Europace Advance Access originally published online on April 28, 2006
Europace 2006 8(6):438-442; doi:10.1093/europace/eul037
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ACCESSORY PATHWAYS
Pacing site and bradycardia dependent retrograde conduction block over an atrioventricular accessory pathway
1 Department of Cardiovascular Science, Ospedale di Circolo e Fondazione Macchi, University of Insubria-Varese, Varese, Italy; 2 Department of Cardiology, Tong-Ji Hospital, Tong-Ji Medical College, Huazhong University of Science and Technology, Wuhan, China; 3 Department of Cardiology, Istituto Clinico Mater Domini, Castellanza, Varese, Italy
Manuscript submitted 19 August 2005. Accepted after revision 28 February 2006.
* Corresponding author. Tel: +39 332 278 937; fax: +39 332 393 309. E-mail address: jorge.salerno{at}ospedale.varese.it
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Abstract |
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Intermittent retrograde conduction over an accessory pathway (AP) is an uncommon phenomenon. We report a case of Wolff–Parkinson–White syndrome in which retrograde conduction of the bypass tract was present only during right ventricular (RV) outflow tract and left ventricular pacing or during RV inflow tract pacing with a fast pacing rate (pacing site and bradycardia dependent conduction block). The interaction between different branches/fibres of the bypass tract might explain the mechanism of this phenomenon. The AP was successfully ablated at the lateral aspect of mitral valve annulus. It is suggested that careful evaluation by decremental ventricular stimulation should be applied from multiple sites both during baseline study and after apparent AP ablation in order to detect such uncommon cases of intermittent conduction.
Key Words: Atrioventricular accessory pathway, Catheter ablation, Pacing site dependent, Phase 4 block, Retrograde conduction
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Introduction |
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The vast majority of atrioventricular (AV) bypass tracts conduct bidirectionally and retrograde conduction is present in almost 95% of the accessory pathways (APs),1
usually behaving in an all-or-none fashion. Intermittent antegrade conduction over a bypass tract is not uncommonly observed, but only few cases have previously been published about unstable retrograde conduction properties of AP resulting from a gap or gap-like phenomenon or supernormal excitability.2–6 We report a case of Wolff–Parkinson–White syndrome with a pacing site and bradycardia dependent retrograde conduction block of the AV bypass tract. |
Case report |
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A 33-year-old man who had recurrent episodes of palpitation was referred to our centre for diagnosis and subsequent management. One of his series of ECGs revealed ventricular pre-excitation through a left lateral AP, but no arrhythmias were recorded. No overt heart disease was detected on non-invasive investigation.
Electrophysiological study (EPS) was performed in a non-sedated, fasting state in the absence of any antiarrhythmic drug and after written informed consent was obtained. A decapolar and a quadripolar diagnostic catheter were positioned in the coronary sinus (CS, distal electrodes were in the middle of the CS) and at the His bundle region, respectively. Another 4-mm tip steerable catheter (Polaris T, Boston Scientific, Natick, MA, USA) was also inserted initially in the right atrium and then moved to the right ventricle (RV) for further pacing and recording. One type of narrow QRS supraventricular tachycardia (Figure 1), with a cycle length (CL) of 276 ms, was easily induced by atrial programmed stimulation. During the tachycardia, an eccentric ventricular-atrial (VA) activation was demonstrated and the earliest retrograde atrial potential localized at the distal CS region. Premature ventricular beats introduced during the antegrade refractoriness of the His bundle reset the tachycardia and, therefore, the diagnosis of ‘orthodromic AV re-entry tachycardia’ was established. No antegrade AP conduction was observed throughout the study either in sinus rhythm or during atrial pacing from different sites, even during isoprenaline infusion.
