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Arrhythmia Rounds Section Editor: George J. Klein, M.D.

Repetitive Oscillating Atrial Activation During Supraventricular Tachycardia JAMES E. IP, M.D., DAVID P. DOBESH, M.D., CHRISTOPHER F. LIU, M.D., and BRUCE B. LERMAN, M.D. From the Division of Cardiology, Department of Medicine, Cornell University Medical Center, New York, New York, USA

atrionodal extensions, atrioventricular nodal reentrant tachycardia Case Presentation A 63-year-old man presented with frequent episodes of paroxysmal supraventricular tachycardia (SVT) at a rate of 150/minutes. He underwent an invasive electrophysiology study during which SVT was induced with single atrial extrastimuli during isoproterenol infusion. The cycle length of tachycardia was 392 milliseconds. During tachycardia, spontaneous repetitive changes in earliest atrial activation were observed without any changes in tachycardia cycle length (Fig. 1A, B). What is the mechanism for the oscillating atrial activation? Commentary The near simultaneous ventricular and atrial activation during tachycardia suggested the diagnosis of atrioventricular (AV) nodal reentrant tachycardia (AVNRT). This diagnosis was confirmed based on the initiation of tachycardia with a critical AH delay, dissociation of the atria and ventricles during tachycardia, and by the inability to advance atrial activation with premature ventricular extrastimuli delivered during His bundle refractoriness. However, the repetitive oscillation of atrial activation, with a transition from concentric to eccentric coronary sinus (CS) activation observed during tachycardia is unusual. This can be due to spontaneous atrial premature depolarizations (APDs) that are dissociated from the tachycardia or due to altered preferential activation along atrionodal lower extensions (passive activation of the CS musculature). However, the constant HA interval of the premature beats during tachycardia (HA linking), the unchanging tachycardia cycle length despite a change in the A–A J Cardiovasc Electrophysiol, Vol. 25, pp. 1137-1139, October 2014. Dr. Liu reports research support from Biosense Webster and speaker honoraria from St. Jude Medical. Other authors: No disclosures. Address for correspondence: Bruce B. Lerman, M.D., Division of Cardiology, Cornell University Medical Center, 525 East 68th Street, Starr 4, New York, NY 10021, USA. Fax: 212-746-6951; E-mail: [email protected] Manuscript received 5 June 2014; Revised manuscript received 17 June 2014; Accepted for publication 20 June 2014. doi: 10.1111/jce.12489

interval as shown in Figure 1A, and the absence APDs during sinus rhythm and following ablation make the former possibility unlikely. Careful inspection of the intervals between the ventricular and atrial activation shows that the tachycardia cycle length remains unchanged despite changes in the AV interval (Fig. 1B), which is consistent with bystander activation of atrionodal extensions rather than coincidentally timed APDs. Delivery of radiofrequency energy in the typical area of the slow pathway at the base of the triangle of Koch resulted in accelerated junctional rhythm with intact ventriculoatrial conduction. However, despite multiple ablation lesions, abolition of slow pathway conduction was not achieved and sustained AVNRT remained inducible. Delivery of progressively anterior RF lesions resulted in transient PR prolongation, suggestive of encroachment upon the fast pathway. Ablation within the proximal CS was ineffective. Transseptal puncture was performed and ablation at the posteroseptal mitral annulus resulted in accelerated junctional rhythm and abolition of slow pathway conduction. Tachycardia was no longer inducible following ablation. The findings in this case delineate the permutations of AVNRT and identify 2 important principles. The first confirms that AVNRT can be a completely left-sided arrhythmia, comprising both left-sided fast and slow atrionodal extensions, and that ablation of the left-sided posterior slow extension may be inaccessible from within the CS and require transseptal access and ablation from the region of the posterior mitral annulus. The second principle is that left-sided atrionodal extensions can serve as a critical component of the AVNRT circuit as well as a non-participatory bystander extension. Recognizing and distinguishing between these 2 possibilities facilitates appropriate targeting of critical reentrant tissue and precludes inappropriate ablation of bystander fibers. Histologically, the compact AV node is a discrete structure that is comprised of specialized myocardium that expresses HCN4.1 While the compact AV node is generally confined to the apex of the triangle of Koch along the anterior paraseptal right atrium, AV nodal tissue extends well beyond the compact AV node, with posterior extensions that can extend to right and left atrium.2,3 Tissue anisotropy as well as these anatomic AV nodal extensions may contribute to and constitute the anterograde and retrograde limbs of the AVNRT

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Journal of Cardiovascular Electrophysiology

Vol. 25, No. 10, October 2014

Figure 1. A: Spontaneous changes in earliest retrograde atrial activation during tachycardia. Surface leads 1, aVF, and V1 are shown as well as intracardiac recordings from the high right atrium (HRA), His bundle, and proximal to distal coronary sinus (CS) and right ventricular apex (RVA). Earliest atrial activation was recorded at the pCS (concentric activation) in the majority of beats, with the exception of the second and seventh beats where earliest conduction shifted to the adjacent and more lateral coronary sinus bipole electrodes (eccentric activation; asterisks). Note the fixed HA coupling interval of the premature beats. B: Zoomed in view of the changing atrial activation pattern (from pCS to the adjacent and more lateral CS bipole pair of electrodes) and A–V relationship of the third atrial beat (asterisk), which is dissociated from the tachycardia, which has a fixed H–H interval of 392 milliseconds. For a high quality, full color version of this figure, please see Journal of Cardiovascular Electrophysiology’s website: www.wileyonlinelibrary. com/journal/jce

circuit. Left atrial inputs to the AV node originating from the region of the mitral annulus have been demonstrated in humans.2 The presence of both rightward and leftward posterior atrionodal extensions in patients with AVNRT may account for (1) the presence of persistent slow pathway conduction and single AV node echo beats despite the inability to induce AVNRT after ablation of a right-sided slow AV

nodal pathway, and (2) the need to consider left-sided slow pathway ablation in patients who do not respond right-sided ablation. AVNRT in our case comprised a circuit that included leftsided fast and slow atrionodal extensions.4 The anterograde slow pathway was ablated from the region of the left posteroseptal mitral annulus, and earliest atrial activation was

