Heart Vessels DOI 10.1007/s00380-014-0579-3
CASE REPORT
Paradoxical responses to pacing maneuvers differentiating atrioventricular node reentrant tachycardia and junctional tachycardia Michifumi Tokuda · Teiichi Yamane · Seiichiro Matsuo · Kenichi Tokutake · Kenichi Yokoyama · Mika Hioki · Ryohsuke Narui · Shin‑ichi Tanigawa · Seigo Yamashita · Keiichi Inada · Michihiro Yoshimura
Received: 10 February 2014 / Accepted: 5 September 2014 © Springer Japan 2014
Abstract A 40-year-old female presented at our hospital because of heart palpitations. During an electrophysiological study, atrioventricular (AV) conduction showed dual AV nodal physiology. Three types of supraventricular tachycardia (SVT) were induced. The initiation of SVT was reproducibility dependent on a critical A–H interval prolongation. An early premature atrial contraction during SVT repeatedly advanced the immediate His potential with termination of the tachycardia, indicating AV node reentrant tachycardia (AVNRT). However, after atrial overdrive pacing during SVT without termination of the tachycardia, the first return electrogram resulted in an AHHA response, consistent with junctional tachycardia. The mechanism of paradoxical responses to pacing maneuvers differentiating AVNRT and junctional tachycardia was discussed. Keywords Catheter ablation · Paroxysmal supraventricular tachycardia · Atrioventricular node reentrant tachycardia · Junctional tachycardia
Case presentation A 40-year-old female presented at our hospital because of heart palpitations. She underwent an electrophysiological study and catheter ablation for the tachycardia. During the electrophysiological study, three types of tachycardia were M. Tokuda (*) · T. Yamane · S. Matsuo · K. Tokutake · K. Yokoyama · M. Hioki · R. Narui · S. Tanigawa · S. Yamashita · K. Inada · M. Yoshimura Department of Cardiology, The Jikei University School of Medicine, 3‑25‑8 Nishi‑shinbashi, Minato‑ku, Tokyo 105‑8461, Japan e-mail: [email protected]
observed. At baseline, atrioventricular (AV) conduction showed dual AV nodal physiology, and no VA conduction was observed. Narrow QRS tachycardia (supraventricular tachycardia (SVT-1), Fig. 1a) with an irregular rhythm was spontaneously initiated. Intracardiac recordings showed that an irregular His-ventricular rhythm dissociated with atrial rhythm (Fig. 2). The SVT-1 terminated spontaneously and has never been initiated. After isoproterenol infusion, HA conduction appeared. SVT-2 (Fig. 1b) was reproducibly induced by programmed atrial stimulation with a finding of an atrio-His (AH) jump. A paced premature atrial contraction (PAC) during tachycardia when the His bundle was refractory advanced the subsequent His potential by 36 ms (Fig. 3a). After atrial overdrive pacing from the high right atrial catheter at a CL of 30 ms shorter than the tachycardia CL, without termination of the tachycardia, the first return electrogram resulted in an AHA response (Fig. 3b). Subsequently, wide QRS tachycardia (Fig. 4a) with a CL of 480 ms was induced by atrial premature stimulation. Since the His potential preceded the simultaneous A and V potentials during tachycardia (Fig. 4b), the mechanism of this tachycardia was considered to be SVT with aberrant conduction, rather than ventricular tachycardia. SVT-3 was reproducibility initiated depending on a critical A–H interval prolongation. An early PAC from the proximal coronary sinus during SVT-3 repeatedly advanced the immediate His potential with termination of the tachycardia (Fig. 5a). However, after atrial overdrive pacing during SVT-3 without termination of the tachycardia, the first return electrogram resulted in an AHHA response (Fig. 5b). What are the mechanisms underlying these tachycardias?
