus at the same site where conduction over the accessory pathway had previously been eliminated.
Radiofrequency energy delivered at this site eliminated the VT. The wide QRS tachycardia was subsequently not inducible and the patient remained asymptomatic during a 3 year follow-up period.
Discussion To our best knowledge, this is the first case report of the late occurrence of a focal VT originating from the ventricular end of an A–V accessory pathway in the absence of any residual conduction across the pathway. That the VT originated from the ventricular end of the pathway is supported by the fact the repeat ablation was successfully performed at the same site and the QRS morphology during VT was similar to the pre-excited QRS noted before. We
C.S. Sriram et al. / Journal of Electrocardiology 48 (2015) 445–449
447
Fig. 2. A. 12-lead electrocardiogram of pre-excitation during sinus rhythm recorded at the first electrophysiology study. Lead V1 shows a dominant S wave. Isoelectric delta waves are seen in leads V1, II, III, and aVF. This suggests a septal pathway. B. The intra-cardiac electrograms confirm pre-excitation during sinus rhythm with a short H-V interval.
speculate that enhanced automaticity or triggered activity from the ventricular remnant of the previously ablated pathway was responsible for the VT. Przybylski et al. [1]
first reported on automaticity arising from A–V accessory pathways during carotid sinus massage in 3 out of their 23 patients. They suggested that, similar to injured fascicles in
500 ms Fig. 3. Induction of the ventricular tachycardia with isorhythmic A–V dissociation following atrial burst pacing during isoproterenol infusion at a rate of 8 micrograms per minute.
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C.S. Sriram et al. / Journal of Electrocardiology 48 (2015) 445–449
Conducted QRS beats during atrial pacing
Fusion beat
VT beat
VT beat
His
Sinus beat
His
Fig. 4. Right ventricular septal ablation site: Surface leads, intracardiac electrograms from right atrium (RAA), His bundle (HB), coronary sinus (CS), mapping catheter with bipolar (Map P—proximal, Map D—distal) and unipolar (UNI 1—distal, UNI 2—proximal). The earliest local electrogram of the ventricular tachycardia (VT) beat on the Map D is 22 milliseconds (ms) prior to the onset of the surface QRS. There is His bundle dissociation on the HBED electrode demonstrated on the 2nd VT beat. The right atrium (RAA) to His interval of 92 ms is the same as the next sinus beat.
which intermittent bundle branch block can coexist with abnormal automaticity, accessory pathways can also give rise to enhanced automaticity [1,2]. Subsequently pathway related automaticity has been confirmed during invasive electrophysiological studies. Deam et al. [3] reported successful ablation of a right posterolateral, bidirectionally conducting A–V accessory
His
pathway which was also the source of an automatic incessant wide QRS tachycardia. The QRS morphology of both the tachycardia and pre-excited beats was similar and ablation of the pathway also eliminated automaticity. Macle et al. [4] described the appearance of spontaneous automatic accessory pathway activity dissociated from the atrium and ventricle after successful ablation of a concealed left sided pathway. The
His
His
Fig. 5. Lead arrangement is similar to Fig. 4. There is non-sustained ventricular tachycardia with His bundle-QRS dissociation.
C.S. Sriram et al. / Journal of Electrocardiology 48 (2015) 445–449
EP Study#1
449
EP Study#2
Maximally pre-excited QRS during atrial fibrillation
Ventricular tachycardia 500 ms
Fig. 6. The 12 lead electrocardiographic morphology of the maximally pre-excited QRS beats during atrial fibrillation noted during electrophysiology (EP) study#1 closely resembled that of the ventricular tachycardia noted during EP study#2 performed 18 months after elimination of accessory A–V pathway conduction.
