EP ROUNDS
Diagnostic Dilemma in a Narrow Complex Tachycardia RAJA J. SELVARAJ, M.D., D.N.B., VIVEK RAJ SINGH, M.D., and JAYARAMAN BALACHANDER, M.D., D.M. From the Department of Cardiology, Jawaharlal Institute of Postgraduate Medical Education and Research, Puducherry, India
atrioventricular nodal reentrant tachycardia, junctional tachycardia, atrial extrastimulus, supraventricular tachycardia
Case A 24-year-old woman presented with episodic palpitations usually associated with exertion. A narrow complex tachycardia was documented during one prolonged episode associated with a febrile illness. Electrocardiogram at rest showed occasional junctional ectopic beats and no preexcitation. During electrophysiology study, dual atrioventricular (AV) nodal physiology in the form of atrial-His (AH) jump was demonstrated and there was no evidence of accessory pathway conduction. No tachycardia could be induced with single and double atrial extrastimuli or atrial burst pacing. During isoprenaline infusion, repeated spontaneous initiation of tachycardia was seen without preceding premature beats or AH prolongation (Fig. 1). This was a regular narrow complex tachycardia at a cycle length of 365 ms with 1:1 ventriculo-atrial (VA) relationship, central VA conduction, and a VA interval of –10 ms. Premature atrial extrastimuli were introduced from the proximal coronary sinus scanning diastole. Shown in Figures 2 and 3 are two extrastimuli. What is the mechanism of the tachycardia based on the response to these extrastimuli? Discussion Narrow complex tachycardia with a very short VA interval and central atrial activation is most commonly atrioventricular nodal reentrant tachycardia (AVNRT), especially in the presence Disclosures and financial support: None declared. Address for reprints: Raja J. Selvaraj, Department of Cardiology, JIPMER, Puducherry – 605006, India. Fax: 91-413-2272067; e-mail: [email protected] Received February 10, 2015; revised March 8, 2015; accepted March 9, 2015. doi: 10.1111/pace.12633
of dual AV nodal physiology. However, unusual for AVNRT in this patient are inability to induce with programmed stimulation and induction during isoprenaline infusion without AH prolongation. Automatic junctional tachycardia (JT) needs to be considered in this situation. In the top panel in Figure 2, the atrial extrastimulus is delivered from the proximal coronary sinus about 10 ms before the His signal. The timing of the His signal is unaltered and the local atrial activation on the His catheter occurs after the His signal. The subsequent atrial activation is advanced by this extrastimulus. Although the advancement is small, the preceding cycle lengths were very stable and this finding was reproducible during a repeat attempt. Perturbation of the subsequent atrial activation by an atrial extrastimulus delivered at His refractoriness has been considered to indicate AVNRT.1 In the bottom panel in Figure 2, with an earlier extrastimulus, advancement of the immediate His signal is seen without interruption of the tachycardia. This finding, which was reproducible, is inconsistent with AVNRT and is typical of JT.1 Since the responses to the early and late extrastimuli are inconsistent with each other, an explanation needs to be found. Although Padanilam et al. did not find either a patient with JT who showed advancement of subsequent His by a late premature atrial complex (PAC) or a patient with AVNRT who showed advancement of the immediate His with continuation of tachycardia with an early PAC, they recognized that these responses could be seen under certain conditions.1 Thus, an early PAC could advance the immediate His by capturing the fast pathway in AVNRT and still not result in tachycardia termination if it also conducts by the slow pathway, producing a dual response and effectively reinducing tachycardia (Fig. 3, panel B). However, as noted by them, in this scenario dual response should also be
©2015 Wiley Periodicals, Inc. PACE, Vol. 38
July 2015
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SELVARAJ, ET AL.
demonstrable during programmed stimulation in sinus rhythm. In patients with JT, on the other hand, advancement of the subsequent His by a late PAC can occur because of conduction through the slow pathway (Fig. 3, panel A). As discussed by Padanilam et al., while possible in the presence of a dual AV nodal physiology, this response would be uncommon because of the precise set of circumstances required. The PAC must be late enough for the His to be refractory, yet early enough to engage the slow pathway and preexcite the subsequent His without too much decrement
in the slow pathway. We found that this response, while reproducible, was seen only within a narrow window of 5–10 ms before the His signal. Thus, the findings in this patient could be seen in both AVNRT and JT. However, with the history of palpitations associated with exercise, presence of junctional ectopics, and tachycardia induction with isoprenaline infusion without preceding premature beats, we considered it more likely that this patient had JT. With this diagnosis, no ablation was done and the patient was treated with beta blockers. At 6 months follow-up, she is free of recurrences on β-blockers.