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Heart Vessels
Fig. 1 a The 12-lead ECG of SVT-1 and b SVT-2
Fig. 2 Intracardiac electrogram during SVT-1. HA dissociation was observed. The measurements of CL are expressed in milliseconds. HRA High right atrium, CS coronary sinus, d distal, m middle, p proximal, RV right ventricle
Discussion In recent years, most supraventricular and ventricular arrhythmias can be cured by ablation [1, 2]. However, nonreentrant junctional tachycardia (JT) may be difficult to
13
distinguish from atrioventricular nodal reentrant tachycardia (AVNRT) during electrophysiology study. The observation of HA dissociation during SVT rules out orthodromic reciprocating tachycardia and atrial tachycardia as the mechanism underlying these SVTs.
Heart Vessels Fig. 3 The response to pacing maneuvers during SVT-2. a A paced PAC during SVT-2, which was delivered when the His was refractory and advanced the next His by 36 ms. b After atrial overdrive pacing at a CL of 30 ms shorter than the tachycardia CL, the first return electrogram resulted in an AHA response. SVT Supraventricular tachycardia, PAC paroxysmal atrial contraction. The abbreviations are the same as those used in the previous figure
Fig. 4 a The 12-lead ECG and b intracardiac electrogram of SVT-3. The abbreviations are the same as those used in the previous figure
The mechanisms of the SVT are narrowed down to JT or AVNRT. HA dissociation during AVNRT can occur in the presence of an upper common pathway, as had been reported in several clinical studies [3, 4]. However, no histologic data have supported this notion so far. AVNRT is the most common SVT, while JT is a rare SVT that occurs
mostly in children or in the postoperative period [5]. These arrhythmias share many common characteristics, including a His bundle deflection prior to the atrial and ventricular electrograms and nearly simultaneous activation of the atrium and ventricle. Although several maneuvers to identify the mechanism of tachycardia have been previously
13
Heart Vessels
Fig. 5 The response to pacing maneuvers during SVT-3. a An early PAC from the proximal coronary sinus advanced the immediate His potential with termination of SVT-3. b After atrial overdrive pacing during SVT-3, the earliest return signal is His, resulting in an AHHA (A-H2-H3-A) response. The abbreviations are the same as those used in previous figures
reported [6, 7], differentiating two arrhythmias is often challenging. A cycle length variability during SVT-1 suggested the mechanism of the SVT-1 was focal rather than reentrant. Thus, JT is most likely. However, detailed electrophysiological study to investigate the mechanism of SVT-1 could not be performed due to instability of tachycardia. The paced beat timed just after the His potential during SVT-2 advanced the immediate His potential and the AHA response following atrial overdrive pacing, suggesting that the mechanism of SVT-2 was AVNRT. It was previously reported that early PACs that advance the immediate His potential without terminating the SVT indicate a diagnosis of JT with a specificity of 100 % [6]. Additionally, JT was identified with an AHHA response after atrial overdrive pacing in 100 % of cases [7]. Other features of SVT-2 were compatible with slow–slow AVNRT, including central atrial activation, an AH interval > HA interval, a short septal VA interval and the earliest atrial activation during SVT-2 which was posteroseptum. The initiation of SVT-3 was dependent on a critical A–H jump, indicating that the mechanism of SVT-3 was AVNRT. The advancement of the immediate His by early PAC must be caused by anterograde conduction of the PAC over the AV nodal fast pathway, making it refractory. Since the AVNRT circuit requires the AV nodal fast pathway for its retrograde limb, this phenomenon is frequently observed in AVNRT than JT (Fig. 6a). However, termination of SVT in response to an early PAC may occur in focal tachycardia and is not a specific phenomenon to distinguish AVNRT and JT [6].
