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Arrhythmia Rounds

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

Activation Sequence Change During Left Free Wall PathwayAblation: What is the Mechanism?

RAJIV MAHAJAN, M.D., D.M., MANOJ K. ROHIT, M.D., D.M.,and KEWAL K. TALWAR, M.D., D.M.

From the Department of Cardiology, PGIMER, Chandigarh, India

Case Summary

A 35-year-old male with a 6-year history of recurrent pal-pitation and documented paroxysmal supraventricular tachy-cardia was referred to us for catheter ablation. He had sev-eral episodes of supraventricular tachycardia despite beingon adequate drug therapy. A standard 12-lead electrocardio-gram (ECG) during sinus rhythm revealed no abnormalities.Echocardiogram revealed a structurally normal heart. The pa-tient was taken up for electrophysiology study and catheterablation. The electrophysiology study was performed inpostabsorptive state. Three quadripolar catheters were in-serted via femoral venous access and advanced to the highright atrium, His bundle, and right ventricle under fluoro-scopic control. A decapolar catheter was inserted via theright internal jugular vein and advanced into the coronarysinus (CS) with the proximal bipole at the ostium (os).Programmed atrial stimulation revealed a continuous atri-oventricular (AV) node function curve. Incremental rightventricular pacing revealed nondecremental ventriculoatrial(VA) conduction, with the earliest atrial activation at thedistal bipole CS (1–2). Programmed ventricular stimulationeasily and repeatedly induced a regular narrow QRS com-plex tachycardia with a cycle length (CL) of 280 ms. Theactivation sequence on the CS during tachycardia was ec-centric (Fig. 1A). A diagnosis of orthodromic A V reen-trant tachycardia (AVRT) using a left-sided free-wall acces-sory pathway (AP) was made. The retrograde transaortalapproach was used for ablation. The ablation catheter waspositioned above the mitral valve at the left AV annulus.Radiofrequency (RF) energy was delivered to the earliestatrial activation site just above the CS12 catheter electrodeat the mitral annulus. The RF energy was applied duringtachycardia. Figure 1B and C shows the intracardiac trac-ings after the second and third burn, respectively. What hashappened?

J Cardiovasc Electrophysiol, Vol. 20, pp. 1174-1175, October 2009.

Address for correspondence: Rajiv Mahajan, M.D., D.M., 54 Sec-tor 21A, Chandigarh, 160022, India. Fax: +91-172-2744401; E-mail:rajivmahajan20@yahoo.co.in

doi: 10.1111/j.1540-8167.2009.01519.x

Commentary

There is a change in activation in the CS activation, dur-ing ongoing tachycardia, from eccentric to concentric on RFenergy application. This can happen due to transition to asecond tachycardia. A significant change in tachycardia CLwould have suggested a second tachycardia. However, thetachycardia CL (280 ms) did not change in this case, suggest-ing otherwise. Still, transition to a second tachycardia can oc-cur without much change in tachycardia CL (<25 ms).1 Thefollowing arguments suggest that it is the same tachycardiacontinuing despite change in CS activation sequence. Boththe tachycardia CL and VA interval HIS remained constantdespite the change in CS activation sequence. Moreover, thechange in activation from eccentric to concentric was gradualand the activation sequence after the second burn (Fig. 1B)was intermediate to that before any burn (Fig. 1A) and afterthe third burn (Fig. 1C). Finally, the retrograde atrial activa-tion at the lateral left AV annulus at the final successful ab-lation site remained the earliest. The persistence of the sameVA HIS with VA in proximal and mid-CS longer than at theHis and earliest retrograde A at the left mitral annulus suggestthe occurrence of an intraatrial conduction block, along themitral annulus, medial to the insertion of the pathway, andthe atrial depolarization proceeds along the superior mitralannulus to His and, subsequently, the proximal and mid-CS.The intermediate activation sequence (Fig. 1B) occurs be-cause of incomplete intraatrial conduction block medial tothe insertion of the pathway. Occasionally, a change in CSactivation sequence can also happen during ventricular pac-ing, after the pathway has been damaged due to RF energydelivery, due to conduction through the His. However, theVA HIS would not be the same and persistence of the changedactivation sequence during orthodromic tachycardia wouldexclude the above.

Luria et al. have reported 11 cases with intraatrial conduc-tion block during left free wall ablation.2 They postulated thepresence of a narrow isthmus between the left inferior pul-monary vein and the inferolateral mitral annulus. Of these11 cases only 6 had complete intraatrial block, medial to thepathway, leading to reversal of CS activation sequence. Insome of them progression to complete block was gradual(like in our case). Cheng et al. explained this phenomenonof protected circumferential conduction with the presence ofinferoposterior muscle bundle in the posterior AV vestibule.3

They explained that the width of this bundle was the sizeof a typical RF lesion. A discrete RF lesion could interrupt

Mahajan et al. Arrhythmia Rounds 1175

Figure 1. Gradual change in atrial activation sequence after radiofrequency (RF) energy delivery. (A) Orthodromic tachycardia prior to ablation. Thetachycardia cycle length (CL) is 280 ms with earliest A at the ablation catheter placed just distally to CS12 and eccentric activation of the CS. (B) Orthodromictachycardia after the second burn. The tachycardia CL is 280 ms with eccentric activation of the coronary sinus (CS). Modest local ventriculoatrial (VA)prolongation. (C) Orthodromic tachycardia after the third burn. The tachycardia CL is 280 ms with concentric activation of the CS. Note that the tachycardiaCL and the VAHIS do not change even after the third burn.

conduction through this bundle and cause reversal of se-quence of activation. Also, advancing the CS catheter be-yond the site of intraatrial block would demonstrate doublepotentials.2-4

The clinical implication of recognizing this phenomenonis that the successful ablation site will be lateral to the siteof RF energy delivery that resulted in intraatrial conductionblock.

References

1. Kuo JY, Tai CT, Chiang CE, Yu WC, Chen YJ, Tsai CF, Hsieh MH,Chen CC, Lin WS, Lin YK, Tsao HM, Ding YA, Chang MS, Chen SA:

Mechanisms of transition between double paroxysmal supraventriculartachycardias. J Cardiovasc Electrophysiol 2001;12:1339-1345.

2. Luria DM, Nemec J, Etheridge SP, Compton SJ, Klein RC, ChughSS, Munger TM, Shen WK, Packer DL, Jahangir A, Rea RF, HammillSC, Friedman PA: Intra-atrial conduction block along the mitral valveannulus during accessory pathway ablation: Evidence for a left atrial“isthmus.” J Cardiovasc Electrophysiol 2001;12:744-749.

3. Cheng J, Yang Y, Ursell PC, Lee RJ, Dorostkar PC, Boahene KA, Schein-man MM: Protected circumferential conduction in the posterior atrioven-tricular vestibule of the left atrium: Electrophysiologic and anatomiccorrelates. Pacing Clin Electrophysiol 2005;28:692-701.

4. Huang XM, Cao J, Qin YW, Hu JQ: Reversal of the activation se-quence along the coronary sinus during RF application with a single leftlateral pathway: What is the mechanism? Pacing Clin Electrophysiol2009;32:106-107.