Europace Advance Access originally published online on September 5, 2007
Europace 2007 9(10):920-922; doi:10.1093/europace/eum183
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ABLATION
Functional bundle branch block and orthodromic reciprocating tachycardia cycle length: do not bet on accessory pathway location
Lariboisière Hospital, APHP, Paris 7 University, Paris, France
Manuscript submitted 21 May 2007. Accepted after revision 2 August 2007.
* Corresponding author: Department of Cardiology, Lariboisière University Hospital, 2 rue Ambroise Paré—75475 Paris Cedex 10, France. Tel: +33 1 49 95 86 74; fax: +33 1 49 95 84 39. E-mail address: fabrice.extramiana{at}lrb.aphp.fr
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Abstract |
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Aims To show 2 examples in which the analysis of the effect of bundle branch block on orthodromic reciprocating tachycardia cycle length was misleading.
Methods and results We performed an electrophysiological study in two patients with orthodromic reciprocating tachycardia showing a transition from wide to narrow QRS during tachycardia. Our two cases of left bundle branch block during reciprocating tachycardia using infero-septal pathways show that ventricular to atrial conduction time prolongation may be larger than 30 ms and may be concealed by a shortening of atrial to ventricular conduction time. In the 2 cases, the atrial insertion of the accessory pathway could be successfully ablated from the right atria at the ostium of the coronary sinus.
ConclusionsThe observation of the association between left bundle branch block and cycle length prolongation during reciprocating tachycardia may be associated with a successful ablation at the ostium of the coronary sinus.
Key Words: Accessory pathway, Ablation, Bundle branch block
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Introduction |
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The effect of a functional bundle branch block (BBB) on the cycle length of an orthodromic atrio-ventricular reciprocating tachycardia (AVRT) has been of interest because of its usefulness in the localization of accessory pathways (APs). The association of a functional BBB and orthodromic AVRT cycle length prolongation due to an increase in ventriculo-atrial conduction time (VA interval) is thought to be diagnosis of an ipsilateral AP.1
–5 We show two examples in which the analysis of the effect of BBB on ORT cycle length was misleading.
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Cases description |
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Patient 1
A 26-year-old man was referred to our department after a first episode of documented wide QRS tachycardia (Figure 1). An electrophysiological study was performed as part of the treatment. No dual nodal pathway, nor anterograde conduction through an AP, could be evidenced.
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During right ventricular pacing, the earliest atrial activation was recorded at the ostium of the coronary sinus. No re-entrant tachycardia was induced under baseline conditions. After isoproterenol infusion, atrial-programmed stimulation induced the clinical wide QRS tachycardia with the left bundle branch block (LBBB) pattern. An extra-stimulus applied from the right ventricle during His bundle refractory period could reset the tachycardia, thus supporting the diagnosis of AVRT.
Figure 2 shows the intracardiac recording at the time of the transition from wide to narrow QRS tachycardia associated with a shortening in the AVRT cycle length from 290 to 250 ms. Endocardial recordings during this shift to a faster AVRT showed a 40 ms shortening of the VA interval without any change in the AH or HV intervals (Figure 2). In addition, ventricular far-field signals recorded through the coronary sinus catheter showed that the wide QRS tachycardia was associated with a delay between RV and LV signals that was reduced during the narrow QRS period of the AVRT (Figure 2).
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During orthodromic tachycardia, the earliest atrial activation was recorded at the lower limb of the coronary sinus ostium. The AP was successfully ablated at this position using a 4 mm-tip ablation catheter. No VA conduction could be evidenced and no tachycardia was inducible after AP ablation.
Patient 2
An 18-year-old man was referred for exercise-induced palpitation. The Holter ECG recording during exercise showed a transition from a wide QRS, suggesting an LBBB pattern to a narrow QRS associated with a shortening of the tachycardia cycle length from 265 to 230 ms (Figure 3). During EP study, two types of orthodromic AVRT (with wide and narrow QRS) showing identical atrial activation sequence could be induced. During the wide QRS tachycardia (LBBB), the HA interval was 165 ms and the AH interval 100 ms (Figure 4, left panel). During the narrow QRS tachycardia, the HA interval was shorter (HA = 125 ms) but the AH interval longer (140 ms) (Figure 4, right panel). Therefore, despite a delay in retrograde conduction, the shortening of the AH interval led to an unchanged cycle length of the orthodromic AVRT with LBBB. In contrast to the His to right ventricle interval that remained unchanged, the interval from the His to the local ventricle increased during LBBB AVRT (Figure 4).