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Fig. 6 Ladder diagrams recorded during the pacing maneuvers for SVT-3. a Early PAC (star) was conducted down the fast pathway, advancing the immediate His (X-n) and terminating the AVNRT. b Following atrial overdrive pacing during SVT-3, simultaneous AV nodal conduction, one conducting via the fast pathway and another via the slow pathway, caused the AHHA response. The dotted arrow indicates conduction via the slow pathway. AVN Atrioventricular node, FP fast pathway, SP slow pathway, SR sinus rhythm. Other abbreviations are the same as those used in previous figures
The fact that the atrial overdrive pacing during SVT-3 resulted in an AHHA response was not consistent with AVNRT and favors a diagnosis of JT. Why did the
Heart Vessels
paradoxical responses occur? One explanation is a pseudo AHHA response where all entrained His potentials are activated by the slow pathway. However, a pseudo AHHA response is less likely since the morphology of H3 is different from H1 and H2 and activation time between H2 and H3 is longer than that between H1 and H2, indicating H3 is not driven by pacing rate. Another possible explanation is that there is a double ventricular response to a single atrial depolarization via dual AV nodal pathways [8, 9]. After atrial overdrive pacing during SVT-3, simultaneous AV nodal conduction may cause an AHHA response: one conducting via the fast pathway and another via the slow pathway (Fig. 6b). A sufficient conduction delay in the slow pathway will allow the distal tissue to recover and respond for the second time. The difference of His morphology between H2 and H3 may indicate that the His bundle was activated in a different direction. However, the His catheter was unstable during the procedure. In this case, radiofrequency application targeting the antegrade slow pathway resulted in the elimination of tachycardias. There has been no tachycardia recurrence during the 1 year of follow-up. Acknowledgments We are grateful to Dr. Brian Quinn (Japan Medical Communication Inc.) for linguistic comments on the manuscript. Conflict of interest None.
References
initiating atrial fibrillation eliminated by catheter ablation using a non-contact mapping system. Heart Vessels 27:221–226 2. Tokuda M, Yamane T, Matsuo S, Ito K, Narui R, Hioki M, Tanigawa S, Nakane T, Yamashita S, Inada K, Shibayama K, Miyanaga S, Yoshida H, Miyazaki H, Date T, Sugimoto K, Yoshimura M (2011) Different strategies for performing pulmonary vein isolation in patients with pulmonary vein rhythm. Heart Vessels 26:667–671 3. Otomo K, Nagata Y, Uno K, Fujiwara H, Iesaka Y (2007) Atypical atrioventricular nodal reentrant tachycardia with eccentric coronary sinus activation: electrophysiological characteristics and essential effects of left-sided ablation inside the coronary sinus. Heart Rhythm 4:421–432 4. Otomo K, Okamura H, Noda T, Satomi K, Shimizu W, Suyama K, Kurita T, Aihara N, Kamakura S (2006) Unique electrophysiologic characteristics of atrioventricular nodal reentrant tachycardia with different ventriculoatrial block patterns: effects of slow pathway ablation and insights into the location of the reentrant circuit. Heart Rhythm 3:544–554 5. Rosen KM (1973) Junctional tachycardia. Mechanisms, diagnosis, differential diagnosis, and management. Circulation 47:654–664 6. Padanilam BJ, Manfredi JA, Steinberg LA, Olson JA, Fogel RI, Prystowsky EN (2008) Differentiating junctional tachycardia and atrioventricular node re-entry tachycardia based on response to atrial extrastimulus pacing. J Am Coll Cardiol 52:1711–1717 7. Fan R, Tardos JG, Almasry I, Barbera S, Rashba EJ, Iwai S (2011) Novel use of atrial overdrive pacing to rapidly differentiate junctional tachycardia from atrioventricular nodal reentrant tachycardia. Heart Rhythm 8:840–844 8. Suzuki F, Tanaka K, Ishihara N, Hirao K, Kawara T, Hiejima K (1994) Double ventricular responses during extrastimulation of atrioventricular nodal reentrant tachycardia. Eur Heart J 15:285–288 9. Lane C, Veenhuyzen GD, Quinn FR (2013) A conflict of evidence: AVNRT or junctional tachycardia? Heart Rhythm 10:767–769
