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Arrhythmia Rounds Section Editor: George J. Klein, M.D.
An Irregular Supraventricular Tachycardia: What is the Mechanism? SHINSUKE MIYAZAKI, M.D., TAKASHI UCHIYAMA, M.D., and YOSHITO IESAKA, M.D. From the Tsuchiura Kyodo Hospital, Ibaraki, Japan
atrial tachycardia, AV node reentry, catheter ablation, double tachycardia, junctional tachycardia, noncoronary cusp Introduction A 56-year-old woman with regular narrow QRS complex tachycardia without any structural heart disease was referred to our center for electrophysiological study and catheter ablation. A baseline electrophysiological test demonstrated a normal AH/HV interval during sinus rhythm and a dual atrioventricular (AV) nodal physiology of the antegrade pathway. The clinical tachycardia was repeatedly inducible following a jump during atrial extrastimuli, and the retrograde earliest atrial activation occurred from the His region during the tachycardia. The ventriculoatrial (VA) conduction exhibited decremental properties with the same atrial activation sequence as that during the tachycardia, and ventricular extrastimuli during His refractory period did not advance atrial excitation. Figure 1 shows the spontaneous fluctuation of this tachycardia. What is the mechanism of this phenomenon? Commentary The differential diagnosis of this irregular tachycardia includes irregular atrial tachycardia (AT), AV nodal reentrant tachycardia (AVNRT) with variable block to atrium and/or ventricle, and AVNRT over multiple retrograde AV node pathways. Although the results of electrophysiological study favor typical slow-fast AVNRT, the irregular tachycardia like Figure 1 cannot be explained. Figure 2 shows the transition
J Cardiovasc Electrophysiol, Vol. 26, pp. 231-232, February 2015. No disclosures. Address for correspondence: Shinsuke Miyazaki, M.D., Cardiology Division, Cardiovascular Center, Tsuchiura Kyodo Hospital, 11–7 Manabeshinmachi, Tsuchiura, Ibaraki 300-0053, Japan. Fax: 81-29-826-2411; E-mail: [email protected] Manuscript received 2 September 2014; Revised manuscript received 4 September 2014; Accepted for publication 9 September 2014. doi: 10.1111/jce.12541
of the tachycardia. Another tachycardia was provoked following ventricular pacing during stable AVNRT (Fig. 2A). The earliest atrial activation occurred from the His region during the tachycardia like AVNRT; however, it was provoked by V-A-A-V response following ventricular pacing, which suggested that the mechanism of the tachycardia was AT. The AT was also inducible by atrial extrastimuli without a jump, and terminated by 4 mg bolus injection of adenosine triphosphate. The AVNRT was more stable than the AT, and spontaneous transition from AT to AVNRT was observed several times (Fig. 2B); however, spontaneous transition from AVNRT to AT was not observed. The cycle length of the AT was longer than that of AVNRT. Slow pathway ablation completely eliminated the AVNRT, and stable AT was easily inducible after eliminating AVNRT. After the detail mapping at right ventricular mid septum and coronary cusps, the AT terminated by a 4.0 seconds of radiofrequency application at the noncoronary cusp, which resulted in inability to induce the AT. Previous studies have demonstrated that focal ATs originating from the septal regions can be reproducibly induced and terminated by programmed atrial stimulation, and are sensitive to intravenous adenosine in most patients.1 The earliest atrial activation site is close to the His bundle, while it could be eliminated by radiofrequency applications from the noncoronary cusp in a part of the patients.2 A recent study has shown that the mechanism of AT was due to reentry, and that adenosine-sensitive atrial tissue close to the AV node but not the AV nodal conducting system forms the tachycardia circuit of the AT.3 In the present case, two different tachyarrhythmias in the vicinity of the His bundle and spontaneous transition were observed. That is, when antegrade impulse reached at lower turnaround while the retrograde fast pathway was refractory, AT was provoked. On the other hand, when antegrade impulse reached at lower turnaround while the retrograde fast pathway was not refractory, slowfast AVNRT was provoked. Both the circuits of the tachycardia were in the vicinity of the His bundle; however, the electrophysiological findings and ablation results are clearly different. The case highlighted the dual tachycardia in the vicinity of the His bundle and the spontaneous transition like “ping-pong phenomenon.”