Figure 1. Spontaneous tachycardia initiation. Electrocardiogram and intracardiac electrograms are shown during spontaneous initiation of a regular, narrow complex tachycardia with a short ventriculo-atrial interval.
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Figure 2. Effect of premature atrial complexes. In the top panel, a late extrastimulus is delivered from the proximal coronary sinus. The pacing spike is seen just before the His signal and does not alter its timing. His to His intervals are marked for each of the inter-beat intervals. In the bottom panel, a late extrastimulus is delivered from the proximal coronary sinus earlier in diastole. Again, all the His to His intervals are marked.
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Conclusion JT is a rare clinical arrhythmia in adults outside the postoperative period. Response to late and early PACs is very useful in differentiating this arrhythmia from AVNRT. In the presence of a dual AV nodal physiology, possiblity of atrial preexcitation by a His refractory PAC should be anticipated and does not exclude the diagnosis of JT.
Figure 3. Ladder diagram showing the mechanism of unusual responses to PACs in the presence of dual AV nodal physiology. In panel A, a late PAC advances the subsequent His activation in junctional tachycardia because of conduction through the slow pathway. In panel B, an early PAC advances the immediate His in AVNRT due to capture of the fast pathway. However, there is no apparent termination of tachycardia because this same PAC also conducts by the slow pathway, producing a double ventricular response, and reinitiating tachycardia. AV = atrioventricular; AVNRT = atrioventricular nodal reentrant tachycardia; PACs = premature atrial complexes.
Reference 1. Padanilam BJ, Manfredi JA, Steinberg LA, Olson JA, Fogel RI, Prystowsky EN. Differentiating junctional tachycardia and
890
July 2015
atrioventricular node re-entry tachycardia based on response to atrial extrastimulus pacing. J Am Coll Cardiol 2008; 52:1711–1717.
PACE, Vol. 38
Diagnostic Dilemma in a Narrow Complex Tachycardia RAJA J. SELVARAJ, M.D., D.N.B., VIVEK RAJ SINGH, M.D., and JAYARAMAN BALACHANDER, M.D., D.M. From the Department of Cardiology, Jawaharlal Institute of Postgraduate Medical Education and Research, Puducherry, India
atrioventricular nodal reentrant tachycardia, junctional tachycardia, atrial extrastimulus, supraventricular tachycardia
Case A 24-year-old woman presented with episodic palpitations usually associated with exertion. A narrow complex tachycardia was documented during one prolonged episode associated with a febrile illness. Electrocardiogram at rest showed occasional junctional ectopic beats and no preexcitation. During electrophysiology study, dual atrioventricular (AV) nodal physiology in the form of atrial-His (AH) jump was demonstrated and there was no evidence of accessory pathway conduction. No tachycardia could be induced with single and double atrial extrastimuli or atrial burst pacing. During isoprenaline infusion, repeated spontaneous initiation of tachycardia was seen without preceding premature beats or AH prolongation (Fig. 1). This was a regular narrow complex tachycardia at a cycle length of 365 ms with 1:1 ventriculo-atrial (VA) relationship, central VA conduction, and a VA interval of –10 ms. Premature atrial extrastimuli were introduced from the proximal coronary sinus scanning diastole. Shown in Figures 2 and 3 are two extrastimuli. What is the mechanism of the tachycardia based on the response to these extrastimuli? Discussion Narrow complex tachycardia with a very short VA interval and central atrial activation is most commonly atrioventricular nodal reentrant tachycardia (AVNRT), especially in the presence Disclosures and financial support: None declared. Address for reprints: Raja J. Selvaraj, Department of Cardiology, JIPMER, Puducherry – 605006, India. Fax: 91-413-2272067; e-mail: [email protected] Received February 10, 2015; revised March 8, 2015; accepted March 9, 2015. doi: 10.1111/pace.12633