1. Hioki M, Matsuo S, Yamane T, Tokutake KI, Ito K, Narui R, Tanigawa SI, Yamashita S, Tokuda M, Inada K, Date T, Yoshimura M (2012) Adenosine-induced atrial tachycardia and multiple foci
13
CASE REPORT
Paradoxical responses to pacing maneuvers differentiating atrioventricular node reentrant tachycardia and junctional tachycardia Michifumi Tokuda · Teiichi Yamane · Seiichiro Matsuo · Kenichi Tokutake · Kenichi Yokoyama · Mika Hioki · Ryohsuke Narui · Shin‑ichi Tanigawa · Seigo Yamashita · Keiichi Inada · Michihiro Yoshimura
Received: 10 February 2014 / Accepted: 5 September 2014 © Springer Japan 2014
Abstract A 40-year-old female presented at our hospital because of heart palpitations. During an electrophysiological study, atrioventricular (AV) conduction showed dual AV nodal physiology. Three types of supraventricular tachycardia (SVT) were induced. The initiation of SVT was reproducibility dependent on a critical A–H interval prolongation. An early premature atrial contraction during SVT repeatedly advanced the immediate His potential with termination of the tachycardia, indicating AV node reentrant tachycardia (AVNRT). However, after atrial overdrive pacing during SVT without termination of the tachycardia, the first return electrogram resulted in an AHHA response, consistent with junctional tachycardia. The mechanism of paradoxical responses to pacing maneuvers differentiating AVNRT and junctional tachycardia was discussed. Keywords Catheter ablation · Paroxysmal supraventricular tachycardia · Atrioventricular node reentrant tachycardia · Junctional tachycardia
Case presentation A 40-year-old female presented at our hospital because of heart palpitations. She underwent an electrophysiological study and catheter ablation for the tachycardia. During the electrophysiological study, three types of tachycardia were M. Tokuda (*) · T. Yamane · S. Matsuo · K. Tokutake · K. Yokoyama · M. Hioki · R. Narui · S. Tanigawa · S. Yamashita · K. Inada · M. Yoshimura Department of Cardiology, The Jikei University School of Medicine, 3‑25‑8 Nishi‑shinbashi, Minato‑ku, Tokyo 105‑8461, Japan e-mail: [email protected]
observed. At baseline, atrioventricular (AV) conduction showed dual AV nodal physiology, and no VA conduction was observed. Narrow QRS tachycardia (supraventricular tachycardia (SVT-1), Fig. 1a) with an irregular rhythm was spontaneously initiated. Intracardiac recordings showed that an irregular His-ventricular rhythm dissociated with atrial rhythm (Fig. 2). The SVT-1 terminated spontaneously and has never been initiated. After isoproterenol infusion, HA conduction appeared. SVT-2 (Fig. 1b) was reproducibly induced by programmed atrial stimulation with a finding of an atrio-His (AH) jump. A paced premature atrial contraction (PAC) during tachycardia when the His bundle was refractory advanced the subsequent His potential by 36 ms (Fig. 3a). After atrial overdrive pacing from the high right atrial catheter at a CL of 30 ms shorter than the tachycardia CL, without termination of the tachycardia, the first return electrogram resulted in an AHA response (Fig. 3b). Subsequently, wide QRS tachycardia (Fig. 4a) with a CL of 480 ms was induced by atrial premature stimulation. Since the His potential preceded the simultaneous A and V potentials during tachycardia (Fig. 4b), the mechanism of this tachycardia was considered to be SVT with aberrant conduction, rather than ventricular tachycardia. SVT-3 was reproducibility initiated depending on a critical A–H interval prolongation. An early PAC from the proximal coronary sinus during SVT-3 repeatedly advanced the immediate His potential with termination of the tachycardia (Fig. 5a). However, after atrial overdrive pacing during SVT-3 without termination of the tachycardia, the first return electrogram resulted in an AHHA response (Fig. 5b). What are the mechanisms underlying these tachycardias?