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Journal of Cardiovascular Electrophysiology
Vol. 26, No. 2, February 2015
Figure 1. Spontaneous fluctuation of the tachycardia is show. CS = coronary sinus; d = distal; H = His bundle potential; His = His region; HRA = high right atrium; p = proximal; RVA = right ventricular apex.
Figure 2. A: The transition of tachycardia by burst ventricular pacing is shown. B: The spontaneous transition of tachycardia is shown. For a high quality, full color version of this figure, please see Journal of Cardiovascular Electrophysiology’s website: www.wileyonlinelibrary.com/journal/jce
References 1. Iesaka Y, Takahashi A, Goya M, Soejima Y, Okamoto Y, Fujiwara H, Aonuma K, Nogami A, Hiroe M, Marumo F, Hiraoka M: Adenosinesensitive atrial reentrant tachycardia originating from the atrioventricular nodal transitional area. J Cardiovasc Electrophysiol 1997;8: 854-864. 2. Tada H, Naito S, Miyazaki A, Oshima S, Nogami A, Taniguchi K:
Successful catheter ablation of atrial tachycardia originating near the atrioventricular node from the noncoronary sinus of Valsalva. Pacing Clin Electrophysiol 2004;27:1440-1443. 3. Yamabe H, Tanaka Y, Morihisa K, Uemura T, Enomoto K, Kawano H, Ogawa H: Analysis of the anatomical tachycardia circuit in verapamil-sensitive atrial tachycardia originating from the vicinity of the atrioventricular node. Circ Arrhythm Electrophysiol 2010;3:5462.
Arrhythmia Rounds Section Editor: George J. Klein, M.D.
An Irregular Supraventricular Tachycardia: What is the Mechanism? SHINSUKE MIYAZAKI, M.D., TAKASHI UCHIYAMA, M.D., and YOSHITO IESAKA, M.D. From the Tsuchiura Kyodo Hospital, Ibaraki, Japan
atrial tachycardia, AV node reentry, catheter ablation, double tachycardia, junctional tachycardia, noncoronary cusp Introduction A 56-year-old woman with regular narrow QRS complex tachycardia without any structural heart disease was referred to our center for electrophysiological study and catheter ablation. A baseline electrophysiological test demonstrated a normal AH/HV interval during sinus rhythm and a dual atrioventricular (AV) nodal physiology of the antegrade pathway. The clinical tachycardia was repeatedly inducible following a jump during atrial extrastimuli, and the retrograde earliest atrial activation occurred from the His region during the tachycardia. The ventriculoatrial (VA) conduction exhibited decremental properties with the same atrial activation sequence as that during the tachycardia, and ventricular extrastimuli during His refractory period did not advance atrial excitation. Figure 1 shows the spontaneous fluctuation of this tachycardia. What is the mechanism of this phenomenon? Commentary The differential diagnosis of this irregular tachycardia includes irregular atrial tachycardia (AT), AV nodal reentrant tachycardia (AVNRT) with variable block to atrium and/or ventricle, and AVNRT over multiple retrograde AV node pathways. Although the results of electrophysiological study favor typical slow-fast AVNRT, the irregular tachycardia like Figure 1 cannot be explained. Figure 2 shows the transition
J Cardiovasc Electrophysiol, Vol. 26, pp. 231-232, February 2015. No disclosures. Address for correspondence: Shinsuke Miyazaki, M.D., Cardiology Division, Cardiovascular Center, Tsuchiura Kyodo Hospital, 11–7 Manabeshinmachi, Tsuchiura, Ibaraki 300-0053, Japan. Fax: 81-29-826-2411; E-mail: [email protected] Manuscript received 2 September 2014; Revised manuscript received 4 September 2014; Accepted for publication 9 September 2014. doi: 10.1111/jce.12541