of dual AV nodal physiology. However, unusual for AVNRT in this patient are inability to induce with programmed stimulation and induction during isoprenaline infusion without AH prolongation. Automatic junctional tachycardia (JT) needs to be considered in this situation. In the top panel in Figure 2, the atrial extrastimulus is delivered from the proximal coronary sinus about 10 ms before the His signal. The timing of the His signal is unaltered and the local atrial activation on the His catheter occurs after the His signal. The subsequent atrial activation is advanced by this extrastimulus. Although the advancement is small, the preceding cycle lengths were very stable and this finding was reproducible during a repeat attempt. Perturbation of the subsequent atrial activation by an atrial extrastimulus delivered at His refractoriness has been considered to indicate AVNRT.1 In the bottom panel in Figure 2, with an earlier extrastimulus, advancement of the immediate His signal is seen without interruption of the tachycardia. This finding, which was reproducible, is inconsistent with AVNRT and is typical of JT.1 Since the responses to the early and late extrastimuli are inconsistent with each other, an explanation needs to be found. Although Padanilam et al. did not find either a patient with JT who showed advancement of subsequent His by a late premature atrial complex (PAC) or a patient with AVNRT who showed advancement of the immediate His with continuation of tachycardia with an early PAC, they recognized that these responses could be seen under certain conditions.1 Thus, an early PAC could advance the immediate His by capturing the fast pathway in AVNRT and still not result in tachycardia termination if it also conducts by the slow pathway, producing a dual response and effectively reinducing tachycardia (Fig. 3, panel B). However, as noted by them, in this scenario dual response should also be
©2015 Wiley Periodicals, Inc. PACE, Vol. 38
July 2015
887
SELVARAJ, ET AL.
demonstrable during programmed stimulation in sinus rhythm. In patients with JT, on the other hand, advancement of the subsequent His by a late PAC can occur because of conduction through the slow pathway (Fig. 3, panel A). As discussed by Padanilam et al., while possible in the presence of a dual AV nodal physiology, this response would be uncommon because of the precise set of circumstances required. The PAC must be late enough for the His to be refractory, yet early enough to engage the slow pathway and preexcite the subsequent His without too much decrement
in the slow pathway. We found that this response, while reproducible, was seen only within a narrow window of 5–10 ms before the His signal. Thus, the findings in this patient could be seen in both AVNRT and JT. However, with the history of palpitations associated with exercise, presence of junctional ectopics, and tachycardia induction with isoprenaline infusion without preceding premature beats, we considered it more likely that this patient had JT. With this diagnosis, no ablation was done and the patient was treated with beta blockers. At 6 months follow-up, she is free of recurrences on β-blockers.
Figure 1. Spontaneous tachycardia initiation. Electrocardiogram and intracardiac electrograms are shown during spontaneous initiation of a regular, narrow complex tachycardia with a short ventriculo-atrial interval.
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Figure 2. Effect of premature atrial complexes. In the top panel, a late extrastimulus is delivered from the proximal coronary sinus. The pacing spike is seen just before the His signal and does not alter its timing. His to His intervals are marked for each of the inter-beat intervals. In the bottom panel, a late extrastimulus is delivered from the proximal coronary sinus earlier in diastole. Again, all the His to His intervals are marked.
PACE, Vol. 38
July 2015
889
SELVARAJ, ET AL.
Conclusion JT is a rare clinical arrhythmia in adults outside the postoperative period. Response to late and early PACs is very useful in differentiating this arrhythmia from AVNRT. In the presence of a dual AV nodal physiology, possiblity of atrial preexcitation by a His refractory PAC should be anticipated and does not exclude the diagnosis of JT.
Figure 3. Ladder diagram showing the mechanism of unusual responses to PACs in the presence of dual AV nodal physiology. In panel A, a late PAC advances the subsequent His activation in junctional tachycardia because of conduction through the slow pathway. In panel B, an early PAC advances the immediate His in AVNRT due to capture of the fast pathway. However, there is no apparent termination of tachycardia because this same PAC also conducts by the slow pathway, producing a double ventricular response, and reinitiating tachycardia. AV = atrioventricular; AVNRT = atrioventricular nodal reentrant tachycardia; PACs = premature atrial complexes.
Reference 1. Padanilam BJ, Manfredi JA, Steinberg LA, Olson JA, Fogel RI, Prystowsky EN. Differentiating junctional tachycardia and
890
July 2015
atrioventricular node re-entry tachycardia based on response to atrial extrastimulus pacing. J Am Coll Cardiol 2008; 52:1711–1717.
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