13
Heart Vessels
Fig. 1 a The 12-lead ECG of SVT-1 and b SVT-2
Fig. 2 Intracardiac electrogram during SVT-1. HA dissociation was observed. The measurements of CL are expressed in milliseconds. HRA High right atrium, CS coronary sinus, d distal, m middle, p proximal, RV right ventricle
Discussion In recent years, most supraventricular and ventricular arrhythmias can be cured by ablation [1, 2]. However, nonreentrant junctional tachycardia (JT) may be difficult to
13
distinguish from atrioventricular nodal reentrant tachycardia (AVNRT) during electrophysiology study. The observation of HA dissociation during SVT rules out orthodromic reciprocating tachycardia and atrial tachycardia as the mechanism underlying these SVTs.
Heart Vessels Fig. 3 The response to pacing maneuvers during SVT-2. a A paced PAC during SVT-2, which was delivered when the His was refractory and advanced the next His by 36 ms. b After atrial overdrive pacing at a CL of 30 ms shorter than the tachycardia CL, the first return electrogram resulted in an AHA response. SVT Supraventricular tachycardia, PAC paroxysmal atrial contraction. The abbreviations are the same as those used in the previous figure
Fig. 4 a The 12-lead ECG and b intracardiac electrogram of SVT-3. The abbreviations are the same as those used in the previous figure
The mechanisms of the SVT are narrowed down to JT or AVNRT. HA dissociation during AVNRT can occur in the presence of an upper common pathway, as had been reported in several clinical studies [3, 4]. However, no histologic data have supported this notion so far. AVNRT is the most common SVT, while JT is a rare SVT that occurs
mostly in children or in the postoperative period [5]. These arrhythmias share many common characteristics, including a His bundle deflection prior to the atrial and ventricular electrograms and nearly simultaneous activation of the atrium and ventricle. Although several maneuvers to identify the mechanism of tachycardia have been previously
13
Heart Vessels
Fig. 5 The response to pacing maneuvers during SVT-3. a An early PAC from the proximal coronary sinus advanced the immediate His potential with termination of SVT-3. b After atrial overdrive pacing during SVT-3, the earliest return signal is His, resulting in an AHHA (A-H2-H3-A) response. The abbreviations are the same as those used in previous figures
reported [6, 7], differentiating two arrhythmias is often challenging. A cycle length variability during SVT-1 suggested the mechanism of the SVT-1 was focal rather than reentrant. Thus, JT is most likely. However, detailed electrophysiological study to investigate the mechanism of SVT-1 could not be performed due to instability of tachycardia. The paced beat timed just after the His potential during SVT-2 advanced the immediate His potential and the AHA response following atrial overdrive pacing, suggesting that the mechanism of SVT-2 was AVNRT. It was previously reported that early PACs that advance the immediate His potential without terminating the SVT indicate a diagnosis of JT with a specificity of 100 % [6]. Additionally, JT was identified with an AHHA response after atrial overdrive pacing in 100 % of cases [7]. Other features of SVT-2 were compatible with slow–slow AVNRT, including central atrial activation, an AH interval > HA interval, a short septal VA interval and the earliest atrial activation during SVT-2 which was posteroseptum. The initiation of SVT-3 was dependent on a critical A–H jump, indicating that the mechanism of SVT-3 was AVNRT. The advancement of the immediate His by early PAC must be caused by anterograde conduction of the PAC over the AV nodal fast pathway, making it refractory. Since the AVNRT circuit requires the AV nodal fast pathway for its retrograde limb, this phenomenon is frequently observed in AVNRT than JT (Fig. 6a). However, termination of SVT in response to an early PAC may occur in focal tachycardia and is not a specific phenomenon to distinguish AVNRT and JT [6].