of the tachycardia. Another tachycardia was provoked following ventricular pacing during stable AVNRT (Fig. 2A). The earliest atrial activation occurred from the His region during the tachycardia like AVNRT; however, it was provoked by V-A-A-V response following ventricular pacing, which suggested that the mechanism of the tachycardia was AT. The AT was also inducible by atrial extrastimuli without a jump, and terminated by 4 mg bolus injection of adenosine triphosphate. The AVNRT was more stable than the AT, and spontaneous transition from AT to AVNRT was observed several times (Fig. 2B); however, spontaneous transition from AVNRT to AT was not observed. The cycle length of the AT was longer than that of AVNRT. Slow pathway ablation completely eliminated the AVNRT, and stable AT was easily inducible after eliminating AVNRT. After the detail mapping at right ventricular mid septum and coronary cusps, the AT terminated by a 4.0 seconds of radiofrequency application at the noncoronary cusp, which resulted in inability to induce the AT. Previous studies have demonstrated that focal ATs originating from the septal regions can be reproducibly induced and terminated by programmed atrial stimulation, and are sensitive to intravenous adenosine in most patients.1 The earliest atrial activation site is close to the His bundle, while it could be eliminated by radiofrequency applications from the noncoronary cusp in a part of the patients.2 A recent study has shown that the mechanism of AT was due to reentry, and that adenosine-sensitive atrial tissue close to the AV node but not the AV nodal conducting system forms the tachycardia circuit of the AT.3 In the present case, two different tachyarrhythmias in the vicinity of the His bundle and spontaneous transition were observed. That is, when antegrade impulse reached at lower turnaround while the retrograde fast pathway was refractory, AT was provoked. On the other hand, when antegrade impulse reached at lower turnaround while the retrograde fast pathway was not refractory, slowfast AVNRT was provoked. Both the circuits of the tachycardia were in the vicinity of the His bundle; however, the electrophysiological findings and ablation results are clearly different. The case highlighted the dual tachycardia in the vicinity of the His bundle and the spontaneous transition like “ping-pong phenomenon.”
232
Journal of Cardiovascular Electrophysiology
Vol. 26, No. 2, February 2015
Figure 1. Spontaneous fluctuation of the tachycardia is show. CS = coronary sinus; d = distal; H = His bundle potential; His = His region; HRA = high right atrium; p = proximal; RVA = right ventricular apex.
Figure 2. A: The transition of tachycardia by burst ventricular pacing is shown. B: The spontaneous transition of tachycardia is shown. For a high quality, full color version of this figure, please see Journal of Cardiovascular Electrophysiology’s website: www.wileyonlinelibrary.com/journal/jce
References 1. Iesaka Y, Takahashi A, Goya M, Soejima Y, Okamoto Y, Fujiwara H, Aonuma K, Nogami A, Hiroe M, Marumo F, Hiraoka M: Adenosinesensitive atrial reentrant tachycardia originating from the atrioventricular nodal transitional area. J Cardiovasc Electrophysiol 1997;8: 854-864. 2. Tada H, Naito S, Miyazaki A, Oshima S, Nogami A, Taniguchi K:
Successful catheter ablation of atrial tachycardia originating near the atrioventricular node from the noncoronary sinus of Valsalva. Pacing Clin Electrophysiol 2004;27:1440-1443. 3. Yamabe H, Tanaka Y, Morihisa K, Uemura T, Enomoto K, Kawano H, Ogawa H: Analysis of the anatomical tachycardia circuit in verapamil-sensitive atrial tachycardia originating from the vicinity of the atrioventricular node. Circ Arrhythm Electrophysiol 2010;3:5462.