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During ventricular pacing, the earliest atrial activation was recorded at the ostium of the coronary sinus. The AP was successfully ablated at this position. No VA conduction could be evidenced and no tachycardia was inducible after AP ablation.
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Discussion |
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We describe two cases of orthodromic AVRT with concealed infero-septal APs showing during tachycardia a ventricular-to-atrial conduction time prolongation when associated with a functional LBBB. In these two cases, the atrial insertion of the AP could be successfully ablated from the right atria at the ostium of the coronary sinus.
In our two cases, we could evidence the change in tachycardia cycle length during the same tachycardia episode (during EP study in Patient 1 and on the Holter recording in Patient 2). This is important since a reciprocating tachycardia may have different cycle lengths due to autonomic modulation, thus making the interpretation of cycle length changes induced by a BBB difficult. A functional block may be due to either changes in refractory periods or slowing in velocity, or a combination of both phenomena. However, the actual mechanism of QRS functional aberrancy observed in our two cases cannot be definitely determined from our data.
In both cases, we could demonstrate a prolongation in the VACT associated with the LBBB. This VACT prolongation was further supported by the prolonged delay between right and left ventricles observed during the wide QRS tachycardias.
In both cases, the LBBB was associated with a VACT prolongation around 40 ms. This result was surprising since it has been published that in case of septal APs, the VACT prolongation associated with an LBBB is never longer than 25 ms.5,6 This VACT prolongation led to a 40 ms orthodromic AVRT cycle length prolongation in Patient 1. In Patient 2, the VACT prolongation associated with LBBB was ‘concealed’ since at the same time the anterograde conduction through the AV node was enhanced as evidenced by the AH interval shortening.
The mechanism of the phenomenon we describe here is not clear. From a theoretical point of view, the prolongation of the ventricle to atria conduction time may be the consequence of a prolonged pathway, a slowing in conduction velocity or any combination of both phenomena.
Our recordings did not support the hypothesis of an oblique AP with a ventricular insertion at the left ventricular free wall. In addition, oblique APs are more often oriented from the left atria free wall to the infero-septal part of the left ventricle.7
The influence of QRS axis deviation with or without BBB has been extensively evaluated.6 The consequence of the association of an LBBB with a right axis deviation on septal APs has, however, not been described in detail. It has been shown that the activation of the posterior para-septal area was provided by the left posterior fascicle.8 Thus, it seems reasonable to expect a VACT prolongation during reciprocating tachycardia with functional left posterior fascicular block in patients with infero-septal AP. In Patient 1, the ventricular conduction defect (LBBB morphology with rightward axis) was associated with a longer time to activate the entire infero-postero-basal left ventricle as evidenced by the lack of change in CS ventricular activation sequence, yet prolongation of the QRS-V time (Figure 2). One can hypothesize that the QRS widening was a consequence of an intra ventricular conduction defect mimicking an LBBB associated with a left posterior fascicular block.
The right axis deviation was however not observed in the other patient. In Patient 2, the interval from the His to the local ventricle increased during LBBB AVRT, whereas right ventricle activation was not delayed. This phenomenon suggests that the ventricle close to the His bundle was activated from the left bundle branch, thus making sense why the LBBB induced a delay to activate the postero-septal AP.
Another possible explanation would be that the AP had an epicardial ventricular insertion in a location activated through the left bundle. This could, however, not be demonstrated since no anterograde conduction through the AP was present. Finally, it cannot be excluded that the observed conduction block is due to a conduction velocity difference between both bundle branches and that the part of VACT prolongation is a consequence of bundles' conduction velocity changes.
More studies are required to elucidate the mechanism(s) of the phenomenon we have described.
Our two cases of LBBB during reciprocating tachycardia using infero-septal pathways show that ventricular-to-atrial conduction time prolongation may be larger than 30 ms and may be concealed by a shortening of atrial-to-ventricular conduction time. In addition, the observation of the association between LBBB and cycle length prolongation during reciprocating tachycardia may be associated with a successful ablation at the ostium of the coronary sinus.
Conflict of interest: none declared.
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References |
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