Wide QRS Complex After Catheter Ablation
A 20-year-old man with recurrent supraventricular tachycardia (Figure 1) was referred for catheter ablation. The baseline ECG (Figure 2) showed sinus rhythm with a PR interval of 0.20 seconds and QRS duration of 0.085 seconds. Application of irrigated radiofrequency current to a site 8 mm below the apex of Koch’s triangle was terminated after 18 seconds because of an accelerated junctional rhythm. After radiofrequency delivery, there was sinus rhythm with a markedly widened QRS complex (Figure 3). What is the cause of the wide QRS complex after ablation?
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Response to ECG Challenge
The mechanism of the supraventricular tachycardia was orthodromic atrioventricular reciprocating tachycardia utilizing an obliquely coursing, midseptal accessory pathway (AP) with poor antegrade but rapid retrograde conduction. Programmed ventricular stimulation demonstrated nondecremental retrograde conduction with earliest atrial activation at the apex of Koch’s triangle. The antegrade and retrograde effective refractory periods of the AP measured 470 ms and 360 ms, respectively. Radiofrequency current was delivered to the site of earliest ventricular activation 8 mm inferior to the apex of Koch’s triangle, where earliest retrograde atrial activation was recorded. After ablation, the anterograde AP effective refractory period was shortened to 320 ms with a retrograde AP effective refractory period of 270 ms. The procedure was terminated, and over the next 24 hours, the PR interval remained short with maximal preexcitation. However, after 48 hours, an intermittent block in AP conduction with intact AVN conduction was observed during sinus pauses (Figure 4).
The interesting question is, why did an iatrogenic block of AVN conduction enhance antegrade AP conduction?
Concealed APs with rapid retrograde but no antegrade conduction are relatively common. In contrast, antegrade-only APs are far less common. This difference in antegrade and retrograde conduction properties has been attributed to a source-sink mismatch.1 Thus, when a wavefront of depolarization conducting over a narrow strand of myocardial fibers comprising an AP (the source) encounters the much larger mass of ventricular myocardium (the sink), a conduction block may occur at the interface because the current is insufficient to generate a self-propagating wavefront in the ventricle.1 Source-sink mismatch has also been demonstrated in cell culture models when a narrow isthmus of myocytes encounters a larger mass of cells.2
We hypothesize that thermal damage to AVN conduction resulted in improved antegrade AP conduction because the depolarizing wavefront was no longer divided between the AVN and the AP. Thus, a larger current was able to traverse the AP overcoming the source-sink mismatch. Another possibility is a branching AP, where the block of one branch by radiofrequency current may have allowed the other branch to successfully depolarize the ventricle. Paradoxical improvement in impulse conduction has been demonstrated at the junction of a narrow isthmus of ventricular myocytes that encounters a larger mass of ventricular myocytes when partial cellular uncoupling is induced by palmitoleic acid.3 The fact that the AP demonstrated antegrade block only at longer cycle lengths associated with recurrent AVN conduction a day after ablation also suggests an inhibiting effect of AVN conduction on the AP, although phase 4 block in the AP is another plausible explanation.
- © 2018 American Heart Association, Inc.