automaticity was accelerated during isoproterenol infusion, but remained dissociated from atrium and ventricle. Tseng et al. [5] reported on transient residual pathway mediated automaticity with antegrade conduction to the ventricle in the first hour after the successful ablation of a manifest para-Hisian pathway. Automaticity was triggered after pauses induced by atrial overdrive pacing during isoproterenol challenge. Arias and Sanchez [6] published a case report of thermal induced transient automaticity arising from a left sided concealed accessory pathway immediately following the ablation of its atrial insertion. The automaticity resulted in both regular and irregular wide complex tachycardia with similar morphology. In all reported cases of accessory pathway related automaticity, there exist either intact conduction over the pathway or acute injury to the pathway [1,3–6]. The absence of any automaticity during the initial study and the prolonged hiatus between successful ablation of the pathway and onset of focal ventricular tachycardia from the same site as presented here has not been previously reported. The fact that automaticity was unmasked only after elimination of conduction over the accessory A–V pathway resembles the ventricular rhythms that originate from injured fascicles observed in patients with bundle branch block. In fact, abnormal conduction and abnormal automaticity frequently coexist in the same region both under experimental and clinical conditions [2]. A micro re-entrant circuit secondary to a myocardial scar from the previous ablation could explain latent VT. However, the circumstances suggest a focal mechanism rather than re-entry. First, we delivered only a single radiofrequency current pulse at the time of initial pathway ablation. This would imply that the anatomical scar created
should be small. Second, the tachycardia was not inducible with ventricular extra stimuli testing. Third, the tachycardia could only be triggered by high dose Isoproteronol and atrial burst pacing followed by a pause. Entrainment could not be performed because of the non-sustained nature of the VT. Conclusions We report the unique case of remote onset of catecholamine sensitive focal ventricular tachycardia arising from the ventricular end of an accessory A–V pathway after successful elimination of conduction. The mechanism of VT may be similar to the occurrence of automaticity in fascicles showing bundle branch block. References [1] Przybylski J, Chiale PA, Halpern MS, Lazzari JO, Elizari MV, Rosenbaum MB. Existence of automaticity in anomalous bundle of Wolff–Parkinson–White syndrome. Br Heart J 1978;40:672–80. [2] Rosenbaum MB, Elizari MV, Chiale P, Levi RJ, Nau GJ, Halpern MS, et al. Relationships between increased automaticity and depressed conduction in the main intraventricular conducting fascicles of the human and canine heart. Circulation 1974;49:818–28. [3] Deam AG, Burton ME, Walter PF, Langberg JJ. Wide complex tachycardia due to automaticity in an accessory pathway. Pacing Clin Electrophysiol 1995;18:2106–8. [4] Macle L, Shah DC, Jais P, Haissaguerre M. Accessory pathway automaticity after radiofrequency ablation. J Cardiovasc Electrophysiol 2002;13:285–7. [5] Tseng ZH, Yadav AV, Scheinman MM. Catecholamine dependent accessory pathway automaticity. Pacing Clin Electrophysiol 2004;27:1005–7. [6] Arias MA, Sanchez AM. Automaticity with anterograde conduction of a concealed accessory pathway due to radiofrequency energy application. Int J Cardiol 2008;129:e30–4.
ScienceDirect Journal of Electrocardiology 48 (2015) 445 – 449 www.jecgonline.com
Late onset of exercise induced focal ventricular tachycardia originating from the ventricular end of an A–V accessory pathway after elimination of conduction☆,☆☆,★,★★ Chenni S. Sriram, MD, Mario D. Gonzalez, MD, PhD, FHRS, Gerald V. Naccarelli, MD, FHRS, Jerry C. Luck, MD⁎ Division of Electrophysiology, Heart & Vascular Institute, Penn State Milton S. Hershey Medical Center, Hershey, PA, United States
Abstract
The authors report the unique case of remote onset of exercise induced focal ventricular tachycardia in a 40-year old male patient that originated from the ventricular end of an accessory atrioventricular pathway 18 months after a successful ablation. There was no residual conduction across the pathway after the first ablation. The ventricular tachycardia (VT) was mapped to and successfully ablated at the same site where the ventricular end of the pathway was previously ablated. The VT morphology was similar to that of the pre-excited QRS beats noted before. Thus far, in all reported cases of accessory pathway related automaticity there was intact conduction over the pathway or acute injury to it. To the best of our knowledge a case similar to our patient is not yet reported. © 2015 Elsevier Inc. All rights reserved.
