© 2003 by European Society of Cardiology
ISSUE CARDIOGRAM
Unusual form of AV nodal Wenckebach block
Cardiovascular Research and Teaching Institute Aalst Aalst, Belgium
Manuscript submitted 21 November 2002. Accepted after revision 29 March 2003.
Correspondence: Pedro Brugada, Cardiovascular Center, OLV Hospital, Moorselbaan 164, 9300 Aalst, Belgium. Fax: +32-53-72-4185; E-mail: pedro.brugada{at}pi.be
Abstract
A 73 year-old man had a fast atrioventricular (AV) nodal pathway accidentally ablated 4 years before, while attempting to ablate a septally located concealed accessory pathway (AP). After initiation of treatment with beta-blockers, because of systemic arterial hypertension, the patient presented to the emergency room complaining of a markedly diminished exercise tolerance. The 12 lead ECG showed an interesting AV nodal Wenckebach sequence, interrupted by P waves retrogradely conducted through the AP. The mechanisms explaining the ECG are discussed.
Key Words: Fast pathway ablation, AV block, Wenckebach block, concealed accessory pathway
Case presentation
A 73 year-old man, presented to the emergency room (ER) complaining of a markedly diminished exercise tolerance, 3 weeks after initiation of treatment with a beta-blocker because of systemic arterial hypertension. The patient had a fast atrioventricular (AV) nodal pathway accidentally ablated 4 years before, while unsuccessfully attempting to ablate a septally located concealed accessory pathway (AP). He had remained asymptomatic ever since. The first ECG, recorded in the ER (Fig. 1), showed an interesting sequence.
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Electrophysiological (EP) investigation using standard techniques was performed. The AH interval was 150 ms and the HV 50 ms. During atrial stimulation no dual AV nodal pathways were documented and the AV node's Wenckebach point was reached at 800 ms (Fig. 2). During ventricular stimulation the retrograde refractory period of the AP was reached at 300 ms. What are the mechanisms explaining the ECGs?
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Discussion
Two interesting EP phenomena are observed in the present case. First, the mechanism involved in the AV delay pattern and second, the mechanism of intermittent retrograde AV conduction. There are many potential mechanisms that can explain the presented ECGs. First of all, there is prolongation of the PR interval between consecutive beats (Fig. 1). Although a higher incidence of late AV block following fast pathway ablation has already been described[1,
2], this AV interval prolongation could correspond either to an AV Wenckebach block or to a jump of AV conduction from the fast to the slow AV nodal pathway. Considering that the P–P interval is not altered during normal sinus rhythm and that no dual pathways were documented during EP investigation, the AV delay and later echo beat cannot be explained by a jump of conduction from the fast to the slow pathway. The fact that retrograde depolarization of the atrium in the third beat resets the sinus node and generates a compensatory pause, gives time for the AV node to recover and the next (delayed) P wave is normally conducted, instead of being blocked. In this way the AV Wenckebach sequence is interrupted.
Why are only beats after an AV conduction delay retrogradely conducted to the atrium?
This has two potential mechanisms. The first one, is that the atrium may be refractory after a normally conducted beat, and only after a prolonged AV delay the atrium has time to recover and can now be depolarized retrogradely through the AP.
The second potential mechanism, is that there is antegrade AP concealed conduction, and with an AV delay shorter than the AP's retrograde refractory period there is no retrograde conduction of the impulse. While with an AV delay greater than the AP's retrograde refractory period, the AP recovers and can retrogradely depolarize the atrium.
By carefully analyzing Fig. 2, we see that the Wenckebach point is reached at 800 ms and that the first conducted beat has no retrograde conduction. However, the interval between the retrograde P wave and the following paced P wave is 280 ms. That means that the atrial refractory period is less than 280 ms and that the mechanism of retrograde block during the first beat of the sequence is not due to atrial refractoriness, but to concealed antegrade conduction over the AP. Note that retrograde P wave morphology on the surface ECG is very helpful to localize the AP, in this case an inferiorly (negative P wave in leads II, III and aVF) and septally (positive P wave in aVR and aVL and isodiphasic in I) located AP.
References
[1] Hindricks G. on behalf of the Multicenter European Radiofrequency Survey (MERFS) Investigators. The Multicenter European Radiofrequency Survey (MERFS)—Complications of radiofrequency catheter ablation of arrhythmias. Eur Heart J 1993; 14: 1644–1653.
[2] Fenelon G, Malacky T, Manios E, Geelen P, Andries E, Brugada P. Radiofrequency ablation of atrioventricular node reentrant tachycardia: fast or slow pathway ablation? In Farre J and Moro C (Eds.). Ten Years of Radiofrequency Catheter Ablation 1998; Futura Publishing Armonk, NY pp. 103–114.
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