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To check the VA conduction in detail, decremental pacing was delivered from the RV inflow tract (RVIT) at a high septal position, starting from a CL of 600 ms and decreasing by steps of 10 ms. At pacing CLs ranging between 600 and 540 ms, decremental VA conduction with the earliest atrial activation recorded from the proximal CS channel (probably sustained by an AV nodal ‘slow pathway’) was observed (Figure 2A). Subsequently, VA dissociation occurred while decreasing the pacing CL. However, the VA conduction, with fixed VA intervals and the same activation sequence as that during the tachycardia, recovered with a 2:1 or 3:2 conduction ratio when the pacing CL was further shortened to 370 ms and transiently improved to 1:1 conduction after the pacing CL reached 290 ms (Figure 2B). Similar results were achieved during single extra-stimulation from the RVIT as VA conduction over the bypass tract only occurred at coupling intervals
400 ms, whereas VA nodal retrograde conduction or VA conduction block occurred at longer coupling intervals. Accordingly, retrograde conduction through the AP in this patient presented a ‘bradycardia dependent block’. This AP conduction behaviour was also observed when the refractoriness of the atrium close to the presumed insertion site of the AP was ‘peeled-back’7 by means of a special AV sequential pacing protocol consisting of eight beats atrial drive (S1) delivered from the distal CS channel (at different CLs) and one premature beat (S2) delivered from the RVIT. Intravenous isoprenaline challenge alone or with hand-grip manoeuvre did not change these results. To examine the impact of a different direction of ventricular activation on this phenomenon, S1S2 pacing and single extra-stimulation were repeated from the RV outflow tract (RVOT) and the left ventricular (LV) anterior wall after a transseptal puncture. In contrast, VA conduction over the AP was constant during RVOT or LV pacing irrespective of the pacing CL (Figure 3A and B), and the refractory period of the bypass tract was 250 ms. So, this AP was also believed to conduct retrogradely in a ‘pacing site dependent’ pattern. Throughout the EPS, no inter- or intra-ventricular conduction delays were noted.
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Endocardial mapping was performed on the atrial aspect of the mitral valve annulus during RVOT pacing, and the AP was successfully ablated within 2.5 s in the lateral wall region during the first radiofrequency current application. After ablation, VA nodal conduction or VA dissociation was confirmed by different programmed stimulation protocols from both RVOT and LV. No additional APs or other electrophysiological disorders were detected.
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Discussion |
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This case report describes a phenomenon of pacing site and bradycardia dependent block of retrograde conduction over a left-sided AP in a patient with intermittent antegrade ventricular pre-excitation and orthodromic AV re-entry tachycardia.
Intermittent retrograde conduction through a Kent fibre is very rare and only reported in some isolated cases2–5 secondary to a previous attempt at radiofrequency ablation of the same or of another bypass tract. In our case, this phenomenon was recognized before catheter ablation, it was dependent on the pacing site, and it was unresponsive either to adrenergic drive augmentation or to atrial refractoriness peeling-back. ‘Pseudo-supernormal’ conduction was excluded in our patient, as there was no inter- or intra-ventricular conduction delay with ventricular extra-stimulation and ‘true supernormal’ conduction was also unlikely because we failed to demonstrate a ‘conduct-block-conduct’ pattern of retrograde atrial activation during decremental ventricular pacing. Moreover, the term ‘phase 4 block’ probably is inadequate to describe the mechanism of conduction block in our case, as it has been reported to occur in His–Purkinje fibres or, sometimes, also in the Kent bundles exhibiting spontaneous automaticity,8–10 a condition not seen in our case.
Anatomically, some AV bypass tracts have multiple branches or fibres at their ventricular insertion sites possibly interconnecting as a three-dimensional network.11 At this level, propagation might be discontinuous because of non-uniform anisotropy or possible interactions between branches.12,13 Sometimes (e.g. RVIT pacing and longer pacing CL), retrograde conduction over the AP is prevented because of the interaction within the fibres and/or of an impaired conduction safety factor; on the other hand, the impulse can reach the atrial side only under some critical conditions (e.g. RVOT or LV pacing and shorter pacing CL). For example, if a current-to-load mismatch existed in this geometrical network, a non-symmetric effect of uncoupling on the current source and the current sink in some branches of the AP might paradoxically improve the conduction in the overall bypass tract at higher rates.14 However, direct recording of the AP activation through properly designed catheters15 could be helpful to understand better the mechanism of this phenomenon.
Another alternative explanation of our case is that the pathway had two branches with different ventricular insertions, one of which was much closer to the RVIT but with inconstant activation to the atrium through the final common trunk because of its slow rate-dependent conduction block properties. Additionally, propagation through this fibre was supposed to inhibit electrotonically or to have concealed penetration into the other bundle when the ventricular impulse came from the RVIT at lower pacing rates. If the ventricular activation direction or sequence changed, as during RVOT or LV pacing, the impulse would go directly through the other branch and retrogradely conduct to the atrium over the main trunk regardless of the block in this fibre.6
The clinical implication of this case report is that intermittent AP retrograde conduction, although exceptional, may mask the presence of the bypass tract or lead to a ‘false success’ after radiofrequency ablation. Therefore, careful evaluation by decremental ventricular stimulation should be applied from multiple sites both during baseline study and after apparently successful AP ablation. Finally, in these cases, ablation from the atrial aspect by transseptal approach should be considered because the common main strand of an AP usually starts from its atrial insertion above the plane of the mitral valve annulus.11,16
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Footnotes |
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Fellows of training programme ‘Level 2 Master of Cardiac Electrophysiology and Pacing’ (University of Insubria and University of Brescia, Italy). 
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References |
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