Keywords:
Accessory pathway; Automaticity; Pre-excitation; Ventricular tachycardia; Wide QRS tachycardia
Case report A 40-year-old male who underwent a successful radiofrequency ablation of a mid-septal atrioventricular (A–V) accessory pathway presented 18 months later with exercise induced palpitations and documented wide complex tachycardia (Fig. 1A). He had a 22 year history of ventricular pre-excitation and narrow complex tachycardia with a structurally normal heart. He underwent an electrophysiological study 18 months earlier at our institution because of recurrent symptomatic narrow complex tachycardia refractory to flecainide therapy as well as rapid pre excited atrial fibrillation. Both orthodromic A–V reentrant tachycardia and atrial fibrillation were induced. The ☆ Disclosures: Dr. Mario D. Gonzalez is a consultant for Biosense Webster and Janssen Pharmaceuticals. He has also received research grants and fellowship support from Biosense Webster. Dr. Gerald V. Naccarelli is a consultant for Daiichi-Sankyo, Biosense-Webster, Janssen, Otsuka Pharmaceutical, Bristol Myers Squibb, Glaxo-Smith-Kline, Boehringer-Ingelheim, Pfizer, and Sanofi Aventis. However, none of these entities provided any support for this study. ☆☆ None of the other listed authors have any financial interest to disclose. ★ The authors report no conflicts of interest. The authors alone are responsible for the content and writing of this paper. ★★ Acknowledgments and Sources of Funding: None. ⁎ Corresponding author at: Penn State Heart & Vascular Institute, Milton S. Hershey Medical Center, Penn State University, 500 University Drive, Hershey, PA 17033, United States. E-mail address: [email protected]
http://dx.doi.org/10.1016/j.jelectrocard.2014.10.001 0022-0736/© 2015 Elsevier Inc. All rights reserved.
shortest pre-excited RR interval during atrial fibrillation was 250 milliseconds. The earliest antegrade ventricular activation was recorded just across the tricuspid annulus, 5 mm above of the superior edge of the coronary sinus ostium. The earliest retrograde atrial activation was just above the ostium, 5 mm below the catheter recording the His bundle potential. A single application of radiofrequency energy targeting the ventricular insertion site of the mid-septal A–V accessory pathway eliminated both antegrade and retrograde conduction. There was no residual pathway conduction or automaticity even during isoproterenol administration (8 micrograms per minute). After a long asymptomatic period of 18 months, he began to experience palpitations during exercise. A treadmill exercise stress test showed no evidence of pre-excitation either at baseline or up to stage 5 of a Bruce treadmill test protocol. However, 90 seconds into the recovery phase he developed a wide QRS tachycardia consistent with a ventricular tachycardia (Fig. 1A). Sinus P waves were followed by progressively shorter P-R intervals and progressive ventricular fusion. Since the rate of the ventricular tachycardia (VT) and sinus tachycardia were similar, both rhythms alternated with each other. Abrupt transition from sinus tachycardia to VT occurred after spontaneous premature ventricular complexes (Fig. 1B). The morphology of the VT resembled the pre-excited QRS noted during sinus rhythm prior to the first ablation. In Fig. 2A and B, we show the pre-excited QRS morphology prior to first ablation.
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C.S. Sriram et al. / Journal of Electrocardiology 48 (2015) 445–449
A
B
Fig. 1. A. Exercise induced ventricular tachycardia. Onset of ventricular tachycardia occurs 90 seconds into recovery of exercise stress test (stage 5, Bruce protocol). The first 6 sinus P waves in the figure (small arrows) have a cycle length of 410 ms and are followed by a progressively shorter P-R interval and progressive ventricular fusion (large arrow). The P waves are eventually buried in the QRS. B. Transition for ventricular tachycardia into sinus tachycardia and back into ventricular tachycardia. Note that since the sinus cycle length was similar to the ventricular tachycardia cycle length, both rhythms alternated with each other. A ventricular premature complex (arrow) facilitates the conversion from sinus to ventricular tachycardia.
