Europace Advance Access originally published online on January 10, 2006
Europace 2006 8(2):134-137; doi:10.1093/europace/euj033
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ELECTROPHYSIOLOGY
Atrioventricular nodal re-entrant tachycardia with QRS voltage and cycle length alternation and aberrant conduction due to two distinct antegrade slow pathways
Department of Cardiology Gulhane Military Medical Academy, 06018 Etlik, Ankara Turkey
Manuscript submitted 25 March 2005. Accepted after revision 9 November 2005.
Corresponding author. Tel: +90 312 304 2390; fax: +90 312 304 4250. E-mail address: dramasyali{at}yahoo.com
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Abstract |
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QRS voltage and cycle length alternation can be seen during supraventricular re-entrant tachycardias, especially in atrioventricular (AV) re-entrant tachycardia. We present a case of a 20-year-old man, in which AV nodal re-entrant tachycardia (AVNRT) shows alternation of QRS voltage and cycle length, as well as right bundle branch block aberration due to a re-entrant circuit using two distinct, beat-to-beat alternating slow AV nodal pathways antegradely and a single fast pathway retrogradely. Although more than one antegrade slow pathway exists, creation of a single lesion at the right posterior atrial septum using the conventional right-sided approach successfully eliminated AVNRT.
Key Words: Atrioventricular nodal re-entrant tachycardia, Cycle length alternation, QRS alternation, Right bundle branch block
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Introduction |
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QRS voltage and cycle length alternation can be seen during supraventricular re-entrant tachycardias, especially in atrioventricular (AV) re-entrant tachycardia (AVRT).1
–4 In this report, we present a case with AV nodal re-entrant tachycardia (AVNRT). |
Case presentation |
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A 20-year-old man with a history of recurrent sudden-onset tachycardia refractory to multiple antiarrhythmic drugs, including oral verapamil, metoprolol, and propafenone, was referred to our institution for electrophysiological (EP) study. Physical examination, resting ECG, chest X-ray, and echocardiography were normal.
In the EP study, basal intervals were within normal limits, AV interval=90 ms and His-ventricular (HV) interval=40 ms. Programmed atrial stimulation revealed dual AV nodal physiology with an atrio-His (AH) jump of 125 ms followed by reproducible induction of a narrow complex tachycardia with two different cycle lengths alternating between 406 and 341 ms. The tachycardia intermittently showed RBBB morphology with QRS alternans, the cycle length alternation persisting (Fig. 1). The HV interval of the tachycardia was constant at 40 ms and the earliest atrial activation was recorded at the His-bundle site. During tachycardia, the VA interval was 64 ms at the high right atrial catheter and was fixed in all RR cycles (Fig. 2). Overdrive ventricular pacing during tachycardia did not affect the alteration in the AA interval and there is no regular relation between ventricular and atrial activations. We also noted that there were fusion beats resulting from the ventricular depolarization due to tachycardia and ventricular pacing in the second and fourth QRS complexes (Fig. 3).
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During tachycardia, the His–His (HH) intervals were also alternating between 341 and 406 ms, the same cycle lengths as those of the RR intervals. The reason for the short and long RR cycle lengths was the alternation of the AH intervals, which were 255 ms in the shorter cycles and 320 ms in the longer cycles.
The differential diagnosis in this case included AVNRT, orthodromic AVRT, and atrial tachycardia with alternating slow and fast AV nodal pathway conduction. In the case of atrial tachycardia, a relatively fixed AA interval with alternating longer and shorter AV and VA intervals would be expected. However, in the present case, the VA interval was fixed and the change in HH intervals preceding the change in AA intervals indicated that atrial tachycardia could not be the mechanism. Premature ventricular extrastimuli delivered during His-bundle refractoriness did not pre-excite the atrium and failed to terminate the tachycardia, thus not favouring re-entrant tachycardias using a concealed accessory pathway. Besides, the response to overdrive ventricular pacing during tachycardia led us to consider that the ventricles were not part of the tachycardia. It is generally accepted that a distal common pathway exists in AVNRT and the ventricles are not essential parts of the re-entrant circuit.5 Therefore, AVRT was excluded and AVNRT was favoured.
Thus, a diagnosis was made of common AVNRT with alternating QRS voltage and cycle length and right bundle branch block due to a re-entrant circuit using two distinct, beat-to-beat alternating slow AV nodal pathways antegradely and a single fast pathway retrogradely.
Radiofrequency ablation of the slow pathway in the common posteroseptal location was accomplished using an ablation catheter with a 4 mm tip electrode (Marinr, Medtronic Inc., Minneapolis, MN, USA). Runs of junctional beats were observed during radiofrequency energy delivery and the tachycardia could be no longer induced with standard pacing manoeuvers, even after isoprenaline infusion. The patient has been asymptomatic without any antiarrhythmic therapy during a follow-up of 9 months.
