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Parsing a perplexing paroxysmal pathwayElaine Wan, MD, José Dizon, MD, William Whang, MD, Hasan Garan, MD

From the Cardiac Electrophysiology, Cardiology Division, Department of Medicine, Columbia University,New York, New York.

IntroductionCatheter ablation is an effective and often preferred treatmentfor supraventricular tachycardia (SVT). Successful ablationis predicated on a precise diagnosis of the arrhythmiamechanism.1 The initial pacing maneuvers during electro-physiologic study (EPS) are often able to narrowthe differential diagnosis immediately.2 We report anunusual case of SVT in which the initial findings at EPSwere inconsistent with the eventual mechanism of thetachycardia.

Case reportA 34-year-old man with a history of high blood pressure andhyperlipidemia and 5 years of intermittent self-limitedpalpitations presented to the emergency room with an SVTat 220 beats per minute (Figure 1). His symptoms includedchest pain and dyspnea. The tachycardia terminated sponta-neously, and the patient was admitted to the hospital forfurther evaluation. His workup showed no structural cardiacabnormalities. Given his youth, otherwise good health, andrapid tachycardia with moderately severe symptoms, he wasreferred for catheter ablation.

Electrode catheters were placed within the right atrium(RA), right ventricle (RV), His-bundle position (HIS), andcoronary sinus (CS). The baseline conduction intervalsincluded a sinus cycle length of 680 milliseconds, anatrial-His interval of 67 milliseconds and His-RV intervalof 32 milliseconds. Pacing the RV at both the apex and baserevealed ventriculoatrial (VA) dissociation at cycle lengthsfrom 350 to 650 milliseconds (Figure 2A). Programmedatrial stimulation did not reveal ventricular preexcitationor dual atrioventricular (AV) nodal physiology. TheAV Wenckebach cycle length was 280 milliseconds.

KEYWORDS Atrioventricular reciprocating tachycardia; Lateral bypass tract;Orthodromic reciprocating tachycardia; Retrograde conduction; Supraven-tricular tachycardiaABBREVIATIONS AV ¼ atrioventricular; CS ¼ coronary sinus; ECG ¼electrocardiogram; EPS¼ electrophysiological study; HIS¼His bundle;

LV ¼ left ventricle; PVC ¼ premature ventricular complex; RA ¼ right

atrium; RV ¼ right ventricle; SVT ¼ supraventricular tachycardia;

VA ¼ ventriculoatrial (Heart Rhythm Case Reports 2015;1:453–456)

Address reprint requests and correspondence: Dr Elaine Wan, P&S9-511, 630 West 168th Street, New York, NY 10032. E-mail address:eyw2003@columbia.edu.

2214-0271 B 2015 Heart Rhythm Society. Published by Elsevier Inc. This is an o(http://creativecommons.org/licenses/by-nc-nd/4.0/).

Tachycardia was easily induced with either rapid ventricularpacing or atrial premature extrastimuli. The atrial activationsequence during tachycardia was distal to proximal in the CSleads (Figure 2B).

Pacing maneuvers were performed in an attempt toelucidate the mechanism of the tachycardia. Prematureventricular complexes (PVCs) were able to terminate thetachycardia without activating the atrium (Figure 2C).Entrainment of the tachycardia with RV pacing demon-strated a VAV response on termination of pacing(Figure 2D). Notably, during multiple terminations of thetachycardia and immediate ventricular burst pacing, VAdissociation persisted. When isoproterenol was infused andventricular pacing repeated, only a concentric and decre-mental retrograde atrial conduction pattern was present,which was consistent with AV nodal conduction.

Fortuitously, it was noted that spontaneous PVCs duringsinus rhythm would occasionally conduct in an eccentricactivation pattern, similar to the activation sequenceobserved during the tachycardia. This phenomenon wasfurther examined and replicated using programmed PVCsduring sinus rhythm, which revealed eccentric retrogradeactivation of the atrium within a window of couplingintervals or during ventricular reentrant beats (Figures 3Aand 3B). Finally, during the manipulation of catheterswithin the left ventricle (LV) near the mitral annulus, VAconduction with an eccentric pattern was also seen(Figure 3C).

Given these contradictory findings, what was the mech-anism of the tachycardia?

DiscussionThe common differential diagnosis of SVT in a patientwithout structural heart disease is AV nodal reentranttachycardia (AVNRT), AV reentrant tachycardia (AVRT),or atrial tachycardia (AT). Convention at electrophysiologicstudy for SVT dictates that RV pacing be performed first, asthe nature of retrograde atrial conduction lends immediateinsight into the mechanism of the tachycardia. AVRT, inwhich retrograde conduction up an accessory pathway is anecessary part of the circuit, is essentially eliminated whenthere is lack of retrograde conduction, and AVNRT becomesless likely as well.

pen access article under the CC BY-NC-ND licensehttp://dx.doi.org/10.1016/j.hrcr.2015.06.013

KEY TEACHING POINTS

� Right ventricular pacing eliciting ventriculoatrialdissociation does not necessarily rule outatrioventricular reentrant tachycardia in uniquecases in which the sinus conduction may arrive atthe accessory pathway at the same time, resultingin summation.

