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Wide QRS complex tachycardia with a 1:1 AV relationship
Journal of Arrhythmia 28 (2012) 78–79
Contents lists available at SciVerse ScienceDirect
Journal of Arrhythmia journal homepage: www.elsevier.com/locate/joa
EPS for Resident Physicians
Wide QRS complex tachycardia with a 1:1 AV relationship Teiichi Yamane n Division of Cardiology, Department of Internal Medicine, Jikei University School of Medicine, 3-25-8 Nishi-shinbashi, Minato-ku, Tokyo 105-8461, Japan
1. Case A 45-year-old man was referred for the management of sudden-onset tachycardia. He had experienced 3 episodes of palpitation attacks, lasting for a couple of hours each, during the last 6 months. A regular, wide QRS complex tachycardia (WCT) at 150 beats/min with a prominent retrograde P wave on the surface electrocardiogram (ECG) was documented during the last attack, which was terminated by drip infusion of pilsicainide administered at another hospital. He did not experience loss of consciousness or dizziness during his palpitation attacks. The findings of other investigations, including physical examination, two-dimensional echocardiography, chest radiography, and laboratory tests, were unremarkable. Cardiac electrophysiological study (EPS) was performed after written informed consent was obtained. Venous access was performed via the right femoral and subclavian veins. Three 5-French quadripolar catheters were advanced to the right ventricular apex, right atrial appendage, and His-bundle region. A 5-French decapolar catheter was placed within the coronary sinus (CS), with a proximal electrode located at its ostium. During the EPS study, a WCT with a cycle length of 330 ms was induced by a ventricular extrastimulus. The morphology of the 12-lead ECG was consistent with that of the clinical tachycardia and showed the right bundlebranch block pattern and left axis deviation. Intracardiac ECG showed a 1:1 atrioventricular (A-V) relationship (Fig. 1). What is the cause of this tachycardia?
2. Commentary Our first impression in this case was AV nodal reentry tachycardia (AVNRT) with aberrant ventricular conduction, n
Tel.: þ 81 3 3433 1111x3261; fax: þ 81 3 3459 6043. E-mail address: [email protected]
since both right atrium and ventricle were activated almost simultaneously after the sharp His-potential. A radio frequency (RF) energy application was attempted at a slowpathway lesion, which did not generate junctional rhythm or affect the inducibility of the tachycardia. During EPS, the differential diagnosis of the WCT between the supraventricular and ventricular origin is not difficult if A-V dissociation is observed. However, a WCT with a 1:1 AV relationship necessitates careful observation and EP techniques to clarify the mechanism underlying the tachycardia. Several techniques have been described for determining the mechanism underlying tachycardia [1–3]. Shortening of the HV interval or a change of the His and RBB activation sequence will favor ventricular tachycardia (VT) or pre-excited supraventricular tachycardia (SVT). A shorter His-atrial (HA) interval during tachycardia than during RV pacing is consistent with AVNRT with aberration or bystander accessory pathway (AP) [1]. Abdelwahab et al. reported that atrial overdrive pacing during the tachycardia is useful for these differentiations [2]. They demonstrated that the presence of both a narrowing of the QRS complex during the atrial overdrive pacing and an AVVA response upon cessation of atrial overdrive pacing are suggestive of ventricular tachycardia as the mechanism of WCT. In this case, transient ventricular capture during overdrive atrial pacing resulted in marked narrowing of the QRS (Fig. 2). The AVVA response was also observed upon the termination of atrial pacing. Since these findings suggested a ventricular origin of tachycardia, we explored the left ventricular chamber through the transaortic approach. A sharp, discrete potential, probably of Purkinje origin, was recorded before the ventricular electrogram and the localized RF application at this site successfully terminated and eliminated the tachycardia. A WCT with a 1:1 AV relationship is sometimes observed during the EPS for WCT. Burst atrial pacing is
1880-4276/$ - see front matter & 2012 Japanese Heart Rhythm Society. Published by Elsevier B.V. All rights reserved. doi:10.1016/j.joa.2012.02.013
T. Yamane / Journal of Arrhythmia 28 (2012) 78–79
79
Fig. 1. Wide Complex Tachycardia (CL: 320 ms).
Fig. 2. Atrial pacing (CL: 240 ms) during Wide Complex Tachycardia.
a simple and reliable technique to identify the tachycardia mechanism and should be borne in mind by all doctors seeking expertise in EP. References [1] Josephson ME. Pre excitation syndromes. In: Josephson ME, editor. Clinical cardiac electrophysiology. Philadelphia: Lippincott Williams and Wilkins; 2002. p. 322–424.
[2] Abdelwahab A, Gardner MJ, Basta MN, et al. A technique for the rapid diagnosis of wide complex tachycardia with 1:1 AV relationship in the electrophysiology laboratory. Pacing Clin Electrophysiol 2009;32:475–83. [3] Kadish AH, Morady F. The response of paroxysmal supraventricular tachycardia to overdrive atrial and ventricular pacing: can it help determine the tachycardia mechanism? J Cardiovasc Electrophysiol 1993;4:239–52.
