February 5th Question
A 64-year-old man with frequent symptomatic premature ventricular complexes is brought to the electrophysiology laboratory for premature ventricular complex ablation. Earliest site of activation during premature ventricular complex is noted at location of ablation catheter (ABL; Figure), a consistent far-field signal 48 ms ahead of onset of QRS. Irrigated radiofrequency ablation (40 watts; 30 mL/min) is performed at this site. What structure could sustain collateral injury during ablation?
A. Left anterior descending coronary artery
B. Left circumflex coronary artery
C. Right coronary artery
D. Atrioventricular node
E. Right bundle branch
Answer to January 29th Question
C. Accessory pathway (atriofascicular/nodofascicular) is not participatory in the tachycardia
This tracing (Figure 1) shows a wide complex tachycardia (WCT) transitioning to a narrow complex tachycardia. The differential diagnosis of WCT includes ventricular tachycardia, supraventricular tachycardia (SVT) with preexcitation over accessory pathway, or SVT with aberrant conduction. SVT with aberrant conduction and without ventricular preexcitation is ruled out because of His-ventricular (HV) interval ≈0 ms. The WCT QRS has a left bundle branch block morphology, late precordial transition, and left axis consistent with antegrade right atriofascicular (Mahaim) pathway conduction.1 Alternatively, an antegradely conducting nodofascicular tract or fascicular ventricular tachycardia from the right bundle branch or moderator band may have a similar morphology and HV interval.
The narrow complex tachycardia with a normal HV interval (48 ms) excludes ventricular tachycardia and preexcited SVT, leaving a differential diagnosis of atrial tachycardia, atrioventricular nodal reentry tachycardia (AVNRT), orthodromic reentry tachycardia, or junctional tachycardia. Septal ventriculo-atrial (VA) interval −13 ms excludes orthodromic reentry tachycardia.2 Atrial tachycardia usually has shorter AH interval but is possible with slow pathway atrionodal conduction resulting in long AH (≈268 ms) with each A generating a QRS timing with subsequent A activation (green arrows). Junctional tachycardia is epidemiologically unlikely in this clinical situation but is a possibility. AVNRT will be statistically most likely (solid red arrows).
The main finding of this tracing is that transition from WCT to narrow complex tachycardia occurs without any change in atrial activation pattern or cycle length. It would be quite coincidental and unlikely for an unrelated WCT due to ventricular tachycardia or antidromic reentry that terminates, to have the exact same cycle length as the subsequent SVT (making statements A and B wrong). It has to be assumed that the WCT at the same cycle length as the uninterrupted SVT is being driven by the SVT, that is, bystander preexcitation over a right atriofascicular (or nodofascicular) tract. Antidromic reentry tachycardia is not the mechanism of this tachycardia because the SVT continues uninterrupted despite inhibition of antegrade accessory pathway conduction, presumably related to mechanical injury during catheter manipulation, proving the accessory pathway is not participatory in the tachycardia (statement C). Because the differential diagnosis of the SVT still includes AVNRT, atrial tachycardia, and junctional tachycardia, statements D and E cannot be stated as being correct.
With further maneuvers, this tachycardia was determined to be AVNRT with bystander preexcitation using a right atriofascicular tract (Figure 2).3 As shown in the figures, the preceding atrial activations are driving the wide QRS complexes, with retrograde activation of the His bundle from the insertion of the atriofascicular tract (dotted red arrows). The asterisk in Figure 1 denotes the absence of the expected bystander ventricular activation because of inhibition of accessory pathway conduction. Slow pathway ablation eliminated the AVNRT. Subsequently, antidromic reentry tachycardia using the accessory pathway was inducible, and the accessory pathway potential at the lateral tricuspid annulus was ablated with elimination of accessory pathway conduction.
I thank Paul A. Friedman, MD for his teaching and contribution to the case presented in February 5th Question.
Circ Arrhythm Electrophysiol is available at http://circep.ahajournals.org.
- © 2018 American Heart Association, Inc.
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