� Programmed premature ventricular complexesduring sinus rhythm may be used for mapping thebypass tract in unique cases in which there isbaseline ventriculoatrial dissociation.

� In rare cases of atrioventricular reentranttachycardia, paroxysmal retrograde conductionalong the bypass tract can be seen.

Heart Rhythm Case Reports, Vol 1, No 6, November 2015454

In this unique case that we report, initial RV pacing from2 RV sites and at various cycle lengths revealed VAdissociation, thus leading one to a potential diagnosis ofAT. However, entrainment maneuvers revealed a VAVresponse during RV pacing, which was inconsistent withAT, and the result of PVCs terminating the tachycardiawithout activating the atria coupled with an eccentricretrograde atrial activation sequence strongly point towardAVRT as the diagnosis.

How can one reconcile the fact that AVRT might exist inthe presence of VA dissociation in the baseline state? Aconduction block can be fixed or functional, and it can occurunder tachycardic (Phase 3) or bradycardic (Phase 4)conditions.3 VA conduction was evidently robust during

Figure 1 A 12-lead electrocardiogram

rapid tachycardia, and the functional block that we observedwas not strictly present during bradycardic conditions,arguing against these mechanisms. One could postulate thata “gap” phenomenon involving myocardial tissue interven-ing between the RV and accessory pathway was occurring.This mechanism might be supported by the observation inFigure 3C, where LV PVCs could conduct up the accessorypathway. However, arguing against this mechanism is thefact that the patient had no evidence of structural heartdisease and so there was no reason to suspect diseasedmyocardial conduction. The observation of spontaneousPVCs occasionally activating the atria suggests a conceal-ment phenomenon, where anterograde penetration of theaccessory pathway during sinus rhythm precludes retrogradeconduction unless the PVCs were critically timed so that theaccessory pathway was not refractory from the sinusimpulse. We were able to demonstrate this effect withprogrammed PVCs during sinus rhythm (Figures 3A and3B). Alternatively, it can be postulated that the sinus wave-front that conducts down the AV node may arrive at theaccessory pathway at nearly the same time as the wavefrontconducting in a retrograde fashion from the PVC, withappropriate timing such that their combined impulses wouldresult in summation.4

We proceeded to insert a mapping catheter via theretrograde aortic approach. Because of the lack of retrogradeatrial activation in the baseline state, mapping occurredduring tachycardia. The earliest retrograde atrial electrogramwas located on the anterolateral mitral annulus. Radiofre-quency energy at this site was able to terminate thetachycardia during the first few seconds of application. VAdissociation persisted after ablation and no other arrhythmias

of supraventricular tachycardia.

Figure 2 A: Right ventricular (RV) pacing at 600 milliseconds at the start of the study showed ventriculoatrial dissociation. B: Tachycardia with intracardiacelectrograms showing eccentric atrial activation sequence. C: Programmed premature ventricular complexes were able to terminate the tachycardia withoutactivating the atrium. D: Entrainment maneuvers by pacing from the RV demonstrated a VAV response.

Figure 3 A: Programmed premature ventricular complexes (PVCs) appropriately timed during normal sinus rhythm demonstrated retrograde conduction overthe accessory pathway. B: A programmed PVC during normal sinus rhythm resulting in ventricular reentrant beat and conduction up the accessory pathway. C:Catheter-induced PVC in the left ventricle shows retrograde conduction over the accessory pathway.

455Wan et al Paroxysmal Pathway

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were inducible in the native state or after the infusion ofisoproterenol at 2 mcg/min. There was no evidence ofanterograde or retrograde accessory pathway activity follow-ing bolus infusion of 12 mg of adenosine. The patient hasbeen free of arrhythmias for up to 6 months of follow-upthus far.

We conclude that this was a supraventricular tachycardiautilizing a pathway with intermittent retrograde conduction,which is a perfect example of why there are exceptions toevery rule in electrophysiology.

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Strickberger SA, Morady F. Diagnostic value of tachycardia features and pacingmaneuvers during paroxysmal supraventricular tachycardia. JACC 2000;36:574–582.

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3. Watanabe Y. Terminology and electrophysiologic concepts in cardiac arrhythmias.V. Phase 3 block and phase 4 block. Part 1. PACE 1979;2:335–344.

4. Watanabe Y. Terminology and electrophysiologic concepts in cardiac arrhythmias.IV. Fusion beats and summation of impulses. PACE 1979;2:76–87.