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Discussion |
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In this report, we present a patient with AVNRT with QRS voltage and cycle length alternation and right bundle branch block pattern. To the best of our knowledge, such a combination, although occasionally seen separately in AVNRT, has not previously been reported.
In such cases with short RP narrow complex tachycardias, the differential diagnosis includes AVNRT, orthodromic AVRT, atrial and junctional tachycardias. Using the aforementioned differential diagnosis manoeuvers together with presence of concentric retrograde atrial activation and absence of an accessory pathway, a diagnosis of common AVNRT using two different antegrade slow pathways was made. Also, the non-inducibility of tachycardia after successful ablation of the slow pathway supported the diagnosis.
QRS alternans has been considered to be strongly suggestive of AVRT.3,4 However, it is not specific for AVRT and it may also occur during AVNRT.6 Additionally, junctional or ventricular bigeminy could also cause ORS alternans. However, both were excluded by the presence of normal and constant HV interval during tachycardia.
The mechanism of the QRS alternans is controversial. It seems to be a rate-related phenomenon and results from oscillations in action potential duration within the His-Purkinje system or ventricular myocardium.6,7 Alternating tachycardia cycle length may have led to oscillations in action potential duration within the His-Purkinje system or ventricular myocardium in the present case. Also, alternation of the tachycardia cycle length is very rare in AVNRT.1,2 Although changes in His-Purkinje refractoriness and functional block in the His-Purkinje system could also rarely cause cycle length alternation during tachycardia, this was not the case in this patient, as HV intervals remained constant and there was no detectable beat-to-beat change in the QRS axis.
In the present case, a single radiofrequency delivery to the right posteroseptal region successfully eliminated AVNRT. Although it is possible to eliminate two or more anatomically close, yet, distinct slow pathways even with a single burn with an ablation catheter moving with cardiac and respiratory cycles, anisotropic conduction-induced functional pathways with a single anatomic localization are more likely to be responsible for the cycle length alternation in this patient.8–10 However, because of complexity of the AV node, cycle length alternation, which may result solely from decremental conduction properties of the AV node, cannot be completely excluded.2
In conclusion, AVNRT, the most frequent narrow-complex tachycardia with regular RR intervals in adults, can rarely present with unusual manifestations such as cycle length and QRS voltage alternation and right bundle branch block aberration. Although more than one antegrade slow pathway may exist, creation of a single lesion in the right posterior atrial septum using the conventional right-sided approach successfully eliminated AVNRT.
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References |
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[1] Surawicz B and Fisch C. Cardiac alternans. Diverse mechanisms and clinical manifestations. J Am Coll Cardiol 1992; 20: 483–99.[Abstract]
[2] Maury P, Raczka F, Piot C, Davy JM. QRS and cycle length alternans during paroxysmal supraventricular tachycardia: what is the mechanism? J Cardiovasc Electrophysiol 2002; 13: 92–3.[CrossRef][Web of Science][Medline]
[3] Green M, Heddle B, Dassen W, et al. Value of QRS alternation in determining the site of origin of narrow QRS supraventricular tachycardia. Circulation 1983; 68: 368–73.
[4] Chen SA, Tai CT, Chiang CE, Chang MS. Role of the surface electrocardiogram in the diagnosis of patients with supraventricular tachycardia. Cardiol Clin 1997; 15: 539–65.[Medline]
[5] Mendez C and Moe GK. Demonstration of a dual A-V nodal conduction system in the isolated rabbit heart. Circ Res 1966; 19: 378–93.
[6] Morady F, DiCarlo LA Jr, Baerman JM, de Buitleir M, Kou WH. Determination of QRS alternans during narrow QRS tachycardia. J Am Coll Cardiol 1987; 9: 489–99.[Abstract]
[7] Tchou PJ, Lehmann MH, Dongas J, Mahmud R, Denker ST, Akhtar M. Effect of sudden rate acceleration on the human His-Purkinje system: adaptation of refractoriness in a dampened oscillatory pattern. Circulation 1986; 73: 920–9.
[8] Anderson RH, Janse MJ, van Capelle FJ, Billette J, Becker AE, Durrer D. A combined morphological and electrophysiological study of the atrioventricular node of the rabbit heart. Circ Res 1974; 35: 909–22.
[9] Wu J. Nondiscrete functional pathways and asymmetric transitional zone: a new concept for AV nodal electrophysiology. J Cardiovasc Electrophysiol 2001; 12: 487–8.[CrossRef][Medline]
[10] Spach MS and Josephson ME. Initiating reentry: the role of nonuniform anisotropy in small circuits. J Cardiovasc Electrophysiol 1994; 5: 182–209.[Web of Science][Medline]
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