A repeat electrophysiological study showed no evidence of pre-excitation or retrograde conduction over an accessory pathway during parahisian and differential ventricular pacing. Nonsustained runs of VT (cycle length 400–430 milliseconds) were repeatedly induced with atrial burst pacing during isoproterenol infusion at 8 micrograms per minute (Fig. 3). Isorhythmic dissociation was clearly documented (Fig. 3). His bundle and VT beat dissociation is shown in Figs. 4 and 5. This would eliminate the possibility of AVNRT with left bundle branch block aberrancy as an alternative explanation. The QRS morphology of the VT was similar to that of maximally pre excited beats during atrial fibrillation documented during the first electrophysiological study (Fig. 6). Mapping of the right ventricle during VT identified a focal origin (Fig. 4) at the tricuspid annulus at the same site where conduction over the accessory pathway had previously been eliminated.
Radiofrequency energy delivered at this site eliminated the VT. The wide QRS tachycardia was subsequently not inducible and the patient remained asymptomatic during a 3 year follow-up period.
Discussion To our best knowledge, this is the first case report of the late occurrence of a focal VT originating from the ventricular end of an A–V accessory pathway in the absence of any residual conduction across the pathway. That the VT originated from the ventricular end of the pathway is supported by the fact the repeat ablation was successfully performed at the same site and the QRS morphology during VT was similar to the pre-excited QRS noted before. We
C.S. Sriram et al. / Journal of Electrocardiology 48 (2015) 445–449
447
Fig. 2. A. 12-lead electrocardiogram of pre-excitation during sinus rhythm recorded at the first electrophysiology study. Lead V1 shows a dominant S wave. Isoelectric delta waves are seen in leads V1, II, III, and aVF. This suggests a septal pathway. B. The intra-cardiac electrograms confirm pre-excitation during sinus rhythm with a short H-V interval.
speculate that enhanced automaticity or triggered activity from the ventricular remnant of the previously ablated pathway was responsible for the VT. Przybylski et al. [1]
first reported on automaticity arising from A–V accessory pathways during carotid sinus massage in 3 out of their 23 patients. They suggested that, similar to injured fascicles in
500 ms Fig. 3. Induction of the ventricular tachycardia with isorhythmic A–V dissociation following atrial burst pacing during isoproterenol infusion at a rate of 8 micrograms per minute.
448
C.S. Sriram et al. / Journal of Electrocardiology 48 (2015) 445–449
Conducted QRS beats during atrial pacing
Fusion beat
VT beat
VT beat
His
Sinus beat
His
Fig. 4. Right ventricular septal ablation site: Surface leads, intracardiac electrograms from right atrium (RAA), His bundle (HB), coronary sinus (CS), mapping catheter with bipolar (Map P—proximal, Map D—distal) and unipolar (UNI 1—distal, UNI 2—proximal). The earliest local electrogram of the ventricular tachycardia (VT) beat on the Map D is 22 milliseconds (ms) prior to the onset of the surface QRS. There is His bundle dissociation on the HBED electrode demonstrated on the 2nd VT beat. The right atrium (RAA) to His interval of 92 ms is the same as the next sinus beat.
which intermittent bundle branch block can coexist with abnormal automaticity, accessory pathways can also give rise to enhanced automaticity [1,2]. Subsequently pathway related automaticity has been confirmed during invasive electrophysiological studies. Deam et al. [3] reported successful ablation of a right posterolateral, bidirectionally conducting A–V accessory
His
pathway which was also the source of an automatic incessant wide QRS tachycardia. The QRS morphology of both the tachycardia and pre-excited beats was similar and ablation of the pathway also eliminated automaticity. Macle et al. [4] described the appearance of spontaneous automatic accessory pathway activity dissociated from the atrium and ventricle after successful ablation of a concealed left sided pathway. The
His
His
Fig. 5. Lead arrangement is similar to Fig. 4. There is non-sustained ventricular tachycardia with His bundle-QRS dissociation.