Figure 2. Earliest retrograde atrial activation recorded at the proximal coronary sinus before anteroseptal right atrium (His) during ventricular pacing. Abbreviations as previously described. For a high quality, full color version of this figure, please see Journal of Cardiovascular Electrophysiology’s website: www.wileyonlinelibrary. com/journal/jce

Ip et al. Arrhythmia Rounds

Figure 3. Proposed mechanism of AVNRT incorporating left-sided fast and slow AV node extensions and left-sided passive bystander. Right-sided anterior atrionodal extension, left-sided midseptal fast pathway atrionodal extension, and 2 posterior (right and left) slow atrionodal extensions are shown. Retrograde atrial activation proceeds predominantly over fast atrionodal extension and activates the muscular sleeve of the proximal coronary sinus (red). However, there is also intermittent conduction over fibers from these extensions that preferentially breakthrough to the muscular fibers of the middle coronary sinus (green), corresponding to atrial beats denoted by asterisks in Figures 2 and 3. These are considered bystander fibers. Anterograde slow conduction proceeds over the posterior left-sided atrionodal extension, which was subsequently ablated. Black bar denotes previously ablated right-sided slow atrionodal nodal extension. (Although the CS catheter recorded earliest retrograde atrial conduction during AVNRT, the fast pathway extension is drawn at a midseptal location in recognition that its exact site cannot be discerned because a left-sided His bundle was not recorded.)

recorded in the proximal CS, demonstrating a retrograde fast pathway exit on the left side of the interatrial septum. Also of note, was that the retrograde fast pathway exit on the left side had a fixed oscillation, with earliest CS activation fluctuating between the proximal and mid-CS during tachycardia (Fig. 1A, B). Although eccentric CS activation is observed in patients with retrograde slow pathway conduction in atypical fast–slow AVNRT, successful ablation is typically achieved with a standard right-sided approach, suggesting that these left-sided extensions are not always critical to the reentrant circuit.5 There are few data that confirm whether left-sided fast pathway extensions are critical components of the reentrant circuit. To this end, one small study found that earliest retrograde activation during typical slow–fast AVNRT could be recorded from the left side of the septum in approximately 50% of patients.6 In addition to the presence of a retrograde left-sided fast pathway bystander extension, there was also an essential

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left-sided fast pathway extension that comprised an integral part of the AVNRT circuit. During tachycardia, earliest retrograde fast pathway activation was recorded on the CS catheter, and preceded atrial activation recorded by the right-sided His bundle catheter (Fig. 1). Also consistent with this finding was that retrograde atrial activation during ventricular pacing demonstrated earliest retrograde activation at the proximal CS (Fig. 2). Although we did not record a left-sided His bundle, it is improbable that a right-sided fast pathway would have activated the CS before the right anteroseptum (as recorded on the His catheter). However, it is possible that, had we recorded a left-sided His bundle, atrial activation from this region may have preceded CS activation.6 Our electrophysiologic findings are supported by the anatomical study of Inoue et al., who showed that in human hearts the compact AV node contains rightward and leftward posterior extensions.2 These posterior extensions also likely provide the anatomic substrate for the variable CS activation we observed during AVNRT. The complex pattern of retrograde atrial activation of fast pathway conduction is consistent with different breakthrough sites from the same left-sided atrionodal extension. A schematic of the AVNRT circuit incorporating left-sided bystander activation, as well as the 2 left-sided atrionodal extensions that comprise the tachycardia circuit is shown in Figure 3.

References 1. Yanni J, Boyett MR, Anderson RH, Dobrzynski H: The extent of the specialized atrioventricular ring tissues. Heart Rhythm 2009;6:672680. 2. Inoue S, Becker AE: Posterior extensions of the human compact atrioventricular node: A neglected anatomic feature of potential clinical significance. Circulation 1998;97:188-193. 3. Widran J, Lev M: The dissection of the atrioventricular node, bundle and bundle branches in the human heart. Circulation. 1951;4:863-867. 4. Ja¨ıs P, Ha¨ıssaguerre M, Shah DC, Coste P, Takahashi A, Barold SS, Cl´ementy J: Successful radiofrequency ablation of a slow atrioventricular nodal pathway on the left posterior atrial septum. Pacing Clin Electrophysiol. 1999;22:525-527. 5. Nam GB, Rhee KS, Kim J, Choi KJ, Kim YH: Left atrionodal connections in typical and atypical atrioventricular nodal reentrant tachycardias: Activation sequence in the coronary sinus and results of radiofrequency catheter ablation. J Cardiovasc Electrophysiol 2006;17:171–177. 6. Katritsis DG, Ellenbogen KA, Becker AE: Atrial activation during atrioventricular nodal reentrant tachycardia: Studies on retrograde fast pathway conduction. Heart Rhythm 2006;3:993-1000.

Repetitive oscillating atrial activation during supraventricular tachycardia.

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