Contents lists available at SciVerse ScienceDirect
Journal of Arrhythmia journal homepage: www.elsevier.com/locate/joa
EPS for Resident Physicians
Wide QRS complex tachycardia with a 1:1 AV relationship Teiichi Yamane n Division of Cardiology, Department of Internal Medicine, Jikei University School of Medicine, 3-25-8 Nishi-shinbashi, Minato-ku, Tokyo 105-8461, Japan
1. Case A 45-year-old man was referred for the management of sudden-onset tachycardia. He had experienced 3 episodes of palpitation attacks, lasting for a couple of hours each, during the last 6 months. A regular, wide QRS complex tachycardia (WCT) at 150 beats/min with a prominent retrograde P wave on the surface electrocardiogram (ECG) was documented during the last attack, which was terminated by drip infusion of pilsicainide administered at another hospital. He did not experience loss of consciousness or dizziness during his palpitation attacks. The findings of other investigations, including physical examination, two-dimensional echocardiography, chest radiography, and laboratory tests, were unremarkable. Cardiac electrophysiological study (EPS) was performed after written informed consent was obtained. Venous access was performed via the right femoral and subclavian veins. Three 5-French quadripolar catheters were advanced to the right ventricular apex, right atrial appendage, and His-bundle region. A 5-French decapolar catheter was placed within the coronary sinus (CS), with a proximal electrode located at its ostium. During the EPS study, a WCT with a cycle length of 330 ms was induced by a ventricular extrastimulus. The morphology of the 12-lead ECG was consistent with that of the clinical tachycardia and showed the right bundlebranch block pattern and left axis deviation. Intracardiac ECG showed a 1:1 atrioventricular (A-V) relationship (Fig. 1). What is the cause of this tachycardia?
2. Commentary Our first impression in this case was AV nodal reentry tachycardia (AVNRT) with aberrant ventricular conduction, n
Tel.: þ 81 3 3433 1111x3261; fax: þ 81 3 3459 6043. E-mail address: [email protected]
since both right atrium and ventricle were activated almost simultaneously after the sharp His-potential. A radio frequency (RF) energy application was attempted at a slowpathway lesion, which did not generate junctional rhythm or affect the inducibility of the tachycardia. During EPS, the differential diagnosis of the WCT between the supraventricular and ventricular origin is not difficult if A-V dissociation is observed. However, a WCT with a 1:1 AV relationship necessitates careful observation and EP techniques to clarify the mechanism underlying the tachycardia. Several techniques have been described for determining the mechanism underlying tachycardia [1–3]. Shortening of the HV interval or a change of the His and RBB activation sequence will favor ventricular tachycardia (VT) or pre-excited supraventricular tachycardia (SVT). A shorter His-atrial (HA) interval during tachycardia than during RV pacing is consistent with AVNRT with aberration or bystander accessory pathway (AP) [1]. Abdelwahab et al. reported that atrial overdrive pacing during the tachycardia is useful for these differentiations [2]. They demonstrated that the presence of both a narrowing of the QRS complex during the atrial overdrive pacing and an AVVA response upon cessation of atrial overdrive pacing are suggestive of ventricular tachycardia as the mechanism of WCT. In this case, transient ventricular capture during overdrive atrial pacing resulted in marked narrowing of the QRS (Fig. 2). The AVVA response was also observed upon the termination of atrial pacing. Since these findings suggested a ventricular origin of tachycardia, we explored the left ventricular chamber through the transaortic approach. A sharp, discrete potential, probably of Purkinje origin, was recorded before the ventricular electrogram and the localized RF application at this site successfully terminated and eliminated the tachycardia. A WCT with a 1:1 AV relationship is sometimes observed during the EPS for WCT. Burst atrial pacing is
1880-4276/$ - see front matter & 2012 Japanese Heart Rhythm Society. Published by Elsevier B.V. All rights reserved. doi:10.1016/j.joa.2012.02.013
T. Yamane / Journal of Arrhythmia 28 (2012) 78–79
79
Fig. 1. Wide Complex Tachycardia (CL: 320 ms).
Fig. 2. Atrial pacing (CL: 240 ms) during Wide Complex Tachycardia.
a simple and reliable technique to identify the tachycardia mechanism and should be borne in mind by all doctors seeking expertise in EP. References [1] Josephson ME. Pre excitation syndromes. In: Josephson ME, editor. Clinical cardiac electrophysiology. Philadelphia: Lippincott Williams and Wilkins; 2002. p. 322–424.
[2] Abdelwahab A, Gardner MJ, Basta MN, et al. A technique for the rapid diagnosis of wide complex tachycardia with 1:1 AV relationship in the electrophysiology laboratory. Pacing Clin Electrophysiol 2009;32:475–83. [3] Kadish AH, Morady F. The response of paroxysmal supraventricular tachycardia to overdrive atrial and ventricular pacing: can it help determine the tachycardia mechanism? J Cardiovasc Electrophysiol 1993;4:239–52.