C.S. Sriram et al. / Journal of Electrocardiology 48 (2015) 445–449
EP Study#1
449
EP Study#2
Maximally pre-excited QRS during atrial fibrillation
Ventricular tachycardia 500 ms
Fig. 6. The 12 lead electrocardiographic morphology of the maximally pre-excited QRS beats during atrial fibrillation noted during electrophysiology (EP) study#1 closely resembled that of the ventricular tachycardia noted during EP study#2 performed 18 months after elimination of accessory A–V pathway conduction.
automaticity was accelerated during isoproterenol infusion, but remained dissociated from atrium and ventricle. Tseng et al. [5] reported on transient residual pathway mediated automaticity with antegrade conduction to the ventricle in the first hour after the successful ablation of a manifest para-Hisian pathway. Automaticity was triggered after pauses induced by atrial overdrive pacing during isoproterenol challenge. Arias and Sanchez [6] published a case report of thermal induced transient automaticity arising from a left sided concealed accessory pathway immediately following the ablation of its atrial insertion. The automaticity resulted in both regular and irregular wide complex tachycardia with similar morphology. In all reported cases of accessory pathway related automaticity, there exist either intact conduction over the pathway or acute injury to the pathway [1,3–6]. The absence of any automaticity during the initial study and the prolonged hiatus between successful ablation of the pathway and onset of focal ventricular tachycardia from the same site as presented here has not been previously reported. The fact that automaticity was unmasked only after elimination of conduction over the accessory A–V pathway resembles the ventricular rhythms that originate from injured fascicles observed in patients with bundle branch block. In fact, abnormal conduction and abnormal automaticity frequently coexist in the same region both under experimental and clinical conditions [2]. A micro re-entrant circuit secondary to a myocardial scar from the previous ablation could explain latent VT. However, the circumstances suggest a focal mechanism rather than re-entry. First, we delivered only a single radiofrequency current pulse at the time of initial pathway ablation. This would imply that the anatomical scar created
should be small. Second, the tachycardia was not inducible with ventricular extra stimuli testing. Third, the tachycardia could only be triggered by high dose Isoproteronol and atrial burst pacing followed by a pause. Entrainment could not be performed because of the non-sustained nature of the VT. Conclusions We report the unique case of remote onset of catecholamine sensitive focal ventricular tachycardia arising from the ventricular end of an accessory A–V pathway after successful elimination of conduction. The mechanism of VT may be similar to the occurrence of automaticity in fascicles showing bundle branch block. References [1] Przybylski J, Chiale PA, Halpern MS, Lazzari JO, Elizari MV, Rosenbaum MB. Existence of automaticity in anomalous bundle of Wolff–Parkinson–White syndrome. Br Heart J 1978;40:672–80. [2] Rosenbaum MB, Elizari MV, Chiale P, Levi RJ, Nau GJ, Halpern MS, et al. Relationships between increased automaticity and depressed conduction in the main intraventricular conducting fascicles of the human and canine heart. Circulation 1974;49:818–28. [3] Deam AG, Burton ME, Walter PF, Langberg JJ. Wide complex tachycardia due to automaticity in an accessory pathway. Pacing Clin Electrophysiol 1995;18:2106–8. [4] Macle L, Shah DC, Jais P, Haissaguerre M. Accessory pathway automaticity after radiofrequency ablation. J Cardiovasc Electrophysiol 2002;13:285–7. [5] Tseng ZH, Yadav AV, Scheinman MM. Catecholamine dependent accessory pathway automaticity. Pacing Clin Electrophysiol 2004;27:1005–7. [6] Arias MA, Sanchez AM. Automaticity with anterograde conduction of a concealed accessory pathway due to radiofrequency energy application. Int J Cardiol 2008;129:e30–4.