13
Fig. 6 Ladder diagrams recorded during the pacing maneuvers for SVT-3. a Early PAC (star) was conducted down the fast pathway, advancing the immediate His (X-n) and terminating the AVNRT. b Following atrial overdrive pacing during SVT-3, simultaneous AV nodal conduction, one conducting via the fast pathway and another via the slow pathway, caused the AHHA response. The dotted arrow indicates conduction via the slow pathway. AVN Atrioventricular node, FP fast pathway, SP slow pathway, SR sinus rhythm. Other abbreviations are the same as those used in previous figures
The fact that the atrial overdrive pacing during SVT-3 resulted in an AHHA response was not consistent with AVNRT and favors a diagnosis of JT. Why did the
Heart Vessels
paradoxical responses occur? One explanation is a pseudo AHHA response where all entrained His potentials are activated by the slow pathway. However, a pseudo AHHA response is less likely since the morphology of H3 is different from H1 and H2 and activation time between H2 and H3 is longer than that between H1 and H2, indicating H3 is not driven by pacing rate. Another possible explanation is that there is a double ventricular response to a single atrial depolarization via dual AV nodal pathways [8, 9]. After atrial overdrive pacing during SVT-3, simultaneous AV nodal conduction may cause an AHHA response: one conducting via the fast pathway and another via the slow pathway (Fig. 6b). A sufficient conduction delay in the slow pathway will allow the distal tissue to recover and respond for the second time. The difference of His morphology between H2 and H3 may indicate that the His bundle was activated in a different direction. However, the His catheter was unstable during the procedure. In this case, radiofrequency application targeting the antegrade slow pathway resulted in the elimination of tachycardias. There has been no tachycardia recurrence during the 1 year of follow-up. Acknowledgments We are grateful to Dr. Brian Quinn (Japan Medical Communication Inc.) for linguistic comments on the manuscript. Conflict of interest None.
References
initiating atrial fibrillation eliminated by catheter ablation using a non-contact mapping system. Heart Vessels 27:221–226 2. Tokuda M, Yamane T, Matsuo S, Ito K, Narui R, Hioki M, Tanigawa S, Nakane T, Yamashita S, Inada K, Shibayama K, Miyanaga S, Yoshida H, Miyazaki H, Date T, Sugimoto K, Yoshimura M (2011) Different strategies for performing pulmonary vein isolation in patients with pulmonary vein rhythm. Heart Vessels 26:667–671 3. Otomo K, Nagata Y, Uno K, Fujiwara H, Iesaka Y (2007) Atypical atrioventricular nodal reentrant tachycardia with eccentric coronary sinus activation: electrophysiological characteristics and essential effects of left-sided ablation inside the coronary sinus. Heart Rhythm 4:421–432 4. Otomo K, Okamura H, Noda T, Satomi K, Shimizu W, Suyama K, Kurita T, Aihara N, Kamakura S (2006) Unique electrophysiologic characteristics of atrioventricular nodal reentrant tachycardia with different ventriculoatrial block patterns: effects of slow pathway ablation and insights into the location of the reentrant circuit. Heart Rhythm 3:544–554 5. Rosen KM (1973) Junctional tachycardia. Mechanisms, diagnosis, differential diagnosis, and management. Circulation 47:654–664 6. Padanilam BJ, Manfredi JA, Steinberg LA, Olson JA, Fogel RI, Prystowsky EN (2008) Differentiating junctional tachycardia and atrioventricular node re-entry tachycardia based on response to atrial extrastimulus pacing. J Am Coll Cardiol 52:1711–1717 7. Fan R, Tardos JG, Almasry I, Barbera S, Rashba EJ, Iwai S (2011) Novel use of atrial overdrive pacing to rapidly differentiate junctional tachycardia from atrioventricular nodal reentrant tachycardia. Heart Rhythm 8:840–844 8. Suzuki F, Tanaka K, Ishihara N, Hirao K, Kawara T, Hiejima K (1994) Double ventricular responses during extrastimulation of atrioventricular nodal reentrant tachycardia. Eur Heart J 15:285–288 9. Lane C, Veenhuyzen GD, Quinn FR (2013) A conflict of evidence: AVNRT or junctional tachycardia? Heart Rhythm 10:767–769
1. Hioki M, Matsuo S, Yamane T, Tokutake KI, Ito K, Narui R, Tanigawa SI, Yamashita S, Tokuda M, Inada K, Date T, Yoshimura M (2012) Adenosine-induced atrial tachycardia and multiple foci
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